Adverse Drug Reaction Reporting
The successful person has the habit of doing the things failures don't like to do.
They don't like doing them either necessarily. But their disliking is subordinated to
the strength of their purpose.
E. M. Gray
1. Which one o f the following statements
is FALSE
I.
'
II.
III.
A.
B.
C.
D.
E.
adverse drug reactions(ADRs)
are a cause o f significant
morbidity and mortality in
patients in all arenas o f health
care
it is estimated that 1/3 to as high
as V2 o f ADRs are believed to
be preventable
adverse drug reactions (ADRs)
are not a cause o f significant
morbidity and mortality in
patients in all arenas o f health
care
if 1 only is correct
if 111 only is correct
if I and II are correct
if II and III are correct
if I, II and III are correct
2. “One which is unintended, and which
occurs at doses normally used in man for
the prophylaxis, diagnosis or therapy o f
disease, or for the modification of
physiological function” is the definition
given by the WHO for
A.
B.
C.
D.
E.
Adverse drug reaction
side effect
adverse drug event
A&C
all
3. Which one o f the following is included
in an adverse drug event
A. an event occurring from a drug
overdose
B. an event occurring from drug abuse
C. an event occurring from drug
withdrawal
D. any significant failure o f expected
pharmacological action
E. All o f the above
4. All the following are included in type A
adverse drug reactions, except one
A. they are extensions o f known
pharmacology
B. are responsible for the majority o f
ADRs
C. are usually dose dependent and
predictable
D. reactions include idiosyncratic
reactions immunological or allergic
reactions
E. none
5. Which one o f the following is TRUE
about type A ADRs
A. to minimize type A reactions
understanding the pharmacology o f
the drug is important
B. drugs with narrow therapeutic
window should be monitored
C. polypharmacy should be avoided if
possible
D. All o f the above
■
E. None
6. Which one o f the following statements
is TRUE
A. recognition o f ADRs are often
subjective
B. Nomograms are useful in
assessment o f causality in ADRS
C. pharmacy departments should take
the lead in the collection o f
information
D. ADR reporting information should
be incorporated into institutional
quality improvement programs
E. All o f the above
7. Which one o f the following questions
help in assessing the determination of
causality
A. whether the onset o f symptoms
occur after the drug was taken
B. the time interval between taking the
drug and the onset o f symptoms
C. whether the symptoms resolve after
the drug was discontinued
D. whether the symptoms reoccur after
the drug was reintroduced
E. All of the above
8. What is NOT involved in surveillance
program?
A. monitoring patients using high-risk
agents
B. reviewing patients who have
received “antidote’’ type drugs
C. report appropriately identified
ADRs to the FDA
‘
D. developing the use o f computer
system to track ADRs
E. reporting adverse events following
the administration of vaccine.
9. The center for biological evaluation and
research (CBER) ensures the safety and
efficacy o f all the following, EXCEPT
A.
B.
C.
D.
E.
blood products
allergenics
somatic cell therapy
dietary supplements
none
10.The national vaccine adverse event
reporting system(VAERS) is co­
administered by
A. department o f health and human
services (DHHS)
B. the CBER o f the FDA
C. the centers for disease control and
prevention (CDC)
D. all except B
E. all
11 .Any adverse events after administration
o f vaccines is reported to
A. DHHS
B.
C.
D.
E.
CBER
CDC
A&B
A& C
12.The VAERS depends on voluntary
reporting by health professionals to
A. identify rare adverse reactions
not detected in pre licensing
studies
B. monitor for increase in already
known reactions
C. identify risk factors or pre
existing conditions that
promote reactions
D. identify particular vaccine lots
with unusually high rates or
unusual types o f events
E. all the above
13. All the following should be reported to
Med Watch, EXCEPT
A. serious ADRs even if causality
is not proven
>
B. malfunctioning devices
C. problems with nutritional
„
products
D. mislabeling and poor
packaging
E. all o f the above
14. Which one o f the following statements
is true?
A. confidentiality o f both the
reporter and the patient whose
case is reported are protected
by the FDA
B. OTC products marketed with
out New Drug Application(
NDA) strongly require
reporting
C. reporting to manufacturers is
described in the FDA’s
guidelines
D. A & C
E. all
ANSWERS
Adverse Drug Reaction Reporting
1. Answer: B. Ill is correct
Explanation.
Adverse drug reactions are a cause o f significant morbidity and mortality in patients in all arenas
o f health care today. There is wide variation in the current health care literature, but it has been
estimated that from 1/3 to as high as V2 o f ADRs are believed to be preventable.The suffering that
patients experience because o f drug related events cannot be quantified.
2. Answer: A. Adverse drug reaction
Explanation
The terms adverse drug reaction, adverse drug event, untoward drug reaction, drug misadventure,
side effects or drug related problems are many times used interchangeably but do not always
describe the same situation.
3. Answer: E. All o f the above
Explanation.
The united states FDA’s definition o f adverse drug event is any adverse event associated with the
use o f drug in humans, whether or not considered drug related including the following: an adverse
event occurring from a drug overdose, whether accidental or intentional; an adverse event
occurring from drug abuse, an adverse event occurring from drug withdrawal and any significant
failure o f expected pharmacological action.
4. Answer: D. reactions include idiosyncratic reactions immunological or allergic reactions.
Explanation.
Type A ADRs are extensions o f the drug’s known pharmacology and are responsible for the
majority o f ADRs. They are usually dose dependent and predictable but can be due to
concomitant disease states, drug -d ru g interactions, or drug-food interactions. And type B ADRs
include idiosyncratic reactions, immunological or allergic reactions and carcinogenic/teratogenic
reactions. Type B reactions are usually not due to a known pharmacology o f the drug, but seem to
be a function o f patient susceptibility. They are rarely predictable, are usually not dose dependent,
and seem to concentrate in certain body systems such as liver, blood, skin, kidney, nervous
system and other body systems.
5. Answer: D. All o f the above
Explanation:
Ways to minimize type A reactions include understanding the pharmacology o f the drug being
prescribed, monitoring drugs with a narrow therapeutic window and avoiding polypharmacy
when possible. In type B ADRs, except for immediate hypersensitivity reactions, it usually takes
5 days before the patient demonstrates hypersensitivity to a drug. There is no maximum time for
the occurrence o f a reaction, but most occur with in 12 weeks o f initiation o f therapy.
6. Answer: E. All o f the above
Explanation.
All the above statements are included in recognition and surveillance programs for ADRs.
7. Answer: E. All o f the above
Explanation:
Besides all the above other factors like, whether the patient actually ingested the drug, did drugdrug interactions contribute to the symptoms, were the drugs measured in “toxic levels” in the
patient’s serum, has the reaction been previously seen with the use o f the drug and the personal
experience o f the clinician is included.
8. Answer: E. reporting adverse events following the administration o f vaccine.
Explanation.
Developing the use o f computer system to track ADRs is part o f the national vaccine adverse
event reporting system(VAERS). Other programs involved in surveillance programs include,
encouraging all health care professionals to be involved in reporting and notifying prescribing o f
suspected ADRs, and encourage thorough documentation o f the description o f the reaction as
well as the outcome in patients’ medical records.
9. Answer: D. dietary supplements.
Explanation.
The center for biological evaluation and research (CBER) ensures the safety and efficacy o f blood
products , vaccines, allergenics, biological therapeutics, somatic cell therapy, gene therapy, and
banked human tissue. The center for food safety and applied Nutrition (CFSAN) established the
CFSAN adverse events reporting systems ( CAERS) in 2002 to identify potentially serious
problems secondary to the non-FDA approved herbs, minerals, vitamins, dietary supplements,
and other substances.
10.Answer: E. All.
Explanation.
The VAERS is co-administered by the department o f health and human services( DHHS), the
CBER o f the FDA, and the centers for disease control and prevention(CDC).
11 .Answer: A. DHHS
Explanation.
The National Childhood Vaccine Injury Act(NCVIA) o f 1989 requires health professionals and
manufacturers o f the vaccines to report to the DHHS adverse events following the administration
o f vaccines specified in the act.
12.Answer: E. All the above.
Explanation.
VAERs is the national vaccine adverse event reporting system that depends on voluntary
reporting by health professionals to monitor known reactions, identify rare adverse reactions, risk
factors for pre-existing conditions and identifying vaccine lots with unusually high rates or
unusual types o f events.
13.
Answer: E. all of the above
Explanation.
Serious ADRs( like death, life threatening events, prolonged hospitalization, disability and
congenita] anomaly); malfunctioning devices ( such as heart valves, latex gloves, dialysis
machines and ventilators); problems with nutritional products and product problem that can result
in compromised safety or quality( product contamination, mislabeling, unclear labeling, poor
packaging, potency problems and questionable stability).
14. Answer: A. confidentiality of both the reporter and the patient whose case is reported are
protected by the FDA
Explanation.
Reporting o f problems with OTC medications are required when the product has been marketed
with the new drug application. Reporting to manufacturers is not described in the FDA’s
guidelines although a section o f the Med Watch form can be checked off to inform the FDA that a
copy o f the report has been forwarded into the manufacturer by the reporter.
Reviewing, Dispensing, and Compounding Prescription
“A deadline is negative inspiration. Still, it's better than no inspiration at all. ”
Rita Mae Brown
3.
Which o f the following is NOT true about prescriptions?
A.
B.
C.
D.
E.
nondrug products could be ordered by prescriptions
prescriptions should be presented in written form only
pharmacists are allowed to order new medications
pharmacist are allowed to change the dose o f existing medication
none
2.
A prescription should necessarily include the following information, EXCEPT
A.
B.
C.
D.
E.
patient information, including full name and address
date on which the prescription was issued
the strength o f the product for a combination o f active ingredients
name and dosage form o f the product
none
3. The name of the product written on the prescription can be
I . proprietary name
II .generic name
III .chemical name
A.
B.
C.
D.
E.
I only
I or IJ only
I, II or III
II only
II or III only
4.
“ As needed” [pro re nata (pm)] refills are usually interpreted as allowing for refills for
A.
B.
C.
D.
E.
1 month
4 months
6 months
] 0 months
3 year
5.
Direction for the pharmacist in the prescription should include the following
A.
B.
C.
D.
E.
preparation (e.g., compounding)
labeling
explicit instruction on the quantity, schedule and duration for proper use
A and B
All of the above
6.
The Drug Enforcement Administration (DEA) number is written in the prescription in
cases
A.
B.
C.
D.
E.
7.
I.
II.
III.
where the prescription is written by midlevel practitioner
where the drug is categorized with the controlled substances
where the prescription is presented electronically
where refills are required
all but D
Which o f the following is NOT true about medication orders?
only the generic name o f the drug should be written
they are intended for ambulatory patients
they may be presented electronically
A.
B.
C.
D.
E.
if I only is correct
if III only is correct
if I and II are correct
if II and III are correct
if I, II and III are correct
8.
Which o f the following information given in prescriptions should be interpreted to know
the intent o f the prescriber.
A.
B.
C.
D.
E.
the name and address o f the prescriber
the patient’s disease or condition requiring treatment
the reason the order is indicated relative to the medical need o f the patient
unit o f measurement and Latin abbreviations
all o f the above
9.
One o f the following need NOT be considered when evaluating prescription
appropriateness?
A. the patient’s disease or condition requiring treatment
B. whether a licensed practitioner, acting in the course and scope o f practice, issued the
prescription in good faith, for a legitimate medical purpose
C. the prescriber’s hand writing
D. possible drug-drug, drug-disease, or drug-food interaction
E. the prescribed route o f administration
10. Pharmacists are required to review medication profiles to ensure the appropriateness of
prescriptions or medication orders. This is called
A.
B.
C.
D.
E.
therapeutic intervention
drug utilization review
prescription review
avoiding errors
prescription control
11. When performing a therapeutic intervention, the following information should be
provided EXCEPT
A.
B.
C.
D.
E.
A brief description o f the problem
A reference sourcc that documents the problem
A description o f the clinical significance o f the problem
Informing other staff members that an error was made
A suggestion o f a solution to the problem
12. Out o f the possible resolutions that can help solve a problem or concern, documentation
o f the results o f the intervention are required if
A.
B.
C.
D.
E.
the prescription or medication order is dispensed as written
the prescription or medication order is not dispensed
the prescription or medication order is altered and dispensed
A and B
B and C
13. When processing prescriptions and medication orders, the pharmacist may come across
product preparation which include all the following EXCEPT,
A.
B.
C.
D.
E.
calculating and providing the correct amount/number o f the medication
generic substitution o f a drug product
assembling the different parts o f drug delivery units
compounding o f extemporaneous prescription
reconstitution o f a powdered drug to make suspensions or solutions
14. The reason for proper selection o f a packaging material or container include
A. legal requirements
B. to make it easier for the patients to take the medication so that they will be encouraged to
stick to the treatment regimen
C. to prevent deterioration of the drug product
D. all o f the above
E. all but C
15. The labeling o f the prescribed drug product must include all the following EXCEPT
A.
B.
C.
D.
name and address o f the pharmacy
initials o f the prescriber
expiration date
product’s brand or generic name
E. the number o f the prescription
16. Auxiliary and cautionary labels are required for the following reasons EXCEPT
A.
B.
C.
D.
E.
to enhance compliance
to make sure that the medication is properly stored
to make sure that the medication is taken properly
to make sure the patient follows the advice given to him by the pharmacist
none
17. One o f following information is NOT included in the patient profile system in the
prescription files and records kept by the pharmacist
A.
B.
C.
D.
E.
birth date o f the patient
weight o f the patient
the pharmacological action o f the prescribed medication
disease state o f the patient
OTC medication used
18. The patient profile should also contain information from each prescription or medication
order, which include all the following EXCEPT
A.
B.
C.
D.
E.
dosage form
direction for the pharmacist
amount o f the medication to be dispensed
prescriber’s name
pharmacist’s initials
19. When advising a patient about potential adverse effects, which o f the following
instructions should the patient be given
I.
II.
III.
A.
B.
C.
D.
E.
how frequent the adverse effect occurs
ways to alleviate the adverse effect
how severe the adverse effect could be
if I only is correct
if III only is correct
if I and II are correct
if II and III are correct
if I, II and III are correct
20. In order to administer a medication properly, a health professional should have all the
following information EXCEPT
A.
B.
C.
D.
E.
dosage and dosage regimen
drug-drug and drug-nutrition interaction
mechanism o f action o f the drug
possible incompatibilities
potential adverse effects
21. Which o f the following is NOT a drug-related prblems?
A.
B.
C.
D.
E.
incorrect dose o f a drug
wrong assessment
inappropriate compliance
adverse drug reactions
unnecessary drug use
22. Which of the following statements about compounding is NOT true?
A. it involves the preparation, mixing, assembling, packaging, or labeling o f a drug or
device
B. it is initiated based on the pharmacist/patient/prescriber relationship in the course o f
professional practice
C. it may be done for the purpose o f research, teaching, or chemical analysis
D. it could not be carried out unless there is a definite prescription order from a practitioner
E. none
23. Manufacturing involves:
A. packaging and repackaging o f substances
B. production, preparation, propagation, conversion or processing o f a drug or device
C. extraction o f drugs from substances o f natural origin or the chemical or biological
synthesis o f drugs
D. labeling or relabeling o f containers
E. All o f the above
24. Which o f the following is NOT true about manufacturing and compounding?
A. compounded drugs are not meant for reselling while the main objective manufacturing is
resale o f drugs
B. like in compounding, manufacturers are required to and provide oversight o f individual
patients
C. compounded drugs are produced and administered by the patient’s health care
professionals, which is not in manufacturing
D. in manufacturing the drug produced are through normal channels o f interstate commerce
to individuals known to the company, while in compounding there is direct relationship
between the pharmacist/prescriber/patient
E. none
25. Extemporaneous compounding by the pharmacist or a prescription order from a licensed
practitioner is controlled by
A.
B.
C.
D.
E.
FDA
USP/NF
State board o f pharmacy
Department o f health
All
26. One o f the following is NOT a responsibility o f a pharmacist
A.
B.
C.
D.
E.
preparing a quality pharmaceutical product
providing proper instructions regarding its storage
advising the patient of any adverse effects
ensuring the correct drug, dose and directions
to decide the products, which should not be prepared extemporaneously
27. The beyond-use day according to the current USP criteria for non aqueous liquid and
solid formulations (where a manufactured drug product is the source o f active
ingredients) is not later than 50% o f the time remaining until the product’s expiration date
or 1 year, which ever is earlier
A. not later than 25% o f the time remaining until the product’s expiration date or 6 months,
whichever is earlier
B. not later than 50% o f the time remaining until the product’s expiration date or 6 months,
whichever is earlier
*
C. not later than 25% o f the time remaining until the product’s expiration date or 3 months,
whichever is earlier
D. not later than 90% o f the time remaining until the product's expiration date or 1
year, whichever is earlier
28. The beyond-use day according to the current USP criteria for nonaqueous liquid and solid
formulations where a USP or NF substance is the source o f active ingredients is
A.
B.
C.
D.
E.
not
not
not
not
not
later than
later than
later than
later than
later than
3 months
1 year
6 months
1 month
2 weeks
29. For water-containing products, prepared from ingredients in solid form and stored in cold
temperatures, the beyond-use date is not later than
A.
B.
C.
D.
1 month
3 weeks
10 days
14 days
E. 45 days
30. All the following quality control tests are required for ointments/creams /gels EXCEPT
A.
B.
C.
D.
E.
pH
specific gravity
rheological properties
dissolution characteristics
active drug assay
31. One o f the following tests is NOT required for suppositories, troches, lollipops, and sticks
A.
B.
C.
D.
E.
melting test
weight
disintegration test
dissolution test
physical stability
32. Which o f the following tests are common to both oral and topical liquids as well as
parenteral preparations?
I.
II.
III.
IV.
weight/volume
osmolality
pH
pyrogenicity
A.
B.
C.
D.
E.
I and III
II and III
I and IV
Ill only
I only
33. Which o f the following does NOT need special consideration in the compounding o f
solutions?
A.
B.
C.
D.
E.
pH
stability
uniformity o f the dosage
solubility o f the drug or chemicals
packaging
.
34. Which o f the following solutions require special attention for their preparation?
A. oral solutions
B. topical solutions
C. otic solutions
D. ophthalmic solutions
E. all o f the above
35. One of he following statements is NOT true aboutthe preparation o f solutions?
I.
flavoring and sweetening agents should be prepared while preparing the solution
II.
a salt should be directly added to a syrup
III.
the free acid or base form o f the drug should be used
IV.
if an alcoholic solution o f a poorly water-soluble drug is used, no water should be
added
A.
B.
C.
D.
E.
I only
II only
Ill only
IV only
I, II, III, and IV
36. Choose the CORRECT statement about the compounding procedure o f the following
medication order.
Phenobarbital Ig
Belladonna Tr 5ml
Preserved flavored syrup q.s. 120ml
I.
the free-base form o f phenobarbital should be used
II.
the phenobarbital should first be dissolved in the tincture
III.
the phenobarbital should first be dissolved in the preserved flavored syrup
A.
B.
C.
D.
E.
I only
I and II only
II only
I and III only
Ill only
•
37. Why should a pharmacist use caution when preparing the following medication order?
Salicylic acid 2%
Lactic acid 6ml
Flexible collodion ad 30ml
A.
B.
C.
D.
E.
salicylic acid and lactic acid are incompatible
flexible collodion is incompatible with acids
flexible collodion is inflammable
the amount o f lactic acid is too high
C and D
38. Which is the correct order o f mixing the components o f the medication order in question
No. 17/96?
A. salicylic acid; lactic acid; flexible collodion
B. salicylic acid; flexible collodion, lactic acid
C. lactic acid, flexible collodion, salicylic acid
D. flexible collodion, lactic acid, salicylic acid
E. A and B
39. In compounding the following medication order, a plastic or rubber spatula should be
used. Why?
Iodine 2%
Sodium iodide 2.4%
Alcohol q.s. 30ml
A.
B.
C.
D.
E.
because alcohol reacts with iron
because alcohol catalyses the reaction between iodine and iron
because iodine is corrosive
because there iron and sodium iodide are incompatible
C and D
40. Which o f the following is NOT true about suspensions?
A.
B.
C.
D.
E.
some suspensions should contain an antimicrobial agent as a preservative
particle settling could be avoided by using suspending agents
tight containers are necessary to ensure the stability of the final product
the suspension should be viscous
insoluble powders should be small and uniform in size to decrease settling
41. Which o f the following does NOT help minimize the physical instability of suspensions
after their formation?
A.
B.
C.
D.
E.
reducing the particle size o f the powders
using thickening agents
using levigating agents
using preservatives
using flavoring agents
,
42. One o f the following is NOT a levigating agent?
A.
B.
C.
D.
E.
glycerin
methylcellulose
propylene glycol
alcohol
water
43. Which o f the following is a WRONG procedure in the preparation o f suspensions?
A. the insoluble powders should be triturated into fine powders
B. the final mixture should be transferred to a “tight” bottle for dispensing to the
patient
C. the water soluble ingredients should be added at the end o f the preparation
process
D. suspensions should be labeled “shake well”
E. suspensions should never be filtered
44. One o f the following does NOT help prevent the two phases o f an emulsion from
separating into two layers,
A.
B.
C.
D.
E.
proportion o f oil and water
emulsifying agent
freezing
use o f hand homogenizer
none
45. The percentages o f methylparaben and propylparaben that can be used together as
preservatives in emulsions are, respectively
A.
B.
C.
D.
E.
1% and 2 %
0.1% each
0.2% and 0.02%
0.2% and 0.1%
0.2% each
46. Which o f the following can be used for preparing only o/w emulsions?
I.
II.
III.
IV.
gums
methylcellulose
soaps
nonionic emulsifying agents
A.
B.
C.
D.
E.
I only
I and II
II and III
II and IV
Ill and IV
47. The correct ratio o f acacia to fixed oil and acacia to volatile oil used in the preparation of
emulsions is
A.
B.
C.
D.
E.
lg
lg
lg
lg
lg
to
to
to
to
to
4ml
2ml
2ml
4ml
3ml
and
and
and
and
and
1g to
1g to
1g to
lg to
1g to
8ml
4ml
3ml
2ml
6ml
respectively
respectively
respectively
respectively
respectively
48. Which o f the following is CORRECT about the formation and preparation o f emulsions?
A.
B.
C.
D.
most o f the time a mortar and pestle are the only equipments required
a rapid motion should be avoided while triturating
a mortar with rough surface should be avoided
the size o f the mortar should be exactly equal to the volume o f the emulsion to be
prepared
E. to create an emulsion trituration o f at least 10 minutes is required
49. Which o f the following methods used for compounding emulsions is different from the
others?
A.
B.
C.
D.
E.
dry gum method
wet gum method
bottle method
beaker method
C and D
50. Which o f the following is NOT true about the preservation of emulsions?
I.
II.
III.
refrigeration is usually sufficient to keep emulsions for extended period o f time
the product could be frozen for better preservation
if preservative is used, it must be soluble in the oilphase of the emulsion
A.
B.
C.
D.
E.
1 ,11 and III
II and III
I and III
I and II
II only
-
51. Given the following medication order,
Mineral oil 18ml
Acacia q.s. Distilled water q.s. ad 90ml
Sig: ltbspq.d.
I f a dry gum method is used for preparing the primary emulsion, the amount o f the oil,
gum and water required is respectively
A.
B.
C.
D.
E.
36ml, 18g, and 9ml
9ml, 18g, and 36ml
18ml, 9g, and 4.5ml
9ml, 18g, and 4.5ml
18ml, 4.5g, and 9ml
52. Given the medication order,
mineral oil 50ml
water q.s. 100ml
sig: 2.5ml p.o. h.s.
One o f the following precautions should NOT be mentioned on the label affixed to the
container?
A.
B.
C.
D.
E.
shake well
for external use only
should be kept below 0°C
protect from light
none
53. Which o f the following can NOT be a reason for using powdered dosage forms?
A.
B.
C.
D.
E.
powders can overcome stability and solubility problems
they can be used to dispense unpleasant tasting medications
they may be used when the powders are too bulky to make into capsules
they may be used if the patient has problem with swallowing capsules
they may be used for internal and external purposes
54. All o f the following statements are true about the blending o f powders EXCEPT
A. when heavy powders are mixed with lighter ones, the heaviest powders should be
placed on the top o f the lighter ones
B. stirring using a spatula is one o f the methods o f blending powders
C. light powders are mixed best by using mortar
D. the mortar and pestle method is preferred when pulverization and a thorough
mixing of ingredients are desired
E. when mixing two or more powders, it is very important that each powder should
be pulverized separately to about the same particle size before blending together
55. Bulk powders include which o f the following
A.
B.
C.
D.
E.
dusting powders
douche powders
laxatives
insufflations
all of the above
56. A container with a sifter top is intended for
A.
B.
C.
D.
E.
effervescent powders
hygroscopic powders
dusting powders
eutectic mixtures
insufflations
57. Eutectic mixtures may cause problems because
~
A.
B.
C.
D.
E.
they can absorb moisture
they deteriorate very easily
they are not water soluble
they liquefy when mixed
all of the above
58. Which o f the following statements about powder papers is NOT true?
A. they are also called divided powders
B. glassine lining is required in case o f hygroscopic, effervescent and deliquescent
powders
C. the amount o f the ingredients required for one dose are weighed separately and
the blended
D. plastic bags or envelopes with snap-and-seal closures can also be used for
packaging powders
E. none
59. All o f the following are correct about the compounding procedure o f the medication
order given below EXCEPT
camphor 1OOmg
menthol 200mg
zinc oxide 800mg
talc 1900mg
M foot powder
Sig: apply to feet
A.
B.
C.
D.
E.
the camphor and menthol may be triturated in glass mortar
geometric dilution may be used
the product may be dispensed in a container with sifter top
the final powder may be passed through a wire mesh sieve
none
60. Which o f the following is the largest capsule in size?
A.
B.
C.
D.
E.
capsule No.l
capsule No.2
capsule No. 00
capsule No. 0
capsule No. 5
61. The largest capsule size suitable for patient use is
A.
B.
C.
D.
No. 0
No. 1
No. 2
No. 3
E. No. 4
62. What would be the best solution, if the amount o f the drug to be encapsulated under fills
a larger capsule and over fills a smaller capsule?
A.
B.
C.
D.
E.
to use both capsule sizes
to use the smaller one
to use the larger one
to avoid the use o f capsules
all the above are possible
63. Which o f the following dosage forms does NOT match with its description?
A.
B.
C.
D.
E.
ointments; oleaginous
creams; o/w or w/o emulsions
jellies; suspensions
gels; high content o f solids
A and B
64. Ointments, creams, pastes and gels are intended
A.
B.
C.
D.
E.
to act on the surface o f the skin
to carry drugs that penetrate into the skin
to carry drugs that will be absorbed systemically
A and B
A,B&C
65. One o f the following statements about ointment bases is NOT true
A.
B.
C.
D.
E.
hydrophobic bases contain a mixture o f fats, oils, and waxes
hydrophobic bases are emulsion bases
the o/w emulsions can easily be washed o ff with water
hydrophobic bases cannot be washed o ff using water
C and D
66. The most suitable container for ointments is
A.
B.
C.
D.
E.
jars
collapsible tubes
chartulae
narrow mouthed bottles
A and B
67. Suppositories are inserted into the following human body orifices EXCEPT
A.
B.
C.
D.
E.
vagina
rectum
mouth
Urethra
None
68. The suppository base, which is fat-soluble mixture o f triglycerides that is most often used
for rectal suppositories is
A.
B.
C.
D.
E.
Cocoa butter
PEG
Carbowax
Glycerinated gelatin
A and C
69. Suppository molds could be made from:
A.
B.
C.
D.
E.
stainless steel
aluminum
plastic
rubber
All o f the above
70. The fusion method o f preparing suppositories involves
A. dissolving the all the ingredients in a volatile solvent, pouring these into a special
mold and finally evaporating the solvent
B. triturating the ingredients in a mortar to form a plastic like material and molding
the suppositories using your fingers
C. triturating the ingredients in a mortar to form a plastic like material and putting
the this plastic like material in suppository compression device
D. melting the suppository base, incorporating the medication and finally pouring
the mixture into a mould
E. A and D
71. Given the following medication order, calculate the amount o f suppository base required
to make 10 suppositories o f 2g (hint: calculate for two extra suppositories, the density
factor o f aspirin is 1.1)
aspirin 300mg
Cocoa butter q.s.
Dispense 10 suppositories
Sig: insert one supp once daily
A.
B.
C.
D.
30.5g
20.73g
25.43g
19.74g
E. 23.32g
72. Which of the following is a WRONG procedure in reconstitution of a dry powder from a
vial?
A. the surface o f the vial containing the sterile powder should be cleaned using
alcohol pad
B. after dissolving the powder, the vial should be in the inverted position to
withdraw the desired volume
C. the volume o f the syringe used for reconstitution should be exactly equal to the
volume required for reconstitution
D. a sterile cap or seal should be applied over the port o f the container
E. none
73. A 5jam filter should be attached to the syringes when removing fluids from
A.
B.
C.
D.
E.
vials
ampoules
IV bags
Prefilled cartridges
All but A
74. Which of the following is NOT true about parenteral preparations?
A. special knowledge and training is required to prepare parenterals
B. they must be prepared using aseptic techniques
C. all parenteral products must be administered directly from their container without
further processing
D. parenteral preparations could be prepared outside hospital pharmacies
E. C and D
75. Which of the following is a WRONG procedure in the removal o f drug solutions from
vials?
A.
B.
C.
the surface of the rubber closure should be swabbed with alcoholprep pad
the needle must be inserted into the rubber closure at 90 [I
a sterile air should be inserted into the vial to help remove the drug and to
prevent the formation of negative vacuum pressure
D. the rubber closure must be opened only for very brief period o f time to allow the
removal of the drug solution
E. B and D
Answers
Reviewing and Dispensing Prescriptio
1. Answer: B. prescriptions should be presented in written form only.
Explanation:
Prescriptions are orders for medications, non drug products, and services that are written by a
licensed practitioner or midlevel practitioner who is authorized by state law to prescribe.
Pharmacists are increasingly being given prescribing privileges by enactment o f state
collaborative drug therapy management (CDTM) legislation. This allows pharmacists to order
new medication or change the dose existing medication under established protocols or guidelines
agreed upon by the pharmacist and physician. Prescriptions may be written, presented orally (by
telephone), or presented electronically (i.e., via fax or computer network) to the pharmacist.
2. Answer: C. the strength o f the product for a combination o f active ingredients.
Explanation:
The strength o f the product is not required if only one strength is commercially available or if the
product contains a combination o f active ingredients. It is advisable to include the strength to
reduce the chance o f misinterpretation the prescription. If the dose is to be calculated by the
pharmacist, then the pharmacist can decide the strength o f the product dispensed after calculating
the patient’s dose.
3. Answer: C. I, II or III.
•
Explanation:
The name o f the product written on the prescription can be any o f the three mentioned above.
4. Answer: E. 1 year
Explanation:
I f refill is not supplied, it is generally assumed that no refills are authorized. “ As needed” [pro re
nata (pm)] refills are usually interpreted as allowing for refills for 1 year.
5. Answer: D. A and B
Explanation:
The explicit instructions on the quantity, schedule and duration for proper use are the directions
intended for the patient. “As directed” should be avoided when giving instructions to the patient.
If the directions vary, a minimum and maximum dose can be used.
6. Answer: B. where the drug is categorized with the controlled substances.
Explanation:
Prescriber information written on the prescription should include the name, office address,
signature o f the prescriber, and the Drug Enforcement Administration (DEA) number should be
mentioned for controlled substances only.
7. Answer: C. 1 and II are correct
Explanation:
Medication orders are orders for medications by an individual authorized to prescribe and are
intended for use by patients while in an institutional setting. They may be written, presented
orally (by telephone), or presented electronically (i.e., via fax or computer network) to the
pharmacist. The name o f the drug written on the prescription can be brand name, generic name,
or chemical name. Medication orders do not have directions for patients. Instead, instructions are
given to the administration, which includes quantity, route o f administration, schedule, and
duration.
8. Answer: E. All o f the above.
Explanation:
A complete understanding o f all information contained in prescription or medication orders is
required. Upon arrival o f the prescription or the medication order the pharmacist must read the
entire prescription or medication order carefully to determine the prescriber’s intent by
interpreting all the above mentioned information. Moreover, the name and address o f the patient,
and the name o f the product, the quality prescribed, and instruction for use should also be studies
carefully.
9. Answer: C. the prescriber’s hand writing.
Explanation:
Although the handwriting o f some prescribers can create certain difficulties, it is not considered
when evaluating the appropriateness of the prescription. The pharmacist is more concerned about
the appropriateness o f the prescription to the particular patient.
10. Answer: B. drug utilization review.
Explanation:
Pharmacists are required to review medication profiles to ensure the appropriateness o f
prescriptions or medication orders. This is commonly called drug utilization review (DUR).
Pharmacist should not fill prescriptions or medication orders that they have concerns with or that
are considered inappropriate, but rather, should contact the prescriber. The process o f calling a
prescriber to discuss concerns identified during a DUR is commonly called therapeutic
intervention.
11 .Answer: D. Informing other staff members that an error was made.
Explanation:
Informing other staff members that an error was made by some prescriber may affect the pride o f
the prescriber and may lead to loss o f confidence in the prescriber. This can lead to confrontation
as well as lack o f cooperation and this will not help resolve the problem.
12 .Answer: C. the prescription or medication order is altered and dispensed.
Explanation:
Documentation o f the results o f a therapeutic intervention are required if the prescription or
medication order is changed. The name o f the prescriber, date o f the communication, issues
discussed, and resolution should be included in the documentation. This information should be
kept for same time period as the prescription or medication order.
13.
Answer: B. generic substitution of a drug product.
Explanation:
Generic substitution o f a drug product is not classified as product preparation. It is part o f product
selection.
14. Answer: D. all o f the above.
Explanation;
The reasons for the proper selection o f a packaging material or container is that it is required by
the law that each drug product should be packaged in a container that is appropriate for it; to
make the patients more compliant since packaging material or container that is properly designed
would make it easier for them to take the prescribed medication; and to ensure the drug product is
protected from the external environment to prevent its deterioration and thus enhance its stability.
15. Answer: B. initials o f the prescriber.
Explanation:
The prescriber’s initials cannot be included in the prescription label, since s/he cannot be
available when the medication is dispensed. Instead the initials of the pharmacist must be
included. Other information that should be included are the name o f the patient, the date o f
filling, instructions on how to use the medication, manufacturer’s name, the name o f the
prescriber, the amount o f the medication dispensed, and product strength if more than one
strengths are available.
16.Answer: E. none.
Explanation:
Auxiliary and/or cautionary labels are affixed to ensure the proper use o f medication, to
encourage patient compliance, to inform the patient that the medication need to be stored in a
proper place, and to reinforce the information given to the patient by the pharmacist during
dispensing the medication.
17.
Answer: C. the pharmacological action o f the prescribed medication.
Explanation:
Birth date and weight o f the patient are important to make sure that the proper dose is given. The
disease state o f the patient helps to assess if the proper medication was prescribed and to avoid
the possibilities o f drug-disease interaction. OTC medication use is important to avoid drug-drug,
as well as drug-disease interactions, to assess the effectiveness o f the medication taken, and to
identify the occurrence o f any adverse effect. Other information that need to be included are
patient’s name; patient’s address; previous allergies, sensitivities, or idiosyncratic reactions; and
occupation o f the patient that will help to identify the conditions associated with a particular
occupation and to help determine if the patient may have any problem complying with the
prescribed prescription.
18. Answer: B. direction for the pharmacist
Explanation:
The information obtained form each prescription or medication order that should be included in
the patient profile include, name o f the product, dosage form and strength o f the product,
prescription number, instruction for use, the amount o f the drug to dispensed, prescriber’s name,
the initials o f the pharmacist, dispensing date, and the number o f the refills authorized and the
number o f the refills left.
19.Answer: E. I, II and III.
Explanation:
It is the responsibility o f the pharmacist to make sure that the patient knows all the potential
adverse effects o f the medication. Moreover, the pharmacist must ensure that the patient
understands the frequency of occurrence o f the adverse effect (this will help the patient to identify
the common adverse effects); the ways o f alleviating the adverse effects and their consequences
(this will enable the patient to manage the adverse effects properly); and the severity o f the
adverse effects (so that the patient could give proper attention to the most severe adverse effects).
20.
Answer: C. mechanism o f action o f the drug.
Explanation:
It is not necessary that a health professional need to know the mechanism o f action o f a drug in
order to administer the medication properly. Other information that the health professional need
to know include the proper choice o f the drug product, the route o f administration, appropriate
handing o f the drug product, potential interference o f the drug with laboratory results, the overall
cost o f the drug product, nutritional requirements as well as the safe way o f disposing the
medication.
21.Answer: B. Wrong assessment.
Explanation:
Although it is possible that wrong assessment o f a patient condition could lead to drug-related
problems, it is not by itself a drug related problem.
22.
Answer: D. it could not be carried out unless there is a definite prescription order from a
practitioner.
Explanation:
Compounding includes the preparation o f drugs and devices in anticipation o f prescription drugs
based on routine, regularly observed patterns.
23. Answer: E. All o f the above
Explanation:
In addition to this, manufacturing involves the promotion and marketing o f drugs and devices. It
also includes the preparation and promotion o f commercially available products from bulk
compound for resale by pharmacies, practitioners, or other persons.
24. Answer: B. like in compounding, manufacturers are required to and provide oversight o f
individual patients.
Explanation:
Manufacturers are not required to, and do not, provide oversight of individual patients.
Compounded drugs on the other hand are personal and responsive to the patient’s immediate
needs.
25. Answer: C. State board o f pharmacy.
Explanation:
As with the dispensing o f any other prescription, extemporaneous compounding by the
pharmacist or a prescription order from a licensed practitioner is controlled by the state broads of
pharmacy.
26. Answer: E. to decide the products, which should not be prepared extemporaneously
Explanation:
The FDA determines the list products that are not safe and/or effective to be prepared
extemporaneously. It is important to note that certain dosage forms o f one drug are allowed to be
prepared extemporaneously while other dosage forms of the same drug are not allowed.
27. Answer: B. not later than 25% of the time remaining until the product’s expiration date or 6
months, whichever is earlier.
Explanation: The beyond-use day according to the current USP criteria for non aqueous liquid
and solid formulations (where a manufactured drug product is the source o f active ingredients) is
not later than 25% o f the time remaining until the product’s expiration date or 6 months,
whichever is earlier.
28. Answer: C. not later than 6 months.
Explanation: The beyond-use day according to the current USP criteria for non aqueous liquid
and solid formulations where a USP or NF substance is the source o f active ingredients is not
later than 6 months.
29. Answer: D. 14 days.
Explanation:
For water-containing products, prepared from ingredients prepared from ingredients in solid form
and stored in cold temperatures, the beyond-use date is not later than 14 days.
30. Answer: D. dissolution characteristics.
Explanation:
Testing the dissolution characteristics is not required in case o f ointments/creams /gels. Other
tests to be considered include physical observation (color, clarity, texture-surface, texture-spatula
spread, appearance, feel) and theoretical weight compared to actual weight.
31. Answer: C. disintegration test.
Explanation:
The quality control tests required for suppositories, troches, lollipops, and sticks include weight,
specific gravity, active drug assay, physical observation (color, clarity, texture of surface,
appearance, feel), melting test, dissolution test, and physical stability.
32. Answer: A. 1 and III.
Explanation:
Osmolality and pyrogenicity tests are not required for oral and topical preparations, because these
preparations are not sterile.
33. Answer: C. uniformity o f the dosage.
Explanation:
By definition, solutions are liquid preparations that contain one or more chemical substances
dissolved (i.e., molecularly dispersed) in a suitable solvent or mixture o f mutually soluble
solvents. Therefore, the uniformity o f the dosage form in a solution may be assumed. However,
the stability, pH, solubility o f the drug or chemicals, tastes (for oral solutions), and packing need
special attention.
34. Answer: D. ophthalmic solutions.
Explanation:
Parenteral and ophthalmic solutions should be sterile. Therefore, they need special attention when
being prepared. The others are all non-sterile solutions.
35. Answer: E. I, II, III, and IV.
Explanation:
If an alcoholic solution o f a poorly water-soluble drug is used. The aqueous solution is added to
the alcoholic solution to maintain as high an alcohol concentration as possible. The salt form o f
the drug, and not the free-acid or base form, which both have poor solubility, is used. Flavoring
or sweetening agents should be prepared ahead o f time. When adding a salt to syrup, dissolve the
salt in a few milliliters of water first; then add the syrup to volume.
36. Answer: E. Ill only.
Explanation:
The correct compounding procedure for the above medication order is the following. The sodium
salt o f phenobarbital (equivalent to 1g o f the phenobarbital) should be used. This salt should be
dissolved in the preserved, flavored syrup. The solution is then slowly added, in individual
portions, to the tincture contained in a beaker and is stirred continuously.
37. Answer: C. flexible collodion is inflammable.
Explanation:
Pharmacists must use caution when preparing this prescription because flexible collodion is
extremely flammable.
38. A nsw er: A . salicylic acid; lactic acid; flexib le collodion.
Explanation:
The correct procedure o f compounding the above prescription is the following. A 1-oz applicator
tip bottle is calibrated, using ethanol, which is poured out and allowed to evaporate, resulting in a
dry bottle. Salicylic acid is directly added into the bottle, to which is added the 6ml o f lactic acid.
The bottle is agitated or a glass stirring rod is used to dissolve the salicylic acid. Flexible
collodion is added up to the calibrate 30ml mark on the applicator tip bottle.
39. Answer: C. because iodine is corrosive.
Explanation:
In compounding the above medication order, rubber or plastic spatula should be used, because
iodine is corrosive.
40. Answer: B. particle settling could be avoided by using suspending agents.
Explanation:
Particles settle in suspensions even when a suspending agent is added; thus, suspensions must be
well shaken before use to ensure the distribution o f particles for a uniform dose.
41. Answer: E. usine flavoring agents.
Review ing, Dispensing, and Compounding Prescription
Compounding includes the preparation o f drugs and devices in anticipation o f prescription drugs
based on routine, regularly observed patterns.
23. Answer: E. All o f the above
Explanation:
In addition to this, manufacturing involves the promotion and marketing o f drugs and devices. It
42. Answer: B. methylcellulose
Explanation:
A levigating agent aids in the initial dispersion o f insoluble particles. Common levigating agents
include glycerin, propylene glycol, alcohol, syrups and water. Methycellulose is used as
thickening agent in the preparation o f suspensions.
43. Answer: C. the water soluble ingredients should be added at the end o f the preparation
process.
Explanation:
The water-soluble ingredients, including flavoring agents, are mixed in the vehicle before mixing
with insoluble ingredients.
44. Answer: C. freezing.
Explanation:
Emulsions are unstable, and the following steps must be taken to prevent the two phases o f an
emulsion from separating into two layers after preparation. The correct proportions o f oil and
water should be used during preparation. The internal phase should represent about 40%-60% o f
the total volume. An emulsifying agent is needed for emulsion formation. A hand homogenizer,
which reduces the size o f globules o f the internal phase, may be used. Preservative should be
added if the preparation is intended to last longer than a few days. A “shake well” label should be
placed on the final product. The product must be protected from light and extreme temperatures.
Both freezing and heat may have effect on stability.
45. Answer: C. 0.2% and 0.02%.
Explanation:
Generally, a combination o f methylparaben (0.2%) and propylparaben (0.02%) may be used as
preservatives for emulsions
46. Answer: B. I and II.
Explanation:
Gums, such as acacia or tragacanth, are used to form o/w emulsions. Methylcellulose and
carboxymethylcellulose are used for o/w emulsions. Soaps and nonionic emulsifying agents can
be used for both o/w and w/o emulsions depending on their emulsification properties.
47. Answer: D. lg to 4ml and lg to 2ml respectively.
Explanation:
In the preparation o f emulsions, one gram o f acacia powder is used for every 4ml o f fixed oil or
lg to 2 ml for a volatile oil.
48. Answer: A. most o f the time a mortar and pestle are the only equipments required.
Explanation:
A mortar and pestle are frequently the only equipments required for the preparation o f emulsions.
A mortar with rough surface (e.g., Wedgwood) should be used. This rough surface allows
maximal dispersion o f globules to produce a fine particle size. A rapid motion is essential when
triturating an emulsion using a mortar and pestle. The mortar should be able to hold at least three
times the quantity being made. Trituration seldom requires more than 5 minutes to create the
emulsion.
49. Answer: D. beaker method.
Explanation: :
Beaker method is different from the other three methods in that all the other methods (i.e., wet
gum method, dry gum method and bottle method) are for forming emulsions using natural
emulsifying agents and require a specific mixing order. On the other hand, beaker method is used
for forming emulsions using synthetic emulsifying agents and produces a satisfactory product
regardless o f the order o f mixing.
50. Answer: B. II and III.
Explanation:
Emulsions should not be allowed to freeze at any time. If a preservative is used, it must be soluble
in the water phase to be effective, since microorganisms can grow only in the water phase o f an
emulsion.
51. Answer: E. 18ml, 4.5g, and 9ml.
Explanation:
With the dry gum method the amount o f oil, gum, and water required to form the primary
emulsion is: 4 parts o f the oil, 2 parts o f water and 1 part o f gum. Therefore, to prepare the
primary emulsion o f the above medication order, 18ml o f mineral oil, 4.5g o f powdered acacia,
and 9ml o f distilled water is required.
52. Answer: C. should be kept below 0°C.
Explanation:
Since it is not advisable to freeze emulsions, they should not be kept at a freezing temperature.
53. Answer: B. they can be used to dispense unpleasant tasting medications.
Explanation: Powders are not suitable for medications that have unpleasant taste. In fact, this is
one o f the disadvantages o f using powders.
54. Answer: C. light powders are mixed best by using mortar.
Explanation:
Light powders are mixed best by using the sifting method. The sifting is repeated three to four
times to ensure thorough mixing o f the powders.
55. Answer: E. All o f the abvoe
Explanation: Bulk powders, which may be used internally or topically, include dusting powders,
douche powders, laxatives, insufflations, and antacids.
56. Answer: C. dusting powders.
Explanation:
After a bulk powder has been pulverized and blended, it should be dispensed in an appropriate
container. Hygroscopic and effervescent powders should always be placed in a tight, wide­
mouthed jar. Dusting powders should be placed in a container with a sifter top.
57. Answer: D. they liquefy when mixed.
Explanation: Eutectic mixtures are problematic in that, their melting point is decreased when they
are mixed as a result o f which they liquefy upon mixing. One remedy is to add an inert powder,
such as magnesium oxide, to separate the eutectic materials.
58. Answer: C. the amount o f the ingredients required for one dose are weighed separately and
the blended.
Explanation:
Incase o f powder, the entire powder is initially blended. Each dose is then individually weighed.
59. Answer: E. none
Explanation:
The compounding procedure o f the above medication order o f as fol!ows:the camphor and
menthol are triturated in a glass mortar, where a liquid eutectic is formed. The zinc oxide and talc
are blended and mixed with the eutectic, using geometric dilution. This mixing results in a dry
powder, which is passed through a wire mesh sieve. The final product is dispensed in a container
with a sifter top.
60. Answer: C. capsule No. 00.
Explanation:
The capsule size in increasing order o f powder capacity is: No. 5, 4, 3, 2, 1,0, 00, and 000.
Therefore, o f the above given capsules, capsule No.00 is the largest. These capsules are for
human use. Capsules for veterinarians are available in Nos. 10, 11. and 12, containing
approximately 30, 15 and 7.5g , respectively.
61. Answer: A. No. 0.
Explanation:
Capsule No. 0 is usually the largest oral size suitable for patients.
62. Answer: C. to use the larger one.
Explanation:
In such cases, it is advisable to use the larger capsule. The remaining space can be filled with
sufficient amount o f diluents such as lactose.
63. Answer: D. gels; high content o f solids.
Explanation:
Ointments, creams, and pastes are semisolid dosage forms intended for topical application to the
skin or mucous membranes. Ointments are characterized as being oleaginous in nature; creams
are generally o/w or w/o emulsions, and pastes are characterized by their high content o f solids
(about 25%). Gels (sometimes called jellies) are semisolid systems consisting o f suspensions
made up o f either small inorganic particles or large organic molecules interpenetrated by a liquid.
64. Answer: E. A,B &C
Explanation:
Ointments, creams, pastes, and gels are semisolid preparations generally applied externally. They
are applied for the following purposes: act solely on the surface o f the skin to produce local effect
(e.g., antifungal agent); to release the medication, which in turn, penetrates into the skin (e.g.,
cortisol cream); and to release medication for systemic absorption through the skin (e.g.,
nitroglycerin).
65. Answer: B. hydrophobic bases are emulsion bases.
Explanation:
Hydrophilic bases are usually emulsion bases. The o/w type emulsions can easily washed off with
water, but the w/o type is slightly more difficult to remove.
66. Answer: E. A and B.
Explanation:
For easy removal o f the preparation, ointments should be packaged in wide opened jars or in
collapsible tubes.
67. Answer: C. mouth
Explanation:
Suppositories are solid bodies o f various shapes and weights, adapted for introduction into the
rectal, vaginal, or urethral orifices o f the human body. They usually melt or, soften, or dissolve at
body temperature. They may act as protectants to the local tissue at the point o f introduction or as
carrier agents for systemic or local action.
68. Answer: A. Cocoa butter.
Explanation: :
Cocoa butter (theobroma oil), which melts at body temperature, is fat-soluble mixture o f
triglycerides that is most often used for rectal suppositories. Polyethylene glycol (PEG,
Carbowax) derivatives are water-soluble bases suitable for vaginal and rectal suppositories.
Glycerinated gelatin is water-miscible base often used in vaginal and rectal suppositories.
69. Answer: E. All o f the above
Explanation:
All the above materials could be used in the manufacture o f suppository molds.
70. Answer: D. melting the suppository base, incorporating the medication and finally pouring the
mixture into a mould.
Explanation:
In the fusion method o f preparing suppositories, small amount o f the base is melted. The finely
powdered drug is added to this with continuous stirring. The remainder o f the suppository is
added with stirring. The mixture is finally poured into the lubricated molds.
71.Answer:B. 20.73g.
Explanation:
Calculating for two extra suppositories, the total weight o f 12 suppositories would be 24g; and
3.6g (12 x 300mg) o f aspirin will be required. 3.6g o f aspirin divided by 1.1, the density factor of
aspirin, gives 3.27. Therefore, 3.6g o f aspirin displaces 3.27g o f cocoa butter. The amount of
cocoa butter required will be 24-3.27, or 20.73g.
72. Answer: C. the volume of the syringe used for reconstitution should be exactly equal to the
volume required for reconstitution.
Explanation:
The syringe chosen for reconstitution should have a volume which is slightly greater than the
volume required for reconstitution.
73. Answer: B. ampoules.
Explanation:
Because glass particles may become dislodged during ampoule opening, the product must be
filtered before administration. For this purpose, a filter should be attached to the syringe when
removing fluids from ampoules.
74. Answer: C. all parenteral products must be administered directly from their container without
further processing.
Explanation:
Not all parenteral preparations need to be administered directly without further processing. Some
drugs, which are unstable in solution form, are packaged as dry powders. Such drugs are to be
reconstituted into solution with the proper solvent just before they are administered. Moreover,
some drug solutions may be packaged in their concentrated form. These drugs are to be diluted
before they are administered.
75. Answer: E. B and D.
Explanation:
The rubber closure is never to be opened at any time. Drug solutions are removed by injecting a
need through the rubber closure at angle o f 90.
Asthma and Chronic Obstructive Pulmonary Disease
“Failure is the opportunity to begin again, more intelligently”
Henry Ford
1. Which o f the following statements is
FALSE about Asthma?
A. It is a chronic inflammatory disorder
o f the airways.
B. It is a syndrome which develops as a
result o f bacterial infection only.
C. It involves a complex interaction
between many cells and
inflammatory mediators.
D. It is characterized by obstruction
which may be partially or
completely reversible after
treatment
E. None
2. Classification o f asthma based on
severity plays an important role in
determining the most appropriate
pharmacotherapeutic approach and is
determined by:
A. Symptoms
B. Treatment requirements
C. Objective measurement o f lung
function
D. All o f the above
E. A and B only
3. One o f the following symptoms
classifies asthma as Mild intermittent
A. The symptoms occur more than two
times a week but not every day;
exacerbations may affect activity.
B. Daily symptoms; daily use o f
inhaled short-acting (3-agonist;
exacerbations affect activity;
exacerbations more than 2 times a
week and may last days.
C. Symptoms occur less than 2 times a
week; asymptomatic between
exacerbations; exacerbations brief
from a few hours to a few days.
D. Continual symptoms, limited
physical activity and frequent
exacerbations.
4. Asthmatic reactions to drugs may occur
due to:
A. Hypersensitivity
B. As an extension o f the
pharmacological effect.
C. Administration o f a drug to induce
asthmatic syndromes.
D. All o f the above
E. A and B only
5. All o f the following drugs are
implicated in induction o f asthmatic
syndrome EXCEPT:
A.
B.
C.
D.
E.
Aspirin
Ibuprofen
Bethanechol
Ephedrine
None
6. All o f the following characteristics have
been identified on postmortem examination
o f patients with asthma EXCEPT:
A. Hypertrophy o f smooth muscle
B. Vasoconstriction o f the vasculature
C. Collagen deposition in basement
membranes
D. Airway containing plugs consisting
o f inflammatory cells and their
debris . proteins, and mucus.
E. Denuded airway epithelium
7. Which o f the following cells are
involved in secretion o f inflammatory
mediators and influences the airways in
asthmatic conditions?
A.
B.
C.
D.
E.
F.
Mast cells
Eosinophils
Erythrocytes
Reticulocytes
A and B
C and D
8. Which o f the following are causes o f
airway obstruction in asthmatic patients?
A. Bronchoconstriction
B. Air wall edema
C. Mucus plug formation
D. AH o f the above
E. B and C only
9. In asthma, Airway inflammation
contributes to the development of:
A.
B.
C.
D.
E.
Airway widening
Air way hyper-responsiveness
Respiratory symptoms
All o f the above
B and C only
10. Air way remodeling is a condition
which may lead to airway obstruction in
asthma. Which o f the following statements
best describes airway remodeling?
A. It is a condition which occurs due to
inflammation and is characterized
by subbasement collagen deposition
and fibrosis
B. It is bronchoconstriction which
occurs due to increase o f
parasympathetic receptors in the
airways.
C. It is congenital narrowing o f the
airways.
D. It is hypersensitivity which occurs
in patients taking antiasthmatic
drugs.
E. None
11. In the triggering stage o f asthma, after
exposure to an allergic trigger the antigen
binds to:
A.
B.
C.
D.
E.
IgM
IgG
IgE
IgA
IgD
12. Which of the following statements is
NOT TRUE?
A. The early asthmatic response can be
blocked by the administration o f pagonist.
B. The early asthmatic response begins
within 30 minutes o f trigger
exposure.
C. The late asthmatic response is
characterized by persistent airflow
obstruction, airway inflammation,
and bronchial hyperresponsivness.
D. The late asthmatic response does not
respond to administration of
corticosteroids.
E. None
13. Which one o f the following anti­
inflammatory drugs is used in blocking
asthmatic response?
A. Aspirin
B. Ibuprofen
C. Naproxen
D. Cromolyn sodium
E. None
14.The main event(s) in asthma include
A. Triggering
B. Signaling
C. Migration
D. Cel] activation
E. All o f the above
15. All of the following are signaling
chemicals released by signaling cells which
attract additional inflammatory cells to the
airways EXCEPT:
A. Cytokines
B. Eicosanoids
C. Corticosteroids
D. Leukotrienes
E. Chemokines
16. In the migration phase o f an asthmatic
attack, in addition to the migration o f
inflammatory cells, cells in the circulation
are attracted to the airways by:
A. Erythrocytes
B. Adhesion molecules
C. Antibodies
D. Enzymes
E. None
17. Which o f the following chemical signals
appears to be the most important in the cell
activation phase o f asthma?
A.
B.
C.
D.
E.
Chemokines
Eicosanoids
Cytokines
Leukotrienes
None
18. In asthmatic conditions leukotrienes
appear to be important in the development
of:
A. Bronchoconstriction
B. Decreased mucus production
C. Increased vascular permeability
D. All o f the above
E. A and C only
19. All o f the following are common
findings in acute exacerbations o f asthma
EXCEPT:
A. Shortness o f breath
B. Wheezing
C. Bradycardia
D. Cough
E. Chest tightness
20. The symptoms o f severe asthma include
A. Respiratory distress at rest and
marked wheezing
B. Marked respiratory distress, loud
wheezing, coughing, difficulty
speaking, accessory chest muscle
use, and chest hyperinflation
C. Severe respiratory distress,
confusion, lethargy, cyanosis and
disappearance o f breath sounds.
D. Mild dyspnea and wheezing
E. None o f the above
21 .In which o f the following stages o f an
acute asthmatic attack, arterial pH may be
increased?
A. Mild
B. Moderate
C. Severe
D. Respiratory failure
E. A and B
22. Which o f the following pulmonary
function test parameters are increased
during an acute exacerbation o f asthmatic?
A. Forced expiratory volume in 1
second
B. Forced vital capacity
C. Residual volume
D. Total lung capacity
E. C and D
23. Which o f the following statements is
FALSE about peak expiratory flow rate?
A. It correlates well with forced expiratory
volume in 1 second (FEV1).
B. It is used in assessment o f therapy,
trigger identification and assessment o f
the need for referral to emergency care.
C. It is used in making the diagnosis of
asthma.
D. Its monitoring is recommended for
patients who have had severe
exacerbations.
E. FEFR is best measured in early
morning, before medication
administration
24.Airway hyper responsiveness and less
than adequate asthma control is inferred if
the diurnal variation in PEFR measurement
is greater than.
A.
B.
C.
D.
E.
15%
10%
100%
20%
None
25. Which o f the following instruments is
used in assessing the degree o f hypoxemia
during an acute exacerbation o f asthma?
A. Sphygmanometer
B. Viscometer
C. Osmometer
D. Oximeter
E. None
26.Electrocardiogram may be used as a
diagnostic test in asthma. In asthma an
electrocardiogram may show:
A. Sinus tachycardia
B. A trio-ventricular block
C. Sinus Bradycardia
D. Tachyarrthymias
E. None
27. All o f the following are signs of
respiratory distress (in asthma) EXCEPT:
A. Declining mental status
B. Inability to speak
C. Cyanosis
D. Peak expiratory flow rate more than
90%.
E. Absence o f respiratory sounds
28. The goals in the treatment o f asthma
include:
A. Minimal or no chronic symptoms day
or night
B. No limitations o f activities
C. Minimal or no exacerbations
D. Minimal or no adverse effects from
medications.
E. All o f the above
29. Which o f the following statements is
NOT TRUE about the stepped approach in
the management o f asthma?
A. In the step-down approach the
therapy starts one step above the
patient’s assessed asthma severity to
give rapid disease control.
B. In the step-down approach the
therapy starts one step below the
patient’s assessed asthma severity to
give rapid disease control.
C. In the step-up approach the therapy
begins with a treatment regimen at
the same step as the patient's asthma
severity to give rapid disease
control.
D. The more aggressive step-down
approach is advocated by experts.
E. A&C
30. Which o f the following statements is
FALSE about prevention and treatment of
exercise induced bronchospasm in ,
asthmatic patients?
A. Patients should be advised that a
warm-up period might be helpful in
preventing exercise induced
bronchospasm.
B. Exercise induced bronchospasm can
be prevented by administration o f a
short acting P-agonist 15 minutes
before exercise.
C. Cromolyn sodium has been shown to
be ineffective in the management o f
exercise induced bronchospasm.
D. Regardless o f the prophylactic
approach, all patients who
experience exercise induced
bronchospasm should have a short-
acting p-agonist available for
treatment o f breakthrough
symptoms.
E. None
31. Some diseases frequently co-exist with
asthma .Which o f the following diseases
may lead to improved control o f asthma if
they are adequately controlled?
A .Allergic rhinitis
B. Sinusitis
C. Gastro-esophageal reflux disease
D. All o f the above
E. A and B only
32.Condition(s) for which Long acting P~
agonists are indicated is(are):
A. In the prophylaxis o f exercise
induced bronchospasm.
B. In patients with chronic obstructive
pulmonary disease.
C. Maintenance treatment o f moderate
persistent asthma in combination
with corticosteroids.
D. Maintenance treatment o f severe
persistent asthma in combination
with corticosteroids.
E. All o f the above
33. All o f the following are effects o f
stimulation o f p2receptors EXCEPT:
A. Insulin secretion
B. Tremor
C. Glycolysis
D. Activation o f Na+ , K+ -adenosine
triphosphate (ATPase)
E. Gluconeogenesis
34. Which o f the following statements is
NOT TRUE about long acting p-agonists?
A. Systemic administration o f these
agents should be reserved for
patients who cannot use inhalation
therapy.
B. When prescribed with other inhaled
agents, they are usually
administered first.
C. Regimens with long-acting agents
should also include a concurrent
inhaled corticosteroid
D. All regimens containing long-acting
agents should also include a shortacting agent for treatment o f acute
symptoms.
E. They should only be used in
combination with a corticosteroid in
the prevention o f exercise induced
bronchospasm.
35. Which o f the following p-agonists is
associated with induction o f myocardial
ischemia, myocardial necrosis, and
arrhythmias because o f excessive cardiac
stimulation?
A. Albuterol
B. Isoproterenol
C. Bitolterol
D. Pirbuterol
E. None
-
36.Tachyphylaxis can occur with regular
use o f inhaled or oral p-agonists. The
possible mechanisms o f this are:
A. A decrease in the number o f P­
receptors due to movement o f
receptors from the cell surface into
the cell.
B. A decreased sensitivity in the p­
receptors to stimuli, making them
unable to activate adenyl cyclase.
C. An increase in the number o f p­
receptors.
D. An increased sensitivity in the P­
receptors to stimuli.
E. A and B
37. Levoalbuterol HC1 is comprised of:
A. The R-isomer
B. The S-isomer
C. Racemic mixture
C. A and B
D. None
38. Which o f the following statements is
FALSE?
A. If the dose o f Levoalbuterol is
increased to 1.25 mg, the incidence
of adverse reactions is similar to the
corresponding dose o f albuterol.
B. Concomitant use o f systemic 13agonists with monoamine oxidase
inhibitors, tricyclic antidepressants,
or methyldopa may lead to severe
hypotension.
C. P-agonists should not be combined
with other sympathomimetic agents
because of the additive
cardiovascular effects.
D. Systemic adverse reactions when the
recommended starting dose o f
Levoalbuterol is used appear to be
similar to or slightly less frequent
than the effects o f albuterol.
E. None
39. All o f the following are clinical effects
o f corticosteroids EXCEPT:
A. Reduced production o f inflammatory
mediators.
B. Enhanced p-adrenergic receptor
expression.
C. Increased mucus production
D. Prevention of endothelial and
vascular leakage.
E. Decreased mucus production
40. The mechanism(s) by which
Corticosteroids reduce inflammation
include:
I. Inhibition o f transcription genes of
inflammatory genes.
II. Inhibition o f release o f inflammatory
genes.
III. Increased transcription o f anti­
inflammatory genes.
A.
B.
C.
D.
E.
if I only is correct
if III only is correct
i f l & II are correct
if II&III are correct
if 1,11, and III are correct
41 . Which o f the following are desirable
characteristics o f systemic corticosteroids
for the treatment o f asthma?
I. Good glucorticoid activity
II. Minimal mineralocorticoid activity
III. Minimal glucorticoid activity
A.
B.
C.
D.
E.
i f l only is correct
if III only is correct
if I & II are correct
if II&III are correct
if I,II, and III are correct
42. Which o f the following statements is
NOT TRUE?
A. Intravenous corticosteroids are
administered to patients who are
unable to take oral medications.
B. Intravenous corticosteroids are the
first line treatments in all asthmatic
conditions.
C. Oral corticosteroids are acceptable
as emergency treatment if the
patient can tolerate the oral route
and is not believed to be in
imminent danger o f respiratory
arrest.
D. There is no significant difference in
the clinical efficacy o f the
corticosteroid agents currently
available.
E. None
43. Which o f the following are the most
frequently used oral corticosteroids in the
treatment o f asthma?
A.
B.
C.
D.
E.
Beclomethasone
Budesonide
Prednisone
Prednisolone
C and D
44. Inhaled corticosteroids should be used
for chronic treatment o f asthma whenever
possible because:
A. They are less likely to produce
adverse reactions.
B. They are more effective than oral
corticosteroids in all conditions.
C. They are less effective than other
oral corticosteroids.
D. Their action is systemic.
E. None
45. Careful monitoring is required when
systemic corticosteroids are given to
patients with:
A.
B.
C.
D.
E.
Heart failure
Peptic ulcer disease
Immunosuppressi on
Osteoporosis
All o f the above
46.The inhaled corticosteroid associated
with short-term growth suppression o f
approximately 1 cm in the first year o f its
use is:
A.
B.
C.
D.
E.
Beclomethasone
Fluticasone
Flunisolide
Budesonide
None
47. Patients taking inhaled corticosteroids
should gargle, rinse their mouth, and
expectorate after administration. These are
helpful for:
A. minimizing orpharyngeal drug
deposition
B. minimize local adverse reactions
C. minimize gastrointestinal absorption
D. All o f the above
E. A and B only
48. AH o f the following result in a
decreased plasma concentration o f
corticosteroids if they are concurrently
taken EXCEPT:
I. Rifampicin
II. Hydantoins
III.Cyclosporine
A. if I only is correct
B. if III only is correct
C. if I & II are correct
D. if II&III are correct
E. if I,II, and III are correct
49. Which o f the following antibiotics
decrease the clearance o f corticosteroids?
A.
B.
C.
D.
E.
F.
Erythromycin
Clarithromycin
Ampicillin
Amoxicillin
A and B
C and D
50.Concurrent Administration o f
corticosteroids with the following drugs
results in an enhanced Hypokalemia:
I. Thiazides
II. Furosemide
III. Amphotericin
A.
B.
C.
D.
E.
i f l only is correct
if III only is correct
if I & II are correct
if II&III are correct
if 1,11, and III are correct
51 .All o f the following are Leukotriene
receptor antagonists EXCEPT:
L Montelukast
II. Zafirlukast
III. Zileuton
A.
B.
C.
D.
E.
if l only is correct
if III only is correct
i f l & II are correct
if II&III are correct
if I,II, and III are correct
52. Which o f the following statements is
FALSE about Leukotriene antagonists?
I. they have anti-inflammatory activity
II. they have bronchodilator activity
III. they are more effective than inhaled
corticosteroids
A.
B.
C.
D.
E.
i f l only is correct
if 111 only is correct
if I & II are correct
if II&III are correct
if 1,11, and III are correct
53.A serious adverse effect o f Leukotriene
antagonists which occurred in patients
whose chronic steroid regimens is tampered
and discontinued is:
A.
B.
C.
D.
E.
Headache
Dizziness
Eosinophilic vasculitis
Dyspepsia
None
54 .All o f the following drugs decrease
zafirlukast blood concentrations EXCEPT:
A.
B.
C.
D.
E.
Erythromycin
Aspirin
Theophylline
Terfenadine
None
55.Zileuton is inhibitor o f the enzyme
lipoxygenase, thereby inhibiting the
synthesis of:
A.
B.
C.
D.
E.
Prostaglandins
Histamines
Thyroxine
Leukotrienes
None
56.Zileuton increases plasma
concentrations of:
A.Propranolol
B.Terfenadine
C.Theophylline
D.
All o f the above
E. None o f the above
57. Which o f the following statements
is(are) TR U Eabout cromolyn sodium and
nedocromil sodium?
A. They are nonsteroidal anti­
inflammatory drugs.
B. They are less effective in their anti­
inflammatory effects than inhaled
corticosteroids.
C. They are frequently used in children
because they have excellent safety
profile.
D. They prevent asthma induced by
exercise, cold air and sulfur dioxide
when used prophylactically.
E. All o f the above
58.The mechanism o f action o f anti­
inflammatory effects o f Cromolyn sodium
and nedocromil sodium is:
A. They stimulate in vivo synthesis o f
anti- inflammatory steroids.
B. They stabilize mast cells and
thereby inhibit mast cell
degranulation.
C. They inhibit Leukotriene synthesis
D. They antagonize the action o f
Leukotrienes at the receptor level.
E. None
59. In which o f the following conditions are
cromolyn sodium and nedocromil sodium
not effective?
A.
B.
C.
D.
E.
Treatment o f Acute asthma
exacerbation
Maintenance therapy for asthma
Prophylactically for the prevention
o f asthma induced by cold air or
exercise.
Prevention o f exercise induced
bronchospasm.
None
60. Which one o f the following statements
is FALSE about theophylline and its
compounds?
A. Theophylline compounds may be
considered if P-agonists and
corticosteroids fail to control an
acute asthma exacerbation.
B. Theophylline is an alternative to
long-acting P-agonists in the
treatment o f persistent asthma.
C. p-agonists produce bronchodilation
to a lesser extent than theophylline
compounds.
D. Theophylline is most beneficial as
an adjuvant to inhaled
corticosteroids in patients with
nocturnal or early morning
symptoms.
E. None
61 .All o f the following are true about the
suggested mechanisms o f action o f
theophylline EXCEPT:
A. Alteration o f intracellular calcium
B. Increased binding of cAMP to its
binding protein.
C. Adenosine antagonism
D. Decreased circulating
E. Inhibition o f production of
contractile prostaglandins
62. Which o f the following Theophylline
containing products has the highest
theophylline content?
A.
B.
C.
D.
E.
Oxtriphylline
Aminophylline anhydrous
Aminophylline hydrous
Theophylline anhydrous
None
63.All the following drugs increase the
clearance o f theophylline EXCEPT:
A.
B.
C.
D.
E.
Carbamazepine
Phenobarbital
Cimetidine
Rifampin
Phenytoin
64. Which o f the following factors increase
the clearance o f theophylline?
A.
B.
C.
D.
E.
Smoking
High protein diet
High carbohydrate diet
Old age
A and B
65. Which o f the following statements is
NOT TRUE about ipratropium bromide?
A. it is particularly useful in older
asthmatic patients and patients with
coexisting chronic obstructive
pulmonary disease.
B. It is recommended for use in
combination with p-agonists for the
treatment o f severe acute asthma
exacerbation.
C. It is highly recommended in the
chronic management o f asthma.
D. It is an alternative bronchodilator in
some patients who can not tolerate paeonists.
Asthm a and Chronic Obstructive Pulmonary D isease
C. Reduced PaC 02
D. Peak expiratory flow rate less than
C. It is chronic inflammation o f the air
ways especially, the bronchiole.
E. None
C. Triamcinolone
D. Budesonide
E. None
66. Chemically ipratropium bromide is a:
A.
B.
C.
D.
E.
Quaternary ammonium compound.
Tertiary amine
Cyclic amine
Primary amine
None
67. Which o f the following therapies may
precipitate bronchospasm when used in the
treatment o f asthma?
A.
B.
C.
D.
E.
Anti-histamine therapy
Antibiotic therapy
Immunotherapy
Mucolytic therapy
None
68. Which o f the following statements is
FALSE about metered dose inhalers in the
management o f asthma?
A. Their efficacy is similar to that of
nebulizers when administered with
good technique and a spacer.
B. They can be administered to patients
on mechanical ventilation with the
use o f a spacer designed for
mechanical ventilator circuit.
C. The dose of a drug administered with
a metered dose inhaler and a spacer is
larger than that administered by
nebulizers.
D. For small children to be able to use
metered dose inhaler properly, a
spacer with a face mask should be
used.
E. None
69.An inhaled corticosteroid available in
metered dose inhaler that comes with a
spacer is:
A. Flunisolide
B. Fluticasone
70.All o f the following are disadvantages
o f nebulizers in the management o f asthma
EXCEPT:
A.
B.
C.
D.
they are expensive
Longer administration time
Size o f the device
Drug delivery inconsistency between
devices
E. They are cheaper
71 .Which o f the following statements is
FALSE about dry powder inhalers?
A. They are used more frequently
because many patients find them
easier to use than an MDI.
B. Spacers are used with dry powder
inhalers.
C. The patients taking dry powder
inhalers are advised to inhale the
powder rapidly as opposed to slow
inhalation required for MDI
administration.
D. Patients should be advised to keep
dry powder inhalers away from
moisture
E. Avoid exhaling into the mouth piece
before inhalation
72. Heliox is a mixture o f oxygen and:
A.
B.
C.
D.
E.
Hydrogen
Helium
Nitrogen
Holmium
None
73. All o f the following may occur in status
asthmaticus EXCEPT:
A. Altered consciousness
B. Cyanosis
C. Reduced PaC 02
D. Peak expiratory flow rate less than
1OOL/min
E. FEV1 less than 1 liter
74. Accumulation o f air in the pleural spice,
as some times occurs during an acute
asthmatic attack is a condition common
referred to as
A.
B.
C.
D.
E.
Pneumonia
Pneumothorax
Status asthmaticus
Pneumonitis
None
75. Which o f the following statements!
FALSE about atelectasis?
A. It is also known as collapsed liir g
B. Gas exchange is inhibited durii);
respiration
C. It may occur as a result o f airwa
obstruction.
D. In asthmatics it only involves th(e
left middle lobe o f the lungs.
E. In asthmatics it usually involve^ the
right middle lobe o f the lungs
76. Which o f the following is a correct
definition o f chronic obstructive pulmc nary
disease by American thoracic society?
A. It is a disease state characterized by
airflow limitation that is not ful y
reversible. The air flow limitation is
usually both progressive and
associated with an abnormal
inflammatory response o f the lifngs
to noxious particles or gases.
B. It is a disease state characterized by
airflow limitation due to chroni
bronchitis or emphysema; the
airflow obstruction is generally
progressive, may be accompan ed
by airway hyperactivity and m: ,y be
partially reversible.
C. It is chronic inflammation of the air
ways especially, the bronchioles.
The airflow to the lungs is not
affected.
D. It is a transient blockade o f the
airways which occurs due to
bacterial infection.
E. None
77.The two major forms o f chronic
obstructive pulmonary disease (COPD) are:
A.
B.
C.
D.
E.
Chronic bronchitis
Emphysema
Asthma
Allergic rhinitis
A and B
78.
Smoking may lead to chronic
obstructive pulmonary disease because it
prevents a r antitrypsin from binding with
and inactivating the enzyme:
A.
B.
C.
D.
E.
Elastase
Lactase
Dipeptidase
Aminotransferase
None
79. In chronic bronchitis respiratory tissue
inflammation results in vasodilatation,
congestion, mucosal edema, and goblet cell
hypertrophy. These events trigger goblet
cells to produce excessive amounts of:
A.
B.
C.
D.
E.
antibodies
mucus
elastase
oxygen
None
80. Which o f the following organisms
normally colonize sterile airways
A.
B.
C.
D.
Streptococcus pneumoniae
Hemophilus influenzae
Staphylococcus aureus
Pseudomonas aeruginosa
E. All o f the above
81 .All o f the following statements are
TRUE about the events that occur in
chronic bronchitis EXCEPT:
A. Cartilage atrophy, infiltration of
neutrophils and other cells, and
impairment o f cilia.
B. Decrease in P aC 0 2
C. The air ways degenerate and overall
gas exchange is impaired.
D. The cilia are impaired.
E. Airways are blocked by thick mucus
82. Which o f the following characteristics
are common to both chronic bronchitis and
emphysema?
A.
B.
C.
D.
E.
Inflammation
Excessive mucus secretion
Hypercapnia
Respiratory acidosis
A and B
83. Which o f the following types of
emphysema is associated with a r
antitrypsin (AAT) deficiency?
A.
B.
C.
D.
E.
Panlobular emphysema
Centrilobular emphysema
Paraseptal emphysema
Mixed emphysema
None
84. Which o f the following damages are
likely to be present in emphysema which
occurs due to smoking?
A. A destruction which involves all
lung segments
B. A central destruction selectively
involving respiratory bronchioles.
C. The lung periphery adjacent to
fibrotic regions is the site o f alveok r
distention and alveolar wall
destruction.
D. A destruction o f the nasopharyngeal
wall.
E. None
85. In chronic bronchitis productive cough
occurs due to:
A. Blockade o f the airways by thick
mucus secretions.
B. Infiltration o f neutrophils and other
cells to inflamed areas.
C. Relaxation o f smooth muscles in the
airways.
D. Hypoxemia
E. None
86.The term” blue bloater” is frequently
used to describe patients with chronic
bronchitis because:
A. Their sputum is blue colored.
B. They tend to develop cyanosis
C. The radiographic examination o f
their chest shows blue spots
D. The exhaled air is blue.
E. None
87.
Which o f the following pulmonary
function test parameters are decreased in
chronic bronchitis?
A. Vital capacity
B. Residua! volume
C. Forced expiratory volume in 1
second
D. Total lung capacity
E. A and C
88.In chronic bronchitis the number o f
some blood cells may increase. Which of
the following blood cells may increase in
response to hypoxemia?
A.
B.
C.
D.
E.
Neutrophils
Erythrocytes
WBC
Platelets
None
89.Which o f the following pulmonary
function parameters is reduced in both
chronic bronchitis and emphysema?
Residual volume
Total lung capacity
Vital capacity
Forced expiratory volume in 1
second
E. None
A.
B.
C.
D.
90.Treatment objectives endorsed by
GOLD (global initiative for chronic
obstructive lung disease) for the treatment
ofC O PD include:
A. Prevent disease progression.
B. Relieve symptoms and improve
exercise tolerance.
C. Prevent and treat exacerbations.
D. All o f the above
E. A and B only
93. Which o f the following statements is
NOT TRUE about the dosage and
administration o f anticholinergics in the
treatment o f COPD?
A. The dose o f glycopyrrolate is 1-2
mg every 8 hours.(it can be
nebulized in combination with pagonists)
B. An MDI dose o f 40pg o f
Ipratropium bromide four times
daily results in severe systemic
adverse effects.
C. Tiotropium bromide capsules
contain 22.5 pg Tiotropium bromide
monohydrate equivalent to 18 pg
Tiotropium.
D. Ipratropium should be administered
regularly because o f a slower onset
and longer duration o f action.
E. None
94. Which o f the following statements is
FALSE about the use o f p-agonists in the
91.
The most commonly used agents in the management o f COPD?
treatment o f COPD are:
A. They are administered via inhalation
A. Methyl-xanthines
B. p-agonists o f the same duration
B . Corticosteroids
should not be used in combination
C. Anticholinergics
because an adequate dose o f a single
D. p-agonists
agent provides peak
E. C and D
bronchodilation.
C. Long acting P-agonists are
92. Which o f the following statements is
recommended for rescue therapy.
WRONG?
D. Long acting P-agonists may be used
as first-line bronchodilators in the
A. Anticholinergics may be used as
maintenance therapy o f COPD.
first-line bronchodilators or in
E. None o f the above
conjunction with p-agonists in the
treatment o f COPD.
B. Atropine is more potent and has
95. Which one o f the following p-agonists
fewer side effects than ipratropium.
has the shortest duration o f action?
C. Ipratropium bromide and tiotropium
bromide reduce sputum volume.
D. Anticholinergics produce
A. Formoterol
bronchodilation by competitively
B. Salmeterol
inhibiting cholinergic responses.
C. Pirbuterol
E. None o f the above
D. Terbutaline
E. None
96. Theophylline compounds are used in the
management o f COPD because:
I. they increase mucociliary clearance
II. they enhance diaphragmatic
contractility
III. they have potent bronchodilator
activity
A.
B.
C.
D.
E.
i f l only is correct
if III only is correct
if I & II are correct
if II&III are correct
if I,II, and III are correct
97.Serum theophylline levels should be
closely monitored in patients with
congestive heart failure because:
A. There is decreased metabolism of
theophylline in such patients.
B. Theophylline misguides the
diagnosis o f congestive heart
failure.
C. Theophylline worsens preexisting
congestive heart failure.
D. Theophylline leads to increased
levels o f drugs used in the treatment
o f congestive heart failure
E. None
98. Inhaled Corticosteroids which may be
used in the prolonged rrj^nagement o f
COPD should be symptomatic and they
should have a documented spirometric
response. The spirometric responses are:
A. Increase in FEVi o f at least 15 %
and 200mL after 6 weeks to 3
months o f use
B. Decease in FEVi o f at least 20 %
after 5 months o f use
C. A decrease in peak expiratory
volume o f at least 30 %
D. An increase in peak expiratory
volume o f at least 30 %
E. None
99. Antibiotics are used to treat
exacerbations with suspected infection as
evidenced by :
A.
B.
C.
D.
E.
Increase in volume o f sputum
Change in color o f sputum
Viscosity o f the sputum
All o f the above
A and B
100. Which o f the following statements
is WRONG about the use o f antibiotics in
the management o f COPD?
A. Prevention o f infection with chronic
antibiotic therapy is controversial
and should be considered only in
patients with multiple exacerbations
annually.
B. Ambulatory antibiotic treatment o f
exacerbations in patients with
COPD is recommended when there
is evidence o f worsening dyspnea
and cough with purulent sputum and
increased sputum volume.
C. Antibiotic treatment o f pneumonia
in hospitalized patients with COPD
includes either a second or third
generation cephalosporin.
D. Antibiotics may be used in the
management o f COPD even if the
only symptom is fever.
101. In patients with COPD if infection
with C.pneumoniae is suspected the drug o f
choice is:
A.
B.
C.
D.
E.
Doxycycline
Procaine penicillin
Streptomycin
Amikacin
None
102. The drugs o f choice for pneumonia
caused by M.pneumoniae or Legionella
pneumophilia in hospitalized patients with
COPD are:
A.Aminoglycoside antibiotics
B.Macrolide
antibiotics
C.Tetracyclines
D.
Aminopenicillins
E.None
103.
Infections (in patients with COPD)
caused by each o f the following organisms
require treatments for approximately 7-10
days EXCEPT:
A.
B.
C.
D.
E.
S.pneumoniae
H.influenzae
M.pneumoniae
M.catarrhal is
None
104. Which one o f the following drugs
allows shorter duration o f therapy for the
treatment o f infections in patients with
COPD?
A. Erythromycin
B. Ampicillin
C. Azithromycin
D. Clarithromycin
E. None
105. Which one o f the following drugs
may improve sputum clearance and disrupt
mucus plugs?
A. Iodinated glycerol
B. Guaifenesin
C. Potassium iodide
D. N-acetylcysteine
E. None
106. Which one o f the following
vaccines is recommended in COPD because
o f its ability to reduce death and serious
illness by almost 50%?
A.
B.
C.
D.
E.
Polyvalent pneumococcal vaccine
Tetanus immunoglobulin
Varicella zoster immunoglobulin
Influenzae virus vaccine
None
107.
Smoking cessation is one o f the
important nonpharmacological treatments
which improve COPD. All o f the following
are useful in smoking cessation EXCEPT:
A.
B.
C.
D.
E.
Nicotine gum
Patches
Buproprion
Inhaled corticosteroids
Clonidine
108. Chest physiotherapy has all o f the
following effects in patients with COPD
EXCEPT:
A.
B.
C.
D.
E.
Loosens mucus secretions.
Helps re-expand the lungs.
Increases the efficacy o f respiratory,
Has anti-bacterial effect.
None
Answers
Asthma and Chronic Obstructive Pulmonary Disease
1. Answer: B. It is a syndrome which develops as a result o f bacterial infection only
Explanation:
Asthma is a chronic inflammatory disorder o f the airways. It involves complex interactions
between many cells and inflammatory mediators that result in inflammation, obstruction (partially
or completely reversible after treatment or resolves spontaneously, and increased airway
responsiveness (i.e, hyperresponsivness).
2. Answer: D. All o f the above
Explanation:
An asthmatic patient’s severity classification plays an important role in determining the most
appropriate pharmacotherapeutic approach and is determined by:
-Treatment requirements
-Objective measurements o f lung function, including diurnal variations
- Symptoms, and
-Frequency o f nocturnal symptoms
3. Answers: C. Symptoms occur less than 2 times a week; asymptomatic between
exacerbations; exacerbations brief from a few hours to a few days
Explanation:
Choice A is classified as Mild persistent, choice B as Moderate persistent,choice C as Mild
interm ittent, and choice D as severe persistent.
4. Answer:
E. A and B only
Explanation:
Asthmatic reactions to drugs may occur due to hypersensitivity or as an extension o f the
pharmacological effect.
5. Answer: D. Ephedrine
Explanation:
Drugs implicated in asthma include:
Aspirin and other nonsteroidal anti-inflammatory drugs.
Anti-adrenergic and cholinergic drugs (e.g. p-adrenergic blockers , Bethanechol)
Medications (or foods) that contain tartrazine, sulfates, and other preservatives. Ephedrine, a
sympathomimetic is a drug used in the treatment o f nasal congestion. It will not induce asthma.
6. Answer: B. Vasoconstriction o f the vasculature
Explanation:
In postmortem examination o f asthmatic patients, all o f the above characteristics are identified
except choice B. Vasodilatation (rather than vasoconstriction) o f the vasculature is evident.
7. Answer: E. A and B
Explanation:
The involvement o f inflammatory cells is one o f the important contributory factors in the
pathophysiology o f asthma. The inflammatory cells include mast cells, Eosinophils, activated T
cells, macrophages, and epithelial cells.These inflammatory cells secrete mediators and influence
the airways directly or via neural mechanisms. Erythrocytcs and Reticulocytes are not
inflammatory' cells.
8. Answer: D. All o f the above
Explanation:
The airway obstruction in asthmatic patients is believed to be a result o f bronchoconstriction,
airway edema, mucus plug formation, smooth muscle hypertrophy, airway remodeling and
hyperplasia.
9. Answer: E. B and C only
Explanation:
In asthma airway inflammation is crucial to the development o f asthma and contributes to airway
hyperresponsivness, respiratory symptoms, airflow obstruction and disease chronicity.
10. Answer: A. It is a condition which occurs due to inflammation and is characterized by
subbasement collagen deposition and fibrosis
Explanation:
Air way remodeling is a structural change to the lung. It can result from persistent inflammation
when asthma is poorly controlled. The resulting damage can yield permanent airway
abnormalities because o f subbasement collagen deposition and fibrosis.
11 .Answer: C. IgE
Explanation:
After exposure to an allergic trigger, antigen binds to immunoglobulin E(IgE) which is attached
to activated mast cells.
12. Answer; D. The late asthmatic response does not respond to administration o f
corticosteroids
Explanation:
The late asthmatic response can be blocked by administration of corticosteroids or anti­
inflammatory agents such as cromolyn sodium or nedocromil.
13.Answer: D. Cromolyn sodium
Explanation:
Cromolyn sodium or nedocromil are used in blocking early and late asthmatic response.
14.
Answer: E. All o f the above
Explanation:
The five main events that occur in asthma are triggering, signaling, migration, cell activation,
tissue stimulation and damage.
15. Answer:
C. Corticosteroids
Explanation:
Corticosteroids are not signaling molecules. They have anti-inflammatory activity. Cytokines,
Eicosanoids, Leukotrienes and chemokines are chemical signals released by activated mast cells
and other signaling cells.
16.Answer: B. Adhesion molecules
Explanation:
In migration phase, an influx o f inflammatory cells (e.g. Eosinophils, lymphocytes,
monocytes* granulocytes. In addition to the migration o f these cells to the airway, up
regulation o f adhesion molecules begin. These adhesion molecules affix themselves to cells
in the circulation and attract these cells to the air ways.
17.Answer: D. Leukotrienes
Explanation:
Cell activation is required before cells can release inflammatory mediators. Once present in the
airways, Eosinophils are activated. Leukotrienes appear to be important in this cell activation.
18.
Answer: E. A and C only
Explanation:
Leukotrienes appear to be important in the development o f bronchoconstriction, increased mucus
production, increased vascular permeability, and hyperresponsivness.
19.Answer: C. Bradycardia
Explanation:
The cardiac effects o f acute asthmatic exacerbations include tachycardia and tachypnea. (Not
bradycardia)
20.Answers: B. Marked respiratory distress, loud wheezing, coughing, difficulty speaking,
accessory chest muscle use, and chest hyperinflation
Explanation:
Choice A are symptoms o f Moderate asthma,Choice B are symptoms o f severe asthma, Choice C
are symptoms o f respiratory failure,and choice D are symptoms o f mild asthma.
21 .Answer:
E. A and B
Explanation;
Arterial pH may increase in mild and moderate stages o f an acute asthmatic attack
22.Answer: E. C a n d D
Explanation:
Forced expiratory volume in 1 second (FEVi) is maximum volume o f air forcibly exhaled in 1
second (normal value o f 3.8 liters).
Forced vital capacity is the maximum volume o f air that can be forcefully exhaled after inhalation
to total lung capacity.
The volume o f air entering or leaving the lungs during a single breath is called tidal volume.
Residual volume is the volume o f air remaining in lungs at the end o f tidal volume
(Normal value o f 2.4 liters).
Total lung capacity is the volume o f air within both lungs at the end o f a maximal inhalation (6.0
liters).
Forced expiratory volume in 1 second (FEV}) and Forced vital capacity decrease while Residual
volume and total lung capacity may increase during acute asthmatic exacerbations.
23.
Answer:
C. It is used in making the diagnosis o f asthma
Explanation:
Peak expiratory flow rate is not used in the diagnosis o f asthma. All other choices are correct.
24.Answer: D. 20%
Explanation:
Diurnal variation o f greater than 20% in peak expiratory flow rate measured during the day
suggests airway hyperresponsivness.
25.Answer: D. Oximeter
Explanation:
Pulse Oximetry is a noninvasive means o f assessing the degree o f hypoxemia during an acute
exacerbation. The Oximeter measures oxygen saturation in arterial blood and pulse.
26.Answer: A. Sinus tachycardia
Explanation:
In asthmatic attacks, an Electrocardiogram may show sinus tachycardia. An ECG may be
particularly useful in an older patient.
27.
Answer: D. Peak expiratory flow rate more than 90%
Explanation:
The signs o f respiratory distress in asthma include use o f accessory muscles, Declining mental
status .Peak expiratory flow rate o f less than 50% ,Cyanosis, and absence o f respiratory sounds
28. Answer: E. All o f the above
Explanation:
The goal o f therapy in asthma is to provide symptomatic control with normalization o f lifestyle
and to return pulmonary function as close to normal as possible.
29. Answer: B. In the step-down approach the therapy starts one step below the patient’s
assessed asthma severity to give rapid disease control
Explanation:
A stepped approach based on severity o f disease is used to manage persistent asthma. Gaining
control o f asthma may be achieved with either a step-up or step-down approach (determined by
severity o f disease); however, the more aggressive step-down approach is advocated by experts.
The step-down approach starts with treatment one step above the patient’s assessed asthma
severity to give rapid disease control.
The step-up approach begins with treatment regimen at the same step as the patient’s severity.
30.Answer: C. Cromolyn sodium has been shown to be ineffective in the management of
exercise induced bronchospasm
Explanation:
Cromolyn sodium and nedocromil may be used to prevent exercise-induced bronchospasm and
exacerbations related to exposure to other asthma triggers. Cromolyn and nedocromil should be
administered no more than 1 hour before exercise or exposure.
31 .Answer: D. All o f the above
Explanation:
Allergic rhinitis, sinusitis, and Gastro-esophageal reflux disease frequently coexist with asthma.
Asthma control has been shown to improve if these conditions are adequately controlled.
32. Answer: E. All o f the above
Explanation:
Indications for long-acting p-agonists are:
-Maintenance treatment o f moderate and severe persistent asthma in combination with inhaled
corticosteroids, particularly for patients with frequent nocturnal symptoms.
-Prophylaxis o f exercise induced bronchospasm
-Patients with chronic obstructive pulmonary disease (COPD)
33.Answer: C. Glycolysis
Explanation
Stimulation o f p2receptors in skeletal muscle accounts for tremor, gluconeogenesis (synthesis of
glucose), insulin secretion, activation o fN a+, K+-adenosine triphosphate (ATPase).
Glycolysis is break down o f glucose. Glycolysis is not found in stimulation o f p2 receptors.
34.
Answer:
E. They should only be used in combination with a corticosteroid in the prevention
o f exercise induced bronchospasm
Explanation:
Long acting p-agonists can be used alone in the prevention o f exercise induced bronchospasm.
35.Answer: B. Isoproterenol
Explanation:
Nonselective p-agonists (e.g. Isoproterenol) may induce myocardial ischemia, myocardial
necrosis, and arrhythmias because o f excessive cardiac stimulation. Use o f p2-agonists (e.g.,
albuterol, Bitolterol, pirbuterol) is preferred.
36.Answer: E. A and B
Explanation:
Tachyphylaxis can occur with regular use o f inhaled or oral p-agonists. The possible mechanisms
include:
A decrease in the number o f active p-receptors due to movement o f receptors from the cell
surface into the cell.
A decreased sensitivity in the p-receptors, making them unable to activate adenyl cyclase.
37.
Answer: A. the R-isomer
Explanation:
Albuterol is a racemic mixture o f albuterol’s R- and S- isomers, but Levoalbuterol HC1 is
comprised o f R-isomer.
38. Answer:
B. Concomitant use o f systemic (3-agonists with monoamine oxidase inhibitors,
tricyclic antidepressants, or methyldopa may lead to severe hypotension
Explanation:
Concomitant use o f systemic p-agonists with monoamine oxidase inhibitors, tricyclic
antidepressants, or methyldopa may lead to severe hypertension.
39. Answer: C. Increased mucus production
Explanation:
Corticosteroids decrease the production of mucus.
40. Answer: E. if I,II, and III are correct
Explanation:
Increased proliferation o f inflammatory cells leads to worsen inflammation and corticosteroids do
not increase proliferation o f inflammatory cells.
Corticosteroids bind to glucocorticoid receptors on the cytoplasm. The activated receptor
regulates transcription o f target genes.
Corticosteroids reduce inflammation via:
-inhibition o f transcription and release o f inflammatory genes.
-increased transcription of anti-inflammatory genes that produce proteins that participate in or
suppress the inflammatory process.
41 .Answer: C. I & II are correct
Explanation:
Systemic corticosteroids for the treatment of asthma should have the following characteristics:
Good glucorticoid activity (good glucorticoid activity means better anti-inflammatory activity)
Minimal mineralocorticoid activity (mineralocorticoid activity results in an increase o f Na^
reabsorption and increased excretion o f K+and H+). Excessive mineralocorticoid activity causes
marked Na+ and water retention with resultant increase in the volume o f extra-cellular fluid,
Hypokalemia, alkalosis, and hypertension.
Short to moderate duration o f action.( short duration o f action is preferable in order to get faster
response action o f the drug)
42.Answer: B. Intravenous corticosteroids are the first line treatments in all asthmatic
conditions
Explanation:
There is no significant difference in the clinical efficacy of the corticosteroid agents currently
available. The route o f administration is determined by the condition o f the patient.
Intravenous corticosteroids are administered to patients who are unable to take oral medications.
They are also for patients believed to be impending respiratory arrest and for initial treatment o f
exacerbations that require ICU admission.
Oral corticosteroids are acceptable as emergency treatment if the patient can tolerate the oral
route and is not believed to be in imminent danger o f respiratory arrest.
43.Answer:
E. C and D
Explanation:
The most frequently used oral corticosteroids in the treatment o f asthma are prednisone and
Prednisolone. Becolmethasone and Budesonide are available as inhalations.
44. Answer: A. they are less likely to produce adverse reactions
Explanation:
Inhaled corticosteroids are least likely to produce adverse reactions, therefore the inhaled route
should be used whenever possible for chronic treatment. However, these inhaled corticosteroids
should not be used to treat acute exacerbations.
45.Answer:
E. All o f the above
Explanation:
Careful monitoring is necessary in patients with diabetes, hypertension, congestive heart failure(
they may result in sodium retention thus they may worsen the condition ) , peptic ulcer disease,
lmmunosuppression( because they have Immunosuppressive property),osteoporosis, chronic
infections, cataracts, glaucoma, myasthenia gravis , and psychiatric diseases (e.g. depression ,
psychosis ).
46.
Answer: D. Budesonide
Explanation:
Two major publications demonstrated short-term growth suppression o f approximately 1 cm in
the first year of Budesonide treatment, but without long-term effects on the final adult height. To
avoid this child should be treated with the lowest effective dose.
47. Answer: D. All of the above
Explanation:
Spacers should be prescribed for patients who receive moderate to high doses of inhaled
corticosteroids via metered-dose inhalers. Patients should also gargle, rinse their mouth and
throat, and expectorate after administration. Both o f these interventions minimize orpharyngeal
drug deposition, local adverse reactions, and gastrointestinal absorption.
48.Answer: B. Ill only is correct
Explanation:
Rifampicin, Hydantoins, and barbiturates induce hepatic microsomal enzymes resulting in
enhanced corticosteroid metabolism if they are given concurrently.
(The overall result is decreased plasma concentration)
Cyclosporine may increase the plasma concentration o f corticosteroids.
49.Answer: E. A and B
Explanation:
Concurrent use estrogens, oral contraceptives, ketoconazole, or macrolide antibiotics (e.g.
erythromycins, Clarithromycin,) may decrease corticosteroid clearance.
Ampicillin and amoxicillin have not been shown to decrease corticosteroid clearance.
50.Answer: E. 1,11, and III are correct
Explanation:
Administration o f potassium-depleting diuretics (e.g. thiazides, Furosemide) or other potassiumdepleting drugs (e.g. amphotericin) with corticosteroids causes enhanced Hypokalemia. Serum
potassium should be closely monitored, especially in patients on digitalis glycosides.
51 .Answer: C. I & II are correct
Explanation:
- Montelukast, zafirlukast and Pranlukast are Leukotriene receptor antagonists.
Zileuton is a lipoxygenase inhibitor.
52.Answer: C. I & II are correct
Explanation:
Leukotriene antagonists have anti-inflammatory and bronchodilator activity. They may allow
reduction in corticosteroid doses in some patients. Because they are less effective agents than
inhaled corticosteroids, they are considered second-line agents. They may be useful in patients
with concurrent allergic rhinitis.
53.Answer:
C. Eosinophilic vasculitis
Explanation:
Churg-strass syndrome is a form o f Eosinophilic vasculitis, which has been associated with
zafirlukast, Montelukast and Pranlukast. It has usually, but not always, occurred in patients whose
chronic steroid regimens were tampered and discontinued.
54.Answer:
Explanation:
B. Aspirin
Aspirin increases zafirlukast blood concentrations. Others decrease the zafirlukast concentrations.
55.Answer:
D. Leukotrienes
Explanation:
Zileuton is inhibitor o f the enzyme lipoxygenase, thereby inhibiting the synthesis o f leukotrienes.
56.Answer: D. All o f the above
Explanation:
Zileuton has not been shown to increase the plasma concentration o f propranolol,
terfenadine and theophylline.
57. Answer:
E. All o f the above
Explanation:
Cromolyn sodium and nedocromil sodium are nonsteroidal anti-inflammatory drugs. These
medications are less effective in their anti-inflammatory properties than the inhaled
corticosteroids; however, because o f their excellent safety profile, they are frequently used in
children. They prevent asthma induced by exercise, cold air and sulfur dioxide when used
prophylactically.
58.Answer: B. They stabilize mast cells and thereby inhibit mast cell degranulation
Explanation:
Cromolyn sodium and nedocromil sodium are believed to act locally by stabilizing mast cells and
thereby inhibiting mast cell degranulation. There is also evidence for inhibitory effects on
inflammatory cells such as macrophages, Eosinophils, neutrophils, monocytes, and platelets.
59.
Answer:A.
treatment o f acute asthma exacerbation
Explanation:
Cromolyn sodium and nedocromil sodium are not effective during an acute asthma exacerbation.
They should only for the prevention o f persistent asthma or prevention o f exercise induced
bronchospasm.
60.Answer:
compounds
C. P-agonists produce bronchodilation to a lesser extent than theophylline
Explanation:
Theophylline compounds produce bronchodilation to a lesser extent than p-agonists.
61 .Answer:
D. Decreased circulating catecholamines
Explanation:
The suggested mechanism o f action o f theophylline is that it results in increased circulating
catecholamines.
62.Answer:
D. Theophylline anhydrous
Explanation:
The theophylline content o f Theophylline containing products is given below Oxtriphylline (64%)
Aminophylline anhydrous (86%)
Aminophylline hydrous (79%)
Theophylline anhydrous (100%)
63.Answer:
C. Cimetidine
Explanation:
The drugs which increase the clearance o f theophylline (resulting in a decrease o f blood levels)
include: Carbamazepine, Phenobarbital, phenytoin and Rifampin.
The drugs which decrease the clearance o f theophylline (increase the blood level) include
Allopurinol, p-blockers, calcium-channel blockers, cimetidine, clindamycin, fluoroquinolones,
macrolides, oral contraceptives, ticlopidine and zafirlukast?influenza virus vaccine.
64. Answer:
E. A and B
Explanation:
Smoking and high-protein diet are likely to increase theophylline clearance.
It is expected that old age and high-carbohydrate diet decrease the clearance o f theophylline.
Other factors that decrease theophylline clearance are Cor pulmonale, congestive heart failure,
fever/viral illness, liver dysfunction.
65. Answer:
C. It is highly recommended in the chronic management o f asthma
Explanation:
The benefits o f ipratropium bromide in the chronic management o f asthma have not been
established. The other statements are true.
66.Answer:
A. Quaternary ammonium compound
Explanation:
Chemically ipratropium bromide is a quaternary ammonium compound.
hoch
2
HO
C H C H 2 N H C {€H 3)3
OH
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More info:
Quaternary ammonium compounds are salts o f quaternary ammonium cations with an anion.
They are used as disinfectants, surfactants, and fabric softeners.
67. Answer:
D. Mucolytic therapy
Explanation:
Mucus may contribute to airway obstruction in asthma. However, because mucolytics may
precipitate bronchospasm, they should not be used for the treatment o f patients with asthma.
Anti-histamines are useful for asthmatic patients with co-existing allergic rhinitis; however, their
role in the treatment o f asthma remains unclear. Antihistamines compete with histamine for
histamine-receptor sites on effector cells; thus, help prevent the histamine-mediated responses
that influence asthma.
Antibiotics are not used for the treatment o f asthma; however, research is under way to determine
the role o f infection in asthma pathogenesis.
Immunotherapy improves asthma control in some patients and is ineffective in others.
A recent meta-analysis demonstrated that immunotherapy may improve lung function, reduce
symptoms, and decrease medication requirements in a significant number o f patients.
68. Answer: C. The dose o f a drug administered with a metered dose inhaler and a spacer is
larger than that administered by nebulizers.
Spacer
Inhaler
Explanation:
When administered with a good technique and a spacer, the efficacy o f metered dose inhalers is
similar to that o f nebulizers, despite the lower doses administered with an MDI and a spacer.
N e b u lizer
tu b in g
69.Answer: C. Triamcinolone
Explanation:
The only metered dose inhaler that comes with a built-in spacer is the azmacort (triamcinolone)
inhaler.
70.Answer:
E. They are cheaper
Explanation:
Disadvantages o f nebulizers include cost, preparation, and administration time, drug delivery
inconsistencies between devices, and size o f the device.
71 .Answer: B. Spacers are used with dry powder inhalers.
Explanation:
Spacers are not used with dry powder inhalers. The dose is loaded into the delivery chamber and
inhaled by close mouth technique. Except the choice (B), all other choices in this question are
true.
72.Answer:
B. Helium
Explanation:
Heliox is a mixture o f oxygen and helium.
73.Answer: C. Reduced P aC 0 2
Explanation:
The findings in status asthmaticus include altered consciousness,
cyanosis (even with oxygen therapy), elevated PaC 02 PEFR less than 1OOL/min in adults, and
FEV i less than 1 L.
74.Answer:
B. Pneumothorax
Explanation:
During an acute asthmatic attack some times accumulation o f air in the pleural space occurs. This
condition is referred to as Pneumothorax .
The symptoms o f Pneumothorax may include sudden pleuritic chest pain, dyspnea, hacking
cough and anxiety.
75.
Answer:
D. In asthmatics it only involves the left middle lobe of the lungs
Explanation:
Atelectasis or collapsed lung inhibits the gas exchange during respiration and may occur as a
result o f airway obstruction. In asthmatics, Atelectasis usually involves the collapse o f right
middle lobe, but some times affects the entire lung.
The symptoms o f Atelectasis include dyspnea and anxiety.
76. Answer:
B. It is a disease state characterized by airflow limitation due to chronic
bronchitis or emphysema; the airflow obstruction is generally progressive may be accompanied
by airway hyperactivity and may be partially reversible
Explanation:
The national heart, lung and blood institute/world health organization global initiative for chronic
lung disease definition o f chronic obstructive pulmonary disease is “ a disease state characterized
by airflow limitation that is not fully reversible. The air flow limitation is usually both
progressive and associated with an abnormal inflammatory response o f the lungs to noxious
particles or gases.”
The American thoracic society definition is “a disease state characterized by airflow limitation
due to chronic bronchitis or emphysema; the airflow obstruction is generally progressive, may be
accompanied by airway hyperactivity and may be partially reversible.
77.Answer:
E. A and B
Explanation:
The two major forms o f chronic obstructive pulmonary disease (COPD) are chronic bronchitis
and Emphysema. These two coexist very frequently.
78.Answer: A. Elastase
Explanation:
Cigarette smoking is the primary etiologic factor for the development o f chronic obstructive
pulmonary disease.
There is also increased risk o f COPD in people who have di-antitrypsin (AAT) deficiency. One
in three people with genetic AAT deficiency develop emphysema, usually as young adults. AAT
is a serine protease inhibitor, and it is also an acute-phase reactive protein. The major
physiological function of AAT is inhibition of neutrophil elastase.
79.Answer:
B. mucus
Explanation:
Respiratory tissue inflammation in chronic bronchitis results in vasodilatation, congestion,
mucosal edema, and goblet cell hypertrophy. These events trigger goblet cells to produce
excessive amounts o f mucus.
80.
Answer:E.Allo f
the above
Explanation:
Normally sterile airways become colonized with Streptococcus pneumoniae, Hemophilus
influenzae, Staphylococcus aureus, Pseudomonas aeruginosa species and Moraxella catarrhal is.
81 .Answer:
B. Decrease in PaC 02
Explanation:
In chronic obstructive pulmonary disease the hypoxemia results in increased carbon dioxide
tension (i.e. increasing P aC 02).0 th er choices are true.
82.Answer:
E.A and B
Explanation:
In both chronic bronchitis and emphysema there is inflammation and excessive mucus
secretion.
In chronic bronchitis hypercapnia (i.e. increasing P aC 0 2) is common but in emphysema
hypercapnia and respiratory acidosis are uncommon because the imbalance in ventilation to
perfusion ratio is compensated for by an increased respiratory rate.
In chronic bronchitis sustained hypercapnia desensitizes the brain’s respiratory control center
chemoreceptors. As a result, compensatory action to correct hypoxemia and hypercapnia (i.e.
a respiratory rate or depth increase) does not occur. Instead hypoxemia serves as the stimulus
for breathing.
83.Answer:
A. Panlobular emphysema
Explanation:
There are specific lung regions in which characteristic anatomical changes of emphysema occur.
In Panlobular emphysema, all lung segments are involved. The alveoli enlarge and atrophy, and
the pulmonary vascular bed is destroyed. This form o f emphysema is associated with ctr
antitrypsin (AAT) deficiency.
In centrilobular emphysema destruction is central, selectively involving respiratory bronchioles.
Typically, bronchioles and alveolar ducts become dilated and merge.
In Paraseptal emphysema, the lung periphery adjacent to fibrotic regions is the site o f alveolar
distention and alveolar wall destruction.
84.Answer:
B. A central destruction selectively involving respiratory bronchioles
Explanation:
Cigarette smoking causes centrilobular emphysema in which the destruction is central,
selectively involving respiratory bronchioles. Typically, bronchioles and alveolar ducts become
dilated and merge. Destruction of the nasopharyngeal wall does not occur in any type of
emphysema.
85. Answer:
A. Blockade o f the airways by thick mucus secretions.
Explanation:
In chronic bronchitis, respiratory tissue inflammation results in vasodilatation, congestion,
mucosal edema, and goblet cell hypertrophy. These events trigger goblet cells to produce
excessive amounts o f mucus.
Airways become blocked by thick, tenacious mucus secretions, which trigger a productive
cough.
86.Answer:
B. they tend to develop cyanosis
Explanation:
The term ” blue bloater” is frequently used to describe patients with chronic bronchitis because
they tend to develop cyanosis.( a condition characterized by blue coloring o f skin which occurs
due to inadequate oxygenation o f blood).
87.Answer:
E. A and C
Explanation:
Pulmonary function may be normal in the early disease stages. Later, they show an increased
residual volume, a decreased vital capacity, and a decreased F E V ,. Unlike emphysema, chronic
bronchitis patients have normal diffusing capacity, normal static lung compliance, and normal
TLC (total lung capacity).
88.Answer:
B. Erythrocytes
Explanation:
In response to hypoxemia (shortage o f oxygen), erythropoiesis (production of erythrocytes)
results an increase in the number of erythrocytes.
WBC count may be increased if there is bacterial infection. (But not in response to hypoxemia).
89. Answer:
D. Forced expiratory volume in 1 second
Explanation:
In emphysema pulmonary tests show normal or increased lung compliance, reduced FEV, and
diffusing capacity and increased Total lung capacity (TLC) and residual volume (RV).
90. Answer:
D. All o f the above
Explanation:
The treatment objectives endorsed by GOLD for treatment o f COPD include:
-Relieve symptoms and improve exercise tolerance (enable the patient to perform normal daily
activities)
-Prevent disease progression (smoking cessation)
-Improve health status
-Prevent and treat exacerbations
-Reduce mortality
- Prevent and treat complications
91 .Answer: E. C and D
Explanation:
Anticholinergics and [3-agonists are the most commonly used agents.
Methyl-xanthines are usually added when the response to other agents is inadequate.
Corticosteroids are beneficial when an allergic component has been demonstrated.
92.Answer:
B. Atropine is more potent and has fewer side effects than ipratropium
Explanation:
Ipratropium bromide is three to five times more potent and has significantly fewer side effects
than atropine.
93.
Answer: B. An MDI dose o f 40pg o f Ipratropium bromide four times daily results in severe
systemic adverse effects
Explanation:
Initial MDI dosing o f Ipratropium bromide is two inhalations (40 pg) four times daily, but dosing
can be increased to six inhalations four times daily without significant risk.
94. Answer:
C. Long acting p-agonists are recommended for rescue therapy
Explanation:
The P-agonists used for rescue therapy in COPD should be short acting. Other choices are true.
95.Answer: D .Terbutaline
Explanation:
The duration o f action o f some P-agonists is as given in the following table.
S.No
1
2
3
4
Name of a (3-agonist
Formoterol
Salmeterol
Pirbuterol
Terbutaline
Duration o f action (hr)
10-12 hr
10-12 hr
5 hr
3-6 hrs ( I), 1.5-4 hr (P),
4-8 hr (O)
Note-I= Inhalational route P= Parenteral 0= oral route
Salmeterol and formoterol (long acting p-agonists) are administered twice daily. They may also be
used in combination with ipratropium bromide or tiotropium. Neither agent is used on an as-needed
basis for rescue therapy, although Formoterol does have a rapid onset of action.
96.Answer:
C I& II are correct
Explanation:
In general the methyl-xanthines (Theophylline and related compounds) do not have good
bronchodilator activity.
In COPD, theophylline compounds are used because they increase mucociliary clearance,
stimulate the respiratory drive, and enhance diaphragmatic contractility, improve the ventricular
ejection fraction, and stimulate renal diuresis.
97. Answer:
A. There is decreased metabolism o f theophylline in such patients
Explanation:
Serum theophylline levels should be closely monitored in patients with Congestive heart failure
or Cor pulmonale due to decreased metabolism of theophylline.
98.Answer:
A. Increase in FEVI o f at least 15 % and 200mL after 6 weeks to 3 months o f use
Explanation:
Inhaled Corticosteroids play a less prominent role in COPD than in asthma.
Candidates for prolonged use o f inhaled Corticosteroids therapy should:
Be symptomatic and have a documented spirometric response (i.e. increase in FEVi o f at least
15% and 200 mL after 6 weeks to 3 months o f use.
Have an FEV] < 50% predicted with a history o f repeated exacerbations requiring systemic
Corticosteroids or antibiotics.
99.Answer:
D. All o f the above
Explanation:
Antibiotics are used to treat exacerbations with suspected infection as evidenced by an increase in
volume or change in color or viscosity of the sputum.
100. Answer: D. Antibiotics may be used in the management o f COPD even if the only
symptom is fever
Explanation:
Fever does not always indicate infection; it may also due to noninfectious causes (e.g. drug
interactions, phlebitis, neoplasms, metabolic disorders, arthritis). Antibiotics are used to treat
acute exacerbations with suspected infections as evidenced by an increase in volume or change in
color or viscosity.
101.
Answer:
A. Doxycyclinc
Explanation:
If infection with C.pneumoniae is suspected, oral Doxycycline is the drug o f choice.
102.
Answer:
B. Macrolide antibiotics
Explanation:
Antibiotic treatment of pneumonia in hospitalized patients with COPD includes either a second or
third generation cephalosporin (e.g. Cefuroxime, ceftriaxone, Cefotaxime)or a p~lactamase
inhibitor(e.g. ampicillin/sulbactam piperacillin/Tazobactam)
If infection with M.pneumoniae or Legionella pneumophilia is a concern, a macrolide (e.g.
erythromycin, Clarithromycin, Azithromycin) may be added.
103.
Answer:
C . M .pneumon iae
Explanation:
S.pneumoniae, H.influenzae and, M.catarrhalis infections should be treated for approximately 7­
10 days. Cases o f M.pneumoniae may require longer therapy ranging from 10-14 days.
104.
Answer:
C. Azithromycin
Explanation:
Azithromycin has a uniquely long half-life (68 hours), thereforefTt allows a therapy o f 5 days.
105.
Answer:
A. lodinated glycerol
Explanation:
Mucolytics (e.g. iodinated glycerol) may improve sputum clearance and disrupt mucus plugs, but
their benefits are small, and they are not recommended.
Antioxidants such as N-acetylcysteine may reduce exacerbation frequency. However, routine use
cannot be recommended based on currently available data.
Expectorants such as Guaifenesin may be used, but the evidence o f effectiveness is anecdotal.
106.
Answer:
D. Influenzae virus vaccine
Explanation:
Influenzae virus vaccination is recommended because o f its ability to reduce death and serious
illnesses by almost 50%.
Polyvalent pneumococcal vaccine is not currently recommended due to lack o f evidence for
efficacy.
107.
Answer:
D. Inhaled corticosteroids
Explanation:
Inhaled corticosteroids have not been shown to be effective in smoking cessation and they are not
used in the management o f smoking cessation.
Smoking cessation and avoidance o f other irritants has been shown to slow the rate o f decline in
F E V ]. Nicotine gum, patches, inhalers, buproprion, or clonidine may be useful in smoking
cessation. Behavior intervention significantly enhances the effectiveness o f pharmacological
therapy in smoking cessation.
108.
Answer:
D. Has anti-bacterial effect
Explanation:
Chest physiotherapy loosens secretions, helps re-expand the lungs, and increases the efficacy o f
respiratory muscle use.
It does not have any effect against infective organisms.
Basic Pharmacokinetics
“Losers visualize the penalties o f failure. Winners visualize the rewards of success.”
Dr. Rob Gilbert
1. The order o f a reaction is
A. The velocity with which the reaction
occurs.
B. The way in which temperature
affects the rate of the reaction
C. The way in which the concentration
o f the reactants affects the rate of
reaction
D. The way in which the concentration
o f the products affects the rate o f
reaction
E. C and D
2. Which o f the following is true about
zero-order reactions?
A. The reactants concentration
decreases with respect to time at a
constant rate
B. The reactants concentration
increases with respect to time at a
constant rate
C. The reactants concentration
decreases with respect to time at a
variable rate
D. The reactants concentration
increases with respect to time at a
variable rate
3. Which o f the following equations
represents zero-order reactions, where C is
the drug concentration, K0 is the zero-order
rate constant, C0 is the drug concentration
at time 0 and t is the time?
A.
B.
C.
D.
E.
dC/dt - - K0 or C = - K0t + C0
dC/dt = K0 or C = - K0t + C0
dC/dt ~ K0 or C = K0t + C0
dC/dt = - K0 or C = K0t + C0
A and C
4. Which o f the following equations
doesn’t represent the first-order reaction in
which drug concentration changes with
respect to time, where C is the drug
concentration, K0 is the zero-order rate
constant, C0 is the drug concentration at
time 0 and t is the time?
A. dC/dt = -kC
B. C = C0e kt
C.In C = -kt/2.30 + In C0
D.log C - -kt/2.30 + log C0
E.
B and D
5. The half-life (ty2) o f a reaction is
A. the time required for the
concentration o f a drug to decrease
by one-half
B. the time required for the
concentration of a drug to be half
that o f the product.
C. the time that indicates the reaction is
not half complete
D. dependent on concentration o f the
reactant given by 693/2k
E. C and D
6. A compartment is
A. not a real physiologic or anatomic
region
B. is a mathematic description o f a
biologic system and is used to
express quantitative relationship
C. is a group o f tissues with similar
blood flow and drug affinity
D. A and C
E. A and B
7. Which o f the following tissues/organs
will have the slowest distribution o f drugs?
A.
B.
C.
D.
E.
Liver
Kidney
Heart
Adrenals
Fat
8. drugs rapidly cross capillary' membranes
into tissues due to
A. active diffusion
B. passive diffusion
c. hydrostatic pressure
D. osmotic pressure
E. B and C only
9. the distribution o f drugs to body tissues
is affected by
A. the physiology o f the tissue
B. the physicochemical characteristics
o f the drug
C. plasma protein binding o f drugs
D. special affinity o f the tissue for the
drug
E. All o f the above
10. Which o f the following is true about
one-compartment open model assumes
A. the entire drug dose enters the body
rapidly
B. the rate o f absorption is not put into
account in doing the calculations
C. the body acts like a single, uniform
compartment
D. the drug distributes instantaneously
and homogenously throughout the
body/compartment
E. all o f the above
11 .Which o f the following is NOT true
about the pharmacokinetic parameters in
one compartment model after IV bolus
injection?
A. drug elimination is a first-order
kinetic process
B. the biological half-life can be
calculated form the elimination rate
constant using the equation Un =
0.693/K, where K is the elimination
rate constant
C. AUCo-,, = clearance /dose
D. The first order elimination rate
constant is the sum o f all rate
constant involved in elimination
E. All but A
12. Which o f the following is NOT true
about apparent volume o f distribution?
A. it helps in determining the amount
o f drug in the body relative to the
amount o f the drug in the plasma
B. it does not represent any actual
physical volume inside the body
C. the volume o f distribution decreases
as the drug distributes more
extravascularly into the tissues
D. it can be much larger than body
volume
E. A and C
13. which o f the following is not true in the
one-compartment pharmacokinetic model
o f a drug administered as an oral dosage
form,
A. drug absorption is a first order
process
B. elimination is a first order process
C. the time for maximum drug
absorption depends only on the
constant rate o f elimination and
absorption
D. lag-time happens only with delayedrelease dosage forms
E. none
14. Which o f the following is NOT true
about the plasma profile o f an intravenous
infusion?
A. Like in the IV bolus injection, the
plasma level is at its peak
immediately after administration
B. The absorption is a zero-order
process
C. Elimination is first order process
D. Upon termination o f infusion, the
plasma drug concentration declines
by first order process
E. It is possible to calculate the
elimination rate constant and
elimination half life from the
declining plasma drug concentration
versus time curve
15.The plasma drug concentration at any
time after the start o f an infusion is
calculated by the formula
A.
B.
C.
D.
E.
Cp = [R7k][ 1-e'kt]
Cp = [R/VDk] [l-e"kt]
C p = [R /V D] [ l- e kt]
C p = [2R/k][l - e kt]
C p = tRVD/k ][l-e k']
16.
Which o f the following is the correct
formula for calculating the infusion rate
required to reach the steady state
concentration?
A.
B.
C.
D.
E.
R
R
R
R
B
= [Css|[ VDk]/ [l-e 'k1]
= Css VDk
= CssCl
= Css/ V Dk
and C
17.The formula for calculating the loading
dose to obtain the steady state concentration
as soon as possible is
I.
II.
III.
Dl = CssVD
D l = R/k
DL = Rk
A. I only is correct
B. Ill only is correct
C. I and II are correct
D. II&III are correct
E. I,II&III are correct
18.
Which o f the following is NOT true
about the intermittent IV infusion?
A. The drug is infused for relatively
long period of time
B. it is used for a few drugs
C. steady-state drug concentrations are
not achieved
D. A and B
E. None
19.All the following are correct about
multiple drug dosing EXCEPT
A. it is used in the treatment o f chronic
diseases
B. in multiple dosing, the plasma drug
concentration fluctuates between a
maximum and minimum values at
the steady-state
C. all drugs that are given as multiple
doses follow the superimposition
principle
D. the principle o f superimposition
assumes that early doses o f drug do
not affect the pharmacokinetics of
subsequent doses
E. according to the superimposition
principle, the total plasma drug
concentration is obtained by adding
the residual drug concentrations
found after each previous dose
20. Which o f the following parameters can
be adjusted in developing a dosage
regimen?
A.
B.
C.
D.
E.
elimination half life
the size o f the dose
the apparent volume o f distribution
the frequency o f doing
B and D
21 .Which o f the following is NOT true?
I .as long as the dosing interval is
unchanged, the expected average
drug concentration at steady-state is
the same
II .changing the dosing rate will change
the values o f C"max and C'r'mm
III. for a larger dose given over a longer
interval there will be smaller
fluctuation between C'°max and C°°m;n
A. I only is correct
B. Ill only is correct
C. I and II are correct
D. II&III are correct
E. I,II&III are correct
22. What is the correct formula for
calculating C"m3X at steady state
concentration after multiple rapid IV bolus
injection?
I.C “max=[D o/V D] / ( l - e kT)
II . r max = C V (l-e -kT)
III -C"max = [VD /D o]/(l- e‘kT)
A. I only is correct
B. Ill only is correct
C. I and II arc correct
D. II&III are correct
E. I,II&III are correct
23.The loading dose for multiple oral
doses, D l is calculated by the formula
A.
B.
C.
D.
D l —D m/ e
Dl = D m | l / ( l - e kT)]
DL = DM [e-kT]
D L = DM- [ e 'kT]
B. after IV bolus injection, the drug
distributes rapidly throughout the
body
C. in this model the drug distributes
between the central compartment
and tissue compartment
D. the drug distributes rapidly and
uniformly in the tissue compartment
E. all the above
26.For a drug administered orally, twocompartment characteristics are seen if
I. the drug is rapidly absorbed
II . the drug is distributed slowly
III . the drug is absorbed slowly
A.
B.
C.
D.
E.
I only
I and II
I and III
II and III
1,11 and III
27. Which o f the following is NOT true
about the kinetics o f multicompartments?
24. Which o f the following is true about
drugs that exhibit multi compartment
models?
A. they distribute into different tissue
at different rates
B. highly perfused tissue groups
equilibrate more rapidly than poorly
perfused tissue groups
drugs that bind to proteins are
expected to accumulate in skeletal
muscles
D. the physicochemical properties of
the drug and the characteristics of
the tissue determine the distribution
o f the drug into the different tissues
E. none
25. Which o f the following about twocompartment model (IV bolus injection) is
correct?
A. the plasma drug concentration
declines monoexponentially
A. drug elimination is presumed to take
place from the peripheral
compartments
B. if additional one compartment is
added, one more first-order plot is
required
C. pharmacokinetic analysis gets
simpler as the number o f .
compartments is increased
D. dosage regimens are calculated from
the rate constant o f the elimination
phase
E. A and C
28. Which o f the following is NOT true
about nonlinear pharmacokinetics?
A. it is also called capacity limited or
dose dependent or saturation
pharmacokinetics
B. it may result from saturation of an
enzyme or carrier-mediated system
C. it does not follow first-order kinetics
as the dose increases
D. It is relatively easier to calculate the
dose for drugs that follow nonlinear
pharmacokinetics
E. A and B
29.Non-linear pharmacokinetics is
characterized by all the following EXCEPT
A. the elimination half-life remains
constant even if the dose is
increased
B. the AUC is not proportional to the
dose
C. presence o f other drugs may affect
pharmacokinetics o f the drug in
question
D. the composition and/or ratio o f the
metabolites o f a drug may be
affected by a change in the dose
E. none
30. Which o f the following is NOT true
about the Michael-Menten kinetics?
A. it describes the velocity o f enzyme
reactions
B. it describes the elimination o f drug
by a saturable process
C. the Michael-Menten equation
describes the rate o f change o f
plasma drug concentration after IV
bolus injection
D. the Michaelis constant (KM) equals
the elimination constant
E .A and D
31 .Drugs that follow nonlinear
pharmacokinetics may show
A. zero-order elimination rates at low
drug concentrations
B. a mix o f zero- and first-order
elimination rates at intermediate
drug concentrations
C. first-order elimination rates at high
drug concentrations
D r A and C only
E. All the above
32. Which of the following is the correct
unit for clearance?
A.
B.
C.
D.
E.
volume /time
mass/time
mass2/time
mass/volume
mass2/volume
33. Which o f the following equations
correctly expresses the measurement of
total body clearance?
A.
B.
C.
D.
E.
CIt = F Dcok/AUC
ClT = VDk
C1t = FD m/AUC
[dDe/dt]/Cp
All but A
34.Renal excretion is the major route o f
drug elimination for all the following
EXCEPT
A.
B.
C.
D.
polar drugs
water-soluble drugs
gaseous drugs
drugs with molecular weight less
than 500
E. drugs that are biotransformed slowly
35.
Which o f the following substances can
be used to estimate GFR?
A.
B.
C.
D.
E.
mannitol
sodium thiosulfate
inulin
creatinine
all the above
36. Which o f the following transport
mechanisms is active process?
A. GF
B. Tubular reabsorption
C . Tubular secreti on
D. A and B
E. B and C
37. Which ofthe following conditions will
decrease the tubular reabsorption o f a
weakly acidic drug?
A.
B.
C.
D.
E.
the use o f a diuretic
if it exists in the nonionized form
if the urine is made more alkaline
A and C
none
38. Which of the following is NOT true
about the active tubular secretion?
A. It is the process in which a drug is
passed from blood into glomerular
filtrate
B. it involves the transport o f drugs in
accordance with the concentration
gradient
C. there are two active secretion
systems in the kidneys; one for
weak acids and one for weak bases
D. it shows a competitive effect which
can be employed to provide longer
biological half-life o f some drugs
E. none
39. Which o f the following is NOT true
about the renal clearance?
A. it is defined as the volume o f drugcontaining plasma that is cleared of
drug by the kidney per unit time.
B. It is expressed in units o f volume
per time
C. It puts in consideration the
physiological mechanism o f
excretion
D. A and B
E. None
40. Which o f the following is a WRONG
match between the value a clearance ratio
and the most probable mechanism o f drug
clearance?
A. clearance ratio >1; filtration plus
active tubular secretion
B. clearance ratio = 1; tubular secretion
plus reabsorption
C. clearance ratio < 1; filtration plus
reabsorption
D. A and B
E. None
41 .Which o f the following is NOT true
about the hepatic clearance?
A. It is the volume of drug containing
plasma that is cleared by the liver
per unit time
B. hepatic clearance is equivalent to
nonrenal clearance
C. hepatic clearance is the ratio of
blood flow and the extraction ratio
D. it can calculated as the product of
blood flow and the extraction ratio
E. none
42.Extraction ratio is
A. the fraction o f drug that enters a
particular tissue
B. the fraction o f drug that leaves a
particular tissue
C. the amount o f drug that enters a
particular tissue minus the amount
that leaves that particular tissue
D. the fraction o f the drug that is
removed irreversibly by a particular
tissue as the plasma containing drug
perfuses the tissue
43.
What will be the fraction o f drug
removed by the liver if the arterial plasma
concentration o f a drug entering the liver is
2.35 mg/ml and the venous plasma
concentration o f the drug is 2.1 lmg/ml?
A.
B.
C.
D.
E.
0.10
0.12
0.34
0.29
0.43
44.Blood enters the liver through
A.
B.
C.
D.
E.
hepatic vein
hepatic portal vein
hepatic artery
mesenteric vessels
B and C
45. Which o f the following is most affected
by sudden changes in protein binding?
A. hepatic clearance o f drugs that have
high extraction ratios and high
intrinsic clearance values
B. hepatic clearance o f drugs that have
low extraction ratios and high
intrinsic clearance values
C. drugs that are highly plasma
protein-bound and have low
intrinsic clearance
D. drugs that are not highly plasma
protein-bound and have low
intrinsic clearance
E. A and C
46. Which o f the following is NOT true
about biliary drug excretion?
A. it is an active process
B. it is a type o f hepatic clearance
C. it involves drugs with molecular
weight greater than 500, polar drugs
and glucuronide conjugates o f
various drugs
D. there is competition between weakly
acidic drugs and weakly basic drugs
for the secretion systems
E. none
in the GI tract may hydrolyze the
glucuronide moiety allowing the
released drug to be reabsorbed
D. from the bile drugs may empty back
(through the bile duct) into the GI
tract for absorption once again
E. all o f the above
48.First pass effect usually occurs with
those drugs that are administered
A.
B.
C.
D.
E.
Orally
IV
IM
Rectally
Topically
49.
The most common mechanism o f first
pass effect is
A. metabolism o f drugs by GIT
mucosal cells
B. metabolism o f drugs by the
intestinal flora
C. biliary secretion o f drugs
D. rapid biotransformation o f drugs by
the liver enzymes
50.In order to have a better bioavailability
for a drug that is affected by first pass
effect, one should.
A. use other routes o f administration
that avoid the first pass effect
B. increase the dose o f the drug
C. use a delayed release dosage form o f
the drug
D. A and B only
E. All the above
47. Which o f the following is/are correct
about the enterohepatic circulation?
A. it is the reabsorption o f drug after
the hepatic pass
B. it is responsible for the drug being
recycled
C. for those drugs emptied into GIT as
glucuronide metabolite, the enzymes
51 .Which o f the following is NOT true
about mean residence time?
A. it is also called mean transit time or
mean sojourn time
B. it is the average time for the drug
molecule to reside in the body
C. it is independent o f the route o f
administration
D. it is calculated by dividing the total
residence time for all drug
molecules in the body by the total
number o f drug molecules.
E. The mean residence time for a drug
given by a noninstantaneous input is
longer than the MRTiv
52.How is the MRTiv related to the
elimination half-life?
A.
B.
C.
D.
E.
MRTiv
MRTiv
MRTiv
MRTiv
MRTiv
=
=
=
=
=
k2
1/k
2k
Vk
1/2k
53. Which o f the following is NOT true
about clinical pharmacokinetics?
A. it is the application of
pharmacokinetic principles to drug
therapy
B. it deals in individualizing dosage
regimen based on the patient’s
disease state and patient specific
considerations
C. it studies the pharmacokinetic
differences o f drugs in various
populations groups
D. the main objective is to increase the
efficiency and decrease the toxicity
E. none
ANSWERS
Basic Pharmacokinetics
1.
Answer: C. The way in which the concentration o f the reactants affects the rate o f reaction.
Explanation:
The order o f a reaction refers to the way in which the concentration o f the reactants influences the
rate o f a chemical reaction. The velocity with which the reaction occurs refers to the rate o f the
chemical reaction.
2. Answer: A. The reactants concentration decreases with respect to time at a constant rate.
Explanation:
For every reaction there is no way the concentration o f the reactants increase as the reaction
progress. And in case o f the zero-order reaction the rate o f the reaction is independent of
concentration.
3. Answer: A. dC/dt = - K0 or C = - K0t + C0.
Explanation:
If the amount of a drug decreases at a constant time interval (ie. Zero-order reaction), then the
rate o f disappearance o f the drug is expressed as dC/dt = - K0. Integration o f this equation gives C
= - K0t + Co. The negative sign indicates that the amount o f the drug is decreasing.
4. Answer: C. In C = -kt/2.30 + In CO
Explanation:
In first-order reaction, the drug concentration changes with respect to time equals the product o f
the rate constant and the concentration o f drug remaining according to the relation dC/dt = -kC;
integrating this equation between the limits concentration at time 0 (Co) and any time t (C ) gives,
InCo —InC = -k(O-t); InC = -kt + InCo. Natural logarithm can be converted into common
logarithm by multiplying the above equation by 2.303 to give the equivalent equation log C = kt/2.3 + log Co.
5. Answer: A. Is the time required for the concentration o f a drug to decrease by one-half.
Explanation:
H alf life is the time necessary for the amount of drug in the body to be reduced to 50 percent. The
relation between half life and k can be determined by the formula
- 0.693/k.
6. Answer: D. A and C
Explanation:
A compartment is a group o f tissue with similar blood flow and drug affinity. A compartment is
not a real physiologic or anatomic region. A mathematic description o f a biologic system is
known as the model and is used to express quantitative relationships.
7. Answer: E. fat.
Explanation:
Drugs distribute rapidly to tissues with high blood flow and more slowly to tissues with low
blood flow. From the tissues/organs listed above, the adrenals have the highest blood flow
followed by the kidneys, liver and the heart. Fat tissues have the least blood flow, therefore they
will have the slowest distribution o f drugs.
8. Answer: E. B and C only.
Explanation:
Passive diffusion and hydrostatic pressure are the two processes by which drugs transverse
capillary membranes.
9. Answer: E. all o f the above
Explanation:
The distribution o f drug into body fluids and tissues is an important determinant o f therapeutic
effect o f the drug. Although there are exceptions, most drugs are not distributed in the plasma
alone but appear to be also distributed in other body fluids and/or tissues. Among the many
factors that affect distribution o f drugs; the physiology o f the tissue, the physicochemical
characteristics o f the drug, plasma protein binding o f drugs, and special affinity o f the tissue for
the drug are some examples.
10. Answer: E. all o f the above
Explanation:
The one-compartment open model is the simplest way o f describing the process of drug
distribution and elimination in the body. This model assumes that the drug can enter or leave the
body, and the body acts like a single, uniform compartment. The simplest route of drug
administration that gives such a model is IV bolus. The drug is injected all at once into a box
(therefore, no absorption rate considered) or compartment, and that the drug distributes
instantaneously and homogenously throughput the compartment.
11 .Answer: C. AUC0-OT= clearance /dose.
Explanation:
In one-compartment model, after IV bolus injection, the total area under curve is determined
using one o f the following equations: AUC0.» = dose/clearance, or AUC0.„, = Co/ K, where Co is
the extrapolated drug concentration at zero time on the y-axis o f the semi-logarithmic plot of
concentration versus time, and k is the first order elimination rate constant.
12. Answer: C. the volume o f distribution decreases as the drug distributes more extravascularly
into the tissues.
Explanation:
The apparent volume o f distribution is the term used to describe the volume o f fluids that would
be required to account for all drug in the body. Its value will be decreased if more of the drug is
contained in the plasma, and its value will increase if the drug distributes more to the
extravascular tissues.
13.Answer: D. lag-time happens only with delayed-release dosage forms.
Explanation:
The lag-time is the time that elapses between administration o f the dosage form and appearance
o f drug in systemic circulation. Delayed-release dosage forms are intended to release their content
at a time later than the time o f administration of the dosage form. Although the conventional
dosage forms are intended to release their contents immediately after administration, they exhibit
certain degree o f delayed release due to some factors that may be related to the dosage form, the
patient or the drug.
14.Answer: A. Like in the IV bolus injection, the plasma level is at its peak immediately after
administration.
Explanation:
In IV bolus injection, since the entire dose is placed in plasma at once, the concentration o f drug
in plasma is at its peak level immediately after administration. In IV infusion however, the entire
dosage is not administered all at once. So the concentration of the drug in the plasma is not at its
peak when the infusion is started.
15.Answer: B. Cp = [R/VDk] [1-e-kt],
Explanation:
The change in the amount o f drug in the body at any time (dDB/dt) during the infusion is the rate
o f input minus the rate o f output.
dDB/dt = R - kDB
Where DB is the amount of drug in the body, R is the infusion rate (zero order), and k is the
elimination rate constant (first order). Integration o f the above equation and substitution o f DB CpVDgives
Cp = [R/VDk] [l-e 'kt].
16.Answer: E. B and C.
Explanation:
As the drug is infused, the plasma drug concentration increases to plateau or steady state
concentration (Css). This occurs at infinite time (t = co) and the expression e‘kt approaches zero
and the equation Cp = [R/VDk] [l-e"kl] is reduced to
Css = R/ VDk. Therefore, R = Css VDk and since VDk = Cl, R = CssC).
17.Answer: C. 1 and II are correct
Explanation:
The loading dose is the amount o f drug that, when dissolved in the apparent VD, produces the
desired Css. Therefore, it is given by the equation DL= Css VD. However, Css = R/[VDk], Therefore,
Dl = R/k.
18.
Answer: A. The drug is infused for relatively long period o f time
Explanation:
Intermittent IV infusion involves infusing the drug for a short period o f time so that drug
accumulation and toxicity are avoided.
19. Answer: C. all drugs that are given as multiple doses follow the superimposition principle.
Explanation:
There are situations in which the superimposition principles do not apply, even with those drugs
that are given in multiple doses. In these cases, the pharmacokinetics o f the drug change after
multiple dosing due to various factors, including changing pathophysiology in the patient,
saturation o f drug carrier system, enzyme induction, and enzyme inhibition. Drugs that follow
nonlinear pharmacokinetics generally do not have predictable plasma drug concentrations after
multiple doses using superimposition principle.
20. Answer: E. B and D.
Explanation:
When designing a multiple-dosage regimen, only the dosing rate can be adjusted easily. The
dosing rate involves the size o f the dose and the time interval between doses.
21 .Answer: B. Ill only is correct
Explanation:
For a larger dose given over a longer interval the value o f C"max is lower and the value o f C“mj„ is
higher as compared to a small dose given more frequently. Therefore, the fluctuation between
C”max and C '„lm will be larger.
22.Answer: C. I and II are correct
Explanation:
To determine the concentration o f a drug in the body after multiple doses, the amount o f drug in
the body is divided by the volume in which it is distributed.
Therefore, C"max = D " o/V d
But D o = Do/( 1- e kT). Therefore, C°°max = [D o/Vd]/( 1- e'kT)
Moreover, C°p = D o/'V d. Therefore, C“max = C°p/(1- e'kT)
23.Answer: B. DL = DM [1/(1 -e kT)]
Explanation:
Loading doses are given to achieve desired plasma concentrations as soon as possible. For
multiple oral dose loading dose is calculated by the formula DL = DM [l/(l-e 'kT)], where DM is the
maintenance dose and 1/(1-e‘kT) is the accumulation rate.
24.
Answer: C. drugs that bind to proteins are expected to accumulate in skeletal muscles.
Explanation:
Drugs that bind to proteins are expected to be concentrated in the plasma since there are proteins
in the blood and since drugs bound to proteins do not diffuse into tissues.
25.Answer: C. in this model the drug distributes between the central compartment and tissue
compartment.
Explanation:
The plasma level-time curve for a drug that follows a two-compartment model shows that the
plasma drug concentration declines biexponentially as the sum of twro first-order processesdistribution and elimination. A drug that follows the pharmacokinetics o f a two-compartment
model does not equilibrate rapidly throughout the body, as is assumed for a one-compartment
model. In this model, the drug distributes into two compartments, the central compartment and
the tissue or peripheral compartment. The central compartment represents the blood, extracellular
fluid, and highly perfused tissues. The drug distributes rapidly and uniformly in the central
compartment. The tissue compartment contains tissues in which the drug equilibrates more
slowly.
26.
Answer: B. I and II
Explanation:
A drug with a rapid distribution phase may not show two compartment characteristics after oral
administration. Two-compartment models are seen if the drug is absorbed rapidly but distributes
slowly.
27.Answer: E. A and C.
Explanation:
In a multi compartment systems, elimination is presumed to take place form the centra]
compartment unless other information about the drug is known. This is because major sites of
drug elimination (renal excretion and hepatic drug metabolism) occur in organs, such as the
kidney and liver, which are highly perfused organs. Adequate pharmacokinetic description of
multicompartment models is often difficult and depends on proper plasma sampling and
determination o f drug concentrations.
28. Answer: D. drugs that follow nonlinear pharmacokinetics are relatively easier to calculate the
dose.
Explanation:
Although most drugs follow linear pharmacokinetics, in some drugs steady-state concentrations
do not change proportionally with change in size o f the dose. In such cases, a plot o f steady-state
concentration o f a drug in plasma as a function o f dose is not linear and the drug is said to follow
non-linear pharmacokinetics, dose dependent, capacity limited, or saturation pharmacokinetics.
Drugs that exhibit nonlinear pharmacokinetics are often very difficult to dose correctly.
29. Answer: A. the elimination half-life remains constant even if the dose is increased.
Explanation:
In non-linear pharmacokinetics, the biological half-life changes with increasing dose. Usually,
half-life increases with increasing dose, but in some cases, half-life may decrease with increasing
dose (e.g., carbamazepine).
30.Answer: D. Michaelis constant (KM) equals the elimination constant.
Explanation:
The Michae-Menten equation is given by the formula,
-dCp/dt = Vmax Cp/(KM+ Cp),
Where Vmaxis the maximum elimination rate and KMis the Michaelis constant that reflects the
capacity o f the enzyme system. It is important to note that KMis not an elimination constant, but
actually a hybrid rate constant in enzyme kinetics, representing both the forward and backward
reaction rates and equal to the drug concentration or amount o f drug in the body at 0.5 Vmax.
31 .Answer: B. a mix o f zero- and first-order elimination rates at intermediate drug
concentrations.
Explanation:
At low drug concentrations (Cp), where KM» Cp, Michael-Menten equation is reduced to a
first-order rate equation because both KMand Vmax are constants.
-dCp/dt = Vmax Cp/ K m = k ’Cp
At high drug concentrations, where Cp » K m, the Michael-Menten equation is reduced to a zeroorder rate equation.
-dCp/dt = Vmax
32. Answer: A. volume /time
Explanation:
Clearance is the measure o f drug elimination from the body. Instead o f describing the rate o f
elimination in terms o f a certain quantity or amount o f drug eliminated per unit time, clearance
describes the rate o f elimination in terms o f volume o f fluid that is cleared o f drug per unit time.
Therefore, the units for clearance are volume/time.
33.Answer: E. All but A
Explanation:
Clearance can be calculated using elimination rate constant (k) and apparent volume of
distribution (V d) (both obtained from the plasma profile o f the drug) from the relation, C1t = K
V d. It can also be calculated based on the concept that the amount o f drug excreted in urine per
unit time (rate o f excretion o f the drug in the urine, dDe/dt) is proportional to the concentration o f
the drug in plasma, Cp. The relation is as follows, [dDe/dt]/Cp. In case o f noncompartmental
(model independent) clearance model, clearance is calculated by the equation C1T = FDoo/AUC.
34.
Answer: C. gaseous drugs.
Explanation:
Anesthetic gases, vapors, and volatile drugs are excreted through the lungs (i.e., pulmonary
excretion).
35.Answer: E. all the above
Explanation:
GFR can be determined by measuring the extent o f excretion and plasma level o f a test substance.
The substance used to measure filtration rate should have the following properties; it should be
removed from plasma by filtration only and not be (actively) secreted or reabsorbed by the
tubules. It should not be metabolized, stored, or protein-bound, and not affect filtration rate.
Substances commonly used to measure GFR include mannitol, sodium thiosulfate, inulin, and
creatinine.
36.Answer: C. tubular secretion.
Explanation:
GF is a passive process by which small molecules and drugs are filtered through the glomerulus
o f the nephron. Tubular reabsorption is a passive process that follows Fick’s law o f diffusion.
Tubular secretion on the other hand is a carrier-mediated active transport system that requires
energy.
37.
Answer: D. A and C
Explanation:
The use o f diuretic increases the flow o f urine as a result o f which more o f the drug will be
excreted. If a drug exists primarily in the nonionized form (i.e., lipid soluble form), then it is
reabsorbed more easily from the lumen o f the nephron. Depending on the pKa o f the drug.
alteration o f the urine pH alters the ratio o f ionized to nonionized drug and affects the rate o f drug
excretion. For example alkalization o f urine increases the excretion (decreases tubular
reabsorption) o f a weakly acidic drug.
38.Answer: B. it involves the transport o f drugs in accordance with the concentration gradient.
Explanation:
Tubular secretion is an active transport process whereby the drug is transported against a
concentration gradient from blood capillaries across the tubular membrane into renal tubule. This
active process accounts for the fact that certain drugs, although extensively bound to plasma
proteins, are rapidly eliminated from the body essentially by renal excretion
39.
Answer: C. It puts in consideration the physiological mechanism o f excretion.
Explanation:
Renal clearance describes drug elimination from the body without identifying specific mechanism
o f the process. The probable mechanism o f renal clearance is obtained with a clearance ratio
(which relates the drug clearance to inulin clearance (a measure o f GFR)) or from a plot of
excretion rate vs plasma concentration o f drug.
40. Answer: B. clearance ratio = 1; tubular secretion plus reabsorption
Explanation;
Clearance ratio is the ratio o f drug clearance to inulin clearance (i.e.GFR). Therefore, if the
clearance ratio is 1, then it indicates that the most probabale mechanism o f drug clearance is
filtration only.
-
41. Answer: C. Hepatic clearance is the ratio o f blood flow and the extraction ratio
Explanation:
Hepatic clearance is a product o f blood flow into the liver and the extraction ratio
45/124. Extraction ratio is
42. Answer: D. the fraction o f the drug that is removed irreversibly by a particular tissue as the
drug containing plasma pass through it.
Explanation:
Extraction ratio is the fraction o f drug removed from the plasma by a particular tissue. It is a
measure o f the efficiency with which an organ eliminates a given drug. It is obtained by
measuring the plasma drug concentration entering the liver and the plasma drug concentration
exiting the liver.
43.Answer: A. 0.10
Explanation:
Extraction ratio is given by the formula.
Extraction ratio = [arterial plasma drug concentration - venous plasma drug
concentration]/arterial plasma drug concentration.
Therefore, for the above case, the fraction o f drug removed by the liver (i.e., the extraction ratio)
will be [2.35-2.11]/2.35 = 0.1.
44.Answer: E. B and C
Explanation:
Blood enters liver by hepatic portal vein and hepatic artery, and leaves the liver by hepatic vein.
After oral drug administration, the drug is absorbed from the GI tract into the mesenteric vessels
and proceeds to hepatic portal vein, to liver, and then to systemic circulation.
45.Answer: C. drugs that are highly plasma protein-bound and have low intrinsic clearance.
Explanation:
For a drug that has a low extraction ratio and is less than 75-80% bound, small changes in protein
binding will not produce significant changes in hepatic clearance. Drugs that are highly bound to
plasma protein but with low extraction ratios are considered capacity limited and biding sensitive,
because a small displacement in the protein binding o f these drugs will cause a very large
increase in the free drug concentration.
46.
Answer: D. there is competition between weakly acidic drugs and weakly basic drugs for the
secretion systems.
Explanation:
Because there are separate active secretion systems for weak acids and weak bases, there cannot
be competition between weakly acid drugs and weakly basic drugs.
47. Answer: E . All o f the above
Explanation:
Some drugs are absorbed from the GI tract by the mesenteric and hepatic portal vein into the
liver. The liver may secret some o f the drug (unchanged or as a glucuronide metabolite) into the
bile. Glucuronide metabolite o f the drug may empty from the bile into GI tract where bacteria
may hydrolyze the glucuronide conjugate allowing the released drug to be reabsorbed.
48.Answer: A. orally.
Explanation:
First pass effect is a phenomenon, which usually occurs with orally administered drugs. In this
phenomenon, a portion o f the orally administered drug undergoes elimination before it has a
chance to be systemically absorbed. It is for this reason that this phenomenon is also called presystemic elimination.
49. Answer: D. rapid biotransformation o f drugs by the liver enzymes.
Explanation:
Although the other factors also contribute, first pass effect generally occurs due to rapid drug
biotransformation by the liver enzymes.
50.Answer: E. all the above.
Explanation:
Using other routes o f administration (other than oral) that avoid first pass effect is successfully
employed for such drugs as sublingual nitroglycerin, insulin subcutaneous, and estradiol
transdermal. Increasing the dose makes over for the amount o f drug lost due to the first pass
effect (e.g., penicillin and propranolol). Using delayed release dosage form o f the drug allows the
drug to be absorbed more distally in the GI tract (e.g., enteric-coated aspirin, mesalamine).
51 .Answer: C. it is independent o f the route o f administration.
Explanation:
Actually, MRT is independent o f the route o f administration because the route o f the
administration does not influence the mean time that molecules reside in the body. However, the
interpretation o f the ratio o f AUMC and AUC does change as a function o f administration
because this ratio only yields the MRT when the input is instantaneous (i.e., IV administration).
In other routes o f administration, it does not give MRT. Fro example. In oral administration,
AUMC/AUC = MRT + MAT. Hence, we say MRT is dependent on the route of administration.
52. Answer: B. MRTiv = 1/k.
Explanation;
The MRT can be related to elimination half-life by considering the situation in which a drug
displays monoexponential decline. The MRT can be written as MRT = AUMC/AUC, but AUMC
=( initial concentration)/k2 and AUC = (initial concetration)/k.
Therefore, MRT = (initial concentrationYk2 ^ 1/k
(Initial concentration)/k
53. Answer: C. it studies the pharmacokinetic differences o f drugs in various populations groups.
Explanation:
The study o f pharmacokinetic differences in various population groups is known as population
pharmacokinetics.
Bioavailabilty and Bioequivalence
RH
“Nothing great was ever achieved without enthusiasm ”
Ralph Waldo Emerson
1. For drugs that are not intended to be
absorbed into the bloodstream
bioavailability may be assessed by:
A. Measuring the rate and extent of
absorption o f therapeutically active
drug that is systemically absorbed.
B. Measurements intended to reflect
the rate and extent to which the
active ingredient becomes available
at the site o f action.
C. Measuring the rate o f drug
elimination
D. Measuring the rate o f drug
distribution
E. Measuring the extent o f elimination
2. If two drug products are considered
pharmaceutical equivalents they may differ:
A. In the chemical form o f the active
ingredient.
B. In the dosage form.
C. Packaging
D. Excipients
E. C and D
3. Which one o f the following is NOT
TRUE?
A. Reference drug product is usually
the currently marketed, brand name
product with a full New drug
application approved by the FDA
B. The generic drug product requires
an Abbreviated New Drug
Application for approval by the
FDA
C. Generic drug product is marketed
after patent expiration of the
reference drug product
D. eneric drug products require Full
New drug application for approval
by the FDA
E. Generic drug product can be
manufactured by any
pharmaceutical company
4. All o f the following are TRUE about
therapeutic equivalent drug products
EXCEPT:
A. They are pharmaceutical equivalents
B. They are expected to have the same
clinical effect and safety profile
when administered to patients under
the same conditions.
C. They need not necessarily be
bioequivalent.
D. They should meet an acceptable in
vitro standard.
5. All o f the following are pharmaceutical
alternatives EXCEPT:
A. Tetracycline hydrochloride versus
tetracycline phosphate
B. Sustained release nifedipine versus
immediate release nifedipine
C. Doxycycline hydrochloride capsules
versus Doxycycline tablets
D. Doxycycline hydrochloride versus
Tetracycline hydrochloride
E. Amoxycillin capsules versus syrup
6. Bioavailability and bioequivalence may
be determined using:
A. Pharmacokinetic studies
B. Measurement o f an acute
pharmacodynamic effect
C. Comparative clinical studies.
D. In vitro studies
E. All o f the above
7. In the determination o f bioequivalence
and Bioavailability the choice o f study
method is based up on:
A. The site o f action o f the drug
B. The ability of the study design to
compare drug delivered to that site
by the two products.
C. On the preference o f the person
doing the study.
D. The dose o f drug to be studied
E. A and B
8. Acute pharmacodynamic effects o f a
drag can be used to measure Bioavailability
when:
A. No assay for plasma drug
concentration is available.
B. The plasma drug concentration does
not relate to the pharmacological
response.
C. the plasma drug concentration is
related well to the pharmacological
response.
D. the drug is hydrophobic.
E. A and B
9. The time taken by a drug to achieve
minimum effective concentration after
administration o f drug is:
D. The intensity o f pharmacological
effect is proportional to the number
o f receptors occupied by the drug up
to a maximum pharmacological
response.
E. If two oral products contain the
same amount o f active drug but
different excipients, the dosage form
that yields the faster rate o f drug
absorption has the longer T MAX
(Time for peak plasma drug
concentration)
11 .Area under the concentration versus
time curve (AUC) relates to:
A. Amount or extent o f absorption
B. Duration o f action
C. The maximum plasma concentration
o f the drug.
D. The amount o f drug excreted
E. None
12. Which o f the following is/are true?
A.
B.
C.
D.
E.
Onset time
-Duration o f action
Time for peak plasma concentration
Half-life
None
10. Which one o f the following is
WRONG?
A.
As long as the drug concentration
remains above the minimum
effective concentration,
pharmacological activity is
observed.
B. Minimum toxic concentration is the
plasma concentration o f the drug
above which a toxic or adverse
response is observed.
C. Quantification o f the
pharmacological effect versus time
profile can be used as a measure o f
A. the plasma drug concentration at
Tmax relates to the intensity o f the
pharmacological response
B. ideally, Cmax should be within the
therapeutic window
C. the amount o f systemic drug
absorption is directly related to the
AUC
D. the AUC is calculated by the
trapezoidal rule and is expressed in
units o f concentration multiplied by
time
E. All o f the above
13.Determination o f bioavailability by
measurement o f urinary drug excretion is
most accurate if
A. the active therapeutic moiety is
excreted unchanged in significant
Bioavailability and Bioequivalence
A. all products
B. products in which the bioavailability
o f the active ingredient is affected
by food
n
_i i i
23. Which o f the following statements is
wrong?
B. the active therapeutic moiety has
many metabolites excreted in the
urine
C. the drug is potent
D. the metabolites o f the drug have
pharmacological activity
E. the active therapeutic moiety is
excreted unchanged in small
quantity in the urine
14. All o f the following are TRUE Except:
A. the cumulative amount o f active
drug excreted in the urine is directly
related to the extent o f systemic
drug absorption
B. the rate o f drug excretion in the
urine is directly related to the rate o
systemic drug absorption
C. The time for the drug to be
completely excreted corresponds to
the gap between drug absorption
and determination o f the amount o f
drug absorbed systemically.
D. As a drug is absorbed, the drug
concentration at the receptor rises lti>
a minimum effective concentration
and a pharmacological response is
initiated
E. The time for the drug to be
completely excreted corresponds to
the total time for drug to be
|
systemically absorbed and
completely excreted after
administration.
15. Which o f the following is NOT TRUE
about relative bioavailability?
j
A. it is the systemic availability o f thb
drug from a dosage form as
compared to a reference standard
given by the same route o f
administration
B. it is calculated as the ratio o f the
AUC for the dosage form to the
AUC for the reference dosage forjn
given in the same dose
C. if its value is less than 1, the
reference and the product under
examination have the same
bioavailability
D. it is very important in generic drug
studies
E. if its value is 1? the drug
bioavailability form both test and
standard dosage forms is the same
but does not indicate the
completeness o f systemic drug
absorption
16.The absolute bioavailability is
calculated as
A. the ratio o f the AUC for the dosage
form given orally to the AUC
obtained after IV drug
administration
B. the ratio o f the AUC for the dosage
form given IV to the AUC obtained
after oral administration
C. the ratio o f the AUC for the dosage
form given orally to the AUC
obtained after administration given
by other route
D. The ratio o f the AUC for the dosage
form given 3V to the AUC obtained
after subcutaneous administration.
E. None
17.An F value (absolute bioavailability) o f
0.8 (80%) indicates th a t:
A. 20% o f the drug was systemically
available from the oral dosage form
B. 80% o f the drug was systemically
available from the oral dosage form
C. 180% of the drug was systemically
available from the oral dosage form
D. 120% o f the drug was systemically
available from the oral dosage form
E. None
18.In the bioequivalence studies food
intervention study is recommended for:
A. all products
B. products in which the bioavailability
o f the active ingredient is affected
by food
C. potent drugs
D. A and C
E. "None
19.The type o f food used in food
intervention study is
A.
B.
C.
D.
E.
Fat rich food
Protein rich
Carbohydrate rich food
Any type o f food
None
20.Cross over study may not be practical in
drugs with
A.
B.
C.
D.
E.
long half-life
short half-life
all drugs
A and C
None
21 .Pharmacokinetic analysis of
bioavailability data includes calculation o f
the following parameters for each subject
EXCEPT:
A. AUC to the last quantifiable
concentration (AUC 0-j) and t
infinity (AUCo-oo)
B. Tmax
C. Cmax
D. Elimination rate constant (K)
F C
22.The statistical methodology for
analyzing bioequivalence studies is called
A.
B.
C.
D.
E.
two one sided test procedure
analysis o f variance
cross over studies
parallel studies
none
23. Which o f the following statements is
wrong?
A. the first o f the two sided tests
determine whether a generic product
(test), when substituted for a brand
product (reference) is significantly
less bioavailable
B. the second o f the two sided tests
determine whether a brand name
product when substituted for a
generic product is significantly less
bioavailable
C. The second o f the two sided tests
determine whether a brand name
product when substituted for a
generic product is significantly more
bioavailable
D. The plasma drug concentration
versus time curve is most often used
to measure the systemic
bioavailability o f a drug from a drug
product
E. None
24.In two one sided test procedure the
difference for each o f statistical test
methods was said to be significant if it is
greater than:
A.
B.
C.
D.
E.
80%
40%
20%
60%
none
25.In bioequivalence studies, an analysis o f
variance (ANOVA) should be performed
on
A. AUC and Cmax values obtained
directly from each subject
B. Log transformed AUC and Cmax
values obtained from each subject
C. The relative bioavailability
D. A and C
E. None
may be encountered while determining their
bioequivalence
26.The bioavailability studies
recommended for drug products where
plasma concentrations are not useful to
determine delivery o f the substance to the
site o f activity are:
A. in vitro studies
B. equivalence studies with
pharmacodynamic end points
C. equivalence studies with clinical
end points
D. in vivo bioequivalence studies
E. All except D
27.Bioequivalence study is not required for
all o f the following products except
A.
B.
C.
D.
E.
Parenteral solutions
oral solutions
tablets
ophthalmic solution
none
28.For which o f the following products the
plasma concentrations are not useful to
determine delivery o f the drug substance to
the site o f activity?
A.
B.
C.
D.
E.
inhalers
nasal sprays
topical products applied to the skin
capsules
all except D
29.The confidence interval in ANOVA for
both pharmacokinetic parameters, AUC and
Cmax must be entirely within:
A.
B.
C.
D.
80%
70%
60%
75%
to
to
to
to
125%
130%
135%
140%
DIRECTION [30-34]: Match the
following drugs with the problem, which
A.
B.
C.
D.
E.
propranolol, verapamil
phenytoin
cholestyramine resin, sulcralfate
selegilene
probucol
30.Drugs with non linear pharmacokinetics
31.Drugs with long elimination half-life
32.Drugs with active metabolites
33.Drugs with highly variable
bioavailability
34.Orally administered drugs that are not
systemically absorbed
35. Which one o f the following is wrong
about bioequivalence study using
pharmacodynamic measurements?
A. they aTe difficult to obtain and the
data tend to be variable requiring
large number o f subjects compared
to the bioequivalence studies for
systemically absorbed drugs
B. a bioequivalence study using
pharmacodynamic measurements
tries to obtain a pharmacodynamic
effect versus time profile for the
drug in each subject
C. the area undeT the effect versus time
profile, peak effect and time to peak
effect are obtained for the test and
reference products and are then
statistically analyzed
D. they can be used for drugs in which
plasma concentrations are useful to
determine delivery o f the drug
substance to the site o f activity
E. None
36.A method that has been suggested for
measuring the bioequivalence o f topical
products intended for local activity is
A.
B.
C.
D.
E.
dermatology
dermatopharmacokinetics
pharmacodynamic measurement
toxicokinetics
none
37. Generic drug substitution is the process
o f dispensing
A. a generic product in place o f a brand
name product
B. a generic product in place o f another
generic product
C. a drug from one class to replace a
drug from another class having the
same indication.
D. A and B
E. None
38.Generic drug products that are classified
as therapeutic equivalents by the FDA are
expected
A. to produce the same clinical effects
as the prescribed drug
B. to produce the same safety profile as
the prescribed drug
C. to be products o f the same company
D. A and B
E. None
39. Which o f the following statements are
TRUE about prescribability?
A. it refers to the measurement of
average bioequivalence in which the
comparison o f population means of
the test and reference products falls
within the acceptable criteria
B. it refers to the measurements
pharmacokinetics parameters useful
in bioequivalence studies
C. it is the current basis for FDA
approval o f therapeutic equivalent
generic drug products
D. A and C
E. None
40. Which one o f the following statements
is NOT TRUE about switchability?
A. it refers to the measurement of
individual bioequivalence
B. it requires knowledge o f individual
variability (intra-subject variability)
and subject-by-formulator effect
C. it assures that the substituted generic
drug product produces the same
response in the individual patient
D. It is the method o f determining the
concentration o f a drug in a blood
sample.
E. None
41 .Which o f the following represent a pair
o f therapeutic alternative?
A.
B.
C.
D.
E.
Amoxicillin - ampicillin
Nifedipine - propranolol
Amoxicillin -Rifampicin
Aspirin - celecoxib
None
42. A formulary is
A.
B.
C.
D.
E.
a list of drugs
a list o f industrial chemicals
a list o f poisonous substances
a list o f all laboratory chemicals
None
43.A formulary which lists all the drugs
that may be substituted is
A.
B.
C.
D.
E.
positive formulary
negative formulary
neutral formulary
restrictive formulary
none
44. The FDA annually publishes approved
drug products with therapeutic equivalence
evaluation, the book is known as
A.
B.
C.
D.
E.
Orange book
USP
BP
National formulary
None
45. Which o f the following may have a
formulary that provides guidance for drug
product substitution?
A.
B.
C.
D.
E.
various hospitals
insurance plans
health maintenance organizations
All o f the above
None
Bioavailability and Bioequivalence
B. the active therapeutic moiety has
C. if its value is less than 1. the
Answers
Bioavailabilty and Bioequivalece
]. Answer: B. Measurements intended to reflect the rate and extent to which the active
ingredient becomes available at the site o f action
Explanation:
Bioavailability is the measurement o f the rate and extent to which the active ingredient becomcs
available at the site o f action. Bioavailability is also considered as a measure o f the rate and
extent o f therapeutically active drug that is systemically absorbed .For drug products that are not
intended to be absorbed into the blood stream, bioavailability may be assessed by measurements
intended to reflect the rate and extent to which the active ingredient becomes available at the site
o f action.
2. Answer: E. C and D
Explanation: Pharmaceutical equivalents are drug products that contain the same therapeutically
active drug ingredients(s); same salt, ester or chemical from; are o f the same dosage form; and are
identical in strength, concentration and route o f administration. Pharmaceutical equivalents may
differ in characteristics such as shape , scoring configuration ,release mechanisms, packaging ,and
excipients (including colors ,flavoring, and preservatives).
3. Answer: B. Generic drug products require Full New drug application for approval by the
FDA.
Explanation: The generic drug product requires an Abbreviated New Drug Application for
approval by the FDA.
Reference drug product is usually the currently marketed, brand name product with a full New
drug application approved by the FDA.
Generic drug product is marketed after patent expiration o f the reference drug product
4. Answer: C. They need not necessarily be bioequivalent.
Explanation: Therapeutic equivalent drug products are pharmaceutical equivalents that can be
expected to have the same clinical effect and safety profile when administered to patients under
the same conditions and they are shown to have same bioequivalence.
5. Answer: D. Doxycycline hydrochloride versus Tetracycline hydrochloride.
Explanation: Pharmaceutical alternatives are drug products that contain the same therapeutic
moiety but are different salts, esters, or complexes (e.g tetracycline hydrochloride versus
tetracycline phosphate) or are different dosage forms (e.g tablet versus capsule; immediaterelease dosage forms versus controlled release dosage form) or strengths. Doxycycline
hydrochloride and Tetracycline hydrochloride do not contain the same therapeutic moiety thus
they are not Pharmaceutical alternatives.
6. Answer: E. All o f the above
Explanation: Bioavailability and bioequivalence may be determined using Pharmacokinetic
studies, Measurement o f an acute pharmacodynamic effect, Comparative clinical studies or in
vitro studies.
7. Answer: E. A and B
Explanation: In the determination o f bioequivalence and bioavailability the choice o f study
method is based up on the ability o f the study design to compare drug delivered to that site by the
two products.
The choice should not be based on the preference o f the person doing the study or dose o f the
drug.
8. Answer: E. A and B
Explanation: Acute pharmacodynamic effects, such as changes in heart rate, blood pressure,
electrocardiogram (ECG), clotting time, or forced expiratory volume can be used to measure
bioavailability when no assay for plasma drug concentration is available or when the plasma drug
concentration does not relate to the pharmacological response(e.g a bronchodilator such as
albuterol given by inhalation).
9. Answer: A. Onset time
Explanation: The time taken by a drug to achieve minimum effective concentration after
administration o f drug is Onset time.
Duration o f action is the time for which the drug concentration remains above the minimum
effective concentration.
Time for peak plasma concentration is the time taken by a drug to reach Peak plasma
concentration^ max).
Half-life o f a drug is the time taken for h alf o f the drug to be eliminated.
10. Answer: E. If two oral products contain the same amount o f active drug but different
excipients, the dosage form that yields the faster rate o f drug absorption has the longer T
(Time for peak plasma drug concentration)
m ax
Explanation: If two oral products contain the same amount o f active drug but different excipients,
the dosage form that yields the faster rate o f drug absorption has the shorter T ma* (Time for peak
plasma drug concentration).
11 .Answer: A. Amount or extent o f absorption
Explanation: Area under the concentration versus time curve (AUC) relates to the amount or
extent o f drug absorption.The amount o f systemic drug absorption is directly related to the AUC.
The AUC is usually calculated by the trapezoidal rule and is expressed in units o f concentration
multiplied by time ( eg. mg x hr/ml)
12. Answer: E. All of the above
Explanation: All o f the above statements are true.
13. Answer: A. the active therapeutic moiety is excreted unchanged in significant quantity in
the urine
Explanation: Measurement o f urinary excretion can determine bioavailability from a drug
product. This method is most accurate if the active therapeutic moiety excreted unchanged in
significant quantity in the urine, so the assay will be only to determine the unchanged drug and
this provides more accuracy in determining the amount o f drug excreted.
14. Answer: C. The time for the drug to be completely excreted corresponds to the gap between
drug absorption and determination o f the amount o f drug absorbed systemically.
Explanation: In the measurement o f urinary drug excretion (in the determination of
bioavailability) the time for the drug to be completely excreted corresponds to the total time for
the drug to be systemically absorbed and completely excreted after administration.
15. Answer: C. if its value is less than 1, the reference and the products under examination have
the same bioavailability
Explanation: Relative bioavailability is the systemic bioavailability o f the drug from a dosage
form as compared to a reference standard given by the same route o f administration. Relative
bioavailability is calculated as the ratio o f the AUC for the dosage form to the AUC for the
reference dosage form.
16. Answer: A. the ratio o f the AUC for the dosage form given orally to the AUC obtained after
IV drug administration
Explanation absolute bioavailability is the fraction o f drug systemically absorbed from the dosage
form. It is calculated as the ratio o f the AUC for the dosage form given orally to the AUC
obtained after IV drug administration.
17.Answer: B. 80% of the drug was systemically available from the oral dosage form
Explanation An F value (absolute bioavailability) of 0.8 (80%) indicates that only 80% o f the
drug was systemically available from the oral dosage form.
18. Answer: B. products in which the bioavailability o f the active ingredient is affected by food
Explanation: If the bioavailability o f the active ingredient is known to be affected by food, the
generic drug manufacturer must include a single-dose, randomized, cross over, food effects
study comparing equal doses o f the test and reference products.
19.Answer: A. Fat rich food
Explanation: In food intervention studies the reference and test products are given immediately
after a standard high-fat content breakfast.
20.
Answer: A. long half-life
Explanation: In Cross over studies the drugs are given to the subjects alternatively, thus they can
not be used in drugs with long half-lives (there may be carry over effect i.e the results o f the two
products will interfere with each other). For drugs having long half-lives parallel study design is
recommended.
21 .Answer: E.Cmin
Explanation: Pharmacokinetic analysis o f bioavailability data includes calculation for each
subject o f the AUC to the last quantifiable concentration AUC to the last quantifiable
concentration (AUC 0-t ) and to infinity (AUCo-oo), Tmax, Cmax . Additionally, the elimination
rate constant (K), the elimination half-life, and other parameters may be estimated.
22.Answer: A. two one sided test procedure
Explanation: Cross over and parallel studies are study designs. The statistical methodology for
analyzing bioequivalence studies is called two one sided test procedures.
23.
Answer : C. The second o f the two sided tests determine whether a brand name product when
substituted for a generic product is significantly more bioavailable.
Explanation: In the analysis o f bioequivalence studies two situations are tested by the two one­
sided test procedure.
- the first o f the two sided tests determine whether a generic product (test), when substituted for a
brand product (reference) is significantly less bioavailable.
- the second o f the two sided tests determine whether a brand name product when substituted for
a generic product is significantly less bioavailable.
24.Answer: C. 20%
Explanation: Based on the opinions o f FDA medical experts, a difference o f greater than 20% for
each o f statistical test methods was determined to be significant and therefore, undesirable for all
drug products
25. Answer : B. Log transformed AUC and Cmax values obtained from each subject
Explanation: Jn bioequivalence studies, an analysis o f variance (ANOVA) should be performed
on the Log transformed AUC and Cmax obtained from each subject.
26.Answer: E. All except D
Explanation: Alternate methods such as in vitro studies or equivalence studies with clinical or
pharmacodynamic end points are used for drug products where plasma concentrations are not
useful to determine delivery of the substance to the site o f activity.
27.Answer: C. tablets
Explanation: No bioequivalence study is required for certain drug products given as a solution
such as o ra l,parenteral, ophthalmic , or other solutions because bioequivalence is self-evident.
For solid dosage forms such as tablets, capsules bioequivalence study is a must.
28.Answer: E. all except D
Explanation: Inhalers, nasal sprays and topical products applied to the skin are intended to act
locally, thus plasma concentrations are not useful to determine delivery o f the drug substance to
the site o f activity. For dosage forms such as capsules the plasma concentration is a good measure
o f the extent o f absorption and the amount o f drug which reaches the site o f activity.
29.Answer: A. 80% to 125%
Explanation: The confidence interval for both pharmacokinetic parameters, AUC and Cmax must
be entirely within 80% to 125% boundaries. Because the mean o f the study data lies in the
center o f the 90% confidence interval, the mean o f the data is usually close to 100% (a reference
ratio o f 1).
30.Answer: -[B]
31.Answer: -[E]
32.Answer: -[D]
33.Answer: -[A]
34.Answer: ~[C]
Explanation:
Drugs with non linear pharmacokinetics result in problems o f bioavailability. Nonlinear
pharmacokinetics is also known as capacity-limited, dose-dependent, or saturation
pharmacokinetics. Nonlinear pharmacokinetics does not follow first-order kinetics as the dose
increases. Nonlinear pharmacokinetics may result from the saturation o f an enzyme-or carriermediated system.
,
Characteristics o f non linear pharmacokinetics include:
- The AUC is not proportional to the dose]
- The amount o f drug excreted in the urin^ is not proportional to the dose.
- The elimination half-life may increase at high doses.
The ratio o f metabolites formed changes witli increased dose.
Another problem while
determining bioavailability is long eliminaticjn half-life for some drugs. If the elimination half-life
is long, there may be carry over effects for the products compared and this may result in wrong
figures which in turn leads to wrong conclusion. Determining the bioavailability o f drugs with
active metabolites may be difficult because tne assay methods available can not determine all
metabolites.
35. Answer; D. they can be used for drugs iiji which plasma concentrations are useful to
determine delivery o f the drug substance tojthe site o f activity
Explanation: Pharmacodynamic measurements are more difficult to obtain and the data tend to be
variable requiring large number o f subjects Compared to the bioequivalence studies for
systemically absorbed drugs.
A bioequivalence study using pharmacodynamic measurements tries to obtain a
pharmacodynamic effect versus time profile for the drug in each subject. The area under the
effect versus time profile, peak effect and tijme to peak effect are obtained for the test and
reference products and are then statistically analyzed.
For drugs in which plasma concentrations are useful to determine delivery o f the drug substancc
to the site o f activity direct determination o f the plasma concentration is recommended instead o f
pharmacodynamic measurements.
36.Answer: B. dermatopharmacokinetics
Explanation: In vitro studies may require th<e development o f a reliable marker that may be
correlated with human in vivo bioavailabil ty data. For example, the penetration o f drug into
layers o f skin with respect to time (dermato;pharmacokinetics) has been suggested as a method for
measuring the bioequivalence o f topical drtig products intended for local activity.
37.Answer: D. A and B
Explanation: Generic drug substitution is the process o f dispensing a generic drug product in
place o f the prescribed drug product (e.g., generic product for brand name product, generic
product in place o f another generic product, a brand name product for a generic product).
3 8.Answer: D. A and B
Explanation: Generic drug products that are classified as therapeutic equivalents by the FDA are
expected to produce the same clinical effect and safety profile as the prescribed drug.
39.Answer: D. A and C
Explanation: Prescribability refers to the measurement o f average bioequivalence in which the
comparison of population means o f the test and reference products falls within the acceptable
criteria. Prescribability is the current basis for FDA approval of therapeutic equivalent generic
drug products.
40.
Answer: D. It is the method o f determining the concentration o f a drug in a blood sample.
Explanation: switchability refers to the measurement of individual bioequivalence, which requires
knowledge o f individual variability (intra-subject variability) and subject-by-formulator effect. It
assures that the substituted generic drug product produces the same response in the individual
patient.
It is not a method o f determining the concentration o f a drug in a blood sample.
41 .Answer: A. Amoxicillin - ampicillin
Explanation: Therapeutic substitution is the process o f dispensing a therapeutic alternative in
place o f the prescribed drug product. The substituted drug product is usually in the same
therapeutic class (e.g. calcium channel blocker) and is expected to have the similar clinical
profile. For example amoxicillin is dispensed for ampicillin. Nifedipine (calcium channel blocker)
and propranolol (p-blocker) are antihypertensive drugs, but they are not o f the same class, thus
they are not therapeutic equivalents. Amoxicillin and Rifampicin have different clinical
indications and they do not belong to the same class, thus they are not therapeutic equivalents.
Aspirin (salicylates) and celecoxib (a selective cyclooxygenase inhibitor) are nonsteriodal anti­
inflammatory drugs but they belong to different classes and their clinical profiles are the same,
thus they are not therapeutic equivalents.
42. Answer : A. a list o f drugs
Explanation: A formulary is a list o f drugs.
It is not a list o f all molecules that have pharmacological activity, industrial chemicals or
poisonous substances.
43.Answer: A. positive formulary
Explanation: A positive formulary lists all the drugs that may be substituted (after prescription),
where as a negative formulary lists drugs for which the pharmacist may not substitute.
44.Answer: A. Orange book
Explanation: The FDA annually publishes approved drug products with therapeutic equivalence
evaluation, the book is known as the Orange book.
45. Answer: D. All o f the above
Explanation: Various hospitals, institutions, insurance plans, health maintenance organizations,
and other third-party plans may have a formulary that provides guidance for drug product
substitution.
Bioavailability and Bioequivalence
Explanation
T “r
phannacokineiirs
7
WemS
Nonlinear
dose-dependem, or d u ratio n
Biochemistrty
Organic chemistry is the chemistry of carbon compounds. Biochemistry is the
study of carbon compounds that crawl
M ike Adam
1. Which
of
the
monosaccharide?
A.
B.
C.
D.
E.
following
Sucrose
Maltose
Dextrose
Lactose
Cellulose
2. “Pyranose” is the systematic name for
A. Straight chain mono-saccharides
B. Five membered acyclic mono­
saccharides
C. Cyclic five membered mono­
saccharides
D. Cyclic six membered mono­
saccharides
E. Acyclic di-saccharides
3. “Mutarotation” refers to change in
optical rotation
due to
conversion of
A. Either the pure □- or pure Danomer of a monosaccharide into
an equilibrium
B.
mixture of both forms
C. □ -anomer to □ -anomer
D.
-anomer to -anomer
E. anomer to epimer
F. None
4. Human intestinal tract is able to
secrete enzymes that can hydrolyze
the below mentioned carbohydrates
EXCEPT
A.
B.
C.
D.
E.
Lactose
Cellulose
Maltose
Starch
Sucrose
5. Decarboxylases and Deaminases are
the enzymes, which catalyze the
removal of functional groups by the
process other than hydrolysis, will fall
into the category
A. Ligases
B. Hydrolases
C.
D.
E.
F.
is
6.
Lyases
Transferases
Isomerases
Oxidoreductases
Pyrimidine base that is found only in
RNAis
A.
B.
C.
D.
E.
Thymine
Cytosine
Adenine
Guanine
Uracil
7. Which of the following are building
blocks of Proteins
A.
B.
C.
D.
E.
Amino acids
Pyrimidines
Nucleotides
Monosaccharides
Purines
8. The structure of protein that gives
information regarding sequence of
amino acids and location of disulfide
bonds is
A.
B.
C.
D.
E.
Primary structure
Secondary structure
Tertiary structure
Quaternary structure
None
*
9. Which of the following is Hetero
polysaccharide
A.
B.
C.
D.
E.
Starch
Heparin
Glycogen
Cellulose
None
10. Bonds present in Carbohydrates are
A.
B.
C.
D.
E.
Peptide bonds
Glycosidic bonds
Phosphodiester bonds
Disulfide bonds
Amide bonds
11. Which o f the following serves as a
template for required protein synthesis
A.
B.
C.
D.
E.
rRNA
mRNA
tRNA
DNA
None
12. N-acetyl-D-glucosamine and N-acetylmuramic acid moieties are
alternatively present in the
heteropolysaccharide
A.
B.
C.
D.
E.
Glycogen
Cellulose
Heparin
Hyaluronic acid
Starch
13. Which o f the following are Nucleic
acids?
A.
B.
C.
D.
E.
DNA&RNA
Purines & Pyrimidines
Thymine & Cytosine
Adenine & Guanine
Glycine & Alanine
A. In DNA, three ot-helical strands
are present
B. The strands in DNA are anti­
parallel - the 51. 31 - inter
nucleotide phophodiester bonds
are in opposite directions.
C. Adenine & Thymine are linked by
triple bond whereas Guanine &
Cytosine are linked by double
bonds.
D. AUG & GUG are terminating
codons
E. UAG & UAA are starting codons
17. The phenomenon o f reactions, which
involve consumption of energy to
form new biochemical compounds is
termed as
A.
B.
C.
D.
E.
Anabolism
Catabolism
Amphibolic pathway
Anaplerotic reactions
None
18. Formation of glucose from non­
carbohydrate source is known as
14. Backbone o f Nucleic acids is
A. Pyrimidines
B. Purines
C. Alternating sugar & phosphate
units, each one further attached
with a base
D. Proteins
E. Lipids
15. Which of the following statement is
FALSE
A. DNA doesn’t contains hydroxyl
group at the pentose C2 position
B. DNA contains Thymine instead of
Uracil
C. DNA contains Uracil instead o f
Thymine
D. The successive nucleotides are
joined by phosphodiester bonds.
E. Nucleotides are the backbones of
Nucleic acids
16. Which of the following statement is
TRUE
A.
B.
C.
D.
E.
Glycolysis
Glycogenesis
Glycogenolysis
Gluconeogenesis
None
19. Which o f the following reaction is
coupled with electron transport
system, from which the released
energy is used to form ATP in
mitochondria
A.
B.
C.
D.
E.
Substrate level phosphoiylation
Oxidative phosphorylation
Anabolism
Catabolism
None
20. Upon metabolism, Triglycerides are
converted to
A.
B.
C.
D.
E.
Fatty acids & glycerol
Amino acids
Monosaccharides
Uric acid
None
21. Metabolism of steroids
produce the metabolite
A.
B.
C.
D.
E.
not
27. Aspartate, Glutamate, Glycine, Formyl
tetra hydrofolate and carbon dioxide
involves in synthesize of
Bile acids
Insulin
Vitamin D
Cortisone
Estrogen
22. Human
beings
synthesize
A.
B.
C.
D.
E.
may
are
unable
to
Bile acids
Pyruvic acid
Succinic acid
Linoleic acid
Glycogen
23. Which of the following does not come
under Terpenes
A.
B.
C.
D.
E.
Cholesterol
Vitamin A
Vitamin K
Bile acid
Vitamin C
24. Nitrogen metabolism involves
metabolism of
A.
B.
C.
D.
E.
Steroids
Carbohydrates
Nucleic acids & amino acids
Lipids
Fatty acids
25. Which of the following is essential
amino acid
A.
B.
C.
D.
E.
Glycine
Leucine
Alanine
Tyrosine
Proline
26. In amino acid metabolism, after
removal of amino group, the carbon
skeleton will be metabolized into any
of the below EXCEPT
A.
B.
C.
D.
E.
Ketogenic amino acids
Glycogenic amino acids
Carbon dioxide
Water
Cyanocobalamine
A.
B.
C.
D.
E.
Purines
Pyrimidines
Steroids
Proteins
Carbohydrates
28. Krebs-Henseleit
synthesis of
A.
B.
C.
D.
E.
pathway
involves
Vitamin-B]2
Estrogen
Phosphatidyl choline
Sphingolipids
Urea
29. An enzyme that is complete and
catalytically active is called as
A.
B.
C.
D.
E.
Co-enzyme
Prosthetic group
Holoenzyme
Apoenzyme
Co-factor
30. Drugs like Nitroglycerine and Aspirin
undergo degradation mostly by
A.
B.
C.
D.
E.
Oxidation
Hydrolysis
Reduction
Glucuronization
Sulfation
ANSWERS
Biochemistry
1. Answer: C. Dextrose
Explanation:
Monosaccharide is the simple carbohydrate, which cannot be further hydrolyzed.
Dextrose is D-glucose monohydrate, a monosaccharide usually obtained by the
hydrolysis o f starch. Sucrose, Maltose and Lactose are Di-saccharides, which contains
two monosaccharides joined covalently by glycosidic bonds. Sucrose is composed of
glucose and fructose; Maltose is composed o f two glucose molecules; Lactose also called
as “milk sugar” consists o f glucose and galactose. Whereas Cellulose comes under
Polysaccharides (which are long chain polymers o f monosaccharides may be either linear
or branched) which is linear and unbranched.
H "1
H
HO
H
HU
H
H
= 0
UH
D-galactose
(aldehyde)
H
HU
H
H
Ul i
UH
OH
HU
"H
HO — — H
N
dh
D-glucose
(aldehyde)
.
— OH
UM
H — — OH
OH
D-fructose
(ketone)
D-itunitose
(aldehyde)
2. Answer: D. Cyclic six membered mono-saccharides
Explanation:
The systematic names o f ‘straight chain’ monosaccharides are based on a stem
name indicating the number o f carbon atoms, a prefix indicating the configuration o f the
hydroxy group and either the suffix -ose (aldoses) or -ulose (ketoses). In addition the
name is also prefixed by the D- (dextro rotatory) or L- (Levo) as appropriate according to
the configuration o f their pentultimate CHOH group. In the D form this hydroxy group
projects on the right o f the carbon chain towards the observer whilst in the L form it
projects on the left o f the carbon chain towards the observer when the molecule is viewed
with the unsaturated group at the top.
Five membered ring monosaccharides have the stem name 'furanose whilst six
membered ring compounds have the stem name pyranose together with the appropriate
configurational prefixes indicating the stereochemistry o f the anomers. Monosaccharides
in which one o f the hydroxy groups has been replaced by a hydrogen atom have the
prefix deoxy- with the appropriate locant, except if it is at position 2, when no locant is
given.
Some monosaccharides may also be classified as epimers. Epimers are compounds that
have identical configurations except for one carbon atom. For example, D-D-glucose and
□ -D-fructose are epimers. Another e.g., L-D-glucose and D-D-mannose are also
epimers.
4.
Answer: B. Cellulose.
Explanation:
Cellulose, linear unbranched polymer o f D-glucose, is a water insoluble structural homo
polysaccharide present in plant cell walls. Human beings are unable to digest cellulose
because the human intestinal tract doesn’t secrete any enzyme that can hydrolyze
cellulose. Lactose also called as “milk su g ar’ will get hydrolyzed by the enzyme Lactase
into its components glucose and galactose; Maltose by maltase enzyme into two
molecules o f glucose,; Sucrose by sucrase enzyme into glucose and fructose. Starch a
homo polysaccharide can also be hydrolyzed by salivary or pancreatic enzyme amylase
into monosaccharides (glucose, dextrose) and/or Oligosaccharides (maltose).
5. Answer: C. Lyases
Explanation:
Lyases are the enzymes that catalyze the removal o f functional groups.
E.g., Decarboxylation reaction by decarboxylase enzyme and Deamination reaction by
deaminase enzyme.
I f the reaction involves hydrolysis catalyzed by enzymes like proteolytic enzymes,
amylases, esterases they are classified as Hydrolases.
Ligases are enzymes that catalyze coupling o f molecules. E.g., DNA ligase (Participates
in DNA synthesis by coupling nucleotides).
Transferases catalyze the transfer o f groups E.g., Phosphate and amine groups.
Isomerases catalyze various isomerization reactions. E.g., Conversions like D-form to Lform and Cis-form to Trans-form isomers and vice-versa.
Oxidoreductases catalyze reactions involving oxidation step. E.g., Dehydrogenase,
Peroxidase, Oxidase (Participates in drug metabolism).
6.
Answer: E. Uracil
Explanation:
Uracil is the pyrimidine base found only in RNA. Thymine and Cytosine are also
pyrimidine bases but former is found in both DNA and RNA whereas latter is found only
in DNA. Adenine and Guanine are purine bases that are found in both DNA and RNA.
"N H ^O
Adenine (A)
7.
Guanine (G)
Answer: A. Amino acids.
Thymine (T)
^ tS -T ^ O
Cytosine (C)
"N h f^ O
Uracil (U)
Explanation:
Proteins are polymeric compounds composed o f amino acids (contains both amino group
and carboxylic acid group) as their building blocks linked together by peptide bonds.
Peptide bonds are links between carbonyl carbons ( C — O ) anc| amino nitrogen’s.
Nucleotides are the building blocks o f Nucleic acids. Nucleotides consist o f three
different molecules linked with covalent bonds. (1) Organic heterocyclic base: either
pyrimidine or purine, (2) Sugar moiety: Pentose (Ribose/deoxy-ribose, 5-carbon
monosaccharide) and (3) Phosphoric acid group.
Nucleoside contains only organic base and pentose moiety.
Organic base + Pentose = Nucleoside.
Organic base + Pentose + Phosphoric acid group = Nucleotide.
Linear polymers o f Nucleotides = Nucleic acids.
Nucleic acid types = DNA and RNA.
X
N-—
HO
WH,
1
M
//
\
NH'
W'
Adenine
(Pyrimidine base)
<r
HQ
\ X
p
OH
Adenosine
(Deoxy-nucleoside)
(Base + pentose)
(Deoxyribonucleoside)
(Ribo-nucleoside)
Similarly,
Guanine linked to ribose = riboguanosine
Thymine linked to ribose = Thymidine
Cytosine linked to deoxyribose = Deoxycytidine
Uracil linked to ribose = Uridine
Adenosine mono phosphate (AMP)
(Deoxy-nucleotide)
(Base + pentose + phosphate)
(Ribo-nucleotide)
Monosaccharide is the simple carbohydrate, which cannot be further hydrolyzed and is
the building block o f Oligosaccharides and Polysaccharides.
8.
Answer: A. Primary structure.
Explanation:
Proteins are polymers o f amino acids that are linked together by peptide bonds (i.e., link
between carbonyl carbon and amino nitrogen). Proteins have four structural levels, each
level reveals about particular information:
Primary structure: Sequence o f amino acids and location o f disulfide bonds present in
proteins.
Secondary structure: Spatial arrangement of sequential amino acids (Ex. Helix (aconformation) and Pleated sheet (P-conformation))
Tertiary structure: Three-dimensional structure o f a single protein.
Quaternary structure: Arrangement o f individual subunit chains into complex molecules.
9. Answer: B. Heparin.
Explanation:
Polysaccharides, also called as Glycans, are long chain polymers o f carbohydrates. They
are either homo- or hetero- polysaccharides and linear or branched.
Starch (composed of two glucose polymers: Amylose (linear and water soluble) and
amylopectin (highly branched and water-insoluble)), Glycogen (branched chain o f Dglucose) and Cellulose (Linear, unbranched and water insoluble polymer o f
Dglucose) comes under Homo polysaccharides.
Heparin, an acid muco polysaccharide, comes under Hetero polysaccharide. It consists o f
a variably sulfated repeating disaccharide unit. The main disaccharide units that occur in
heparin are 2-O-sulfated iduronic acid and N-sulfated glucosamine.
10. Answer: B. Glycosidic bonds.
Explanation:
-
Glycosidic bonds are present in carbohydrates to link monosaccharides and produce
Oligosaccharides and polysaccharides. This is a type o f covalent chemical bond that joins
two simple sugars via an oxygen atom (-0-). The bond may be either above the plane of
the ring as in a beta glycosidic bond or below the plane as in an alpha glycosidic linkage
A peptide bond is a chemical bond formed between two molecules when the carboxyl
group o f one molecule reacts with the amino group of the other molecule (-CO-NH-),
releasing a molecule o f water (H 2 O).
Disulfide bonds are also present in proteins. Disulfide bond is a single covalent bond
derived from the coupling o f thiol groups. The linkage is also called an SS-bond or
disulfide bridge (-C-S-S-C-). E.g., Insulin.
Phosphodiester bonds are present in both DNA and RNA to join successive nucleotides
between 5'-hydroxyl group o f one nucleotide’s pentose and S'-hydroxyl group o f the next
nucleotide’s pentose.
11. Answer: B. mRNA.
Explanation:
DNA and RNA are examples of Nucleic acids. RNA will be in three forms.
rRNA (ribosomal RNA): rRNA is a component o f the ribosomes. It consists o f 30S and
50S subunits and acts as framework to bind both messenger and transfer RNA.
mRNA (messenger RNA): mRNA is a copy o f the information carried by a gene on the
DNA. The role o f mRNA is to move the information contained in DNA to the translation
machinery for required protein synthesis and specifies a polypeptide’s amino acid
sequence.
tRNA (transfer RNA): tRNA is the information adapter molecule. It brings the activated
amino acids over the growing polypeptide chain at ribosomes.
12. Answer: D. Hyaluronic acid
Explanation:
Hyaluronic acid is a component o f synovial fluid, and is found in the vitreous humor of
the eye, the synovia of joints, and in subcutaneous tissue where it functions is as a
cementing agent. Hyaluronic acid is a glycosaminoglycan with alternating units o f Nacetyl-D-glucosamine and N-acetyl-muramic acid.
Glycogen (compact branched chain o f D-glucose) and Cellulose (Linear, unbranched &
water insoluble polymer o f D-glucose) comes under Homo polysaccharides.
Heparin, even though Hetero polysaccharide, is an acid muco polysaccharide, consisting
o f sulfate derivatives o f N-acetyl-D-glucosamine and D-iduronate.
13. Answer: A. DNA & RNA
Explanation:
DNA (Deoxyribonucleic acid) and RNA (Ribonucleic acid) are the two main types of
Nucleic acids. They are made up o f Nucleotides (building blocks o f Nucleic acids),
which include pyrimidine and purine bases linked to ribose or deoxyribose sugars
(nucleosides) and bound to phosphate groups.
RNA is o f three types: mRNA (messenger RNA), tRNA (transfer) and rRNA (ribosomal
RNA).
Pyrimidine bases: Cytosine (present in DNA & RNA)
Thymine (present only in DNA)
Uracil (present only in RNA)
Purine bases: Adenine (present in DNA & RNA)
Guanine (present in DNA & RNA)
Glycine and Alanine are the amino acids, which are building blocks o f Proteins.
14. Answer: C. Alternating sugar & phosphate units, each one further attached with a
base
Explanation:
Nucleic acids are made up o f Nucleotides, which contain Nucleosides (Pyrimidine or
Purine base attached to ribose or deoxyribose sugar moiety) attached to phosphate group.
In this the backbone is having alternating sugar (pentose) & phosphate units each one
further attached with a purine or pyrimidine base.
Sugar---- C ------- G — Sugar
,
A
i
I
0
o —P^O
.
i
I
O— P —Q
I
Q
Sugar----- T --------- A — Sugar
1
0
O — i’= G
1
O
I
O
O— P = 0
O
I
I Sugar— G ------- C -J-S u g a r
5’ End | ~—
I 3’ End
Proteins are polymers o f amino acids linked together by peptide bonds.
Lipids are triglyceride esters o f fatty acids.
15. Answer: C.
Explanation:
The successive nucleotides are joined by phosphodiester bonds in both DNA and RNA.
Nucleotides [Nucleosides (Pyrimidine/Purine base + sugar moiety) + phosphate group]
are the building blocks of Nucleic acids
Both RNA and DNA are composed o f repeated units. The repeating units o f RNA are
ribonucleotide
monophosphates
and
of
DNA
are
2'-deoxyribonucleotide
monophosphates. That means DNA doesn’t contains hydroxyl group at the pentose C 2
position and it contains Thymine instead o f Uracil.
16. Answer: B. The strands in DNA are anti-parallel - the 5 1, 31 - inter nucleotide
phophodiester bonds are in opposite directions.
Explanation:
The prime features o f the DNA structure are:
•
•
•
•
•
•
•
•
•
two strands o f DNA wrap around each other
the strand polarities are opposite to each other and are anti-parallel
the sugar-phosphate hydrophilic backbone is on the outside
the hydrophobic bases are in the middle
it is a right-handed helix
there is a 2-fold axis o f symmetry
the bases are perpendicular to the axis o f symmetry
there is a wide (major) and a narrow (minor) groove between the backbones
on
opposite strands.
The 5 1, 3 1 —inter nucleotide phophodiester bonds (Phosphodiester bonds are present
in both DNA and RNA to join successive nucleotides between 5 '-hydroxyl group o f
one nucleotide’s pentose and 3 '-hydroxyl group o f the next nucleotide’s pentose) are
in opposite directions.
ON
V
•
f
?/
The strands are complementary i.e., the base sequence o f one strand determines the
base sequence o f the other.
Hydrogen bonds are present between specific base pairs. Adenine and Thymine are
linked by double bond ( A = T ) whereas Guanine and Cytosine are linked by triple
bond ( G ~ C ) .
<p»>
ti
}
j
O
D&HQritKue
iwktoe
f'i
residue
A -T tea* pair
-A -.
DeoxvriN*w?
re^kkie
n
£**C I*jbw p a r
For each amino acid recognition three codons are required. AUG and GUG are starting
codons whereas UAG (opra), UAA (ochra) and UGA (opal) are ending/terminating
codons also called as non-sense codons.
17. Answer: A. Anabolism
Explanation:
Anabolism is the phenomenon o f reactions (build up reactions involving synthesis of
complex molecules from simple molecules) that consume energy to form new
biochemical compounds e.g., Synthesis of: proteins from aminoacids, Glycogen from
glucose etc.
Catabolism is the phenomenon o f degradation reactions (break down reactions involving
conversion o f complex molecules to simple molecules), which releases energy e.g.,
Breakdown o f glycogen into glucose moieties, glucose into pyruvic acid (aerobic
pathway) or lactic acid (anaerobic pathway) etc.
Amphibolic pathways are those, which are used for both anabolic and catabolic processes
e.g., Krebs cycle involves both synthesis (Anabolism) o f new amino acids or heme (from
succinyl CoA) from the metabolites as well as breakdown o f molecules (Catabolism) to
yield major part o f the energy. Since metabolites are being used for the synthesis o f
amino acids or heme, the metabolite has to be replaced by intermediates from other
sources (e.g., glutamate from the breakdown o f protein forms a-ketoglutarate) also called
as Anaplerotic reactions.
18. Answer: D. Gluconeogenesis.
Explanation:
Gluconeogenesis: Formation o f glucose from non-carbohydrate sources like lactate,
pyruvate, krebs cycle metabolites and amino acids. Fatty acids cannot form glucose.
Glycolysis: Breakdown o f sugar phosphates (glucose, fructose) into pyruvate (aerobic
pathway) or lactae (anaerobic pathway). It takes place in cytoplasm.
Glycogenesis: Formation o f glycogen from glucose. It takes place in liver and muscles
and is controlled by pancreatic hormone insulin.
Glycogenolysis: Breakdown o f glycogen into glucose phosphate. It takes place in liver
and skeletal muscle and is controlled by hormones glucagons and epinephrine
19. Answer: B. Oxidative phosphorylation
Explanation:
Oxidative phosphorylation, which requires oxygen, involves formation of ATP
(Adenosine triphosphate) from the metabolite produced by oxidoreductase enzymes e.g.,
dehydrogenases; that uses FAD (Flavin adenine dinucleotide: obtained from vitamin
riboflavin) or NAD (Nicotinamide adenin dinucleotide: obtained from vitamin
nicotinamide) and coupled with electron transport system and the energy produced is
used to form ATP in the mitochondria.
Electron transport system accepts electron and hydrogen from the metabolites of Krebs
cycle upon oxidation and utilizes the energy produced to synthesize ATP in the
mitochondria.
Substrate level phosphorylation doesn’t need oxygen and involves the formation o f ATP
(Adenosine triphosphate) from metabolite e.g.. phosphoenol pyruvate to pyruvate,
succinyl CoA to succinate.
Anabolism is the phenomenon o f reactions (build up reactions involving synthesis of
complex molecules from simple molecules) that consume energy to form new
biochemical compounds e.g., Synthesis of: proteins from aminoacids, Glycogen from
glucose etc.
Catabolism is the phenomenon o f degradation reactions (break down reactions involving
conversion o f complex molecules to simple molecules), which releases energy e.g.,
Breakdown o f glycogen into glucose moieties, glucose into pyruvic acid (aerobic
pathway) or lactic acid (anaerobic pathway) etc.
20. Answer: A. Fatty acids & glycerol
Explanation:
Triglycerides are metabolized (hydrolysis) by the enzymes lipases into fatty acids and
glycerol. In that, fatty acids undergo beta oxidation and gets breakdown into acetyl CoA,
which further enters into Krebs cycle to complete the oxidation with the release o f energy
finally producing carbon dioxide and water. Excess breakdown o f fatty acids may leads
to Ketogenesis (release o f ketone bodies) whereas glycerol enters glycolysis cycle and
gets oxidized to pyruvate and through Krebs cycle gets oxidized to carbon dioxide and
water.
Upon metabolism proteins release amino acids whereas complex polysaccharides release
oligo- or mono- saccharides.
Purines with the action o f xanthine oxidase enzyme releases uric acid in humans.
21. Answer: B. Insulin
Explanation:
Upon metabolism steroids are converted to bile acids, vitamin-D or steroidal hormones
like estrogens, androgens, cortisone. Anyhow steroids won’t undergo complete broken
down.
Insulin is a pancreatic hormone (polypeptide containing 51 amino acids with two chains
A (21 amino acids) and B (30 amino acids) linked by disulfide bond) that controls
glucose uptake by the cells.
22. Answer: D. Linoleic acid
Explanation:
Linoleic acid is essential fatty acid that means it is not synthesized by the human body, so
it has to be taken by diet.
Bile acids, pyruvic acid, succinic acid and glycogen are formed within the body.
23. Answer: E. Vitamin C
Explanation:
Terpenes are synthesized from acetyl CoA via mevalonate pathway and include:
Cholesterol, other steroids, Fat soluble vitamins (A, D, E & K) and Bile acids. They
contain isoprene units as monomers
Vitamin C also called as Ascorbic acid is a water soluble vitamin that doesn’t contain any
isoprene unit, hence w on’t come under Terpenes.
24. Answer: C. Nucleic acids & amino acids
Explanation:
Nitrogen metabolism involves metabolism o f amino acids and nucleic acids (both
anabolism and catabolism)._________ _______ ______________________________________
Anabolism
Substrates
Products
Citric acid cycle intermediates
Carbonyl phosphate, aspartate, glutamate,
glycine, carbon dioxide and formyl tetra
hydrofolate.
Aspartate and carbamoyl phosphate
Aspartate, glutamate
Purines
Pyrimidines
Catabolism
Product
Metabolites
Amino acids
Purines
Pyrimidines
Acetyl CoA (ketogenic amino acids),
Krebs cycle intermediates (glycogenic
amino acids) and finally gets oxidized to
carbon dioxide and water
Uric acid
Carbon dioxide, ammonia and (3-alanine
25. Answer: B. Leucine
Explanation:
Amino acids can be classified as Essential and Non-essential amino acids.
Essential amino acids are those that cannot be synthesized by our body and hence to be
taken in diet. These include Histidine, Arginine, Methionine [HArM], Leucine, Lysine,
Phenylalanine [LLIP], Valine, Isoleucine, Threonine, Tryptophan [VITT]
Non-essential amino acids are those that are synthesized within our body. These include
Glycine, Alanine, Serine [GAS], Glutamine, Asparagine, Aspartic acid, Tyrosine
[GAAT], Glutamic acid Cystine, and Proline [GCP].
26. Answer: E. Cyanocobalamine
Explanation:
In amino acid metabolism after removal o f amino group, the carbon skeleton will be
metabolized into acetyl CoA (ketogenic amino acids) or to Krebs cycle intermediates
(glycogenic amino acids) and finally get oxidized to carbon dioxide and water for the
generation of energy.
Gluconeogensis involves formation o f glucose from non-carbohvdrate sources like
glycogenic amino acids.
Cyanocobalamine is a water-soluble vitamin also designated as Vitamin B12.
27. Answer: A. Purines
Explanation:
Purines are synthesized from complex reactions involving carbonyl phosphate, aspartate,
glutamate, glycine, carbon dioxide and formyl tetra hydrofolate.
Pyrimidines are synthesized from aspartate and carbamoyl phosphate.
Steroids are synthesized from acetyl CoA via mevalonate pathway.
Proteins are synthesized from amino acids whereas carbohydrates are synthesized from
monosaccharide units.
28. Answer: E. Urea
Explanation:
Krebs-Henseleit pathway involves synthesis of urea mainly in the liver.
Carbamoyl phosphate synthesized from Glutamine (produced from glutamate and
ammonia) and carbon dioxide, enters urea cycle and produces urea. Ammonia is obtained
from amino acids by the action o f enzyme, amino acid transferase (transaminase) using
pyridoxal phosphate (Vitamin B6) as coenzyme.
Phosphatidyl choline is a lipid compound that is important in cell membrane.
Sphingolipids contain sphingenine formed from palmitoyl CoA and serine. Sphingenine
is the backbone for various compounds like cerebrosides, gangliosides or sphingomyelin.
29. Answer: C. Holoenzyme
Explanation:
Enzymes are biocatalysts that enhance the rate o f a specific reaction by lowering its
activation energy. An enzyme may be a complex one in which the protein part is called
Apoenzyme.
A cofactor firmly bound to Apoenzyme is referred as Prosthetic group. Cofactor may be
an inorganic component (metal ion) or a non-protein organic component.
The organic cofactor that is not firmly bound to Apoenzyme but requires its participation
during enzyme catalysis is called as Coenzyme.
An enzyme that is complete and catalytically active is called as Holoenzyme.
All enzymes are proteins but all proteins are not enzymes.
30. Answer: B. Hydrolysis
Explanation:
Drugs undergo biotransformation under two phases. Phase I metabolism include
Oxidation, Hydrolysis and Reduction. Phase II metabolism include conjugation reactions
like Glucuronization, Sulfation, Acetylation, Methylation, Glutathione conjugation and
Amino acid conjugation.
Drugs like Nitroglycerine and Aspirin undergo degradation mostly by Hydrolysis.
Biopharmaceutics
“Fortune knocks but once, but misfortune has much more patience. ”
Laurence Peter
D. Types
1. Biopharmaceutics is the study o f the
relation o f the Physical and chemical
properties o f a drug in relation to its:
A.
B.
C.
D.
E.
Bioavailability
Pharmacokinetics
Pharmacodynamics
Toxicologic effects
All o f the above
2. A drug product contains the active
ingredient in association with which o f the
following:
A.
B.
C.
D.
Excipients
Impurities
Adulterants
Containers
3. The concept that includes the drug
formulation and the dynamic interaction
among the drug, its formulation matrix, its
container, and the patient.
A.
B.
C.
D.
Bioavailability
Drug product
Drug delivery system
Dosage form
4. Bioavailability is a measurement o f the
rate and extent o f which o f the
therapeutically active drug
A.
B.
C.
D.
Distribution
Elimination
Metabolism
Systemic absorption
5. What is studied in pharmacokinetics
about the drug movement in the body
during absorption, distribution, and
elimination is studied.
A. Time course
B. Mechanism
C. Receptors
6. Which one of the following represents a
WRONG pair?
A. Pharmacodynamics - relation o f the
drug concentration or amount at the
site o f action and its pharmacologic
response as a function o f time.
B. Pharmacokinetics - time course of
drug movement in the body during
absorption, distribution, and
elimination
C. Bioavailability - the amount o f drug
entering cells
D. A and C
7. A cell membrane is composed
primarily o f
A. Proteins and lipids
B. Polysaccharides and
monosaccharide
C. Alkaloids and terpenes
D. Tannins and Xanthenes
E. None
8. Which one o f the following is a means
o f transport o f drugs?
A.
B.
C.
D.
E.
Passive diffusion
Carrier mediated transport
Vesicular transport
Para cellular transport
All of he above
9. Which one o f the following drugs can
easily cross cell membranes as compared to
the others?
A.
B.
C.
D.
Polar drug
Drugs bound to Proteins
Drugs having high molecular weight
Non polar lipid -soluble drugs
having low molecular weight
10. Within the cytoplasm or in interstitial
fluid, most drugs undergo transport by:
A.
B.
C.
D.
Simple diffusion
Carrier mediated transport
Facilitated diffusion
Vesicular transport
11 .Passive transport across cell membranes
involves:
A. Successive partitioning o f a solute
between aqueous and lipid phases as
well as diffusion within the
respective phases.
B. Only diffusion across the lipid
bilayer
C. Only partitioning between aqueous
and lipid phases
D. Dissolution and disintegration.
12. Which o f the following have effect on
the ionization o f a weak electrolyte?
A. PH o f the media in which the drug is
dissolved.
B. PKa o f the drug
C. Crystallinity o f the drug
D. A and B
A. The surface area o f the plane across
which transfer occurs.
B. Thickness o f the region across
which diffusion occurs.
C. The difference in concentration o f
drug between the two points.
D. Diffusion coefficient o f the drug.
E. All o f the above
15.Carrier mediated transport includes:
A.
B.
C.
D.
E.
Active transport
Facilitated diffusion
Para cellular transport
Vesicular transport
A and B
16.
Which o f the following the statements is
incorrect about active transport?
A. The drug moves with the direction
o f concentration gradie
B. The process requires energy
C. The carrier system may be saturated
at high concentration.
D. The transport process may be
competitive.
17.Para cellular transport involves the
following across Para cellular channels
13. Which one o f the following statements
is true?
A. Nonionized species o f drugs are
more lipid soluble than the ionized
species
B. Ionized species partition more
readily than nonionized species o f
drugs across cell membranes.
C. Ionization o f drugs does not affect
lipid solubility.
D. Only lipid soluble molecules readily
cross cell membranes.
14. According to Fick’s law o f diffusion the
rate o f diffusion depends up on:
A. Diffusion and the convective flow
o f water and accompanying water
soluble drug molecules
B. Dissolution and disintegration
C. Ionization and dissolution
D. Crystallization and digestion
18.
All o f the following are TRUE about
facilitated diffusion EXCEPT:
A. It is a carrier mediated transport
B. It occurs with the direction o f
concentration gradient.
C. The process does not require energy.
D. It occurs against the direction o f
concentration gradient
23.The side effects with the intravenous
bolus injection are:
19.The two forms o f vesicular transport are
A. Active transport and Para cellular
transport
B. Phagocytosis and pinocytosis
C. Carrier mediated transport
and
Passive diffusion
D. Partitioning
and distribution
E. None
20. Which one o f the following statements
is true?
A. Vesicular transport is the only
transport mechanism that doesn’t
require a drug to be in aqueous
solution to be absorbed.
B. A carrier is involved in vesicular
transport.
C. Pinocytosis is the engulfment o f
large particles or macromolecules.
D. Phagocytosis is the engulfment o f
small solutes or fluids by cells.
21 .An example o f transporter proteins
which are embedded in the lipid bilayer o f
cell membranes is:
A.
B.
C.
D.
P-glycoprotein
Cytochrome P 450 3A4
Adenosine triphosphate
Alanine
22. All o f the following are true regarding
transporter proteins except:
A. They are ATP dependent pumps.
B. They facilitate efflux o f drug
molecules from the c e ll.
C. They are found in conjunction with
metabolizing enzymes such as
Cytochrome P450 3A4
D. They are involved in the translation
o f genetic code
A.
B.
C.
D.
Intense pharmacological response
Anaphylaxis
Overt toxicity
All o f the above
24. A drug has low molecular weight but it
is water soluble. Which one of the
following routes is the most likely
mechanism o f entry for the drug across a
cell membrane?
A.
B.
C.
D.
Passive diffusion
Carrier mediated transport
Para cellular transport
Vesicular transport
25. Which o f the following injections is
used for diagnostic agents and occasionally
for chemotherapy.
A.
B.
C.
D.
E.
Intraarticular injection
Intradermal injection
Intra-arterial injection
Intramuscular injection
Intravenous injection
26. Which one o f the following statements
is true?
A. Intra-articular injection maintains a
relatively constant plasma drug
concentration once the infusion rate
is approximately equal to the drugs’
elimination rate from the body.
B. In subcutaneous injection the drug is
injected beneath the skin.
C. Subcutaneous region o f the skin is
more vascular than muscle tissues,
so the drug absorption is more rapid
by subcutaneous injection.
D. In intravenous injection the drug is
given intravenously at a constant
'Tate.
E. B and D
27. A given drug is known to be
metabolized by liver and in gastrointestinal
tract enzymes. The drug is non polar, very
lipid soluble and its absorption rate in the
epithelial tissues o f the mouth is very high.
If the metabolites of the drug do not have
pharmacological activity which route o f
administration is the best candidate for the
drug to be administered to achieve the
desired outcome o f drug therapy?
A. Sublingual and Buccal
administration
B. Oral administration
C. Respiratory tract administration
D. Ophthalmic route o f administration
28.In the gastrointestinal tract the most
common mechanism o f absorption is:
A.
B.
C.
D.
Passive diffusion and partitioning
Carrier mediated transport
Vesicular transport
Facilitated diffusion
29.The duodenal region is the primary
absorption site in the gastrointestinal tract
for drugs administered orally because:
A. It has large surface area because o f
the villi and microvilli
B. The large blood supply provided by
the mesenteric vessels allows the
drug to be absorbed more
efficiently.
C. There are many phagocytic cells
D. There are many enzymes
E. A and B
30.Gastric emptying time is affected by:
A. Food content
B. Drugs that alter gastrointestinal tract
motility.
C. pH o f the stomach
31 .Which one o f the following drug classes
does not affect gastrointestinal tract
motility?
A.
B.
C.
D.
Anticholinergics
Narcotic analgesics
Prokinetic agents
Antiseptics
32.The absorption rate o f a drug
administered by the oral route may be
erratic because of:
A. Delayed gastric emptying
B. Changes in intestinal motility
C. Changes in temperature o f the
stomach
D. The absorbing cells are few.
E. A and B
33.In intramuscular injection,the rate o f
drug absorption depends on:
A.
B.
C.
D.
Vascularity o f the muscle site
Lipid solubility o f the drug
The formulation matrix
All o f the above
34. Which one o f the following is not a type
o f enteral route o f administration?
A.
B.
C.
D.
E.
Sublingual administration
Per oral administration
Respiratory tract administration
Rectal administration
Buccal administration
35.One drug used in the treatment of
pulmonary infection is to be designed in the
form o f an aerosol. What should be the
particle size o f the formulation so that the
drug can reach the site o f action?
A. Between 100 to 150 pm
B. Between 20 to 30 (am
C. Between 15 to 20 ^m
D. Between 1 and 2 fim
36. Which one of the following drugs is not
readily absorbed from the skin when
administered by transdermal route?
A.
B.
C.
D.
Nitroglycerin
Clonidine
Nicotine
Paracetamol
37.The major factors in the design of
dosage forms include:
A. Route o f administration
B. Absorption site o f the drug
C. Bioavailability o f drug from dosage
form
D. All o f the above
38.The Noyes-Whitney equation describes:
'
A. The change in solubility o f drug
with respect to temperature
B. The change in amount of drug in
solution with respect to time.
C. The change in physicochemical
properties o f the drug with respect
to PH
D. The extent o f Ionization with
respect to PH
E. None
39. As the particle size o f solid drugs
decreases, the particle surface area
A.
B.
C.
D.
E.
Increases
Decreases
Doesn’t change
A and C
None
40. A formulation scientist thought o f
increasing the dissolution o f Griseofulvin (a
hydrophobic drug) by reducing the particle
size o f the active ingredient .The result was
reverse, i.e. the dissolution rate o f the drug
was decreased . What could be the reason
for this result ?
A. Surface area o f the drug particles is
always inversely proportional to the
dissolution rate.
B. After excessive reduction, the small
particles may have aggregated to
form larger particles and the
aggregates are less soluble.
C. The drug is completely insoluble in
the GIT fluids.
D. A and B
41 .Which one o f the following statements
best describes partition coefficient?
A. It is the ratio o f drug soluble in a
given volume o f water.
B. It is the ratio of the solubility of the
drug, at equilibrium, in a non
aqueous solvent to that in an
aqueous solvent.
C. It is the partition o f a drug molecule
in to its polar and non polar
portions.
D. It is a constant related to the
thermodynamic properties o f a drug.
42. All o f the following statements are
correct EXCEPT:
A. Molecular dispersion o f
Griseofulvin in PEG 4000 decreases
dissolution and bioavailability o f the
drug.
B. The potassium salts o f weakly
acidic drugs are more soluble than
their divalent or trivalent cation
salts.
C. Drug solubility in a saturated
solution is a static (equilibrium
property) property.
D. The dissolution rate o f a drug is a
dynamic property related to the rate
o f absorption.
aspirin formulation. What could be the
reason for the better dissolution profile?
43.If the pKa o f a weakly acidic drug
equals the pH o f the medium, then
according to Henderson- Hasselbalch
equation the amount o f ionized and
nonionized species will be:
A.
B.
C.
D.
50
40
40
70
%
%
%
%
ionized and 50 % nonionized
nonionized and 60 % ionized
ionized and 60 % nonionized
nonionized and 30 % ionized
44. The correct form of the HendersonHasselbalch equation for a weak base is
A. pH = pKa + Log {_[salt]____
}
[Nonionized base]
B. pH = pKa + Log {Tnonionized base] I
[Salt]
C. pH = pKa + Log {Tnonionized acidl }
[Base]
A. The buffering agent increases the
surface area o f the aspirin particles.
B. The alkaline medium produced by
the buffering agent makes the
aspirin molecules more polar.
C. The buffering agent forms an
alkaline medium in the
gastrointestinal tract and the drug
dissolves in situ.
D. A and B
47.The effervescence in effervescent tablets
results from:
A. The gas molecules included during
compression.
B. The sodium bicarbonate included in
the formulation results in the
formation o f carbonic acid when
dissolved in water and carbonic acid
decomposes to form carbon dioxide.
C. The glidants in the tablet.
D. A and C
D. B and C
45. Which one o f the following statements
is WRONG?
A. Certain salts are designed to provide
slower dissolution, slower
bioavailability and longer duration
o f action.
B. Sodium aspirin is more stable than
aspirin.
C. The choice o f salt form for a drug
depends on the desired physical,
chemical or pharmacological
properties.
D. Some salts o f drugs are selected for
greater stability.
46.Aspirin was formulated into a solid
dosage form with buffering agents.The
dissolution rate in the gastrointestinal tract
was better as compared with an ordinary
48. All o f the following salts o f weakly
basic drugs are very soluble in water
except:
A.
B.
C.
D.
Hydrochlorides
Sulfates
Stearates
Citrates
49.A drug in its crystalline form was
formulated into a drug product. Quality
control tests have shown that the amount of
the active ingredient was within the
pharmacopieal specifications ,however the
dissolution rate was not satisfactory as
compared to that o f a standard product.
Assuming there is no problem with the non
active ingredient part o f the formulation
what could be the reason for the slower rate
o f dissolution?
A. The crystals have changed to
insoluble forms during the process
o f dissolution.
B. The drug may have different
polymorphs with different physico
chemical properties such as melting
point and dissolution rate. The
polymorph which has relatively
slower rate o f dissolution was
included in the formulation.
C. The crystalline form o f the drug has
been changed to amorphous form
during dissolution.
D. A and C
50. All o f the following statements are true
EXCEPT:
A. Different polymorphs have different
physical properties, including
melting point and dissolution rate.
B. Amorphous or non crystalline forms
o f a drug have faster dissolution
rates than crystalline forms
C. Individual enantiomers may not
have the same pharmacokinetic and
pharmacodynamic properties
D. In ibuprofen only the R-enantiomers
is pharmacologically active
E. None
51 .An analyst compared the dissolution
rates o f anhydrous and hydrated ampicillin
.What results do you expect from the
experimental work?
A. The anhydrous form o f ampicillin
dissolves faster than hydrated form.
B. The hydrated form dissolves faster
the anhydrous form
C. The two forms have equal rates of
dissolution
D. B and C
E. None
52. Which one o f the following statements
best describes chelates?
A. complexes with ring like structure
formed by the interaction between a
partial ring o f atoms and a metal.
B. precipitates formed as result o f a
reaction between anions and cations
C. Byproducts in reaction between
anions and cations
D. Organic compounds formed as a
result o f a reaction between two
inorganic molecules
E. None
53.In which o f the following formulations
is the probability for a bioavailability
problem greater?
A.
B.
C.
D.
E.
Controlled release tablet
Transdermal patch
Conventional tablet
A and B
None
54.The rate limiting step in the
bioavailability o f a drug from a sustained
release product is:
A. The dissolution rate
B. The release o f the drug from the
delivery system
C. The rate o f disintegration
D. The disaggregation o f granules to
fine particles
55.For most conventional solid drug
products (e.g. Capsules, tablets), the rate
limiting step in the bioavailability o f the
drug is:
A. The dissolution rate
B. The rate o f disintegration
C. The release o f the drug from the
delivery system
D. A and B
56. Which one o f the following statements
is WRONG?
A. Compared with other oral
formulations a drug dissolved in an
aqueous solution is in the most
bioavailable form.
B. Per oral drug solutions are often
used as reference preparation for
solid per oral formulations.
C. In aqueous solutions no dissolution
step is necessary before systemic
absorption occurs.
D. A drug dissolved in a hydro
alcoholic solution does not have
good bioavailability.
57. Which one o f the following
formulations provides the slowest rate of
drug absorption as compared with the
others?
A.
B.
C.
D.
Syrup
Elixir
Aqueous solution
Tablet
58. Which one o f the following represents a
CORRECT sequence for the processes
involved in drug release from a per oral
dosage form?
A. Attrition -disintegration dissolution- disaggregation absorption Convection diffusion
B. Dissolution - disaggregationdisintegration- Attrition dissolution- absorption
C. Disintegration - Dissolution disaggregation- Attrition -absorption
D. Attrition- disintegration disaggregation - dissolutionConvection diffusion - absorption
59.The role suspending agents in
suspensions is :
A. To increase viscosity
B. To inhibit agglomeration
C. To decrease the rate at which
particles settle
D. To decrease the rate o f dissolution
E. All except D
60. Which one the following statements is
WRONG about highly viscous
suspensions?
A. They prolong gastric emptying time.
B. They have slower rate o f dissolution
C. They decrease the absorption rate o f
the drug
D. Viscous suspensions o f drug
provides better bioavailability than
less viscous suspensions
61 .All o f the following statements are
TRUE except:
A. Soft gelatin capsules are the
preferred dosage forms for early
clinical trials o f new drugs.
B. Lanoxicaps have better
bioavailability than a compressed
tablet formulation (lanoxin).
C. Soft gelatin capsules may contain a
nonaqueus solution, a powder, or
drug suspension.
D. Soft gelatin capsules that contain a
drug dissolved in a hydrophobic
vehicle (e.g. vegetable oil) may
have poorer bioavailability than a
compressed tablet formulation.
62. Which one o f the following statements
is true?
A. Aging and storage conditions of a
capsule do not affect the
bioavailability o f the drug.
B. At low moisture levels, the capsule
shell becomes brittle and is easily
ruptured.
C. High moisture levels do not affect
the capsule shell.
D. A and C are correct
63.Which of the following statements is/are
true about Excipients:
A. They permit the efficient
manufacture o f compressed tablets
B. They affect the physical and
chemical properties o f the drug.
C. They affect the bioavailability o f the
drug.
D. The higher the ratio o f excipients to
active drug in a given formulation,
the greater the likelihood that the
excipients affect the bioavailability.
E. All o f the above
64.Disintegrants vary in action depending
on their:
A. Their concentration
B. The method by which the
disintegrant is mixed with the
powder formulation.
C. The degree o f tablet compaction.
D. All o f the above
65. All o f the following are used as
disintegrants EXCEPT:
A.
B.
C.
D.
Acacia
Starch
Croscarmellose
Sodium starch glycolate
66. A formulation development section o f a
company used one hydrophobic waterinsoluble substance as a lubricant.
However, the dissolution rate o f the tablet
and its bioavailability was not satisfactory.
The lubricant was replaced by another one
and the rate o f dissolution and its
bioavailability was better. What do you
comment on the nature o f the second
lubricant.
A. It is hydrophobic lubricant
B. The lubricant was water soluble,
thus it does not interfere with the
dissolution or bioavailability o f the
drug.
C. It is a water insoluble substance.
D. None
67. Which one o f the following is WRONG
about glidants?
A. Glidants improve the flow
properties o f a dry powder blend
before it is compressed.
B. They slow the dissolution rate o f
drug from a tablet by reducing
wetting o f the surface o f the solid
particles.
C. They may reduce tablet to tablet
variability and improve product
efficacy.
D. Colloidal silicon dioxide is an
example o f glidants
68.Surfactants enhance drug dissolution
rates and bioavailability by:
A. Increasing the surface area o f solid
drug particles.
B. Reducing the particle size o f the
solid drug particles.
C. Reducing interfacial tension at the
boundary between solid drug and
liquid and improving the wettability
(contact) ofthe solid drug particles
by the solvent.
D. Enhancing the hydrophobicity o f the
drug particles.
69.The coating o f coated compressed
tablets may have the following properties
EXCEPT:
A. It protects the drug from moisture,
light, and air.
B. It masks the taste or odor of the
drug.
C. It improves the appearance o f the
tablet.
D. It enhances the disintegration o f
tablet.
70.Enteric coatings are used to:
A. Minimize irritation o f the gastric
mucosa by the drug.
B. Prevent inactivation o f the
degradation o f the drug in the
stomach.
C. Delay release o f the drug until the
tablet reaches the small intestine,
where conditions for absorption may
be optimal.
D. All o f the above
71 .Dose dumping is:
A. Abrupt or uncontrolled release of a
large amount o f a drug from a
modified release dosage form .
B. A decrease in the dissolution rate of
conventional dosage form.
C. A delay in release o f the drug from a
modified release dosage form.
D. A decrease in the amount o f drug
which reaches the site o f action.
72.Extended release dosage forms include:
A.
B.
C.
D.
E.
Controlled release dosage
Sustained release dosage
Long acting drug delivery system
Delayed release dosage forms
A, B and C
73.In extended release dosage forms, the
extended, slow release o f controlled release
products produces:
A. A randomly fluctuating plasma drug
concentration
B. A lower than average level of
concentration
C. An abnormally high concentration
o f the drug which is out o f the
therapeutic window.
D. Sustained plasma drug
concentration that avoids toxicity.
ANSWERS
Biopharmaceutics
1. Answer: E. All o f the above
Explanation: Biopharmaceutics is the study o f the relation o f the Physical and chemical
properties o f a drug to its Bioavailability, Pharmacokinetics, pharmacodynamics and toxicologic
effects.
2. Answer: A. Excipients
Explanation: A drug product contains the active ingredient in association with excipients , that
make up the vehicle or formulation matrix .Examples o f a drug product include tablets ,capsules,
solutions etc.
3. Answer: C. Drug delivery system
Explanation: The phrase Drug delivery system is used interchangeably with the term drug
product. However,Drug delivery system is a more comprehensive concept that includes the drug
formulation and the dynamic interaction among the drug, its formulation matrix , its container ,
and the patient.
4. Answer: D. Systemic absorption
Explanation: Bioavailability is a measurement o f the rate and extent o f Systemic absorption of
the therapeutically active drug.
5. Answer: A. Time course
Explanation: Pharmacokinetics is the study o f time course o f the drug movement in the body
during absorption, distribution, and elimination. The main parameter studied is time.
6. Answer: C. Bioavailability - the amount o f drug entering cells
Explanation: Bioavailability is a measurement o f the rate and extent o f systemic absorption o f the
therapeutically active drug. It is not the measurement o f the amount o f drug entering cells. The
other pairs are correct hence the correct definitions are given.
7. Answer: A. Proteins and lipids
Explanation: Cell membranes are primarily composed o f lipids and proteins.
8. Answer: E. All o f the above
Explanation: Drugs may be transported by passive diffusion, partitioning, Carrier mediated
transport, Para cellular transport or Vesicular transport.
9. Answer: D. Non polar lipid -soluble drugs having low molecular weight
Explanation: Usually proteins, drugs bound to proteins, and macromolecules do not cross
membranes easily. Non polar lipid -soluble drugs having low molecular weight traverse
membranes more easily than ionic or polar drugs.
10.Answer: A. Simple diffusion
Explanation; Within the cytoplasm or in interstitial fluid, most drugs undergo transport by
simple diffusion .All the others are used in the transport o f drugs across the cell membrane.
11 .Answer: A. Successive partitioning o f a solute between aqueous and lipid phases as well as
diffusion within the respective phases
Explanation: Passive transport across cell membranes involves successive partitioning o f a solute
between aqueous and lipid phases as well as diffusion within the respective phases.
12.Answer: D. A and B
Explanation: The extent o f Ionization o f a weak electrolyte depends up on its pKa and pH o f the
solution in which it is dissolved
13.
A. Nonionized species o f drugs are more lipid soluble than the ionized species
Explanation: Nonionized species are non polar so they are lipid soluble and they easily cross cell
membranes. Small water soluble molecules may cross cell membranes by passing through the
pores which are larger than their diameters.
14. Answer: E. All o f the above
Explanation: Fick’s law o f diffusion is dQ ■=DAK
dt
h
( Cl - C2}
Where dQ is rate o f diffusion D = Diffusion coefficient o f the drug
dt
A= surface area o f the plane across which transfer occurs
(Cl - C2) = the difference in concentration o f drug between the two points
h= Thickness o f the region across which diffusion occurs.
15.Answer: E. A and B
Explanation: Active transport and facilitated diffusion are types o f Carrier mediated transport.
16.
Answer: A. The drug moves with the direction o f concentration gradient
Explanation: Active transport o f the drug across a membrane is a carrier mediated transport that
has the following characteristics:
1. The drug moves against the direction o f concentration gradient
2. The process requires energy
3. The carrier may be selective for certain drugs that resemble natural substrates, or metabolites
that are actively transported.
4. The carrier system may be saturated at high concentration.
5. The transport process may be competitive (i.e. drugs with similar structures may compete for
the same carrier).
17. Answer: A. Diffusion and the convective flow o f water and accompanying water soluble drug
molecules
Explanation: Para cellular transport involves both diffusion and the convective flow of water and
accompanying water soluble drug molecules through the para cellular channels.
18. Answer: D. It occurs against the direction o f concentration gradient
Explanation: Facilitated diffusion occurs with the direction o f concentration gradient and does
not require energy.
19. Answer: B. Phagocytosis and pinocytosis
Explanation: Phagocytosis and pinocytosis are two forms o f vesicular transport.
20. Answer: A. Vesicular transport is the only transport mechanism that doesn’t require a drug to
be in aqueous solution to be absorbed
Explanation: Vesicular transport is process o f engulfing particles or dissolved materials by a cell.
Vesicular transport is the only transport mechanism that does not require a drug to be in an
aqueous solution to be absorbed.
Pinocytosis is the engulfment o f small solutes or fluids by cells while Phagocytosis is the
engulfment o f large particles or macromolecules, generally by macrophages.
21 .Answer: A. P-glycoprotein
Explanation: Various transporter proteins are embedded in the lipid bilayer o f cell membranes
e.g. P-glycoprotein
22. Answer: D. They are involved in the translation o f genetic code
Explanation: Transporter proteins are adenosine triphosphate dependent ‘pumps’ which facilitate
the efflux o f drug molecules from the cell. Because these transmembrane efflux pumps are
often found in conjunction with metabolizing enzymes such as Cytochrome P450 3A4, their net
effect is to substantially reduce intracellular drug concentrations. Thus, they determine, to a large
extent, the pharmacokinetic disposition and circulating drug concentrations o f drugs (e.g
cyclosporine, nifedipine)that are substrates for these proteins.
23. Answer: D. All o f the above
Explanation: In intravenous bolus injection the drug injected directly in to the blood stream,
distributes throughout the body. Any side effects including an intense pharmacological response,
anaphylaxis, or overt toxicity, also occur rapidly.
24.Answer: A. Passive diffusion
Explanation: Low molecular weight drugs diffuse across a cell membrane more easily than drugs
having high molecular weight.
25.Answer: C. Intra-arterial injection
Explanation: Intra-arterial injection is used for diagnostic agents and occasionally for
chemotherapy.
26.Answer: E. B and D
Explanation: In intravenous injection the drug is injected at a constant rate.Constant intravenous
injection maintains a relatively constant plasma drug concentration once the infusion rate is
approximately equal to the drugs’ elimination rate from the body (i.e. steady state is reached ).
In subcutaneous injection the drug is injected beneath the skin. Subcutaneous region o f the skin is
less vascular than muscle tissues so the rate o f drug absorption is less rapid as compared with the
absorption in muscle tissues.
27.Answer: A. Sublingual and Buccal administration
Explanation: In Sublingual routes o f administration a tablet or lozenge is placed under the tongue
(Sublingual) or in contact with the mucosal (Buccal) surface o f the cheek .This type of
administration allows non polar, lipid soluble drug to be absorbed across the epithelial lining of
the mouth .After Buccal or sublingual administration, the drug is absorbed directly into the
systemic circulation, by passing the liver and any first pass effects.
28.Answer: A. Passive diffusion and partitioning
Explanation: Most drugs are xenobiotics or exogenous molecules and consequently are absorbed
from the gastrointestinal tract by passive diffusion and partitioning. Carrier mediated transport,
Vesicular transport, facilitated diffusion play smaller but critical roles, particularly for exogenous
molecules.
29.
Answer: E. A and B
Explanation: Drug molecules are absorbed out the gastrointestinal tract, but the duodenal region,
which has a very large surface area because o f the villi and the microvilli, is the primary
absorption site. The large blood supply provided by the mesenteric vessels allows the drug to be
absorbed more efficiently
30.Answer: D. A and B
Explanation: Altered gastric emptying affects arrival o f the drug in the duodenum for systemic
absorption. Gastric emptying time is affected by food content, emotional state and drugs that alter
gastrointestinal tract motility.
31.
Answer: D. Antiseptics
Explanation :Examples o f drugs that affect gastrointestinal tract motility are Anticholinergics,
Narcotic analgesics, Prokinetic agents.
32. Answer: E .A and B
Explanation: The absorption rate o f a drug administered by the oral route may be erratic because
o f delayed gastric emptying or changes in intestinal motility.
33. Answer: D. All o f the above
Explanation: In intramuscular injection the rate o f drug absorption depends on Vascularity o f the
muscle site, lipid solubility o f the drug and the formulation matrix.
34.Answer: C. Respiratory tract administration
Explanation: Enteral route o f administration includes sublingual administration, Per oral
administration, rectal administration, and Buccal administration.
35.Answer: D. Between 1 and 2 |um
Explanation: In general particles larger than 60 jam are primarily deposited in the trachea.
Particles larger 20 |im do not reach the bronchioles, and particles smaller than 0.6 [*m are not
deposited and are exhaled. Particles between 2 to 6 fim can reach the alveolar ducts, although
only particles o f 1 and 2 |um are retained in the alveoli.
36.Answer: D. Paracetamol
Explanation: Small lipid soluble molecules such as Nitroglycerin, Clonidine, nicotine, Fentanyl
and steroids (e.g. testosterone), are readily absorbed from the skin.
37.
Answer: D. All o f the above
Explanation: The route o f administration, absorption site, bioavailability o f drug from dosage
form,are the major factors in the design o f dosage forms.
38. Answer: B. The change in amount o f drug in solution with respect to time
Explanation: The Noyes-Whitney equation describes the change in amount o f drug in solution
with respect to time .
dm = DA_(CS- C b) dm = change in amount o f drug in solution with respect to time
dt
5
dt
D= Diffusion coefficient o f the solute A= surface area o f the solid undergoing dissolution, d = is
the thickness o f the Diffusion layer, Cs= the concentration o f the solvate at saturation, and C b is
the concentration of drug in the bulk solution phase.
39.Answer: A. Increases
Explanation: Particle size and surface area are inversely proportional .As solid drug particle size
decreases, particle surface area increases.
40.Answer: B. after excessive reduction, the small particles may have aggregated to form larger
particles and the aggregates are less soluble
Explanation: With certain hydrophobic drugs, excessive reduction does not always increase the
dissolution rate. Small particles reaggregate into larger particles to reduce the high surface free
energy produced by particle size reduction.
41. Answer: B. It is the ratio o f the solubility o f the drug, at equilibrium, in a non aqueous solvent
to that in an aqueous solvent
Explanation: Partition coefficient is the ratio o f the solubility o f the drug, at equilibrium, in a non
aqueous solvent to that in an aqueous solvent.
42.Answer: A. Molecular dispersion o f Griseofulvin in PEG 4000 decreases dissolution and
bioavailability o f the drug
Explanation: To prevent the formation o f aggregates, small drug molecules are dispersed in
polyethylene glycol (PEG) dextrose or other agents.For example Molecular dispersion of
Griseofulvin in PEG 4000 enhances dissolution and bioavailability o f the drug.
43.Answer: A.50 % ionized and 50 % nonionized
Explanation: when pKa o f a weakly acidic drug equals the pH o f the medium, then according to
Henderson- Hasselbalch equation
}
0 ~ Log { .[salt]___
[Nonionized base]
Antilog 0 = { [salt]___ _ } -= 1 [salt] = [Nonionized base]
[Nonionized base]
So
50 % ionized and 50 % nonionized.
44.Answer: B
Explanation: The correct form o f the Henderson- Hasselbalch equation for a weak base is pH =
pKa + Log {[nonionized base] }
[Salt]
45.Answer: B. Sodium aspirin is more stable than aspirin
Explanation: Some soluble salt forms are less stable than the nonionized form. For example
sodium aspirin is less soluble than aspirin in the acid form.
46.
Answer: C. The buffering agent forms an alkaline medium in the gastrointestinal tract and the
drug dissolves in situ
Explanation: A solid dosage form containing buffering agents may be formulated with the free
acid form o f the drug (e.g buffered aspirin).
The buffering agent forms an alkaline medium in the gastrointestinal tract and the drug dissolves
in situ.The dissolved salt form o f the drug diffuses into the bulk fluid o f the gastrointestinal tact,
forms a fine precipitate that redissolves rapidly, and becomes available for absorption.
47. Answer: B. The sodium bicarbonate included in the formulation results in the formation of
carbonic acid when dissolved in water and carbonic acid decomposes to form carbon dioxide
Explanation: Effervescent tablets containing the acid drug in addition to sodium bicarbonate,
tartaric acid, citric acid, or other ingredients are added to water just before oral administration
.The excess sodiilm bicarbonate forms an alkaline solution in which the drug dissolves. Carbon
dioxide is also formed by the decomposition o f carbonic acid.
48.Answer: C. Stearates
Explanation: For weak bases, common water soluble salts include the hydrochlorides, Sulfates,
citrates and Gluconates .The estolate, napsylate and Stearates are less water soluble.
49.
Answer: B. The drug may have different polymorphs with different physico chemical
properties such as melting point and dissolution rate. The polymorph which has relatively slower
rate o f dissolution was included in the formulation
Explanation: Polymorphism is the ability o f a drug to exist in more than one crystalline form.
Different polymorphs have different physical properties, including melting points and dissolution
rate.
50. Answer: D. In ibuprofen only the R-enantiomers is pharmacologically active
Explanation:
Amorphous forms o f a drug have faster dissolution rate than crystalline forms. Individual
enantiomers may not have the same pharmacokinetic and pharmacodynamic properties.
Ibuprofen exists as the R and S enantiomers; only the S enantiomer is pharmacologically active.
51 .Answer: A. The anhydrous form o f ampicillin dissolves faster than hydrated form
Explanation:
Drugs may exist as hydrated or solvated form or as an anhydrous molecule.
Dissolution rates differ for hydrated and anhydrous forms. For example the anhydrous form o f
ampicillin dissolves faster and is more rapidly absorbed the than hydrated form
52.Answer: A. complexes with ring like structure formed by the interaction between a partial
ring o f atoms and a metal
Explanation: Chelates are complexes with ring like structure formed by the interaction between a
partial ring o f atoms and a metal.
53.Answer: D. A and B
Explanation: The more complicated the formulation o f the finished product (e.g. Controlled
release tablet, enteric coated tablet, transdermal patch), the greater the potential for a
bioavailability problem.
54.
Answer: B. The release o f the drug from the delivery system
Explanation: The rate limiting step in the bioavailability o f a drug from a sustained release or
controlled release drug product is the release o f the drug from the delivery system.
1 Biopharmaceutics
hydrophobic vehicle (vegetable oil) may have poorer bioavailability than a compressed tablet
fnrmiilntinn
55.Answer: A .The dissolution rate
Explanation: For most conventional solid drug products (e.g. Capsules, tablets), the rate limiting
step in the bioavailability o f the drug is the dissolution rate.
56.Answer: D. A drug dissolved in a hydro alcoholic solution does not have good bioavailability
Explanation: Compared with other oral formulations a drug dissolved in an aqueous solution is in
the most bioavailable and consistent form. Because the drug is already in solution, no dissolution
step is necessary before systemic absorption. A drug dissolved in a hydro alcoholic solution has
good bioavailability. Alcohol aids drug solubility.
57.Answer: D. Tablet
Explanation: A drug dissolved in hydro alcoholic solution (e.g. Elixir) has good bioavailability.
Alcohol aids drug solubility. Compared with other oral formulations a drug dissolved in an
aqueous solution is in the most bioavailable and consistent form. Because the drug is already in
solution, no dissolution step is necessary before systemic absorption
58.
Answer: D. Attrition- disintegration - disaggregation - dissolution- Convection diffusion absorption
Explanation: The release o f a drug from per oral dosage form and its subsequent bioavailability
depends on a succession o f the rate processes .These processes include
1. Attrition -disintegration or disaggregation o f the drug product.
2. Dissolution o f the drug in an aqueous environment.
3. Convection and dissolution o f the drug molecules to absorbing surface.
4. Absorption o f the drug across cell membranes into the systemic circulation.
59. Answer: E. All except D
Explanation: Suspending agents are hydrophilic colloids ( e.g. cellulose derivatives , acacia,
xanthine g u m ) added to increase viscosity, to inhibit agglomeration, and decrease the rate at
which particles settle. They are not added to decrease the rate o f dissolution.
60. Answer: D. Viscous suspensions o f drug provides better bioavailability than less viscous
suspensions.
Explanation: Highly viscous suspensions may prolong gastric emptying time, slow rate o f
dissolution, and decrease the absorption rate of the drug. They decrease bioavailability o f the
drug.
61 .Answer: A. Soft gelatin capsules are the preferred dosage forms for early clinical trials of
new drugs
Explanation: Soft gelatin capsules may contain anonaqueus solution, a powder, or drug
suspension .The vehicle may be water miscible (e.g. PEG).The cardiac glycoside digoxin,
dispersed in a water miscible vehicle (Lanoxicaps), has better bioavailability than a compressed
tablet formulation (lanoxin).However, a Soft gelatin capsules that contains a drug dissolved in a
hydrophobic vehicle (vegetable oil) may ha
formulation.
Hard gelatin capsules are usually filled with a powder blend that contains the drug,
Typically the powder blend is simpler and 1ess compacted than the blend in a compressed tablet
formulation. Encapsulated drugs are release d rapidly and dispersed easily, and the bioavailability
is good. Hard gelatin capsules are the preferired dosage forms for early clinical trials o f new
drugs.
62.Answer: B. At low moisture levels, the capsule shell becomes brittle and is easily ruptured.
Explanation: Aging and storage conditions affect the moisture content o f the gelatin
component o f the shell and the bioavailability o f the drug.
At low moisture levels, the capsule shell becomes brittle and is easily ruptured.At high moisture
levels, the capsule shell becomes moist, soft, and distorted .Moisture may be transferred to the
capsule contents, particularly if the contents are hydroscopic.
63.Answer: E. None
Explanation: Excipients including diluents disintegrants, lubricants, glidants, surfactants, dye,
and flavoring agents, have the following p toperties.
1. They permit the efficient manufacture o compressed tablets,
2. They affect the physical and chemical properties o f the drug
3. They affect the bioavailability o f the di ug. The higher the ratio o f excipients to active drug in
a given formulation, the greater the likelihi )od that the excipients affect the bioavailability.
64.
Answer: D .All o f the above
Explanation: Disintegrants vary in action depending on their concentration, the method by which
the disintegrant is mixed with the powder formulation and the degree o f tablet compression.
Although tablet disintegration is usually not a problem because it often occurs more rapidly than
drug dissolution, it is necessary for dissolution in immediate release formulations. Inability to
disintegrate may interfere with bioavailability.
65.Answer: A. Acacia
Explanation: Starch, croscarmellose, and Sodium starch glycolate are disintegrating agents,
Acacia is not a disintegrant; it is used as a suspending agent.
66. Answer: B. The lubricant was water soluble, thus it does not interfere with the dissolution or
bioavailability of the drug.
Explanation: Lubricants are hydrophobic , water insoluble substances such as stearic acid,
magnesium steartate, hydrogenated oil, an d talc. They may reduce wetting o f the surface o f the
solid particles, slowing the dissolution and bioavailability o f the drug. Water soluble lubricants,
such as L - leucine, do not interfere with dissolution or bioavailability.
67.Answer: B. they slow the dissolutior rate o f drug from a tablet by reducing wetting o f the
surface o f the solid particles
Explanation: Glidants improve the flow properties o f a dry powder blend before it is compressed
Rather than posing a potential problem with bioavailability, glidants may reduce tablet to tablet
variability and improve product efficacy.
68. Answer: C. Reducing interfacial tension at the boundary between solid drug and liquid and
improving the wettability (contact) o f the solid drug particles by the solvent.
Explanation: Surfactants enhance drug dissolution rates and bioavailability by reducing
interfacial tension at the boundary between solid drug and liquid and improving the wettability
(contact) o f the solid drug particles by the solvent.
69. Answer: D. It enhances the disintegration o f tablet
Explanation:
Coated compressed tablets have a sugar coat, a film coat, or an enteric coat with the following
characteristics:
- It protects the drug from moisture, light, and air
- It masks the taste or odor o f the drug.
- It improves the appearance o f the tablet.
- It may affect the release rate o f the drug
70. Answer: D .All o f the above
Explanation: Enteric coatings are used to:
- Minimize irritation o f the gastric mucosa by the drug
- Prevent inactivation o f the degradation o f the drug in the stomach
- Delay release o f the drug until the tablet reaches the small intestine, where conditions for
absorption may be optimal.
71 .Answer: A. Abrupt or uncontrolled release o f a large amount o f a drug from a modified
release dosage form
Explanation: Dose dumping is an abrupt or uncontrolled release o f a large amount o f a drug from
a modified release dosage form.
72.Answer: E. A, B and C
Explanation: Extended release dosage forms include Controlled release dosage, Sustained release
dosage and long acting drug delivery system.
73.Answer: D. Sustained plasma drug concentration that avoids toxicity
Explanation: In extended release dosage forms, the extended, slow release o f controlled release
products produces relatively flat sustained plasma drug concentration that avoids toxicity ( from
high drug concentration ) or lack o f efficacy ( from low drug concentrations).
Biotechnologic Products
“For every failure, there’s an alternative course of action. You just have to find it.
When you come to a roadblock, take a detour. ”
Mary Kay Ash
1. The immunoglobulins whose production
is induced when the host’s lymphoid
system comes in contact with foreign
molecules are
A.
B.
C.
D.
E.
antigens
antibodies
cytokines
lymphokines
haptens
2. What is the molecule, which contains
the genetic instructions of a cell?
A.
B.
C.
D.
E.
antisense DNA
gene
genome
DNA
All the above
B. it is produced by fusing B cells to
myeloma cancer cells
C. it can grow indefinitely like the
cancer cells, yet also produce and
secret antibodies like the B cell
D. a single hybridoma can produce a
variety o f antibodies
E. none
8. What is the class o f glycoproteins
produced by animal cells in response to
viral infection?
A.
B.
C.
D.
E.
interferon
interleukin
lymphokine
colony stimulating factors
all but D
9. Which o f the following is NOT correct
about plasmids?
[3-6] For each statement below, choose the
best enzyme that it most closely describes.
A.
B.
C.
D.
E.
DNA ligase
DNA polymerase
Restriction endonuclease
Reveres transcriptase
DNA topoisomerases
3. The enzyme, which enables DNA
fragments from different sources to be
joined.
4. The enzyme that cleaves double
stranded DNA into smaller fragments.
5. The enzyme that catalyzes the synthesis
o f DNA,
6. The enzymes responsible for removing
supercoils in the helix,
7. Which o f the following is NOT true
about hybridoma?
A. it is a hybrid cell
Biotechnologic Products
A. they are small, circular,
extrachromosomal DNA molecules
B. they can replicate independently
C. they carry genetic information
D. they can be used as vectors fro the
transfer o f DNA in recombinant
DNA technology
E. they are found in some species of
bacteria only
10. Which of the following is a WRONG
match between a protein and its function?
A. hemoglobin; oxygen transport
B. myosin; confer elasticity and
contractility to muscles
C. globulins; drug carriers
D. Albumin; binds to many drugs
E. None
11 .Which o f the following is NOT true
about immunoglobulin?
A. it is a protein
B. it is involved in immunity and
allergic response
C. therapeutically it is used to
modulate or replace antibody in
various immunodeficiency and
disease states
D. immunoglobulin preparations are
given either IM or IV
E. none
B. prolonging the survival o f
neutrophilis
C. induce megakaryocyte formation
D. enhance the phagocytic activity o f
neutrophilis
E. increase the cytotoxic activity o f
neutrophilis
15. Which o f the following is NOT true
about glycoproteins?
12. Which o f the following is NOT correct
about the recombinant human granulocyte
colony-stimulating factor?
A. they are glycoproteins
B. they produce many type o f blood
cells and components in the body
C. they can be used to treat congenita]
disease
D. they are used to treat certain forms
o f cancer
E. none
13. Which o f the following is NOT true
about filgrastim and lenograstim?
A. both o f them selectively promote the
proliferation, differentiation, and
maturation o f blood cell precursor
B. lenograstim is more potent than
filgrastim
C. both are glycosylated at the same
site as natural HuG-CSF
D. lenograstim can reduce the duration
o f neutropenia and the severity o f
infection in patients who are
receiving cytotoxic chemotherapy
fro nonmyeloid malignanc
E. B and D
14. All o f the following activities are shared
by both natural and recombinant
granulocyte CSF EXCEPT
A. They are proteins to which
oligosaccharides are covalently
attached
B. They form the natural structural
membranes in cells o f unicellular
and multicellular organisms
C. It is the extent o f glycosylation of a
protein molecule only, which
determines the physicochemical
properties, stability and specificity
o f surface receptor in a cell
D. Glycoproteins in the cells surface o f
RBC participate in the
determination o f specific blood type
E. B and D
16. The carbohydrates in glycoproteins are
responsible for the following functions
EXCEPT
A. they determine which amino acid
will be glycosylated
B. they participate in cell surface
recognition
C. they participate in cells surface
antigenecity
D. they participate in recognition o f
sialylated, fucosylated
lactosaminoglycans on leukocytes
by E-selection o f endothelial cells
E. none
17.Single stranded DNA are available in
A. stimulating the release o f mature
neutrophilis from hematopoietic
tissue
A. all viruses
B. some viruses
C. some bacteria
D. some fungi
E. none
] 8.DNA is the genetic material o f all the
following EXCEPT
A.
B.
C.
D.
E.
humans
some bacteria
some fungi
some viruses
none
19. Which o f the following is NOT correct
about antisense drugs?
A. they are single stranded, synthetic
oligonucleotides, which could be
used to inhibit gene expression
B. the advantage is that, the antisense
DNA could be made without first
elucidating the nucleotide base
sequence o f a gene that controls a
specific body function
C. the disadvantage is that, it is not
possible to affect the stability and
potency o f these drugs
D. they may be used to treat cancer and
viral diseases
E. B and C
20. Which o f the following is NOT true
about alteplase?
A. it is a thrombolytic agent
B. it is effective in producing
recanalization o f occluded coronary
arteries after acute myocardial
infarction
C. it is effective in the treatment o f
acute massive pulmonary embolism
D. it can cause reperfusion arrhythmias
as an adverse effect
E. it is more liable to cause systemic
fibrinolysis than streptokinase
21 .What is the biotechnologic drug that is
used to treat metastatic renal cell
carcinoma?
A.
B.
C.
D.
E.
aldesleukin
abciximab
edobacomab
muromonab-CD3
nebacumab
22.All the following are correct about
inerIeukin-3 EXCEPT
A. it is a hematopoietic growth factor
B. it is be used to treat bone marrow
failure
C. it improves neutrophil and platelet
count in patients who have
chemotherapy-related bone marrow
failure
D. used alone it is effective in
improving hematopoiesis in patients
who have Aplastic anemia
E. none
23.Campath-l is clinically used to treat all
the following EXCEPT
A. for immunosuppression in patients
who undergo organ transplant
B. to treat refractory autoimmune
disorders
C. vasculitis
D. to treat lymphoid malignancy
caused by immonusuppression in
patients who undergo organ
transplant
E. none
24.zolimomab aritox may be used for the
treatment o f
A. rheumatoid arthritis
B. insulin-dependent diabetes mellitus
C. steroid resistant graft-versus-host
disease after allogeneic bone
marrow transplant fo hematopoietic
neoplasm
D. A and B only
E. All the above
25.Betaseron may administered through all
the following routes o f administration
EXCEPT
A.
B.
C.
D.
E.
intravenously
intramuscularly
orally
topically
intrathecally
26.Betaseron is indicated for the treatment
of
A.
B.
C.
D.
multiple sclerosis
AIDS
Malignant melanoma
Herpes virus and papilloma virus
infections
E. All the above
Answers
Biotechnologic Products
1. Answer: B. Antibodies
Explanation:
Antibodies are a special kind o f blood proteins (chemically they are proteins o f the globulin type),
which are synthesized in the lymphoid tissue in response to the presence o f foreign particles
(antigens) and they circulate in the blood to attack the antigen and render it harmless. Cytokines
are special type o f proteins released by cells to affect the action o f other cells. Haptens are small
particles that are not capable o f inducing immune response by them selves. But they may become
antigenic by combining with and modifying the body’s own proteins.
2. Answer: D. DNA
Explanation:
DNA is the genetic material o f nearly all living organisms, which controls heredity. It is the
molecule that contains the genetic information o f a cell. Antisense DNA is a complementary
strand o f DNA that is specifically synthesized to attach to the sense DNA and prevent genetic
prescription. Gene is the basic genetic material, which is carried at a particular place on a
chromosome. It is the segment o f DNA that codes for a specific polypeptide. Genome is the basic
haploid set o f chromosomes o f an organism and make up the genetic information content o f a
cell.
3. Answer: A. DNA ligase.
Explanation;
DNA ligase is the enzyme that catalyzes the final phosphodiester linkage between the 5’phosphate group on the DNA chain made by polymerase II and the 3’-hydroxyl group on the
chain made by polymerase I. In doing so, the enzyme is capable o f joining DNA fragments from
different sources. DNA 4/208. The enzyme that cleaves double stranded DNA into smaller
fragments.
4. Answer: C. restriction endonuclease.
Explanation:
One o f the major obstacles to molecular analysis o f genomic DNA is the immense size o f the
molecules involved. The discovery o f restriction endonucleases (restriction enzymes) that cleave
the double stranded DNA at sequence-specific site into smaller fragments opened the way for
DNA analysis.
5. Answer: B. DNA polymerase.
Explanation:
DNA polymerases are the enzymes that form the sugar phosphate bond (the phosphodiester bond)
between adjacent nucleotides in a nucleic acid chain. This way they synthesize DNA molecules.
6. Answer: E. DNA topoisomerase.
7. Answer: D. A single hybridoma can produce a variety o f antibodies
Explanation;
The first production o f monoclonal antibodies represents the convergence o f three areas o f basic
medical reseach: immunochemistry, the in vitro cultivation o f cancer cells and the molecular
biology o f malignant transformations. For many years this approach was not technically feasible
because the plasma cells have a short life span and can not be maintained in tissue cultures. In
1975, Georges Kohler and Cesar Milstein devised a solution to this problem by fusing a normal B
cell (plasma cell) with a myeloma (a cancerous plasma cell), called a hybridoma or
heterokaryons, that possessed the proliferating growth properties o f the myeloma cells but
secreted the antibody product o f the B cell. A single hybridoma is capable o f producing a single
type o f antibody only.
8. Answer: A. interferon
Explanation;
Interferone is a substance that is produced by cells infected with a virus and has the ability to
inhibit viral growth. Interleukin is a group of proteins synthesized by macrophages and T
lymphocytes in response to antigens and other stimulation. Lymphokine is any o f a class o f
soluble proteins produced by some white blood cells. These proteins stimulate other white blood
cells as part o f the immune response. Colony stimulating factors are a class o f glycoprotein
hormones that regulate the differentiation and formation o f blood cells from precursor cells.
9. Answer: E. they are found in some species o f bacteria only
Explanation:
Plasmids are found in most species o f bacteria.
10.Answer: C. globulins; drug carriers
Explanation:
Globulins are one group o f simple proteins that are soluble in dilute salt solutions and can be
coagulated by heat. A range o f different globulins is present in the blood (the serum globulins
including alpha, beta and gamma globulins). They are involved in immunological response and
antibody formation. Albumins are the ones that can function as drug carriers.
11 .Answer: A. it is a protein
Explanation:
Immunoglobulin is one o f a group o f structurally related glycoproteins that act as antibodies.
12.Answer: B. they produce many type o f blood cells and components in the body
Explanation:
These factors are involved in regulating the production o f blood cells and other components but
they cannot produce them.
13.Answer: C. both are glycosylated at the same site as natural HuG-CSF
Explanation;
Lenogratism is a recombinant human granulocyte CSF derived from Chinese hamster ovary
cells, which is glycosylated at the same site as natural HuG-CSF. Filgrastim on the other hand,
is obtained from Escherichia coli and is not glycosylated.
14.Answer: C. induce megakaryocyte formation
Explanation;
In addition to the activities it share with natural CSF, rHuG-CSF shows synergism with
interleukin-3 to induce megakaryocyte formation. It also shows synergism with GM-CSF to
stimulate granulocyte-macrophage colonies.
15. Answer: C. It is the extent o f glycosylation o f a protein molecule only, which determines the
physicochemical properties, stability and specificity o f surface receptor in a cell.
Explanation;
Glycoproteins contain highly variable amount o f carbohydrates. The extent as well as the site o f
this glycosylation o f a protein determine the physicochemical properties, stability and specificity
o f surface receptor in a cell.
16.Answer: A. they determine which amino acid will be glycosylated
Explanation;
In glycoproteins, the oligosaccharides are covalently attached to specific amino acid R-groups p f
the protein. It is the three dimensional structure o f the protein which determines whether or not a
specific amino acid R-group is glycosylated.
17.Answer: B. some viruses
Explanation;
With the exception o f some few viruses that contain single-stranded DNA, DNA exists as a
double stranded molecule, where the strands wind each other forming a double helix.
18.Answer: D. some viruses
Biotechnologic Products
Explanation;
With the exception o f some viruses, where the genetic material is contained in RNA, DNA is the
genetic material o f all organisms.
19.Answer: E. B and C
Explanation;
For antisense DNA to be synthesized, the sense DNA that carries the information that affects the
disease process is usually elucidated before antisense drug could be designed. It is possible to
modify the antisense drugs so that they will have better potency and stability. For example,
phosphodiesters (which are susceptible to the esterase enzymes) can be chemically converted to
phosphothioates. This increases the stability o f the drug.
20.Answer: E. it is more liable to cause systemic fibrinolysis than streptokinase
Explanation;
Increased fibrinolysis is effective therapy for thrombolic disease, for which streptokinase and
alteplase are indicated. Systemic fibrinolysis can occur as adverse effect o f both agents. However,
it is more pronounced in streptokinase than alteplase
21 .Answer: A. aldesleukin
Explanation;
Aldesleukin is alymphokine, which is a human recombinant interleukin-2 product that is used to
treat metastatic renal cell carcinoma. Abciximab is a chimeric monoclonal antibody Fab fragment
that is specific fro platelet glycoprotein Ilb-Iia receptors. It is effective in reducing fatalities in
subjects who have unstable angina after they undergo angioplasty. Edobacomab is an immune
globulin directed against gram-negative bacterial endotoxins. Muromonab-CD3 is an
immunosupprresive agent with specific targeting, which effective in reversing acute renal
allograft rejection. Nebacumab is n immune globulin directed against gram-negative bacterial
endotoxins.
22.Answer: D. used alone it is effective in improving hematopoiesis in patients who have
Aplastic anemia.
Explanation:
If used alone it is not effective in improving hematopoiesis in patients who have Aplastic anemia.
Enhanced response can be obtained with sequential combined use o f recombinant human
interleukin-3 and other hematopoietic growth factors such as GM-CSF.
23.Answer: C. vasculitis
Explanation:
Campath is used only experimentally in vasculitis.
24.Answer: E. All the above
Explanation;
;
Zolimomab aritox is an immunoconjugate o f monoclonal anti-CD5 murine IgG and the ricin Achain toxin. It is primarily used fro the treatment of steroid resistant graft-versus-host disease
after allogeneic bone marrow transplant fo hematopoietic neoplasm. It may also be used in the
treatment o f rheumatoid arthritis and insulin-dependent diabetes mellitus.
25.Answer: C. orally
Explanation;
;
Betaseron is administered intravenously!, intramuscularly, topically, subcutaneously,
intrathecally, or intralesionally for a variety o f indications. However, it is ineffective when
administered orally.
;
26.Answer: E. All the above
Explanation;
Betaseron is a glycoprotein with antiviral, antiproliferative, and immunomodulatory activity.
Therefore, it may be used in the treatment o f multiple sclerosis, AIDS, Malignant melanoma, and
Herpes virus and papilloma virus infections.
Biotransformation, Prodrugs and Pharmacogenetics
D©we(£)
If you can imagine it, you can achieve it. If you can dream it, you can become it.
William Arthur Ward
1. Which o f the following is correct about
metabolism?
A. metabolism leads always to different
metabolites that are inactive
B. metabolism refers exclusively to
normal anabolic and catabolic
reactions of the body (protein, fat,
carbohydrate, nucleic acids)
C. all substances entering the body are
finally changed to new substances
before being excreted
D. most o f the time metabolism results
in more than one metabolites
E. all o f the above
D. includes unmasking polar functional
groups
E. none
5. Xenobiotics are
A.
B.
C.
D.
E.
drugs
prodrugs
inactive metabolites
toxic substances
any chemical that is foreign to the
body
6. Which o f the following is the main
organ o f metabolism?
2. Which o f the following is true about
metabolites?
A. metabolites may be inactive
B. metabolites may be less active than
the parent substance
C. metabolites may be more active than
the parent substance
D. metabolites can show activity not
shown by the parent substance
E. all o f the above
3. Prodrugs are
A. inactive metabolites
B. bioactivated metabolites
C. substances whose metabolites have
decreased activity
D. substances whose metabolites are
very toxic
E. all
4. All of the following are true about the
Phase 1 reactions, exccpt
A. convert the parent drug into a more
polar metabolite
B. involves
introducing
polar
functional groups
C. the activity o f the drugs is not
modified
A.
B.
C.
D.
E.
kidney
liver
intestines
pancrease
heart
7. What is the most common phase I
biotransformation?
A.
B.
C.
D.
E.
reduction
oxidation
hydrolysis
hydrogen bond formation
acetylation
8. Which o f the following is not true about
cytochrome P450 enzymes?
A. they carry out the majority o f the
oxidation reactions in the phase I
reaction
B. because they are enzymes, CPY450
oxidases can only be metabolized a
specific type o f substrates
C. they are found bound to the smooth
endoplastic reticulum
D. they require both NADPH and a
porphyrin prosthetic group.
E. none o f the above
9. In the
CYP3A4, the number ‘3’ and
the letter ‘A ’ indicate respectively
A.
B.
C.
D.
E.
individual gene and subfamily
family and subfamily
family and individual gene
subfamily and family
individual gene and family
10. Which of the following is true about the
phase I oxidation reactions?
A. all oxidation reactions are catalyzed
by the CYP450 oxidases
B. some oxidations are catalyzed by
enzymes other than the CYP450
oxidases but located within the
endoplasmic reticulum o f the liver
C. some oxidations are catalyzed by
enzymes other than the CYP450
oxidases which are nonmicrosomal
but
located
in
cytosol
and
mitochondria o f liver cells
D. some oxidations are catalyzed by
nonmicrosomal oxidases located in
cytosol
and
mitochondria
of
extrahepatic tissues.
E. none o f the above
11. The metabolites produced after phase I
oxidation reactions
A. have decreased polarity than the
parent drugs
B. have enhanced water solubility than
the parent drugs
C. their tubular reabsorption in the
kidneys is increased leading to their
reduced excretion
D. do not need to go further
biotransformation by phase II
pathways
E. none o f the above
12.All o f the following are correct
statements about reduction phase I
reactions except one
A. the overall goal is to create polar
functional groups so that their
elimination in the urine will be
facilitated/reduced
B. like
the
oxidation
reactions,
CYP450 play the major role in
carrying out reduction reactions
C. bacteria resident in the GIT are also
involved in reduction reactions
D. reduction reactions are not as
common as oxidation reactions
E. none
13. Which o f the following is not true about
the esterase enzymes?
A. they are usually present in plasma
and various tissues
B. they are very specific
C. they
catalyze
de-esterification,
hydrolyzing relatively non-polar
esters into two polar, more water
soluble compounds; an alcohol and
an acid
D. they are responsible for converting
many prodrugs into their active
drugs
E. none o f the above
14. Which o f the following is NOT true
about the enzymatic hydrolysis o f ester and
amide drugs?
A. amidase enzymes hydrolyze amides
into amines and acids
B. ester drugs are usually longer acting
than structurally similar amide drugs
C. amidase enzymes are mainly located
in the liver
D. lactones are hydrolyzed by esterases
while lactams are hydrolyzed by
amidase
15.All o f the following statements about
the phase II reactions are true, except
A. most phase II conjugates are very
polar
B. during phase II reactions, only the
metabolites formed in phase I
reaction are conjugated
C. the metabolites o f phase II are most
o f the time pharmacologically
inactive
D. phase II conjugates can be excreted
in urine or bile
E. none
16.The high-energy molecule required for
the conjugation reaction consists o f a
coenzyme bound to
A. the parent drug
B. the endogenous substrates like the
glucuronic acid
C. the drug’s phase 1 conjugates
D. the enzyme
E. all but D
17.All o f the following are natural
endogenous constituents involved in phase
II reaction except
A.
B.
C.
D.
E.
cytosine
glucuronic acid
Glycine
Glutamine
Glutathione
18.The enzymes that catalyze conjugation
reactions are called
A.
B.
C.
D.
E.
conjugases
esterases
transferases
amidases
reductases
19. The enzymes responsible for catalyzing
conjugation reactions are found mainly in
A.
B.
C.
D.
intestine
kidneys
blood
pancreas
E. liver
20. Which of the following is not true about
the conjugates produced after the phase II
reaction
A. they are highly polar
B. they are unable to cross cell
membranes
C. they
are
almost
always
pharmacologically inactive
D. they could be toxic
E. they are easily excreted from the
body
21. Which of the six conjugation pathways
is the most common one?
A.
B.
C.
D.
E.
glucuronidation
sulfate conjugation
amino acid conjugation
glutathione conjugation
methylation
22. The high-energy form o f glucuronic acid
is
A. uridine diphosphate glucuronic acid
B. uridine triphosphate glucuronic acid
C. uridine monophosphate glucuronic
acid
D. B and C
23. Which
drugs
glucuronidation?
readily
undergo
A. drugs that possess amide functional
groups
B. drugs that posses a ketone functional
group
C. drugs that possess a carboxyl
functional group
D. drugs that possess a hydroxyl
functional group
E. C and D
24.The high-energy form o f sulfate reacts
with all of the following except
A.
B.
C.
D.
E.
alcohols
arylamines
phenols
N-hydroxy] compounds
Carboxyl acids
29. What are the conjugation reactions in
which the unaltered drug is more polar than
the metabolites?
25.Amino acid conjugation involves the
reaction o f either Glycine or glutamine with
which o f the following to form amides.
A.
B.
C.
D.
E.
carboxylic acids
phenols
arylamines
alcohols
A and C
A. sulfate conjugation and amino acid
conjugation
B. sulfate conjugation and methylation
C. sulfate
conjugation
and
glucuronidation
D. sulfate conjugation and acetylation
E. acetylation and methylation
30. Which o f the following is not correct
about methylation reaction?
26. Which o f the six conjugation reactions
is extremely important in preventing
toxicity from a variety o f harmful
electrophilic agents?
A.
B.
C.
D.
E.
C. fluorine
D. sulfur
E. none
Amino acid conjugation
Glutathione conjugation ■
Methylation
Glucuronidation
Sulfate conjugation
A. the
enzyme
responsible
for
catalyzing the reaction is called
methyl transferase
B. methylation plays major role in the
elimination o f drugs
C. it has a major role in the
biosynthesis
of
endogenous
compounds such as epinephrine
D. it can inactivate certain compounds
like
cathecholamine
neurotransmitters
E. none
27. What is the final product o f glutathione
conjugation?
31 .Acetylation can occur with
A.
B.
C.
D.
E.
urea
C 02
Mercapturic acid derivative
Carboxylic acid derivative
A
dipeptide
derivative
glutathione
I .primary amides
II. sulfonamides
III. hydrazides
of
28.Methylation is most suitable with drugs
containing functional groups that have the
following atoms, except
A. oxygen
B. nitrogen
A.
B.
C.
D.
E.
I only
I and II
I, II and 111
11 and III
I and III
32. In one o f the following, there is a danger
of tissue accumulation that can lead to
crystalluria and subsequent tissue damage.
A. mercapturic acid derivative
B. N-acetylated
metabolites
of
sulfonamides
C. Glucuronides with high molecular
weight
D. Acetyl-CoA
33. The
high-energy
acetylation is
molecule
for
A.
B.
C.
D.
N-acetyl transferase
S-adenosylmethionine
Acetyl-CoA
B’-phosphoadenosine^”phosphoac ety 1ate
E. ATP
34. Which o f the following is not among the
factors that affect drug metabolism?
A.
B.
C.
D.
E.
chemical structure o f the drug
drug administration route
nutritional status
age
none o f the above
35.Qualitative species difference in the
metabolism o f drugs occur primary with
A.
B.
C.
D.
phase 1
phase II
both phase I and phase II
with some people phase I and with
others phase II
D. a difference
in a particular
endogenous substrate
E. a difference in the extent o f
competing reactions
37. Which o f the following is likely to affect
the metabolism o f drugs?
A.
B.
C.
D.
E.
liver disease
congestive heart failure
abnormal albumin level in the blood
A and C
all o f the above
3 8 .Which o f the following statements is
correct?
I. slow acetylators are more prone
hepatotoxicity from isoniazid
II. fast acetylators are less prone to
toxicities from isoniazid
III.slow acetylators are less prone to
toxicities
of
isoniazid
hepatotoxicity
A.
B.
C.
D.
E.
to
all
all
but
I and II
II only
II and III
Ill only
None o f the above
39.
Which o f the following is true about the
influence o f dosage upon drug metabolism?
A. an increase in drug dosage always
results
in
increased
drug
concentrations and hence increased
drug metabolism
36.
Which o f the following is not a cause of
B. at
50%
enzyme
saturation,
quantitative type o f species difference in
metabolism via the enzyme follows
the metabolism o f drugs?
zero-order kinetics
A. difference in the enzyme level
C. at
100%
enzyme
saturation,
metabolism
via
the
enzyme
will be
B. the presence o f species specific
mixture o f both first-order and zeroisozymes
order kinetics.
C. a difference in the amount o f
D. An increase in drug dosage can
endogenous inhibitor
result
in
increased
drug
concentration but the metabolism
increases up to a certain level only
E. A and C
40.Low protein diet can lead to
A. decreased
oxidative
drug
metabolism capacity
B. decreased amino acid conjugation
C. decreased methylation o f drugs
D. A and B
E. B and C
41 .Which o f the following is true about the
metabolism
of
ethyl-morphine
and
hexobarbital?
A. diet deficiency in essential fatty
acids reduces the metabolism of
these drugs
B. low-protein dies results in decreased
metabolism o f these drugs
C. essential fatty acids content o f diet
does not have influence on the
metabolism o f these drugs
D. high-protein
diets
results
in
increased metabolism o f theses
drugs
E. A and B
42.A diet deficient in the mineral calcium
results in
A. increased drug-metabolizing
capacity
B. variable
effect
in the
drug
metabolizing capacity
C. decreased
drug
metabolizing
capacity
D. no change in the drug metabolizing
capacity
E. A & B
43.DealkyIation and hydroxylation o f drugs
is retarded by deficiency in
A.
B.
vitamin A
vitamin B
C. vitamin C
D. vitamin D
E. vitamin E
44.Which o f the following is not true
statement about the effect o f age up on drug
metabolism?
A. since metabolizing enzymes are not
fully developed at birth, all infants
and children require smaller doses
o f drugs than adults in order to
avoid toxic side effects
B. drugs metabolized by glucuronide
conjugation require special attention
when given to infants and children
C. In general the rate o f drug
elimination is lower in elderly
D. In older children, the metabolism o f
some drugs is faster than in adults
E. B and D
45. The
oxidative
propranolol is
metabolism
A.
B.
C.
D.
faster in men than in women
faster in women than in men
not influenced by gender
sometimes faster in men
sometimes in women
E. none o f the above
of
and
46.Which o f the following routes o f
administration does not bypass first-pass
effect?
A.
B.
C.
D.
E.
I .V . administration
Oral administration
Rectal administration
Sublingual administration
None o f the above
47.Which o f the following is true about
first-pass effect?
A. It is o f little clinical significance
B. It causes the inactivation o f drugs
before they reach their site o f action
C. It cannot be offset by increasing the
dose o f the drug
D. A and C
E. A and B
48.Extrahepatic metabolism takes place
A.
B.
C.
D.
E.
in the GI mucosa only
kidneys only
lungs only
throughout the body
B and C
D. doesn’t show
individuals
E. B and C
variation
among
52. Which o f the following affect intestinal
bacteria] flora?
A.
B.
C.
D.
E.
age
disease state
diet
drugs
all o f the above
53.Ulcerative colitis causes
49. Which o f the following is not true about
the metabolism that takes place in the
plasma?
A.
A. the
enzymes
responsible
for
metabolism in the blood are
primarily the esterases
B. simple esters are rapidly hydrolyzed
in the blood
C. metabolism in the blood always
results in loss o f activity
D. A and B
E. None
C.
50. Metabolizing enzymes in the intestinal
mucosa are especially important for drugs
undergoing
A.
B.
C.
D.
E.
microsomal oxidation
glucuronide conjugation
amino acid conjugation
sul fate conj ugati on
all but C
51.Drug
mucosa
metabolism
in
the
intestinal
A. is similar but not comparable in
capacity to a first-pass effect
B. makes the drugs more polar before
they enter the blood
C. occurs during drug absorption
B.
D.
E.
increased bacterial
growth in
intestine
decreased bacterial
growth in
intestine
no effect upon the bacterial growth
in intestine
sometimes increases and some times
decreases bacterial
growth in
intestine
none o f the above
54.Which o f the following statements is
false about the enterohepatic circulation o f
bile acids?
A. It occurs as a result o f the action o f
P-glucuronidase enzyme secreted by
the bacterial flora in the intestine
enzyme upon the polar glucuronide
conjugates o f bile
B. allows free, non-polar bile to be
reabsorbed
C. partially maintains the pools o f bile
acids
D. it applies to the glucuronide
conjugates of bile acids only and not
to conjugates o f drugs.
E. None o f the above
55. Which o f the following is/are caused by
the action o f bacterial flora in the intestine?
A. conversion o f vitamin precursors to
their active forms
B. conversion of some drugs to toxic
substances
C. conversion o f certain prodrugs to
their active forms
D. conversion o f some drug conjugates
to non-polar free drugs
E. all o f the above
56.The acidic environment o f the stomach
contributes
to
the
non-enzymatic
degradation o f all except
A.
B.
C.
D.
E.
protein and peptide drugs
penicillin G
erythromycin
carbenicillin
acetaminophen
57.
Which o f the following is not true about
the metabolism o f drugs in the nasal
passages?
A. the metabolism occurs mainly due
to the presence of high level of
CYP450 activity in the nasal
mucosa
B. it does not result in significant
reduction in the blood level o f drugs
C. nasal decongestant and anesthetics
are examples o f those metabolized
in the nasal passages
D. none
A. the metabolizing enzymes in lungs
have similar specific activities but
are less in amount compared to
those in the liver
B. the metabolizing enzymes in the
lungs are comparable to those found
in the liver in both their specific
activity and amount
C. the metabolizing enzymes in the
lungs are similar in amount to those
found in the liver, but their specific
activity is appreciably different
D. the metabolizing enzymes found in
the liver and the lungs are different
in their specific activity as well as
their amount
60.All o f the following statements about
placenta] metabolism are true except
A. if a drug is lipid soluble enough to
be absorbed into the systemic
circulation, then it can easily pass
the placenta o f a pregnant woman
without being metabolized
B. the placenta present no physical or
metabolic barrier to xenobiotics
C. many drugs get metabolized in the
placenta before passing into the
fetus
D. the only enzyme activity present in
the placenta is that aryl aromatic
hydroxylase, which is inducible in
pregnant women
who
smoke
cigarettes
E. all but C
58.The lung is responsible for the first-pass
metabolism o f drugs administered
A.
B.
C.
D.
E.
Intravenously
Transdermally
Subcutaneously
Intramuscularly
All o f the above
59. Which o f the following is true about the
metabolizing enzymes found in lungs and
liver?
61.The major deficient enzyme activity in
fetus and the neonate is
A.
B.
C.
D.
E.
sulfate conjugating activity
glucuronic acid conjugating activity
oxidative activity
amino acid conjugating activity
A and B
62.Gray baby syndrome results from
A. decrease in bilirubin glucuronide
formation
B. decrease
in
erythromycin
glucuronidation
C. decrease
in
isoniazid
glucuronidation
D. decrease
in
chloramphenicol
glucuronidation
E. A and D
63. Which o f the following is/are true about
the
strategies
of
managing
drug
metabolism?
A. the strategies try to circumvent the
rapid metabolism o f drugs
B. the aim is to improve drug therapy
C. they result in increased duration of
action
D. they can provide increased site
specificity
E. all o f the above
64.The
pharmaceutical
strategy
managing drug metabolism involves
of
A. the concurrent use o f enzyme
inhibitors to drug metabolism
B. the use o f different dosage forms to
either avoid or compensate for rapid
metabolism
C. the addition, deletion, or isosteric
modification o f key functional
groups
D. the use o f additional agents that
prevents the toxicity caused by
metabolites o f the therapeutic agent
E. A and D
65.Nitroglycerin,
a
rapidly
acting
antianginal agent, is essentially ineffective
when given orally, but is very effective in
treating acute attacks o f angina if given
sublingually. This is an example o f
A. a
pharmaceutical
strategy
managing drug metabolism
of
B. a pharmacological strategy o f
managing drug metabolism
C. a chemical strategy o f managing
drug metabolism
D. both pharmaceutical as well as
pharmacological
strategy
of
managing drug metabolism
E. none
66. Which o f the following is not a correct
match between the examples given and the
strategies o f managing drug metabolism?
A. enteric-coated
omeprazole
preparations;
pharmaceutical
strategy
B. clavulanic acid used in conjunction
with penicillin; pharmacological
strategy
C. extended-release
transdermal
patches and ointment formulations
o f nitroglycerin; pharmaceutical
strategy
D. chlorpropamide,
a
structurally
similar compound to tolbutamide,
has a much longer duration o f
action; pharmacological strategy.
E. none
67.The concurrent use o f levodopa and
carbidopa, is an example o f
A. pharmacological
strategy
of
managing drug metabolism
B. pharmaceutical
strategy
of
managing drug metabolism
C. physical strategy o f managing drug
metabolism
D. chemical strategy o f managing drug
metabolism
E. B and C
68.Ifosfamide and mesna make a typical
example o f pharmacological strategy to
avoid toxicity because
A. mesna is a non-toxic derivative o f
ifosfamide
B. mesna prevents the metabolisnf o f
ifosfamide
C. mesna shortens the action o f
ifosfamide
D. mesna reacts with toxic metabolite
o f ifosfamide
E. C and D
69.Ritonavir and lopinavir constitute
A.
B.
C.
D.
E.
a pharmacological
strategy of
extending the action o f ritonav r by
coadministering lopinavir
a pharmacological
strategy of
enhancing
the
pharmacolo jical
action o f lopinavir by concurrent
administration o f ritonavir
a chemical strategy, where lopihavir
is the long-acting derivative of
ritonavir
a pharmacological strategy, \ 'here
lopinavir prevents the metabolism of
ritonavir.
A chemical strategy, where the
metabolism o f lopinavir rebases
less toxic metabolites than th|at o f
ritonavir.
70. Addition o f 17a-methyl groub to
testosterone results in the new corrijound
methyltestosterone. Which o f the following
is not true about testosterone and
methyltestosterone?
A. they make up an example o f a
chemical strategy o f managing drug
metabolism
B. methyltestosterone is only h^lf as
potent as testosterone
C. methyltestosterone is subject to
rapid first-pass metabolism
D. methyltestosterone can be used
orally but not testosterone
E. none
71. Which o f the following is not a eason
for developing
metaproterenol
from
isoproterenol?
A. metaproterenol is orally active while
isoproterenol is not
B. metaproterenol has longer duration
o f action
C. metaproterenol is much more potent
than isopreterenol
D. metaproterenol is less susceptible to
metabolism by catechol O-methyl
transferase (COMT)
E. none o f the above
72. Which o f the following can be
considered as advantages gained from the
use o f prodrugs instead o f the active form
o f the drug?
A.
B.
C.
D.
E.
increased water solubility
increased lipid solubility
site specificity
increased shelf-life
all o f the above
73. Which o f the following ,esters are not
involved
A. in making some water soluble
steroidal produgs
B. in making lipid soluble prodrugs of
estradiol,
which
have
longer
duration o f action
C. in producing nabumetone, a prodrug
with decreased GI irritation than the
other NSAIDs
D. in making steroids which have
increased topical absorption
E. none
74. Which o f the following is true about
enalaprilat and enalapril?
A. enalaprilat is the prodrug, which is
converted to the active enalapril by
plasma esterases.
B. Enalapril is less water soluble than
enalaprilat
C. Enalaprilat is active orally, while
enalapril is not
D. Enalapril is used
administration
E. None
for parenteral
E. none o f the above
79.An anti-prostate cancer agent with less
systemic side effect is
75. The reason for esterification
sulfisoxazole to acetyl sulfisoxazole is
of
A.
B.
C.
D.
to increase oral bioavailability
to increase the duration o f action
to avoid certain adverse effects
to overcome the bitter taste of
sulfisoxazole
E. A and D
76.The prodrug nabumetone is employed to
overcome the GI irritation caused by some
NSAIDs. This is because
A. it has the ability to get dissolved in
the stomach and neutralize the acid
there
B. nabumetone is a ketone
C. it does not inhibit the synthesis of
prostaglandins
D . all o f the ab ove
E .B and C
77. Which o f the following is not true about
the prodrug methenamine?
A. it is stable and nontoxic at norma]
physiological pH
B. it is best if it is used as enteric
coated formulations
C. it is more potent than formaldehyde
D. it
hydrolyzes
and
forms
formaldehyde in the acidic pH o f the
urine
E. none
78. Which o f the following prodrugs is not
developed for its site specificity?
A.
B.
C.
D.
methyldopa
diethylstilbesterol
cefamandole
olsalazine
A.
B.
C.
D.
E.
olsalazine
sulfasalazine
diethylstilbesterol
diethylstilbeterol diphosphate
B and D
80,Cyclophosphamide is different
other nitrogen mustards because
A.
B.
C.
D.
E.
from
it is less toxic
it is site specific
it has longer duration o f action
it is more stable
all o f the above
81 .Which o f the following is not true about
genes?
A. they are discrete segments o f DNA
B. B. they are capable o f reproduction
when the cell replicates
C. C. they are responsible for guiding
the biosynthesis o f specific proteins
D. sometimes they may also be found
in the RNA
E. none o f the above
82.Genes are involved in
A. metabolism o f drugs
B. determining drug response and
toxicity
C. absorption and transports o f drug
molecules
D. in the production o f drug receptors
E. all o f the above
83.A
patient may not respond to or suffer
adverse effects from a drug prescribed for
his/her condition, because o f which o f the
following?
A.
B.
C.
D.
E.
inappropriate dosing
drug allergies
drug-drug interaction
medication errors
all of the above
84. Which o f the following is not true about
pharmacogenetics?
A. it involves identifying the individual
genetic differences
B. it tries to select the right drug for the
right patient
C. it tries to identify individual
predisposition
D. it makes use o f genetic information
to improve drug response and limit
side effects
E. it studies the genetics o f humans
87 .An SNP that could alter the transcription
rate, resulting in either an increase or
decrease in the production o f the target
protein if found in which region?
A.
B.
C.
D.
E.
88.Which o f the SNP located within the
coding region would have a significant
effect?
I. an SNP that did not alter the
amino acid sequence
]]. an SNP that resulted in one
amino acid being replaced by
a similar amino acid
III.
an
SNP
that
resulted in one amino acid
being
replaced
by
a
significantly different amino
acid
85.The genetic variation in the DNA
sequence o f certain individuals can lead
them to which o f the following ?
A. to be more likely to develop specific
disease states
B. to be more likely to follow a
specific path o f disease progression
C. to be more likely to respond to
specific drug therapy
D. to be more likely to develop certain
adverse drug effects
E. all o f the above
86. The genetic variation between any two
unrelated individuals is approximately
A. two base pair change in every 100
base pairs
B. one base pair change in every 100
base pairs
C. three base pair change in every 100
base pairs
D. one base pair change in every 1000
base pairs
E. three base pair change in every 1000
base pairs
coding
splicing control
promoter
outside any o f the above regions
B and C
A.
B.
C.
D.
E.
I only
11 and III
Ill
II
I, II, III
ANSW ERS
Biotransformation, Prodrugs and Pharmacogenetics
1. Answer: D. most o f the time metabolism results in more than one metabolites
Explanation:
Drug metabolism (also called biotransformation) refers to the biochemical changes that drugs and
other foreign chemicals undergo in the body, leading to the formation o f different metabolites
with different effects. Often a mixture o f intermediate metabolites and excreted products,
including unchanged parent drug are produced. Rarely is one metabolite produced from a single
drug.
2. Answer: E. all o f the above
Explanation:
Some metabolites are inactive (i.e., their pharmacologically active parent compounds become
inactivated or detoxified). For example, the oxidation o f 6-mercaptopurine to 6-mercapturic acid
results in a loss o f anticancer activity. Certain metabolites retain the pharmacological activity of
their parent compounds to lesser or greater extent (e.g., imipiramine is demethylated to the
essentially equiactive antidepressant, desipramine). Some metabolites develop activity different
from that o f their parent drugs (e.g., the antidepressant iproniazid is dealkylated to the
antitubercular, Isoniazid).
3. Answer: B. bioactivated metabolites
Explanation:
Prodrugs are molecules that are either inactive or very weakly active and require in vivo
biotransformation to produce the physiologically active drug.
4. Answer: C. the activity o f the drugs is not modified
Explanation:
Phase I reactions are those in which polar functional groups are introduced into the molecule or
unmasked by oxidation, reduction, or hydrolysis. After the phase 1 reaction the drugs are
converted to more polar metabolites that may or may not retain their activity.
5. Answer: E. any chemical that is foreign to the body
Explanation:
Xenobiotics include any compound (drugs, toxic substances, etc) that enter the body and thus is
foreign to it.
6. Answer: B. liver
Explanation:
Since it contains the majority o f the metabolizing enzymes, liver is the main organ o f metabolism.
7. Answer: B. oxidation
Explanation:
The types o f biotransformations that occur during the phase I reactions include oxidation,
reduction and hydrolysis. Among this oxidation is the most common one.
8. Answer: B. because they are enzymes, CPY450 oxidases can only metabolized a specific type
o f substrates
Explanation:
CYP450, unlike most enzymes uses a variety o f oxidase biotransformations to metabolize a
diverse group o f substrates. It exists in multiple isoforms or families. The presence o f these
different isoforms is responsible for the large substrate variation seen with CYP450.
9. Answer: B. family and subfamily
Explanation:
CYP450 isoforms are named using the root ‘CYP’ followed by an Arabic number designating the
family, a letter designating the subfamily, and a second Arabic number indicating the individual
gene.
10.Answer: D. some oxidations are catalyzed by nonmicrosomal oxidases located in cytosol and
mitochondria o f extrahepatic tissues
Explanation:
The vast majority o f oxidations are catalyzed by a group o f mixed-function oxidases known as
cytochrome Plso (CYP450). These oxidases are bound to the smooth endoplasmic reticulum of
the liver and require both NADPH and a porphyrin prosthetic group. Unlike most enzymes,
CYP450 uses a variety o f oxidative biotransformation to metabolize a diverse group of
substances.
11 .Answer: B. have enhanced water solubility than the parent drugs
Explanation:
The metabolites produced after phase I oxidation reactions have increased polarity, which
enhances their water solubility and reduces their tubular reabsorption to some extent, thus
favoring their excretion in the urine. Most o f the time these metabolites undergo further
biotransformation by phase II pathways.
12.Answer: B. like the oxidation reactions, CYP450 play the major role in carrying out reduction
reactions
Explanation:
Although there is evidence suggesting that the CYP450 system might be involved in some
reduction reactions, it cannot be considered to play the major role.
13.Answer: B. they are very specific
Explanation:
Esterase enzymes are generally non-specific when catalyzing de-esterification reactions.
14.Answer: B. ester drugs are usually longer acting than structurally similar amide drugs
Explanation:
Since esterases are mainly located in the plasma, ester drugs are in general shorter acting than
structurally similar amide drug, which are not hydrolyzed until they reach the liver (because
amidase enzymes are mainly found in the liver).
15.Answer: B. during phase II reactions, only the metabolites formed in phase I reaction are
conjugated
Explanation:
During the phase II reactions, the functional groups o f either the original drug or the metabolites
o f the phase I reaction are masked by a conjugation reaction.
16.Answer: E. all but D
Explanation:
Conjugation reactions combine the parent drug (or its metabolite) with certain natural indigenous
constituents, such as glucuronic acid. These reactions generally require both a high-energy
molecule and an enzyme. The high energy molecule consists o f a coenzyme bound to the
endogenous substance, the parent drug, or the drug’s phase I metabolite.
17.Answer: A. cytosine
Explanation:
The natural endogenous constituents involved in phase 11 reactions include, glucuronic acid,
Glycine, glutamine, sulfate, glutathione, the two-carbon acetyl fragment, and the one-carbon
methyl fragment.
18.Answer: C. transferases
Explanation:
The enzymes, which catalyze the conjugation reactions during the phase II reactions are called
transferases.
19.
Answer: E. liver
Explanation:
The enzymes responsible for catalyzing conjugation reactions are found mainly in liver and to
lesser extent in the intestines and other tissue.
20. Answer: D. they could be toxic
Explanation:
In genera], conjugates are polar molecules that are readily excreted and unable to cross the cell
membrane and thus they are often pharmacologically inactive and non-toxic.
21.Answer: A. glucuronidation
Explanation:
Glucuronidation is the most common conjugation pathway because o f a readily available supply
o f glucuronic acid as well as large variety o f functional groups, which can enzymatically react
with this sugar derivative.
22.Answer: A. uridine diphosphate glucuronic acid
Explanation:
The high-energy form o f glucuronic acid is uridine diphosphate glucuronic acid, and reacts with
variety o f functional groups under the influence o f glucuronyl transferase.
23.Answer: E. C and D
Explanation:
Drugs that possess hydroxyl or carboxyl groups readily undergo glucuronidation to form ethers
and esters, respectively. In addition, N-, S-, and C-glucuronides are also possible.
24.Answer: E. Carboxyl acids
Explanation:
The high-energy form o f sulfate, 3’-phosphoadenosine-5’phophosulfate (PAPS), react with
phenols, alcohols, arylamines, and N-hydroxyl compounds under the influence o f sulfotransferase
to form highly polar metabolites.
25.Answer: A. carboxylic acids
Explanation:
Amino acid conjugation involves the reaction o f either Glycine or glutamine with aliphatic or
aromatic acids to forms amides. A drug molecule is first converted to an acyl coenzyme A
intermediate. An N-acyltransferase enzyme then catalyzes the conjugation o f the activated drug
molecule with the amino acid.
26. Answer: B. Glutathione conjugation
Explanation:
Under the influence o f glutathione S-transferase, glutathione can react with halides, epoxides and
other electrophilic compounds to form harmless inactive products.
27.Answer: C. Mercapturic acid derivative
Explanation:
When glutathione has reacted with an electrophile, it undergoes a series o f reaction to produce a
mercapturic acid derivative, which is eliminated.
28.Answer: C. fluorine
Explanation:
Methylation occurs with drugs that have functional groups containing oxygen, nitrogen, and
sulfur and result in metabolites that are usually less polar than the unaltered drugs.
29.Answer: E. acetylation and methylation
Explanation:
Acetylation and methylation o f drugs results in metabolite, which are less polar than the parent
drugs and can retain some pharmacological activity.
30.
Answer: B. methylation plays major role in the elimination o f drugs
Explanation:
Methylation can inactivate certain compounds, but overall it plays a minor role in the elimination
o f drugs.
flir
31 .Answer: C. I, II and III
Explanation:
Acetylation can occur with primary amides, sulfonamides, hydrazides and, occasionally, amides.
It leads to the formation o f N-acetylated products.
„COOH
Q
o
11
H3c %
h 3c c
II
^
^
^ ^ COOH
^
^
ococh
3
o
Alkane
_
Alkyl halide
R -X
X = F, Cl, Br, I
Primary alcohol
—
II
1
R—|- O H
Secondary alcohol
R
1
R— | ' —OH
Alkyl, and occasionally aryl (aromatic) functions are
represented by the RMethyl:
C H 3Ethyl:
CH3CH2Propyl:
CH3CH2CH2Isopropyl:
(CH3)2CHPhenyl: C 6H 5Alkyl halides [haloalkanes] consist o f an alkyl group attached
to a halogen:
F, Cl, Br, 1.
Chloro, bromo and iodo alkyl halides are often susceptible to
elimination and/or nucleophilic substitution reactions.
Primary alcohols have an -OH function attached to an R-CH2group.
Primary alcohols can be oxidised to aldehydes and on to
carboxylic acids. (It can be difficult to stop the oxidation at the
aldehyde stage.)
Primary alcohols can be shown in text as: RCH 20H
Secondary alcohols have an -OH function attached to a R2CHgroup.
Secondary alcohols can be oxidised to ketones.
Secondary alcohols can be shown in text as: R2CHOH
H
Tertiary alcohol
r —| :
-
oh
Aldehyde
1?
R
H
Ketone
Tertiary alcohols have an -OH function attached to a R3Cgroup.
Tertiary alcohols are resistant to oxidation with acidified
potassium dichromate(VI), K.
Tertiary alcohols can be shown in text as: R3COH
Aldehydes have a hydrogen and an alkyl (or aromatic) group
attached to a carbonyl function.
Aldehydes can be shown in text as: RCHO
Aldehydes are easily oxidised to carboxylic acids, and they can
be reduced to primary alcohols.
Ketones have a pair o f alkyl or aromatic groups attached to a
carbonyl function.
Ketones can be shown in text as: RCOR
‘if
r'
\
Carboxylic acid
O
R
/
\
OH
Carbonyl function
o
II
/ C\
Ester
O
II
/ C\
R
O -R
O
II
c
r ' xnh2
Primary amine
r~ ~ n h 2
Secondary amine
,N H
Tertiary amine
R\
—N
R
RX
Acid chloride
O
II
R
The carbonyl group is a super function because many common
functional groups are based on a carbonyl, including:
aldehydes, ketones, carboxylic acids, esters, amides, acyl (acid)
chlorides, acid anhydrides
Esters have a pair o f alkyl or aromatic groups attached to a
carbonyl linking oxygen function.
Esters can be shown in text as: RCOORjDrJoccasioually)_____
ROCOR.
carboxylic acid alcohol -> ester water
This is an acid catalysed equilibrium.
Primary amides (shown) have an alkyl or aromatic group
attached to an amino-carbonyl function.
Primary amides can be shown in text as: RCONH2
Secondary amides have an alkyl or aryl group attached to the
nitrogen: RCONHR
Tertiary amides have two alkyl or aryl group attached to the
nitrogen: RCONR2
+
Amide
R
Carboxylic acids have an alkyl or aromatic groups attached to a
hydroxy-carbonyl function.
Carboxylic acids can be shown in text as: RCOOH
Carboxylic acids are weak Bronsted acids and they liberate
C 02 from carbonates and hydrogen carbonates.
Cl
+
~
+
Primary amines have an alkyl or aromatic group and two hydrogens attached to a nitrogen atom.
Primary amines can be shown in text as: RNH2
Primary amines are basic functions that can be protonated to
the corresponding ammonium ion.
Primary amines are also nucleophilic
Secondary amines have a pair o f alkyl or aromatic groups, and
a hydrogen, attached to a nitrogen atom.
Secondary amines can be shown in text as: R2NH
Secondary amines are basic functions that can be protonated to
the corresponding ammonium ion. Secondary amines are also
nucleoghilic.
Tertiary amines have three alkyl or aromatic groups attached to
a nitrogen atom.
Tertiary amines can be shown in text as: R3N
Tertiary amines are basic functions that can be protonated to
the corresponding ammonium ion.
Tertiary amines are also nucleophilic.
Acid chlorides, or acyl chlorides, have an alkyl (or aromatic)
group attached to a carbonyl function plus a labile (easily
displaced) chlorine. Acid chlorides highly reactive entities are
highly susceptible to attack by nucleophiles.
Acid chlorides can be shown in text as: ROC1
Acid anhydride
?
V nr
I
Ry
Nitrile
R —*C=N
Carboxylate ion or salt
P
R
0
Ammonium ion
r
i+
r
i
LR Xr „
Amino acid
yCOOH
R - C —H
\ Nh2
Alkene
R\
C= C
H7
/H
XH
Ether
R
/(X
R
Acid anhydrides are formed when water is removed from a
carboxylic acid, hence the name.
Acid anhydrides can be shown in text as: (R 0 )2 0
Nitriles (or organo cyanides) have an alkyl (or aromatic) group
attached to a carbon-triple-bond-nitrogen function.
Nitriles can be shown in text as: RCN
Carboxylate ions are the conjugate bases o f carboxylic acids,
ie. the deprotonated carboxylic acid.
Carboxylate ions can be shown in text as: R CO O When the counter ion is included, the salt is being shown.
Salts can be shown in text as: RCOONa
Ammonium ions have a total o f four alkyl and/or hydrogen
functions attached to a nitrogen atom.
[NH4]+
[RNH3]+
[R2NH2]+
[R3NH]+
[R4NJ+
Quaternary ammonium ions are not proton donors, but the
others are weak Bronsted acids (pKa about 10).
Amino acids, strictly alpha-amino acids, have carboxylic acid,
amino function and a hydrogen attached to a the same carbon
atom.
There are 20 naturally occurring amino acids. All except
glycine (R = H) are chiral and only the L enantiomer is found
in nature.
Amino acids can be shown in text as: R-CH(NII2)COOH
Alkenes consist o f a C=C double bond function.
Alkenes can be shown in text as:
Mono substituted: RCH=CH2
1.1-disubstituted: R2C=CH2
1.2-disubstituted: RCH=CHR
Alkanes are planar as there is no rotation about the C=C bond.
Alkenes are electron rich reactive centres and are susceptible to
electrophilic addition.
Ethers have a pair o f alkyl or aromatic groups attached to a
linking oxygen atom.
Ethers can be shown in text as: ROR
32. Answer: B. N-acetylated metabolites o f sulfonamides
Explanation:
N-acetylated metabolites can accumulate in tissue or in the kidneys, as in the case o f certain
antibacterial sulfonamides. Crystalluria and subsequent tissue damage may result.
Sulfonamide Structure
33.Answer: C. Acetyl-CoA
Explanation:
The high-energy molecule for acetylation is acety]-CoA. The reaction is catalyzed by N-acetly
transferase. S-adenosylmethionine is the high-energy molecule for methylation.
Acetyl-CoA
34. Answer: E. none o f the above
Explanation:
The factors which influence drug metabolism include: chemical structure o f the drug, species
difference, physiological or diseases state, genetic variation, drug dosage, diet, age, gender, drug
administration route.
35.Answer: B. phase II
Explanation:
In general qualitative difference occurs primary with phase 11 reactions and quantitative
differences occur primary with phase I reactions.
36.Answer: D, a difference in a particular endogenous substrate
Explanation:
Species difference in drug metabolism could be qualitative difference in the actual metabolic
pathway, which could result from a genetic deficiency o f a particular enzyme or a difference in a
particular endogenous substrate. Species differences, which are quantitative, are differences in the
extent to which the same type o f metabolic reaction occurs. The causes include difference in the
enzyme level, the presence o f species specific isozymes, a difference in the amount o f
endogenous inhibitors or inducer or a difference in the extent o f competing reactions.
37. Answer: E. all o f the above
Explanation:
Because the liver is the major organ involved in the metabolism o f drugs any disease that may
affect its function is likely to affect the metabolism o f drugs. Congestive heart failure affect drug
metabolism through the effect it has on hepatic blood flow. CHF decrease the hepatic blood flow
and thus the extent o f drug metabolism in the liver.
3 8. Answer: E. None o f the above
.
Explanation:
The acetylation rate depends on the amount o f N-acetyltransferase present, which is determined
by genetic factors. The general population can be divided into fast acetylators and slow
acetylators. Fast acetylators are more prone to hepatotoxicity from isoniazid than slow
acetylators, whereas slow acetylators are more prone to isoniazids other toxic effects.
39.Answer: D. An increase in drug dosage can result in increased drug concentration but the
metabolism increases up to a certain level only.
Explanation:
An increase in drug dosage results in increased drug concentrations and can saturate certain
metabolic enzymes. As drug concentration exceeds 50% saturation for a particular enzyme, drug
elimination via this path no longer follows solely first-order kinetics, but rather is a mix o f zeroand first-order kinetics. At 100 % saturation, metabolism via this enzyme follows zero-order
kinetics.
40.Answer: D. A and B.
Explanation:
The level o f some conjugating agents (or endogenous substrates) such as sulfate, glutathione, and
(rarely) glucuronic acid, are sensitive to body nutrient levels. For example, a low-protein diet can
lead to a deficiency o f certain amino acids such as Glycine and decreased oxidative drug
metabolism capacity.
41 .Answer: A. diet deficiency in essential fatty acids reduces the metabolism o f these drugs.
Explanation:
Diets deficiency in essential fatty acids reduces the metabolism o f ethylmorphine and
hexobarbital by decreasing synthesis o f certain drug-metabolizing enzymes.
42.Answer: C. decreased drug metabolizing capacity.
Explanation:
A deficiency o f certain dietary minerals affects drug metabolism. Calcium, magnesium, and zinc
deficiencies decrease drug-metabolizing capacity, whereas iron deficiency appears to increase it.
A copper deficiency leads to variable effects.
43.Answer: E. vitamin E
Explanation:
Deficiencies o f vitamins (particularly vitamins A, C, E, and B group) affect drug metabolizing
capacity. For example, a vitamin C deficiency can result in a decrease in oxidative pathway,
whereas a vitamin E deficiency can retard dealkylation and hydroxylation.
44.Answer: A. Since metabolizing enzymes are not fully developed at birth, all infants and
children require smaller doses of drugs than adults in order to avoid toxic side effects
Explanation:
Since the enzyme systems are not fully developed, all infant and young children require smaller
doses o f drugs than adults. This is particularly true o f drugs that require glucuronide
conjugation. In older children, some drugs are metabolized faster than in adults, particularly if
the dosage is based on weight. The liver develops faster than the increase in general body weight
and thus represents a greater fraction o f total body weight. In the elderly, metabolizing enzyme
systems decline, resulting in decreased metabolism o f drugs and thus slower rate o f drug
elimination.
Elimination o f acetaminophen is principally by liver metabolism (conjugation) and subsequent
renal excretion o f metabolites. Approximately 85% o f an oral dose appears in the urine within 24
hours o f administration, most as the glucuronide conjugate, with small amounts o f other
conjugates and unchanged drug.
In neonates and children (3— 9 years), acetaminophen is excreted primarily as the sulfate
conjugate. The difference in methods o f clearance may be due to a deficiency in glucuronide
formation in younger age groups
N-acetylcysteine is used to treat neonatal acetaminophen toxicity.
45.Answer: B. Faster in women than in men.
Explanation: Metabolic differences between the sexes have been observed for a number o f
compounds, suggesting that androgen, estrogen, and/or adrenocorticoid activity might affect the
activity o f certain CYP450 enzyme isozymes. The metabolism of diazepam, prednisolone,
caffeine, and acetaminophen is faster in women, whereas that o f propranolol, chlordiazepoxide,
lidocaine, and some steroids is faster in men.
46.Answer: B. Oral administration.
Explanation:
After oral administration, drugs are absorbed from the GIT and transported to the liver through
the hepatic portal vein before entering the systemic circulation. Thus, the drugs are subject to
hepatic metabolism (first-pass effect or presystemic elimination) before they reach their site o f
action.
47.
Answer: B. It causes the inactivation o f drugs before they reach their site o f action.
Explanation:
During first-pass effect drugs are metabolized in the liver from their active forms to their inactive
forms. This leads to decreased plasma levels of the drug as well as inactivation o f the drugs
before they reach their site o f action and this can cause significant clinical problems. Therefore,
this effect must be counteracted if the drug is to be effective. The most common way to do this is
to increase the oral dose o f the drug.
48.Answer: D. Throughout the body.
Explanation:
Extrahepatic metabolism means the biotransformation o f drugs that takes place in tissues other
than the liver. The most common sites are portals o f entry (GI mucosa, nasal passages, lungs) and
the portals o f excretion (kidneys). However, metabolism can occur throughout the body.
49.
Answer: C. Metabolism in the blood always results in loss o f activity.
Explanation:
Plasma contains the enzyme esterases, which hydrolyze drugs like procaine and succinylcholine
that are simple esters. Additionally plasma esterases can activate a variety of ester prodrugs in the
blood. So, not all blood metabolisms result in loss o f activity.
50. Answer: E. all but C.
Explanation:
Microsomal oxidation, glucuronide conjugation and sulfate conjugation are the most important
types o f metabolisms that occur in the intestinal mucosa.
51 .Answer: E. B and C.
Explanation:
Drugs are metabolized as they are absorbed from the intestinal mucosa into polar or inactive
metabolites before entering the blood. This intestinal drug metabolism is similar to and
comparable in capacity to first-pass effect, but it shows greater individual variation as it is
exposed to the environment.
52. Answer: E. all o f the above
Explanation:
Age, disease state, diet, and exposure to chemicals and drugs are the factors which can affect the
intestinal bacterial flora, and hence they may also modify drug activity.
53.Answer: A. increased bacterial growth in intestine.
Explanation:
Certain diseases, particularly intestinal diseases, affect intestinal flora. Ulcerative colitis, for
example, promotes bacterial growth while diarrhea reduces the number o f bacteria.
54.
drugs.
Answer: D. It applies to the glucuronide conjugates o f bile acids only and not to conjugates o f
Explanation:
The principle o f enterohepatic circulation applies to certain glucuronide conjugates o f drugs as
well.
55. Answer: E.all of the above
Explanation:
Certain bacterial flora converts vitamin precursors to their active form, as with vitamin k.
Bacterial flora can also convert some drugs to their toxic form, as with the conversion o f the
artificial sweetener cyclamate to produce cyclohexylamine, a suspected carcinogen. Intestinal
bacteria produce the enzyme azoreductase, which reduces the prodrug sulfasalazine to the active
anti-inflammatory aminosalicylic acid and the active antibacterial sulfapyridine. The intestinal
bacteria can also secret the enzyme p-glucuronidase, which can hydrolyze glucuronide conjugate
o f some drugs resulting less polar drugs that can be reabsorbed to the systemic circulation.
56.Answer: E. acetaminophen.
Explanation:
Acetaminophen is not degraded in the stomach.
57.
Answer: B. it does not result in significant reduction in the blood level o f drugs.
Explanation:
Drug metabolism in the nasal passages can result in significant reduction in the blood levels of
drugs.
58.Answer: E. All o f the above
Explanation:
Drugs administered intravenously, intramuscularly, subcutaneously or transdermally have their
first-pass metabolism in the lungs.
59.
Answer: A. the metabolizing enzymes in lungs have similar specific activities but are less in
amount compared to those in the liver
Explanation:
The total amount o f the metabolizing enzymes found in the lungs is less than in the liver;
however, the specific activities o f the enzymes are comparable to those in the liver. Moreover, the
lung provides second-pass metabolism for drugs leaving the liver.
60. Answer: C. many drugs get metabolized in the placenta before passing into the fetus
Explanation:
The placenta is not a physical or metabolic barrier to xenobiotics. Very little metabolizing
enzyme activity has been demonstrated in the placenta. Drugs present in their active form in the
maternal circulation likely pass unchanged into the fetal circulation. An exception to this lack of
enzyme activity in the placenta is the presence o f a small amount o f aryl aromatic hydroxylase,
which is inducible in pregnant women who smoke cigarettes.
61 .Answer: B. glucuronic acid conjugating activity.
Explanation:
In terms o f fetal metabolism, there are varying degrees o f drug-metabolizing activity depending
upon a number o f factors including fetal age. A major deficiency is that o f glucuronic acid
conjugating activity both in fetus and the neonate.
62.Answer: D. decrease in chloramphenicol glucuronidation
Explanation:
Two consequences o f decreased glucuronic acid conjugating activity in the fetus and neonate are
the gray baby syndrome, resulting from decreased chloramphenicol glucuronidation, and neonatal
hyperbilirubinemia, resulting from a decrease in bilirubin glucuronide formation.
63.Answer: E. all o f the above
Explanation:
A variety o f strategies have been used to circumvent the rapid metabolism o f drugs, which results
in increased duration o f action and thus, improve drug therapy. In some instances, these methods
have provided increased site specificity as well.
64.Answer: B. the use o f different dosage forms to either avoid or compensate for rapid
metabolism.
Explanation:
The strategies used to manage drug metabolism can be pharmaceutical, pharmacological or
chemical ones. Pharmaceutical strategies involve the use o f different dosage forms to either avoid
or compensate for rapid metabolism. Pharmacological strategies involve the concurrent use o f
enzyme inhibitors to drug metabolism. In some cases, the concurrent use o f an additional agent
does not prevent metabolism but rather prevents the toxicity caused by metabolites o f the
therapeutic agents. And the chemical strategies involve the addition, deletion, or isosteric
modification o f key functional groups.
65.Answer: A. a pharmaceutical strategy o f managing drug metabolism.
Explanation:
Sublingual tablets are useful for delivering drugs directly into the systemic circulation and
bypassing hepatic first-pass metabolism. Nitroglycerin is ineffective when administered orally
due to an extremely high first-pass-effect but is very effective in treating acute attacks o f angina if
given sublingually.
Hepatic first-pass metabolism:
The first-pass effect (or first-pass metabolism) is a phenomenon o f drug metabolism.
After a drug is swallowed, it is absorbed by the digestive system and enters the hepatic portal
system. The absorbed drug is carried through the portal vein into the liver.
Oral
Medication
o
/
* ■'‘intestinal
Tract
The liver is responsible for metabolizing many drugs. Some drugs are so extensively metabolized
by the liver that only a small amount o f unchanged drug may enter the systemic circulation, so the
bioavailability o f the drug is reduced.
e.g., isoproterenol, meperidine, pentazocine, morphine
Intravenous, intramuscular, sublingual routes avoid the first-pass effect.
66.Answer: D. chlorpropamide, a structurally similar compound to tolbutamide, has a much
longer duration o f action; pharmacological strategy.
Explanation:
Pharmaceutical strategies try to make use o f different dosage forms to either avoid or compensate
for rapid metabolism. For example, enteric coated formulations can protect acid sensitive drugs
(such as omeprazole, erythromycin) as they pass through the acidic environment o f the stomach;
transdermal patches and ointment formulations provide a continuous supply o f drug over an
extended period o f time and are useful for rapidly metabolized compounds such as nitroglycerin.
The use o f clavulanic acid along with (3-lactam antibiotics to inhibit p-lactamase, the enzyme
secreted by certain bacteria and capable o f hydrolyzing the P-lactam ring and inactivate these
antibiotics, is an example o f pharmacological strategy o f overcoming drug metabolism, where the
concurrent use o f enzyme inhibitors is made use o f to decrease drug metabolism. Chemical
strategy involves the addition, deletion or isomeric modification o f key functional groups. For
example, tolbutamide is an oral hypoglycemic and rapidly undergoes oxidation o f its para-methyl
group. Chlorpropamide is similar to tolbutamide but has a nonmetabolizable para-chloro group
and as a result has a much duration o f action.
67. Answer: A. pharmacological strategy o f managing drug metabolism.
Explanation:
Levodopa (L-dopa), the amino acid precursor of dopamine, is used in the treatment o f
parkinsonism. Unlike dopamine, L-dopa can penetrate blood-brain barrier an reach the CNS.
When in brain, it is decarboxylated to dopamine. To ensure that adequate concentrations o f Ldopa reach the CNS, peripheral metabolism o f the drug must be blocked. The concurrent use o f
carbidopa, a dopa carboxylase inhibitor that cannot penetrate the blood-brain barrier, prevents
peripheral formation o f dopamine and allows site-specific delivery o f dopamine to the CNS. So
this is a typical example o f a pharmacological strategy o f managing drug metabolism.
dopamine
levodopa
68. Answer: D. mesna reacts with toxic metabolite o f ifosfamide.
Explanation:
Ifosfamide is an alkylating agent that must undergo in vivo metabolism to produce active nitrogen
mustard. In the process o f this metabolic activation, significant concentrations o f acrolein are
produced. These acrolein molecules react with nucleophiles on renal proteins and produce
hemorrhagic cystitis. To prevent this toxicity, ifosfamide is always coadministered with mesna, a
sulfydryl-containing compound that reacts with and neutralizes any acrolein that is present I the
kidney.
69. Answer: B. a pharmacological strategy o f enhancing the pharmacological action o f lopinavir
by concurrent administration o f ritonavir.
Explanation:
Ritonavir is an HIV protease inhibitor that is ineffective if used alone due to rapid oxidation by
CYP3A isozymes. A combination o f a low dose o f ritonavir with a therapeutic dose o f lopinavir,
results in an inhibition o f CYP3A, the establishment o f adequate levels o f lopinavir, enhancement
of the pharmacological action o f lopinavir, and better therapeutic efficacy without hepatotoxicity
(since at therapeutic doses, ritonavir is known to cause hepatic toxicity).
70. Answer: C. methyltestosterone is subject to rapid first-pass metabolism.
Explanation: Testosterone is not orally active due to rapid oxidation o f its 17-hydroxyl group to a
ketone. Addition o f a 17a-methyl group converts the labile secondary alcohol to a stable tertiary
alcohol. The resulting compound, methyltestosterone, is only half as potent as testosterone;
however, it is not subject to rapid first-pass metabolism and can be used orally. A similar strategy
has been used to make orally active estradiol analogues.
71 .Answer: C. metaproterenol is much more potent than isoproterenol.
Explanation:
Isoproterenol is a potent )3-adrenergic agonist used for the relief o f bronchospasm associated with
bronchial asthma. Because it is a catechol (3,4-dihydroxy-substituted benzene ring), isoproterenol
is subject to rapid metabolism by catachol O-methyl transferase (COMT) and thus, has poor oral
activity. Alteration o f the 3,4-dihydroxy substitution to a 3,5-dihydroxy substitution produces
metaproterenol, a bronchodilator that is not susceptible to COMT, is orally active, and has a
longer duration o f action than isoproterenol. This is an example o f chemical strategy o f managing
drug metabolism.
72. Answer: E. all o f the above
Explanation:
Prodrugs are molecules that are either inactive or very weakly active and require in vivo
biotransformation to produce the physiologically active drug. The advantages that can be gained
form produgs include; increased water solubility, which is useful for the preparation o f
ophthalmic and parenteral preparations. Another advantage is increased lipid solubility, which
leads to increased oral and topical absorption, increased duration o f action, and increased
palatability. Site specificity, which is useful for increasing the concentration of drug at the active
site and for decreasing side effects is also one of the advantages o f prodrugs. Increased shelf life
o f drug products can be obtained by the use o f prodrugs. GI irritation with some drug could also
be decreased by making use of prodrugs o f the drugs.
73.Answer: C. in producing nabumetone, a prodrug with decreased GI irritation than the other
NSAIDs.
Explanation:
Esterification is the common method o f making prodrugs o f various drugs. For example, sodium
succinate esters and sodium phosphate esters have been used to make a number o f water-soluble
steroidal prodrugs. Lipid-soluble esters o f estradiol, such as benzoate, valerate and cypionate, are
used to prolong estrogenic activity. Increased topical absorption of steroids is obtained by
masking hydroxyl groups as esters or acetonides. Unlike other NSAIDs nabumetone does not
have irritant effect on the GI tract because the intestinal mucosa are not exposed to high
concentration o f the active drug during oral administration, plus it is a ketone, not an acid, and
lacks any direct irritant effects.
74.Answer: B. Enalapril is less water soluble than enalaprilat.
Explanation:
Enalaprilat is a potent angiotensin-converting enzyme (ACE) inhibitor that is used for parenteral
administration, but due to its high polarity, it is orally inactive. Its monomethyl ester, enalapril, is
considerably more lipophilic and, thus, provides good oral absorption. This strategy has been
successfully used for a variety o f other compounds, including additional ACE inhibitors, fibric
acid derivatives, ampicillin, and several cephalosporins.
75.
Answer: D. to overcome the bitter taste o f sulfisoxazole
Explanation:
Antibiotics such as sulfisoxazole have a bitter taste and are not suitable for administration to
young children who cannot yet swallow tablets or capsules. Esterification to produce
sulfisoxazole acetyl decreases the water solubility o f the antibiotics and, thus, decreases the
interaction with bitter taste receptors on the tongue. Similar strategies have been used to mask the
bitter taste o f chloramphenicol and other antibiotics.
76. Answer: E. B and C
Explanation:
NSAIDs produce gastric irritation via two mechanisms. A direct irritant effect o f the acidic
molecule and inhibition of gastroprotective prostaglandin production. The prodrugs sulindac and
nabumetone produce less gastric irritation because the gastric and intestinal mucosa are not
exposed to high concentrations o f active drug during oral absorption. Additionally, nabumetone is
a ketone, not an acid, and lacks any direct irritant effects.
77. Answer: C. it is more potent than formaldehyde
Explanation:
Methenamine is the prodrug for the active drug formaldehyde, an effective urinary tract
antiseptic, which due to significant toxicity cannot be given orally. Therefore, methenamine,
which is stable and nontoxic at normal physiological pH but hydrolyzes to form formaldehyde in
the acid urine pH, cannot be more potent than the active drug. It just results in the release o f the
active drug in the desired place. In order to prevent activation before absorption, it should be
given as enteric-coated formulation.
78. Answer: C. cefamandole
Explanation:
Cefamandole is a second generation cephalosporin that is unstable solid dosage forms.
Esterification o f the a-hydroxyl group with formic acid produces cefamandole, a stable prodrug
that is hydrolyzed by plasma esterases to produce the parent antibiotic. Thus, it is developed to
increase stability and shelf life. All the others are developed to deliver the parent drug to its site
o f action and thus, increase site specificity and decrease the adverse effects.
79.Answer: D. diethylstilbeterol diphosphate.
Explanation:
Diethylstilbesterol is a synthetic estrogen that can produce undesirable, feminizing side effects
when used in the treatment o f prostate cancer. These side effects can be avoided by the use o f the
ester prodrug, diethylstibesterol diphosphate. This prodrug is inactive until dephosphorylated by
acid phophatase, an enzyme that is highly active in prostate tumor cells. This allows for a
localized release o f active compound and a decrease in systemic side effects.
80.
Answer: D. it is more stable
Explanation:
Cyclophosphamide is a prodrug that is requires in vivo oxidation, followed by non enzymatic
decomposition, to produce the active phosphoramide mustard. As a result, aqueous solutions o f
cyclophosphamide are much stable than those o f other nitrogen mustards (i.e., mechloethamide).
Mechlorethamide is highly reactive, does not require in vivo activation, and can rapidly
decompose in aqueous environmental before administration.
81 .Answer: D. sometimes they may also be found in the RNA
Explanation:
Genes can be defined as discrete segments o f DNA that are capable o f reproducing during cell
replication and that are responsible for guiding the biosynthesis o f specific proteins and enzymes.
82.Answer: E. all o f the above
Explanation:
Genes encode proteins involved in the absorption, transport, metabolism, and elimination o f drug
molecules. Additionally, they encode proteins that serve as drug receptors. It is obvious then that
a genetic disposition that would result in either an over- or under-expression o f these genes could
significantly alter drug response and toxicity.
83.
Answer: E. all o f the above
Explanation:
Besides the above, genetic predisposition is also a major factor.
84.Answer: E. it studies the genetics ofhum ans.
Explanation:
In its simplistic form, pharmacogenetics can be defined as the use o f genetic information to select
the ‘right drug for the right patient’. This area o f study primary seeks to identify the individual
genetic differences and predisposition that influence drug response and safety.
85.Answer: E. all o f the above
Explanation:
All o f the above mentioned may be caused by genetic variations in the DNA sequence o f certain
population o f individuals.
86.
Answer: D. one base pair change in every 1000 base pairs.
Explanation:
The genetic variation between any two unrelated individuals is approximately one base pair
change in every 1000 base pair. These changes are referred to as single nucleotide polymorphism
(SNPs) and are the most common form o f genetic variation.
87.Answer: C. promoter.
Explanation:
The effects o f SNPs vary based upon the type and location o f the variation. An SNP located
within the coding region o f a gene could produce no discernible effects, negligible effect, or a
significant alteration in effects depending upon how the SNP affected the amino acid sequencing.
An SNP in a splicing control region could result in the formation o f a novel protein that is either
larger or smaller in size than that which is naturally occurring. An SPN in a promoter region
could alter the transcription rate, resulting in either an increase or decrease in the production o f
the target protein. An SNP residing outside o f any o f the above location is genetically silent and
does not produce any observable effects.
88.Answer: C. III.
Explanation:
An SNP located within the coding region o f a gene could produce no discernible effects,
negligible effect, or a significant alteration in effects depending upon how the SNP affected the
amino acid sequencing. An SNP that did not alter the amino acid sequence in a protein would
produce no discernible effects. An SNP that resulted in one amino acid being replaced by a
similar amino acid would have a negligible effect (e.g., changing a portion o f the genetic code
from AUC to GUU would result in isoleucin being replaced by valine, a similar hydrophobic
amino acid). An SNP that resulted in one amino acid being replaced by one with significantly
different chemical properties would cause a significant alteration o f effects. E.g., changing a
portion o f genetic code from GUU to GAU would result in valine being replaced with acidic, and
more hydrophilic, aspartic acid).
Cardiac Arrhythmias
“Success Is a Process for Those with More Heart than Talent”
1. All o f the following are included
under the term cardiac arrhythmias
EXCEPT:
5. Which one o f the following
statements is not true about the impulse
generated by the sinoatrial (SA) node?
A. abnormalities in heart rate
B. conduction disturbances
C. abnormalities in site o f impulse
origin
D. narrowing o f the major epicardial
coronary arteries
E. none o f the above
A. The SA node initiates 60-100
beats/min
B. The impulses generated by the SA
node trigger atrial contraction.
C. The SA node is located in the left
atrium.
D. SA node predominates except when
it is depressed or injured.
E. none o f the above
2. Which o f the following statements
describe the conduction system o f the
heart?
A. The conduction system o f the heart
is comprised o f tissues that are able
only to contract
B. It is comprised o f tissues that can
generate electrical impulses.
C. It is composed o f tissues that can
conduct electrical impulses.
D. B and C
E. none o f the above
3. The two electrical sequences that
cause the heart chambers to fill with
blood and contract are:
A.
B.
C.
D.
E.
impulse generation
impulse transmission
depolarization
A and B
B and C
sinoatrial (SA) node
atrioventricular node
bundle o f His
Purkinje fibers
none o f the above
A. permit completion o f atrial
contraction before ventricular
contraction begins.
B. block the conduction o f the impulse
thus limiting it to the atrial tissues
only.
C. to change the number o f beats per
second set by the sinoatrial node
D. B and C
E. none o f the above
7. Which one o f the following are true
about latent pacemakers?
.
4. Part o f the conduction system o f the
heart that serves as main pace maker o f
the heart is:
A.
B.
C.
D.
E.
6. At the atrioventricular (AV) node
the impulses generated by the Sinoatrial
(SA) node are delayed in order to:
A. They contain AV junction, bundle
o f His, and Purkinje fibers.
B. They contain cells capable o f
generating impulses
C. They have a faster firing rate than
the SA node
D. They are not predominant unless the
SA node is depressed or injured.
E. A ,B and D
8. All o f the following are latent
pacemakers EXCEPT:
A. bundle o f his
B. Purkinje fibers
C. atrioventricular node
D. sinoatrial node
E. all o f the above
9. When the Sinoatrial node (SA) is
depressed or injured, the latent
pacemakers predominate, this is known
as
A.
B.
C.
D.
E.
overdrive suppression
impulse formation
impulse transmission
Underdrive suppression
none o f the above
10. Depolarization and repolarization
result from changes in the electrical
potential across the cell membrane,
caused by the exchange o f which o f the
following?
A.
B.
C.
D.
E.
sodium and potassium
phosphate and bicarbonate
magnesium and phosphorous
iron and barium
none o f the above
13. Potassium ions are pumped out of
the cell as the cell rapidly completes
repolarization and resumes its initial
negativity.
14. Calcium ions enter the cell through
slow channels while potassium ions exit.
As the cell membrane’s electrical
activity temporarily stabilizes, the action
potential reaches a plateau.
15. The cell returns to its resting state
with potassium ions inside the cell and
sodiumand calcium ions outside.
16. A period when a cardiac muscle
cannot respond to any stimulus is:
A.
B.
C.
D.
E.
absolute refractory period
rapid depolarization
slow repolarization
relative refractory period none o f the above
(From Questions 11-15)
Direction: Match the following phases o f
action potential (for a cardiac muscle) with
their description mentioned in questions 11 15
•
A.
B.
C.
D.
E.
Rapid repolarization (phase 0)
Early rapid repolarization (phase 1)
Plateau (phase 2)
Final rapid repolarization (phase 3)
Slow depolarization (phase 4)
11. As fast sodium channels close and
potassium ions leave the cell, the cell
rapidly repolarizes i.e. the cell returns to
resting potential.
12. Takes place as sodium ions enter the
cell through fast channels; the cell
membrane’s electrical charge changes
from negative to positive.
17. Which one o f the following
statements is not true?
A. A cardiac cell’s ability to respond to
stimuli increases as repolarization
continues
B. During the relative refractory
period, which occurs during phase
3, the cell can respond to a strong
stimulus
C. Cells in different cardiac regions
depolarize at various speeds,
depending on whether fast or slow
channels
D. A cardiac cell can not respond to a
stimuli even after it has completely
repolarized
Direction: Match the following patterns in
a normal ECG (Electrocardiograph) for a
cardiac muscle) with their description for
questions from (18-22)
A.
B.
C.
D.
E.
The
The
The
The
The
P wave
PR interval
QRS complex
ST segment
T wave
18. The wave that shows phase 3 o f the
action potential-ventricular
repolarization
C. the cardiac muscle ventricular cells
become pace makers
D. B and C
25. All o f the following may precipitate
cardiac arrhythmias EXCEPT:
A. heart disease such as infection,
valvular heart diseases, ischemic
heart disease
B. myocardial infarction
C. decreased sympathetic tone
D. hyperkalemia
E. hypokalemia
19. The wave that reflects ventricular
depolarization is
20. The segment that represents phase
o f 2 o f the action potential-the absolute
refractory period
21. The wave that represents the spread
o f the impulse from the atria through the
purkinje fibers
22. The wave that reflects atrial
depolarization
23. Arrhythmias are generally classified
by:
A. the type o f action potential
generated
B. severity
C. origin
D. none
24. Supraventricular arrhythmias stem
from:
A. enhanced automaticity o f the SA
node or another pace maker region
B. an ectopic (abnormal) pacemaker
triggers a ventricular contraction
before the SA node fires
26. Abnormal impulse formation,
abnormal impulse conduction, or a
combination of both may give rise to
arrhythmias. Abnormal impulse
formation may result from:
A.
B.
C.
D.
E.
depressed automaticity
increased automaticity
depolarization and triggered activity
B and C
all o f the above
27. Which one o f the following occurs
in tachycardia (increased heart beat)?
A.
B.
C.
D.
E.
depressed automaticity
depolarization and triggered activity
A and B
increased automaticity
none o f the above
28. One cause o f abnormal impulse
conduction (in cardiac arrhythmias) is
reentry. Which o f the following
statements are true about reentry?
A. It occurs when an impulse is
rerouted through certain regions in
which it has already traveled.
B. The rerouted impulse depolarizes
the same tissue more than once,
producing an additional impulse.
C. It occurs when an impulse does not
reach a cardiac tissue and the tissue
generates an impulse by itself.
D. A and B
E. All o f the above
29. The conditions, which must exist for
reentry to occur are;
A. slow conduction area for
depolarization to occur
B. markedly shortened refractoriness
C. unidirectional conduction
D. all o f the above
E. None o f the above
30. Reentry may occur in all o f the
following EXCEPT:
A.
B.
C.
D.
sinoatrial node (SA)
atrioventricular node (AV)
in all cardiac muscle cells
accessories pathways o f the
conducting system located in the
atria and ventricles.
E. None o f the above
31. One sign of cardiac arrhythmias is
anxiety and confusion. This occurs due
to
E. Syncope
33. A patient with cardiac arrhythmia
had serum calcium level of4.00m Eq/L;
which o f the following changes are most
likely to be present in the ECG o f the
patient as compared to a normal ECG?
A.
B.
C.
D.
E.
prolonged QT intervals
flattened T waves
inverted T waves
all o f the above
E. none o f the above
34. The treatment objectives for cardiac
arrthymias include which o f the
following?
A. terminate or suppress the arrhythmia
if it causes hemodynamic
compromise or disturbing
symptoms.
B. maintain adequate cardiac output
and tissue perfusion
C. correct or maintain fluid balance
D. A, B and C
E. increase heart beat above 100 beats
per second regardless o f the type o f
arrthymias
35. Which o f the following are Class 1A
antiarrythmic drugs EXCEPT:
A. reduced brain perfusion
B. the effect o f the electrical impulses
generated in the heart on brain cells.
C. the overall response o f the body to
the cardiac arrhythmias
D. B and C
E. All o f the above
A.
B.
C.
D.
E.
32. All o f the following are signs and
symptoms that typically accompany
arrhythmias EXCEPT:
36. Proacinamide is used more
frequently than Quinidine in the
treatment o f arrhythmia because:
A.
B.
C.
D.
A. Procainamide can be administered
intravenously
Chest pain
Skin pallor or cyanosis
Palpitations
Increased urinary output
Quinidine
Procainamide
Disopyramide
All o f the above
none o f the above
B. Procainamide can be administered
in sustained-release oral
preparations
C. Procainamide can be useful in the
treatment o f more than one type of
arrhythmia as compared to
Quinidine.
D. B and C
E. none o f the above
B.
C.
D.
E.
37. Which o f the following
antiarrythmic drugs result in strong
depression o f conduction?
A.
B.
C.
D.
E.
A.
B.
C.
D.
E.
Flecainide
Mexiletine
Moricizine
Both A and C
Both B and C
38. An anti-epileptic drug commonly
used in the treatment o f digitalisinduced ventricular and supraventicular
arrhythmias is:
A.
B.
C.
D.
E.
Phenobarbitone
Phenytoin
Carbamazepine
Valproic acid
none o f the above
39. A drug closely related to lidocaine,
most commonly used in the treatment of
patients in whom a Class 1 agent has
failed is
A.
B.
C.
D.
E.
Tocainide
Phenytoin
Mexiletine
Quinidine
none o f the above
40. An antiarrythmic agent which has
the properties o f all three class I
antiarrythmic drugs is:
A. Flecainide
Propafenone
Moricizine
Phenytoin
None o f the above
41. A class IC drug reserved for patients
with refractory life-threatening
ventricular arrhythmias who do not have
coronary artery disease is:
Propafenone
Moricizine
Flecainide
Quinidine
None o f the above
42. The mechanism o f action o f Class I
antiarrhythmic agents is:
A. They block the rapid inward sodium
current and thereby slow down the
rate o f the rise o f the cardiac tissue’s
action potential
B. They enhance the entrance of
sodium to its channels.
C. -They block the inward flow o f
calcium
D. They enhance the inward flow o f
calcium
E. none o f the above
43. Which o f the following statements
is not true about Class I antiarrhythmic
agents?
A. Class IA drugs moderately reduce
the depolarization rate and prolong
repolarization (refractory period)
B. Class IB drugs shorten
repolarization (refractory period);
they also weakly affect the
repolarization rate.
C. Class I agents are sub classified
based on their structural similarity
D. Class 1 C drugs depresses
depolarization but have a negligible
effect on the duration o f
repolarization or refractoriness.
E. None o f the above
44. Which o f the following statements
is not true about the dosage and
administration o f procainamide?
A. The usual effective dose is 500­
1000 mg
B. In rapid Intravenous administration
1-1.5 g is given at a rate o f 20-50
mg/min.
C. For acute therapy, intramuscular
therapy is preferred.
D. Procainamide is available for oral,
intravenous, or intramuscular use.
E. None o f the above
45. Which one o f the following Class
1A drugs is given only orally?
A.
B.
C.
D.
E.
Procainamide
Quinidine
Disopyramide
Lidocaine
All o f the above
46. The most important risk associated
with the use o f antiarrhythmic drug
therapy is Proarrythmia. Proarrythmia
is:
A. the ability to cause arrhythmia
B. inability to correct the arrhythmia
for which they are given
C. an increased incidence of
cardiovascular adverse effects.
D. decreasing the heartbeat more than
normal.
E. None o f the above
47. The therapeutic range for serum
levels o f quinidine is:
A. 2-6 jig/mL
B. 1-5 pg/mL
C. 6-lO^ig/mL
D. 20-25 pg/mL
E. None o f the above
48. Which o f the following drugs can be
used in the management o f quinidine
induced ventricular tachyarrhythmias:
A.
B.
C.
D.
E.
catecholamines
glucagon
sodium lactate
lidocaine
A, B and C
49. A patient suffering from atrial
tachyarrhytmias was taking quinidine.
The physician in charge observed the
increased ventricular response and the
increased AV node conduction. To
counteract the response he ordered
administration of a drug that slows AV
conduction .Unfortunately the nurse
gave the patient an overdose o f the drug
and there were signs o f ventricular and
supraventricular arrhythmias. The
physician started intravenous
administration o f phenytoin and the
ventricular and supraventricular
arrhythmias subsided. The drug, which
was given to counteract the increased
ventricular response and the increased
AV node conduction induced by
quinidine, is:
A.
B.
C.
D.
E.
Mexiletine
Propafenone
Moricizine
Digoxin
none o f the above
50. Anticoagulants may be administered
before quinidine therapy begins, because
They enhance the therapeutic effects
o f quinidine
B. They reduce the elimination of
quinidine
C. They prevent or minimize the
embolism that may occur
D. They enhance the gastrointestinal
absorption o f quinidine.
E. none o f the above
B.
C.
D.
E.
diarrhea
urinary retention
A and C
All o f the above
51. Cinchonism due to high serum
concentration o f quinidine is manifested
by
55. A class IB anti-arrhythmic drug
with few untoward cardiovascular
effects, known for its central nervous
system reactions is:
A.
B.
C.
D.
E.
A.
B.
C.
D.
E.
tinnitus
hearing loss
blurred vision
gastrointestinal (GI) disturbances
All o f the above
52. Which o f the following statements
are true about procainamide?
A. Procainamide may cause systemic
lupus erythematosus
B. Procainamide is contraindicated in
patients with hypersensitivity to
procaine and related drugs.
C. Hypotension may occur with rapid
intravenous administration.
D. GI adverse effects are less common
than quinidine therapy.
E. allof the above
53. Procainamide toxicity may cause all
o f the following EXCEPT:
A. SA node block
B. ventricular tachycardia
C. enhanced conduction in all regions
o f heart
D. asystole
E. all o f the above
54. A patient with ventricular
arrhythmia was taking disopyramide.
Which o f the following effects are likely
to be seen in the patient taking
disopyramide?
A. dry mouth
Mexiletine
Phenytoin
Lidocaine
Tocainide
None o f the above
56. A class IB antiarrhythmic drug
contraindicated in patients with
hypersensitivity to lidocaine and related
drugs is:
A.
B.
C.
D.
E.
Phenytoin
Mexiletine
Tocainide
Flecainide
none o f the above
57. An antiarrhythmic drug
contraindicated in patients with sinus
bradycardia or heart block and its
chronic use may lead to vestibular and a
cerebellar effect is:
A.
B.
C.
D.
E.
Phenytoin
Mexiletine
Tocainide
Flecainide
none o f the above
58. The hematological effects o f
phenytoin include which o f the
following?
A.
B.
C.
D.
agranulocystosis
megaloblastic anemia
leukopenia
thrombocytopenia
E. all of the above
59. Treatment o f arrythmia with which
o f the following drugs requires prior
anticoagulant therapy?
A.
B.
C.
D.
E.
Disopyramide and Mexiletine
Flecainide and tocainide
Propafenone and Moricizine
Procainamide and quinidine
none of the above
60. All o f the following drugs
antagonize the activity o f quinidine
EXCEPT:
A.
B.
C.
D.
E.
Phenytoin
Rifamipicin
Barbiturates
Nitroglycerin
none o f the above
61. All o f the following drugs increase
the plasma concentration o f quinidine
EXCEPT: A.
B.
C.
D.
E.
Nifedipine
Antacids
Sodium bicarbonate
Sodium acetazolamide
one o f the above
62. The effect o f cimetidine and
amiodarone on plasma level o f
procainamide is:
A. They increase the plasma
concentration o f procainamide.
B. They decrease the plasma
concentration o f procainamide.
C. They do not have any effect on the
plasma concentration of
procainamide.
D. B and C
E. none o f the above
63. Phenytoin decreases the therapeutic
efficacy o f disopyramide. The possible
mechanism is:
A. Phenytoin decreases the absorption
o f disopyramide
B. Phenytoin inhibits the metabolism
o f disopyramide
C. Phenytoin enhances the metabolism
o f disopyramide
D. Phenytoin decreases the metabolism
o f disopyramide
E. none o f the above
64. Which one o f the following is not
true about the drug interactions o f
phenytoin?
A. Phenytoin may increase the
cardiodeppressant effects o f
lidocaine.
B. Phenytoin accelerates disopyramide
metabolism.
C. Carbamazepine may enhance
phenytoin metabolism and thus
reduce plasma phenytoin levels and
therapeutic efficacy
D. Phenytoin deceases the metabolism
o f carbamazepine
E. Phenytoin may reduce plasma
Mexiletine levels and may decrease
therapeutic efficacy.
65. All o f the following are class II *
antiarrhythmic drugs EXCEPT:
A.
B.
C.
D.
E.
Esmolol
Propranolol
Acebutolol
Amiodarone
none o f the above
66. Which o f the following is not the
action o f class II antiarrhythmic drugs?
A. They reduce sympathetic
stimulation o f the heart
B. They decrease the conduction o f
impulse through the AV node
C. They increase the sinus rhythm
D. They lengthen the refractory period
E. none o f the above
67. The blocking effects o f propranolol
may lead to all o f the following
EXCEPT:
A.
B.
C.
D.
E.
hypotension
hypertension
left ventricular failure
cardiac arrest
none o f the above
68. Which o f the following statements
are not true about propranolol?
j
A. It is contraindicated in patientsjwith
sinus bradycardia, severe CHF|
(congestive heart failure) or asthma
B. It may depress AV node conduction
and ventricular pacemaker activity,
resulting in AV block or asyst6le
C. Sudden withdrawal o f propranolol
may lead to acute MI, arrhythmias,
or angina in cardiac patients i
D. The dose is normally lOOOmgiday
E. none o f the above
69. A class II antiarrhythmic drug), with
a short half life that has been used!in the
treatment o f supraventricular
tachycardia and to control ventricular
response to atrial fibrillation or flitter
during or after surgery is:
A.
B.
C.
D.
E.
Esmolol
Propranolol
Metaprolol
Acebutolol
none o f the above
70. A patient with supraventricular
tachycardia was taking esmolol. After
his heart stabilized the physician in
charge ordered propranolol for the
patient. The possible reason for the
continuation o f the antiarrhythmic
therapy with propranolol is:
A. Esmolol was not effective in
controlling the supraventricular
tachycardia.
B. The adverse effects o f esmolol
could have been troublesome.
C. Esmolol is for short-term use only
and should be replaced by a longacting antiarrhythmic drug once the
patient’s heart stabilizes.
D. A and B
E. none o f the above
71. Which o f the following adverse
effects are common to esmolol and
propranolol?
A.
B.
C.
D.
E.
hypotension
dizziness
headache
vomiting
all of the above
72. Severe vasoconstriction can occur if
propranolol is given concomitantly with:
A.
B.
C.
D.
E.
Epinephrine
Digitalis
Dilitazem
Quinidine
None o f the above
73. Which o f the following statements
best describes the interaction o f esmolol
with morphine?
A. Morphine decreases the plasma
levels o f esmolol
B. Morphine does not have any effect
on the plasma levels o f esmolol
C. Morphine raises the plasma level of
esmolol.
D. Morphine decreases the plasma
~ levels o f esmolol if given by the oral
route, and vice versa if given by the
intravenous route.
E. None of the above
74. The property o f satolol that
distinguishes it from other adrenergic
blockers and classified as a type III
antiarrhythmic drug rather than a type II
agent is that:
A. It antagonizes both (31 and
(3 2 adrenergic receptors
B. It prolongs the phase 3 o f action
potential (in cardiac muscles)
C. It has different therapeutic effects
D. It has different clinical and safety
profile
E. none o f the above
75. Which o f the following statements
is not true about amiodarone?
A. It is given to control malignant
ventricular arrhythmias
B. It is recommended in the treatment
o f ventricular fibrillation and pulse
less ventricular tachycardia.
C. It is used prophylactically against
both atrial and ventricular
tachycardia and fibrillation.
D. It is associated with more
arrhythmic deaths in patients after
an MI (myocardial infarction)
E. none o f the above
76. All of the following are class III
antiarrhythmic agents EXCEPT:
A.
B.
C.
D.
E.
Amiodarone
Bretylium
Ibutilide
Adenosine
Dofetilide
77. A class 111 antiarrhythmic drug used
in the treatment o f life-threatening
ventricular arrhythmias, including
ventricular tachycardia and ventricular
fibrillation, that have not responded to
other agents is:
A.
B.
C.
D.
E.
Satolol
Ibutilide
Dofetilide
Bretylium
none o f the above
78. Which o f the following statements
are true about the mechanism o f action
o f class III antiarrhythmic drugs?
A. they prolong the refractory period
B. they prolong the action potential
C. they increase the force of
myocardial contractility
D. they increase the conduction time
E. A and B
19. Which one of the following class III
antiarrhythmic drugs is not available for
oral administration?
A.
B.
C.
D.
E.
Ibutilide
Dofetilide Satolol
Amiodarone
none o f the above
80. Which o f the following statements
are NOT true about dofetilide?
A. It is only available for oral
administration.
B. Dofetilide should not be given to
those patients with creatinine
clearance values less than 20
mL/min
C. Dofetilide can be given to
outpatients
D. All o f the above
E. None o f the above
81. A nurse wanted to give Dofetilide
tablets to a patient who had atrial
fibrillation. The creatinine clearance o f
88. The main mechanism o f class IV
antiarrhythmics is:
A. They inhibit action potential
generation in all cardiac muscle
cells.
B. They inhibit AV node conduction
by depressing the SA and AV nodes
C. They inhibit cardiac muscle cell
contractility.
D. They selectively inhibit the sodium
channels.
E. none o f the above
89. The most commonly used class IV
antiarrhythmic drugs are:
A.
B.
C.
D.
E.
Verapamil and Diltiazem
Nifedipine and nicardipine
Amlodipine and felodipine
Bepridil and felodipine
none o f the above
90. Which o f the following statements
are WRONG about verapamil and
Diltiazem?
A. They are contraindicated in patients
with AV block; left ventricular
dysfunction, concomitant
intravenous U-blockers; and atrial
fibrillation.
B. They have positive chronotropic
effect
C. They should be used cautiously in
patients with CHF, MI and hepatic
or renal impairment
D. Constipation and nausea have been
reported with verapamil
E. none o f the above
91. Diltiazem may inhibit the
metabolism of:
A. Theophyline
B. Cyclosporine
C. Verapamil
D. Felodipine
E. A and B
92. The mechanism o f action o f
atropine, which enables it to be used as
an antiarrhythmic in the treatment o f
sinus bradycardia is:
A. It blocks vagal effects on the SA
node, thus blocking conduction of
through the AV node and increasing
the heart rate
B. It enhances effects o f the vagus
nerve on the heart
C. It increases the pace maker rhythm
D. It blocks the vagal effects on the SA
node, thus promoting conduction
through the AV node and increasing
the heart rate
E. none o f the above
93. Artopine belongs to which class o f
antiarrhymics?
A.
B.
C.
D.
E.
Class IA
Class HI
Class IB
Class 11
It is unclassified
94. A patient with a problem o f sinus
bradycardia was admitted to an intensive
care unit o f a hospital. The physician in
charge ordered administration of
atropine by intravenous push. When the
first dose o f 0.4 mg was given, the
bradycardia worsened but the symptom
subsided with subsequent doses o f the
drug. What could be the possible reason
for bradycardia, which occurred at the
beginning o f the antiarrhythmic
therapy?
A. The metabolite o f atropine has the
reverse pharmacological activity
and this phenomenon is result o f
that.
B. It is a reflex bradycardia, which
resulted from incomplete
suppression o f vagal impulses.
C. The patient’s heart responded the
opposite way
D. A and C
E. none o f the above
95. Which o f the following statements
is not true about adenosine?
A. It is indicated for the conversion o f
acute supraventricular tachycardia
to normal sinus rhythm.
B. It is a naturally occurring
nucleoside, which is normally
present in all cells o f the body
C. It enhances conduction through the
AV node
D. It restores normal sinus rhythm in
patients with PSVTs
E. none o f the above
Cardiac Arrhythmias
Explanation:
.
The atrioventricular (AV) node, situated in the lower interatrial septum, the impulses are
delayed briefly to permit completion of atrial contraction before ventricular contraction
begins.
Answers
Cardiac Arrhythmias
1. Answer: D. Narrowing o f the major epicardial coronary arteries
Explanation:
Cardiac arrhythmias are deviations from the normal heart rate baet pattern. They include
abnormalities o f impulse formation, such as heart rate, rhythm, or site o f impulse origin,
which disrupt the normal sequence o f atrial and ventricular activation. Narrowing o f the
major epicardial coronary arteries is known as coronary artery disease.
2. Answer: D. B and C
Explanation:
Conduction system o f the heart comprises tissues that can generate and transmit electrical
impulses signaling the heart to contract.
3. Answer: D. A and B
Explanation:
Impulse generation, the first sequence, takes place when an electrical impulse is
generated automatically. Impulse transmission, the second sequence, occurs once the
impulse has been generated, signaling the heart to contract.
4. Answer: A. Sinoatrial (SA) node
Explanation:
The Sinoatrial (SA) node, in the wall o f the right atrium, contains cells that spontaneously
initiate an action potential.
5. Answer: C. The SA node is located in the left atrium
Explanation:
The sinoatrial node is located in the right atrium. The impulses generated by the SA node
trigger atrial contraction. SA node predominates except when it is depressed or injured. In
case o f injuries or when the SA node is not properly working other parts o f the
conducting system take charge.
6. Answer:A. Permit completion of atrial contraction before ventricular contraction begins.
17. Answer: D. A cardiac cell can not respond to a stimuli even after it has completely
repolarized
Explanation:
A cardiac cell’s ability to respond to stimuli increases as repolarization continues. During
the relative refractory period, which occurs during phase 3, the cell can respond to a
strong stimulus. Cells in different cardiac regions depolarize at various speeds, depending
on whether fast or slow channels (i.e when fast channels predominate depolarization
occurs quickly and when Slow channels predominate and depolarization occurs slowly)
When a cardiac cell has been completely repolarized, it can again respond fully to
stimuli.
18.Answer- [E]
19.Answer-[C]
20.Answer-[D]
21.Answer-[B]
22.Answer-[A]
23.Answer:
C. Origin
Explanation:
Arrhythmias are generally classified by origin (i.e., supraventricular or ventricular).
24.Answer: A. Enhanced automaticity o f the SA node or another pace maker region
Explanation:
Supraventricular arrhythmias stem from enhanced automaticity o f the SA node (or
another pace maker region).An ectopic (abnormal) pacemaker triggers a ventricular
contraction before the SA node fires in ventricular arrhythmias.Cardiac muscle cells do
not have the capacity to generate pace maker beats.
25.Answer: C. Decreased sympathetic tone
Explanation:
Arrhythmias may result from various conditions, including:
- An infarction may cause death o f pacemaker cells or conducting tissue
-Heart disease such as infection, valvular heart diseases, ischemic heart disease may
disrupt the conduction network
- Increased sympathetic tone (e.g due to stress, anxiety or smoking)
- Decreased parasympathetic tone
A. Hypothyroidism, hyperthyroidism, hyperkalemia and hypokalemia or other
electrolyte disturbance.
26. Answer: E. All o f the above
Explanation:
All o f the above may result in abnormal impulse formation.
27.Answer: D. Increased automaticity
Explanation:
Increased automaticity causes tachycardia.
28.Answer: D. A and B
Explanation:
Reentry occurs when an impulse is rercjuted through certain regions in which it has already
traveled. Thus, the rerouted impulse depolarizes the same tissue more than once, producing an
additional impulse.
29. Answer: D. All o f the above.
Explanation:
For reentry to occur, the following con ditions must exist:
1. Markedly shortened refractoriness or slow conduction area that allows an adequate delay so
that depolarization occurs. (If the refra tory period is short, the probability of a cardiac cell to
respond to the stimuli again increases)
2. Unidirectional conduction (if the im pulse is conducted in one direction the probability that
one cardiac cell is stimulated repeated y increases).
30. Answer: C. In all cardiac muscle cells
Explanation:
Reentry sites include the sinoatrial nod e (SA), the Atrioventricular node (AV) as well as various
accessory pathways in the atria and v<elntricles. Cardiac muscle is not involved in impulse
conduction, therefore, reentry cannot occur in the cardiac muscle cells.
31 .Answer: A. Reduced brain perfusion
Explanation:
Arrthymias may decrease cardiac output, reduce blood pressure, and disrupt perfusion o f vital
organs. Anxiety and confusion may result from decreased brain perfusion.
32. Answer: D. Increased urinary output
Explanation:
Arrthymias may decrease cardiac output, reduce blood pressure, and disrupt perfusion o f vital
organs. Kidney is one o f the vital organs and decreased perfusion o f vital organs results in
decreased urinary output (urinary output is a directly related to kidney perfusion).
33. Answer: D. All o f the above
Explanation:
A serum calcium level below 4.5 mEq/L signifies hypocalcaemia.
Prolonged QT intervals, Flattened T waves or inverted T waves signal hypocalcaemia.
34.Answer: D. A, B and C
Explanation:
Increasing the heart rate above the maximum does not have any use in the management o f
cardiac arrthymias (the normal heart beat is 60-100 beats per second).
35.Answer: D. all o f the above
Explanation:
Quinidine, Procainamide and disopyramide are Class IA antiarrythmic drugs.
36.Answer: D. B and C
Explanation:
Procainamide is used for the same arrhythmias for which Quinidine is given. It is used more
frequently than Quinidine because it can be administered intravenously and in sustained-release
oral preparations. Quinidine poses added concern when used intravenously because o f increased
cardiovascular effects (i.e. hypotension, syncope, myocardial depression).
37.Answer:
D. Both A and C
Explanation:
Flecainide, Moricizine and propafenone are Class I C drugs. Use o f all Class IC drugs result in
strong depression o f conduction in the cardiac tissues. Mexiletine is a class I B drug and the drugs
in this class result in moderate depression o f conduction.
38.Answer: B. Phenytoin
Explanation:
Phenytoin is anti-epileptic drug commonly used in the treatment o f digitalis-induced ventricular
and supraventicular arrhythmias.
39.Answer:
C. Mexiletine
Explanation:
Mexiletine is closely related to lidocaine, structurally with modifications. It is commonly used to
treat patients in whom a Class I agent has failed and it is moderately effective in suppressing
ventricular ectopy.
40.Answer:
C. Moricizine
Explanation:
Moricizine is a difficult antiarrhythmic agent to classify because it has properties o f all three
class I antiarrhythmic groups. Because it prolongs the QRS interval like other Class IC agents, it
is classified as a class IC agent.
41.Answer: C. Flecainide
Explanation:
Flecainide suppresses premature ventricular arrhythmias and ventricular tachycardia; it may be
used to treat some arrhythmias that are refractory to other agents. Flecainide is reserved for
patients with refractory life-threatening ventricular arrhythmias who do not have coronary artery
disease.
42.Answer: A. They block the rapid inward sodium current and thereby slow down the rate of
the rise o f the cardiac tissue’s action potential
Explanation:
All class I agents work by blocking the rapid inward sodium current and thereby slow down the
rate o f rise o f the cardiac tissue’s action potential.
43.Answer:
C. Class I agents are sub classified based on their structural similarity
Explanation:
Class I agents are not classified based on their structural similarity. They are classified based up
on the differences in EP (electrophysiological) effects.
44.Answer: C. For acute therapy, intramuscular therapy is preferred
Explanation:
For acute therapy, intravenous route is preferred.
45.Answer: C. Disopyramide
Explanation:
Disopyramide is available in oral form. Usually, 300-400mg is given as a loading dose to attain
an effective plasma level rapidly. For maintenance therapy, doses o f 400-800mg/day are given in
four doses every 6 hours (non-sustained capsule) or in two doses every 12 hours (sustained
release capsule)
46. Answer: A. The ability to cause arrhythmia
Explanation:
Proarrythmia is the ability to cause arrhythmia (e.g. Brady arrhythmias and ventricular
tachyarrhythmias)
47. Answer: A. 2-6 |j.g/mL
Explanation:
Serum levels above the maximum result in symptoms of acute toxicity. Toxicity may cause acute
cardiac effects, such as pronounced slowing o f conduction in all heart regions; this in turn, may
lead to SA block or arrest, ventricular tachycardia, or asystole.
48.Answer: A, B and C
Explanation:
Lidocaine is not used in the management o f quinidine induced tachyarrhytmias.
49.Answer: D. Digoxin
Explanation:
In Patients receiving quinidine for atrial tachyarrhytmias, vagolytic effects may increase impulse
conduction at the AV node, resulting in an accelerated ventricular response. To prevent this,
agents that slow AV nodal conduction (e.g. verapamil, Digoxin) may be administered.
Over dose o f Digoxin results in ventricular and supraventricular arrhythmias and phenytoin is the
drug o f choice in digitalis-induced arrhythmias.
50.
Answer: C. They prevent or minimize the embolism that may occur
Explanation:
Embolism (formation o f blood clots within the coronary arteries) may occur upon restoration of
normal sinus rhythm after prolonged atrial fibrillation. To prevent or minimize this complication,
anticoagulants may be administered before quinidine therapy begins.
51 .Answer: E. all o f the above
Explanation:
Quinidine may cause cinchonism at high serum concentrations, manifested by tinnitus, hearing
loss, blurred vision, and gastrointestinal (GI) disturbances. In severe cases, nausea, vomiting,
diarrhea, headache, confusion, delirium, photophobia and psychosis occur.
52. Answer: E. All o f the above
Explanation: All the given choices are true about the drug procainamide.
53.Answer: C. Enhanced conduction in all regions o f heart
Explanation:
Procainamide toxicity may cause acute cardiac effects (e.g Pronounced slowing of conduction in
all regions o f heart), which, in turn, may lead to SA node block or arrest, ventricular tachycardia,
or asystole.
54.Answer: D. A and C
Explanation:
Anticholinergic effects o f dysopyramide include dry mouth, constipation, urinary retention, and
blurred vision.
55.Answer: C. Lidocaine
Explanation:
Generally Lidocaine has few cardiovascular adverse effects. Central nervous system (CNS)
reactions are the most pronounced adverse effects o f lidocaine. These reactions may range from
light-headedness and restlessness to confusion, tremor, stupor, and convulsions.
56.Answer: C. Tocainide
Explanation:
Tocainide is contraindicated in patients with hypersensitivity to lidocaine and relate drugs.
57.
Answer: A. Phenytoin
Explanation:
Phenytoin is contraindicated in patients with bradycardia or heart block. Chronic use may lead to
vestibular and cerebellar effects, behavioral changes, GI distress, gingival hyperplasia,
megablastic anemia, and osteomalalcia.
58.Answer: E. all the above
Explanation:
Hematological reactions include Agranulocystosis, Megaloblastic anemia, Leukopenia,
Thrombocytopenia, and pancytopenia.
59.Answer: D. Procainamide and Quinidine
Explanation:
In antiarrhythmic therapy with procainamide and quinidine, embolism may occur upon
restoration o f normal sinus rhythm after prolonged atrial fibrillation. An anticoagulant is
frequently administered before procainamide or quinidine therapy begins to prevent this
complication.
60.Answer: D. Nitroglycerin
Explanation:
Phenytoin, Rifamipicin and barbiturates may antagonize the activity o f quinidine. Nitroglycerin
does not antagonize the activity o f quinidine but it worsens the orthostatic hypertension if given
concomitantly with quinidine.
61.Answer: A. Nifedipine
Explanation:
Antacids, sodium bicarbonate and sodium acetazolamide may increase quinidine levels possibly
resulting in toxicity. Nifedipine may reduce plasma quinidine levels.
62.
Answer: A. they increase the plasma concentration o f procainamide
Explanation:
Cimetidine and amiodarone may increase plasma procainamide levels, possibly leading to drug
toxicity.
63. Answer: C. Phenytoin enchances the metabolism o f disopyramide.
Explanation:
Phenytoin accelerates the metabolism o f disopyramide, possibly reducing the therapeutic
efficacy.
64. Answer: D. Phenytoin decreases the metabolism o f Carbamazepine.
Explanation:
Carbamazepine may enhance phenytoin metabolism and thus reduce plasma phenytoin levels and
therapeutic efficacy. Phenytoin has the same effect on carbamazepine.
65.Answer: D. Amiodarone
Explanation:
Class II antiarrhythmic drugs are the p-blockers Esmolol, Propranolol, and Acebutolol (EEsmolol, P- Propranolol, A- Acebutolol which can be abbreviated as EPA).Amiodarone is a
class-III antiarrhythmic drug.
66 .Answer: C. They increase the sinus rhythm
Explanation:
Class II antiarrhythmics reduce sympathetic stimulation o f the heart, decreasing impulse
conduction through the AV node and lengthening the refractory period. Additionally, this class o f
antiarrhythmics slow the sinus rhythm without significantly changing the QT or QRS intervals,
resulting in a reduced heart rate and a decrease in myocardial oxygen demand.
67. Answer: B. Hypertension
Explanation:
The (3-blocking effects o f propranolol may lead to marked Hypotension, exacerbation o f CHF
(congestive heart failure) and left ventricular failure, or cardiac arrest.
68.Answer: D. The dose is normally lOOOmg/day
Explanation:
For oral therapy, 10-80mg/day is given in three or four doses.
69.Answer: A. Esmolol
Explanation:
Esmolol is used to treat supraventricular tachycardia: it possesses a very short ( 9 minutes ) half­
life and has been used to control the ventricular response to atrial fibrillation or flutter during or
after surgery.
70.
Answer:. C. Esmolol is for short-term use only and should be replaced by a long-acting
antiarrhythmic drug once the patient’s heart stabilizes.
Explanation:
Esmolol is for short-term use only and should be replaced by a long-acting antiarrhythmic drug
once the patient’s heart stabilizes.
71 .Answer: E. all o f the above
Explanation:
Hypotension, Dizziness, Headache, nausea, vomiting are common to both esmolol and
propranolol.
72.Answer: A. Epinephrine
Explanation:
Severe vasoconstriction may occur with concomitant epinephrine administration.
73.
Answer: C. Morphine raises the plasma level o f esmolol
Explanation:
Morphine raises the plasma level o f esmolol.
74. Answer: B. It prolongs the phase 3 o f action potential(in cardiac muscles).
Explanation:
Satolol is a P-adrenergic blocker.lt prolongs the phase 3 o f action potential in cardiac muscles.
This property distinguishes it from other p-adrenergic blockers and it is the reason why it is
classified as a type III antiarrhythmic drug rather than a type II agent.
75.Answer:
infarction).
D. It is associated with more arrhythmic deaths in patients after an Ml (myocardial
Explanation:
Unlike other agents with the exception o f the p-adrenergic blockers, amiodarone has been shown
to reduce arrhythmic deaths in patients after an M I .
76.Answer: D. Adenosine
Explanation:
Adenosine is not a class III antiarrhythmic drug. It is categorized as unclassified antiarrhythmic
drug. The class III antiarrhythmic agents can be abbreviated as ABIDS ( A-Amiodarone, BBretylium, 1- Ibutilide, D- Dofetilide , S-sotalol).
77.Answer: D. Bretylium
Explanation:
Bretylium is used in the treatment o f life-threatening ventricular arrhythmias, including
ventricular tachycardia and ventricular, that has not responded to other agents.
78.Answer: E. A and B
Explanation:
Class III antiarrhythmic drugs prolong the refractory period and action potential; they have no
effect on myocardial contractility or conduction time.
79.Answer: A. Ibutilide
Explanation:
Ibutilide and bretylium are used for parenteral therapy only.
80.Answer: C. Dofetilide can be given to outpatients
Explanation:
Dofetilide is only available for oral administration and it should be initiated only in a hospital
setting with trained personnel and equipment necessary to provide continuous cardiac monitoring
during initiation o f therapy. It should not be given to those patients with creatinine clearance
values less than 20 mL/min.
81 .Answer: B. 0.25 mg twice daily
Explanation:
A normal dose o f dofetilide for the conversion o f recent onset atrial fibrillation to normal sinus
rhythm is 0.5mg twice daily for patients with creatinine clearance values greater than 60 mL/min.
0.25 mg for those with creatinine values o f 40-60 mL/min, 0.125mg for those with creatinine
clearance values o f 20-40mL/min.
82.Answer: D. 400 mg/day
Explanation: Life threatening pulmonary toxicity may occur during amiodarone therapy,
especially in patients receiving more than 400 mg/day. Baseline as well as routine pulmonary
function tests reveal relevant pulmonary changes.
83.Answer: D. Hypotension and Brady arrhythmias
Explanation:
In amiodarone therapy, blood pressure and heart rhythm must be monitored for Hypotension and
Brady arrhythmias .
84.Answer: C. Amiodarone has a half-life o f up to 60 hours
Explanation:
Amiodarone has an extremely long half-life (up to 60 hours). Therapeutic response may be
delayed for weeks after oral therapy begins; adverse reactions may persist up to 4 months after
therapy ends.
85.Answer:C. sotalol
Explanation:
The side effects described above are directly related to p -blockade and prolongation o f
repolarization and the drug is sotalol.
86.Answer:
C. Ibutilide
F Y n lan atin rv
Cardiac Arrhythmias
93.Answer: E. It is u n classified
Explanation:
Atropine does not belong to any o f the existing classes o f antiarrhymics (i.e. it is unclassified)
87.Answer: D . A m iod aron e has been reported to h ave num erous drug-drug interactions
am ong all ca tegories o f drugs
Explanation:
Amiodarone has been reported to have numerous drug-drug interactions among all categories o f
drugs. To avoid the development of a significant drug-drug interaction a thorough patient
medication profile should be carried out for each patient having amiodarone therapy initiated, as
well as each time a patient currently receiving amiodarone is given an additional drug.
88.Answer: B . T hey inhibit A V n od e conduction b y depressing th e SA and A V n o d es
Explanation:
Class IV antiarrhythmics are calcium channel blockers. They inhibit AV node conduction by
depressing the SA and AV nodes, where calcium channels predominate.
89.Answer: A . Verapam il and D iltiazem
Explanation:
V erapam il and D ilita zem are the calciu m channel block ers m ost com m o n ly used as
antiarrhythm ics. O ther calcium channel blockers include nicardipine, N ifed ip in e,
bepridil, am lodip in e, and felod ip in e, but th ese agents have prim arily been used in the
treatm ent o f angina and hypertension.
90.Answer: B. T h ey h ave p o sitiv e chronotropic effect
Explanation:
Verapamil and Diltiazem have negative chronotropic (a decrease in heart rate) effect, thus they
must be used cautiously in patients who have slow heart rates or who are receiving digitalis
glycosides.
91 .Answer: E . A and B
Explanation:
Dilitazem and verapamil inhibit the metabolism o f Theophyline and Cyclosporine. They require
dosage administration if concomitantly used.
92.Answer: D . It b lo ck s the vagal e ffe c ts on the SA node,thus prom oting conduction
through the A V node and increasing the heart rate
Explanation:
Atropine is therapeutic for symptomatic sinus bradycardia and junctional rhythm. An
anticholinergic atropine blocks vagal effects (a nerve which has inhibitory effect on the heart rate)
on the SA node and increasing conduction through the AV node and increasing the heart rate.
93.Answer: E . It is unclassified
Explanation:
Atropine does not belong to any o f the existing classes o f antiarrhymics (i.e. it is unclassified)
94.Answer: B . It is a reflex bradycardia, w hich resulted from incom plete suppression o f
vagal im pulses
Explanation:
When the patient took the initial doses o f atropine, reflex bradycardia might have resulted from
incomplete suppression o f vagal impulses. Normally effect o f the vagus nerve is to slow down the
heart rate, if there is incomplete suppression o f this effect, bradycardia may result from reflex
action.
95.Answer: C . It enhances conduction th ro u g h the A V node
Explanation:
Adenosine is a naturally occurring nucleoside, which is normally present in all cells o f body. It
has been shown to:
-Slow conduction through the AV nods
- Interrupt re-entry pathways through the AV node
- Restore normal sinus rhythm in patiqnts with paroxysmal supraventricular tachycardia.
Clinical Toxicology
^>e>ive 0
“Hatred is toxic waste in the river o f life.”
Micron
1. Which one o f the following is not
covered under clinical toxicology?
A. Accidental poisoning
B. Intentional overdose o f medications
C. Intentional overdoses o f drugs of
abuse
D. The effect o f industrial chemicals on
the environment.
2. A TOME (toxicologic, occupational
medicine and environmental series)
provides information on:
A.
B.
C.
D.
Prescription drugs
Poison control centers
Industrial chemicals
Drugs o f abuse
3. Which one o f the following is not a
printed publication that provides
information related to poisoning?
A. Poison index
B. Poisoning and toxicology
compendium
C. Diagnosis and treatment o f human
poisoning
D. Toxicologic emergencies
4. The mandatory first steps in the initial
management o f drug ingestions are:
A. Evaluating and supporting vital
functions
B. Identifying the agent responsible for
the poisoning.
C. Laboratory assessment
D. Obtaining past medical history o f
the patient
5. The purpose o f administering 50%
dextrose (IV) in poisoning cases with
depressed mental status is:
A. To remove the poisoning
agent
B. To increase elimination o f
the poisoning agent
C. To treat the hypoglycemia
associated with poisoning
D. A and B
6. A poisoning case has a depressed mental
status. Obtaining a history o f exposure for
the patient includes all o f the following
Except:
A. Establishing the identity o f the
substance.
B. Neurological examination
C. Cardiopulmonary examination
D. Gastrointestinal decontamination
E. Interview with the patient
7. Which one o f the following is not true
about toxicology laboratory tests?
A. all possible intoxicating agents can
be screened
B. critically ill patients supportive
treatment is needed beforelaboratory
results o f the toxicology screen are
available
C. They occasionally help guide
therapy.
D. None
8. A person known to be a narcotic addict
was admitted to an emergency ward o f a
hospital. The patient had a depressed
mental status. In addition to other
supportive measures, an IV injection o f a
drug was given to the patient and the
respiratory depression improved. The drug
is most probably:
A.
B.
C.
D.
Morphine
Methadone
Naloxone
Codeine
9. For which o f the following drugs are
quantitative levels (in the blood) o f the drug
important to guide therapy (in case o f
poisoning by the drugs)?
A.
B.
C.
D.
E.
Acetaminophen
Vitamin C
Vitamin B
Lithium
A and D
10. Which o f the following is
contraindicated in a patient exposed to
sulphuric acid?
A. Removing the patient clothing
B. Irrigating the exposed areas with
water
C. Neutralization o f the acid bums with
sodium bicarbonate
D. A and B
11 .All o f the following are GIT
decontamination procedures EXCEPT:
A. Removal o f the ingested substance
by emesis
B. Removal o f the toxic substance by
gastric lavage.
C. Use o f activated charcoal to bind the
toxic substance
D. Use o f cathartics to hasten removal
o f the toxic substance from the GIT.
E. By inducing diuresis
12. Induction o f emesis is contraindicated in
cases poisoned by which o f the following
agents:
A. Patients who have ingested a strong
alkali or strong acid
B. Patients with compromised airway
protective reflexes(coma and
convulsions)
C. Patients with central nervous system
depression or seizures
D. Patients who have ingested some
type o f hydrocarbon or petroleum
distillates.
E. All o f the above
13. Which one o f the following is NOT
TRUE about syrup o f ipecac
A. When administered to poisoning
cases the onset o f emesis usually
occurs within 30 minutes
B. Prolonged emesis occurs after
administration o f the syrup to
poisoned patients (> 1 hour)
C. There is evidence that syrup o f
ipecac is beneficial even after
delayed administration
D. None.
14. Gastric lavage is used in patients who
are:
A. Not alert or have a diminished gag
reflex
B. Seen early following massive
ingestions.
C. admitted for ingestion o f acids,
alkalis, or hydrocarbons
D. At risk for GI perforation.
E. A and B
15.In gastric lavage a cuffed endotracheal
tube is in place to:
A. Suck the poison out o f the stomach
B. Protect the airways from the
ingested poison.
C. Push the gastric contents down to
the small intestine.
D. A and C
16. Which one o f the following is a correct
order o f the procedures in gastric lavage?
A. Protection o f the airway-Aspiration
o f GIT contents- instillation and
aspiration o f 250 ml o f water or
saline
B. Aspiration o f GIT contents-250 ml
o f water or saline is instilled and
aspirated- protect the airway -
C. Protect the airway- 250 ml o f water
or saline is instilled and aspiratedAspiration o f GIT contents
D. None
] 7. Activated charcoal is available as a
colloidal dispersion with:
A.
B.
C.
D.
E.
Water
Sorbitol
Methanol
Strong acids
A and B
18. Which one o f the following is not TRUE
about activated charcoal when used in the
management o f poisoning?
A. Ethanol, iron, lithium, methanol,
strong acids are strongly adsorbed
on activated charcoal.
B. The adult dose o f activated charcoal
is 25-100 g.
C. Constipation is commonly observed
after administration o f a single dose
o f activated charcoal.
D. Bowel obstruction may occur when
multiple doses o f activated charcoal
are given.
19.Toxic ingestions with drugs having an
enterohepatic circulation (e.g.
carbmazepine, theophylline and
Phenobarbital) generally require that
charcoal be readministered every 6 hours in
order to:
A. Prevent reabsorption during
recirculation
B. Facilitate their metabolism by
interfering with the function o f liver
enzymes
C. To induce vomiting after repeated
administration.
D. B and C
procedure, which employs an
isoosmotic cathartic solution and shown to
be effective under certain conditions
particularly when, activated charcoal lacks
efficacy is:
A.
B.
C.
D.
Whole bowel irrigation
Emesis
Whole bowel irrigation
Gastric lavage
21 .Multiple doses o f any cathartics should
be avoided because:
A. It may enhance the GIT absorption
o f the poison
B. They may interact with some
poisons
C. They may cause electrolyte
imbalance/and dehydration
D. A and B
22. Which one o f the following is NOT
TRUE about forced diuresis and urinary pH
manipulation in the management of
poisoning?
A. They may be used to enhance the
elimination o f substances, when
their elimination is mainly through
the renal route.
B. They may be used in the elimination
o f substances, which have small
volume o f distribution with little
protein binding.
C. Alkaline diuresis facilitates the
excretion o f weak acids
D. Alkaline diuresis facilitates the
excretion o f weak bases
23.A child ingested many aspirin tablets.
As a management strategy, the child was
given 50 mEq o f sodium bicarbonate in 1L
o f 0.25 %-0. 45 % normal saline. But the
child developed complications, and was
referred to an intensive care unit for close
monitoring.
The probable complications o f the alkaline
diuresis may include all o f the following
EXCEPT:
A. Metabolic acidosis
B. Hypernatremia
C. Hyperosmolarity
D. Fluid overload
24. All o f the following are true about
dialysis EXCEPT:
A. Substances that are removed by
hemodialysis generally are lipid
soluble.
B. Most o f the Substances removed by
hemodialysis have low molecular
weight and small volume o f
distribution.
C. It is indicated for life threatening
ingestions o f ethylene glycol,
methanol or paraquat.
D. B and C
25. Which o f the following statements are
not TRUE about hemoperfusion?
A. It is a technique in which
anticoagulated blood is passed
through (perfused) a column
containing activated charcoal or
resin particles.
B. It clears substances from the blood
more rapidly than hemodialysis.
C. It corrects electrolyte abnormalities
associated with poisoning
D. It is more effective in removing
ethanol or methanol.
E. C and D
26. Acetaminophen can produce fatal
hepatotoxicity in untreated patients
through:
A. Generation o f a toxic metabolite
B. Inhibition o f liver’s capacity to
metabolize endogenous compounds.
C. Inhibition o f kidney’s metabolic
capacity.
D. B and C
27.A patient who overdoses on
acetaminophen is admitted to an emergency
ward o f a hospital. The patient has ingested
8 grams o f acetaminophen tabs. If the
patient came to the hospital 1 hour after
ingestion, what is the treatment
recommended?
A. GI decontamination with syrup o f
ipecac or gastric lavage
B. Antidotal therapy with Nacetylcysteine.
C. Alkaline diuresis
D. B and C
28.In acetaminophen poisoning which
phase of the clinical presentation is
asymptomatic?
A.
B.
C.
D.
Phase
Phase
Phase
B and
1
II
III
C
29.During antidotal therapy with in
Acetaminophen poisoning, the purpose of
including metaclopramide is:
A. To counteract severe nausea
secondary to N-acetylcysteine
therapy
B. To increase the rate o f Nacetylcysteine absorption.
C. To synergize the antidotal activity
o f N-acety Icy steine
D. A and B
30.Laboratory data for a patient exposed to
ethylene glycol may include all o f the
following EXCEPT:
A. Severe metabolic acidosis
B. Calcium oxalate crystals in urine
C. Hypercalcemia
D. None
31 .Which one o f the following represents
the correct sequence in the hepatic
metabolism o f ethylene glycol?
A. Ethylene glycol -Glycoaldehydeglycolic acid -G lyoxylic acid Oxalic acid
B. Ethylene glycol - Glyoxylic acidglycolic acid- GlycoaldehydeOxalic acid
C. Ethylene glycol - Oxalic acidglycolic acid- GlycoaldehydeGlyoxylic acid
D. Ethylene glycol - Oxalic acidGlycoaldehyde- Glyoxylic acidglycolic acid.
1
i
i
;
32. A chemistry laboratory technician
drank 2 liters o f ethylene glycol. If he was
brought to emergency department after 20
hours with any prior treatment, what are the
likely symptoms in the clinical presentation
o f the patient?
A.
B.
C.
D.
Bradycardia
Pulmonary edema
Pneumonitis
All except A
33.A man working in a chemical industry
was poisoned with ethylene glycol.
The laboratory data shows that the serum
level o f ethylene glycol was 0.5 mg/dL
What treatment do you suggest in the
management o f the poisoned patient?
A.
B.
C.
D.
Gastric lavage within 30 minutes
IV ethanol
Activated charcoal
B and C
34. Intravenous ethanol is used in the
treatment o f ethylene glycol poisoning
because:
A. It inhibits alcohol dehydrogenase
B. It saturates alcohol dehydrogenase
thus it inhibits the formation o f toxic
metabolites from ethylene glycol.
C. It decreases the absorption o f
ethylene glycol
D. A and C
35. The most toxic metabolite o f glycolic
acid is:
A.
B.
C.
D.
Carbonic acid
Sulphuric acid
Oxalic acid
Glycoaldehyde.
36. Which o f the following is a potent
inhibitor o f alcohol dehydrogenase that can
prevent the formation o f toxic metabolite
from methanol or ethylene glycol.
A.
B.
C.
D.
Pyridoxine
Sodium bicarbonate
Fomepizole
IV ethanol
37.Pyridoxine and thiamine are used in the
management o f ethylene glycol poisoning
because:
A. They convert glyoxylic acid to
nonoxalate metabolites
B. They inhibit the metabolism of
ethylene glycol to glycoaldehyde.
C. They minimize the adverse effects
o f concurrently administered drugs
D. B and C
38.In the management o f ethylene glycol
poisoning, hemodialysis is indicated when:
A. Ethylene glycol levels are more than
50mg/dl
B. Congestive heart failure is present
C. Renal failure is present
D. Severe acidosis is present.
E. All o f the above
39.The laboratory data for methanol may
reveal all o f the following EXCEPT:
A.
B.
C.
D.
Metabolic alkalosis
Hyperglycemia.
Metabolic acidosis
Hyperamylasemia
40.Folic acid is administered at
1 mg/Kg(maximum 50 mg) IV every 4
hours for 6 doses. The possible mechanism
o f folic acid in the management o f
methanol poisoning is :
A. It increases the metabolism o f
formate
B. It inhibits the formation o f formic
acid
C. It inhibits the enzyme alcohol
dehydrogenase
D. None
41 .A patient was admitted to an emergency
department o f a hospital because o f
methanol poisoning. Laboratory data
showed that the serum level o f methanol
was 60mg/dL. The patient had severe
acidosis, which was resistant to the
administration o f sodium bicarbonate.
Moreover, the patient had kidney failure.
What is the most probable mode o f
management for the patient?
A.
B.
C.
D.
Administration o f activated charcoal
Hemodialysis
Induction o f emesis
IV ethanol
42.A patient with coronary disease was
taking IV heparin to prevent the threat o f
clot formation. Unfortunately a clumsy
nurse gave an overdose o f an anticoagulant
and the patient showed some signs of
bleeding. The physician in charge described
the situation as a mild over-anticoagulation.
What is the suggested treatment?
A. Stopping heparin administration and
restarting therapy at a reduced dose
after 1-2 hours.
B. 60 mg o f protamine is
recommended.
C. 150 mg o f protamine should be
administered in any 10-minute
period.
D. B and C
43. Which o f the following statements are
wrong about warfarin?
I. The protein binding is 99 %.
II. The mean half-life is 35 hours
III. Warfarin has poor absorption when
administered through the oral route.
A.
B.
C.
D.
E.
i f l only is correct
if III only is correct
i f l and II are correct
if II and III are correct
if l, II and III are correct
44.The mechanism by which protamine
counteracts the action o f heparin is:
A. Protamine combines with heparin
and neutralizes it
B. Protamine induces the synthesis o f
vitamin K
C. Protamine induces the metabolism
of heparin
D. B and C
45. Which one o f the following statements
is wrong about protamine?
A. One milligram o f protamine
neutralizes 100 units o f heparin.
B. The maximum dose o f protamine is
50mg in any 10-minute period.
C. Protamine is a basic drug.
D. Protamine is an acidic drug.
46. Which one o f the following is TRUE
about tricyclic antidepressants?
i
A. Blood level monitoring o f tricyclic
antidepressants does not correlate
well with clinical sings and
symptoms o f toxicity.
B. Electrocardiographic monitoring is a
better guide for assessing the
severity o f ingestion in tricyclic
antidepressants.
C. Tricyclic antidepressants undergo
enterobepatic recirculation
D. All o f the above
47. As part o f the treatment modality for
TCA poisoning phenytoin was given to the
poisoned in order to control the seizures.
After measuring the blood pressure, the
physician in charge reduced the dose of
phenytoin to 50mg/min. Not satisfied with
the response after reducing the dose o f the
drug, the physician in charge replaced
phenytoin by fosphenytoin. What could be
the reason for reducing the dose of
phenytoin and finally replacing it with
fosphenytoin?
A. Phenytoin has a hypotensive
adverse effect when given in
doses exceeding 25mg/min, but
fosphenytoin has less hypotensive
effect.
B. Phenytoin is less effective in
controlling seizures.
C. Fosphenytoin in addition to
controlling seizures it neutralizes
the acidic environment created by
the poisoning.
D. B and C
48. Which o f the following drugs are used
to control seizures as part o f the
management o f tricyclic antidepressants?
A.
B.
C.
D.
Phenytoin
Benzodiazepines
Physostigmine
Sodium bicarbonate
49.Physostigmine may be used to reverse
the severe anticholinergic toxicity due to
tricyclic antidepressant poisoning, but the
use o f this antidote is declining because:
A. It is not effective
B. It may cause asystole as an
adverse effect.
C. It interacts with the other drugs
used in the management of
tricyclic antidepressants.
D. A and C
50.The
laboratory data recommended for
selective serotonin reuptake inhibitors
poisoning is:
A.
B.
C.
D.
ECG monitoring
Blood level monitoring
WBC counts
Platelet count
51 .Which o f the following are not selective
serotonin reuptake inhibitors?
A.
B.
C.
D.
E.
Fluoxetine
Sertaline
Diazepam
Florazepam
C and D
52.A psychiatric patient with a problem of
depression took an overdose of a
psychotropic drug. The symptoms o f the
patient include mydriasis, urinary retention,
tachycardia, pulmonary edema and
confusion. The most likely cause o f the
poisoning is:
A.
B.
C.
D.
Amitriptyline
Fluoxetine
Sertaline
Diazepam
53.In the treatment o f tricyclic
antidepressant poisoning ipecac syrup is
not recommended because:
A. It has intolerable adverse effect
B. It induces vomiting
C. Patients may quickly become
comatose and increase the risk o f
aspiration.
A. A and B
54.The importance o f alkalinization with
sodium bicarbonate (1-2 mEq/Kg) in the
poisoning by tricyclic anti depressants is:
A. It maintains an arterial pH o f 7.45
to 7.55 and this decreases the
fraction o f absorbed toxins
B. Alkalinization reverses some o f
the cardiac abnormalities
C. To control seizures
D. To reverse the anticholinergic
toxicity associated with tricyclic
antidepressant poisoning.
55.
Which one o f the following is not true
about benzodiazepine poisonining?
A. The clinical presentation includes
drowsiness, ataxia and confusion
B. Supportive treatment includes
gastric emptying, activated
charcoal, and a cathartic
C. Benzodiazepines are hepatically
metabolized
D. Seizure is one symptom o f
benzodiazepine poisonining
56. Which one o f the following is WRONG
about flumazenil?
A. It is given 0.2 mg IV over 30
seconds in the treatment o f
Benzodiazepine poisoning
B. It is contraindicated in mixed
overdose patients.
C. It is indicated in tricyclic
antidepressant poisoning.
D. Flumazenil has a long elimination
half-life.
E. C&D
57. Epinephrine should be used cautiously
in the treatment o f p-blocker overdoses
bccause:
A. Unopposed a-Receptor
stimulation may lead to profound
hypertension
B. It may aggravate the condition o f
poisoning.
C. It may aggravate the
hypoglycemia associated with the
poisoning.
D. It decreases the metabolism o f pblocker
58.A clinical symptom common to
overdose o f all calcium channel blockers is:
A.
B.
C.
D.
Bradycardia
Hypotension
Pulmonary edema
Atrioventricular block
59.Bradycardia and Atrioventricular block
are commonly seen with ingestions of:
A.
B.
C.
D.
E.
Verapamil
Nifedipine
Diltiazem
Isradpine
A and C
60.1n the treatment o f calcium channel
blocker poisoning calcium chloride is given
for the management of:
A.
B.
C.
D.
E.
Hypotension
Bradycardia
Heart block
All o f the above
None o f the above
61 .Cocaine is an alkaloid obtained from:
A.
B.
C.
D.
Digitalis lanata
Papaver somniferum
Erthroxylon coca
Cephalis ipecacunha
vomiting and seizures. The treatment
should include:
!
j
j
A.
B.
C.
D.
E.
Amyl nitrite
Sodium nitrite
Oxygen
All of the above
A and B only
62. Which one o f the following is not TRUE
about cocaine?
A.
Cocaine is well absorbed
following oral administration.
B. Cocaine is metabolized in the
liver
C. Cocaine has poor absorption
following inhalational
administration.
D. In cocaine overdoses, death may
result from respiratory failure,
myocardial infarction, or cardiac
arrest.
63.Which one o f the following drugs is
used in the supportive treatment for the
hypertension in the management o f cocainei
overdose?
A.
B.
C.
D.
Diazepam
Labetolol
Flouxetine
Calcium chloride
64. Which one o f the following is NOT
TRUE about corrosives?
A. The available forms include
strong acids or alkalis.
B. Corrosives are well absorbed
following oral and inhalational
administration.
C. These compounds produce burns
on contact.
D. all o f the above
65.A man working in a nail polish industry
was exposed to traces o f cyanide through
inhalation. He had symptoms o f nausea,
66.Sodium nitrite is included in a cyanide
antidote kit because it:
A. Converts hemoglobin to
methemoglobin
B. It binds to the cyanide ion.
C. It neutralizes the acidosis induced
by the cyanide.
D. B and C
67.For equilibrium between serum digoxin
level and myocardial binding, it requires
approximately:
A.
B.
C.
D.
0.5-0.8 hr
1-2 hr
6-8 hrs
2-3 hrs
68.In mild cases o f digoxin poisoning
confusion, anorexia, are common. In more
severe cases which o f the following is
common.
A.
B.
C.
D.
Hypertension
Hypoglycemia
Cardiac dysrhythmias
Seizures
69.Supportive therapy for digoxin
poisoning includes:
A. Managing hyperkalemia or
hypokalemia
B. Inotropic support
C. Removal by inducing emesis
D. A and B
70.In the treatment o f digoxin over dosage
by digoxin-specific Fab antibodies, the
formula used to determine the dosage is:
A. Dose(vials)={ingested digoxin
(mg)}/0.5
B. Dose= {ingested digoxin (mg) X
0.8 }/0.6
C. Dose = {ingested digoxin (mg)
X0.8J/0.9
D. Dose ={ingested digoxin (mg) X
0.5}/0.8
71 .Which one of the following is not true
about magnesium?
A. Magnesium is found intracellulary
B. Magnesium is eliminated renally.
C. Magnesium containing cathartics
have been reported to produce
hypermagnesmia
D. Magnesium poisoning is classified
as mild if the its plasma
concentration is more than
lOmEq/L
72. In the treatment o f magnesium
poisoning 10 % calcium chloride is given in
order to:
A. Enhance the elimination o f
magnesium.
B. Temporarily antagonize the
cardiac effects o f magnesium.
C. Stimulate the metabolism o f
magnesium o f magnesium ion.
D. A and C
73.An intracellular cation, whose serum
values depends on the pH o f serum and
over dosage o f this cation may result in
cardiac irritabilities, and peripheral
weakness. The cation is
A. Magnesium
B. Potassium
C. Calcium
D. Sodium
74.The purpose o f using sodium carbonate
in the treatment o f potassium over dosage is
A. To increase serum pH and cause
an intracellular shift o f potassium.
B. To increase renal excretion of
potassium.
C. To enhance the metabolism o f
potassium
D. B and C
75.A hypertensive patient was taking a
diuretic regularly .One day the patient took
an overdose o f the drug. He was taken to a
hospital and the laboratory tests showed
severe hypokalemia. The physician in
charge ordered IV KC1 for the patient.
Unfortunately the nurse in charge
administered an overdose o f the potassium,
and the patient started showing symptoms
o f poisoning. As part o f the treatment plan
for the potassium overdose, the patient was
given 6 units o f regular insulin. The insulin
is given because:
A. It decreases the hypoglycemia
associated with potassium
poisoning.
B. It shifts potassium from the extra
cellular fluids in to cells
C. It stimulates the metabolism o f
potassium
D. It is given as a supportive therapy;
it doesn’t affect the concentration
o f potassium
E. in serum.
76.The mechanism o f action o f cation
exchange resins in the treatment of
potassium overdosage is:
A. They bind potassium in exchange
for another cation
B. They nullify the charge o f
potassium in their porous body.
C. They increase the shift of
potassium from extra cellular fluid
into cells.
D. They absorb potassium in their
porous body.
B. Pyridoxine
C. Deferoxime
D. Sodium bicarbonate
I
77.Sodium polystyrene sulfonate
(Kayexelate) is given in a dose o f 15 g/60
mL with:
A. 50ml o f dextrose
B. 50 % ethanol
C. 100 ml o f sterile water
D. 23.5 % sorbitol
78.Toxicity o f iron is based on the amount
o f elemental iron ingested. Which one of
the following represents a wrong pair o f a
salt and the amount of free elemental iron?
A. Sulfate salt- 20 % elemental iron
B. Fumarate salt-13% elemental iron
C. Gluconate salt-12% elemental
iron
D. None
82.The laboratory data for iron poisoning
patients should include:
A.
B.
C.
D.
E.
Serum Fe levels
Liver function tests
Hemoglobin
Hematocrit
All o f the above
83.
Which one of the following is NOT
TRUE regarding the treatment o f iron
poisoning?
A. For ingestions greater than
30mg/Kg, ipecac emesis may be
used within few minutes o f
exposure.
B. Gastric lavage using sodium
bicarbonate is very effective
procedure.
C. Whole-bowel irrigation is used for
large ingestions
D. None
79.Iron is absorbed in the:
A.
B.
C.
D.
Duodenum
Jejunum
Colon
A and B
80.The phase o f clinical presentation in
iron poisoning with nausea, vomiting, and
hypotension is:
A.
B.
C.
D.
Phase I
Phase II
Phase III
None
84. The maximum dose o f Deferoxime in
the treatment o f poisoning is:
A.
B.
C.
D.
6 g/day
5g/day
2g/day
1g/day
85.A cofactor that reverses Isoniazidinduced seizures is:
A.
B.
C.
D.
Thiamine
NADH
Pyridoxine
NADPH
81 .A chelator used in the treatment o f iron
poisoning is :
A. Dimercaprol
86. Emesis should not be used in the
treatment o f isoniazid poisoning because:
A. It is ineffective
B. Patients at high risk o f developing
seizures
C. The drug is corrosive, thus it
damages the GI mucosa.
D. A and C
87.The laboratory data in isoniazid
poisoning shows all o f the following
EXCEPT:
A.
B.
C.
D.
Alkalosis
Hypoglycemia
Mild hyperkalemia
Leukocytosis
88.
A child playing with paint drank half a
litre o f the paint. The symptoms o f the
ingestion include nausea, vomiting,
abdominal pain and convulsion. The most
likely cause o f the poisoning is:
A.
B.
C.
D.
Iron
Lead
Potassium
Magnesium
89.The half-life of lead in the human body
is:
A.
B.
C.
D.
2
3
4
5
months
months
months
months
90. Which of the following are used in the
treatment o f lead poisoning?
A.
B.
C.
D.
E.
Edetate calcium disodium
Dimercaprol
Deferoxamine
Cation exchage resins
A and B
91 .Which one o f the following represents
the range o f concentration in mild lithium
toxicity?
A. 0.6-1.2m Eq/L
B. 1.5-2.5m Eq/L
C. 2.5-3.0 mEq/L
D. More than 3 mEq/L
92.A patient with manic-depressive
disorder took an overdose o f lithium. The
plasma concentration o f lithium in the
patient was 4 mEq/L .The symptoms likely
to be present in the patient are:
A.
B.
C.
D.
E.
Delirium
Slurred speech
Coma
Hypertherima
AH except B
93.In the treatment o f lithium poisoning by
hemodialysis, lithium levels may rise after
dialysis due to:
A. Rebound effect
B. Storage o f lithium outside the
blood
C. Decreased elimination by the
kidneys
D. B and C
94.A cancer patient was taking morphine to
relieve the pain associated with the
malignancy. Hopeless o f his condition the
patient took an overdose o f morphine
intentionally. When he arrived at the
hospital he had symptoms of respiratory
depression and bradycardia. Naloxone was
given in a dose o f 0.3 mg every 5 minutes.
All the symptoms o f poisoning were
relieved after he took naloxone, but there
was a problem o f resedation long after the
occurrence o f poisoning. The most likely
cause o f the resedation is :
A. The patient may have taken a long
acting opiod
B. The patient may have taken a
sustained release dosage form o f
an opiod
C. Naloxone is not effective in
relieving the symptoms o f opiod
poisoning
D. A and B
95,Organophosphates are usually used as:
A.
B.
C.
D.
E.
Pesticides
Chemical warfare agents
Drugs for human use.
A and B
None
D. 40-60mg/dL-plasma concentration
o f salicylates results in tinnitus.
99.A 30-year-old man was admitted to an
emergency ward o f a hospital for aspirin
poisoning (after 2 hours o f ingestion). The
concentration o f aspirin in his blood was
70mg/dL. The patient had a problem o f GI
bleeding, increased prothrombin time,
nausea and vomiting. The main treatment
for the patient includes:
A. Alkaline diuresis
B. Hemodialysis
C. Induction o f Emesis with syrup o f
ipecac.
D. None
96.The clinical presentation o f
organophosphate poisoning includes
A. Excessive anticholinergic
stimulation
B. Excessive cholinergic stimulation
C. Excessive parasympathetic
nervous system stimulation.
D. None
97.The antidote used to reverse the
peripheral muscarinic effects of
organophosphate is:
A.
B.
C.
D.
Naloxone
Atropine
Nalmefene
Dimercaprol
98.
Which one of the following is
WRONG?
A. Salicylates have poor absorption
when given by the oral route, so
they should be given parentally.
B. In overdoses situations, the half­
life o f salicylates may be
prolonged to more than 20 hours.
C. The half-life o f salicylates is 6-12
hours at lower doses.
100. Which o f the following is not TRUE
about snake bite?
A. Onset o f symptomatolgy depends
on the species of snake and the
patient’s underlying medical
conditions.
B. More severe envenomation can
lead to severe tissue injury, and
shock.
C. Bradycardia is one o f the most
common clinical symptoms.
D. Pain and edema become evident at
the site o f snakebite.
101. Which one o f the following is
correct regarding the supportive treatment
o f snakebites?
A. Move the patient away from the
striking distance o f the snake.
B. Constrictive clothing, rings and
watches should be removed.
C. Surgical intervention may be
necessary for severe cases
D. All o f the above
102.
Horse-derived antivenom that has
been reported to produce allergic reaction
is:
103.
In unstable theophylline poisoned
patient who are in status epilepticus, the
recommended technique of
decontamination is:
A. Antivenin polyvalent
B. Crotalidae polyvalent immune
Fab
C. Tetanus antitoxin
D. None
A. Activated charcoal
B. Induction o f emesis with Syrup o f
ipecac
C. Charcoal hemoperfusion
D. Alkaline diuresis
Answers
Clinical Toxicology
1. Answer: D. The effect o f industrial chemicals on the environment
Explanation: Clinical toxicology focuses on the effects o f substances in patients by accidental or
intentional overdoses o f medications, drugs o f abuse, household products, or various other
chemicals.
2. Answer: C. Industrial chemicals
Explanation: TOMES (toxicologic, occupational medicine and environmental series) provides
information on Industrial chemicals
3. Answer: A. Poison index
Explanation: Poison index is a computerized CD-ROM database that is updated regularly and is
a primary source for poison control centers.
4. Answer: A. Evaluating and supporting vital functions
Explanation: Evaluating and supporting vital functions(airway, breathing and circulation) are
the mandatory first steps in the initial management o f drug ingestions.
5. Answer: C. To treat the hypoglycemia associated with poisoning
Explanation: The purpose of administering 50% dextrose (IV) in poisoning cases with depressed
mental status is to treat the hypoglycemia associated with poisoning.
6. Answer: E. Interview with the patient
Explanation: since the patient had a depressed mental status obtaining information through
interview is impossible
7. Answer: A. AH possible intoxicating agents can be screened
Explanation: All possible intoxicating agents cannot be screened by toxicology laboratory tests.
8. Answer: C. Naloxone
Explanation: Morphine, Methadone, Codeine are narcotics (opiod analgesics). Naloxone is an
opiod antagonist which is used in the treatment o f opiod overdosage.
9. Answer: E. A and D
Explanation: For Acetaminophen and lithium the treatment depends up on their blood level, so
the quantitative levels (in the blood) o f the drug important to guide therapy. Vitamins B and C are
not harmful,if taken more than the prescribed.
10. Answer: C. Neutralization o f the acid bums with sodium bicarbonate
Explanation: Neutralization o f the acid bums with sodium bicarbonate will produce an
exothermic chemical reaction, thereby exacerbating the patient’s condition.
11 .Answer: E. By inducing diuresis
Explanation: Inducing diuresis is not a GIT decontamination procedure. It is a procedure, which
enhances removal the toxic substance through the kidneys.
12.Answer: E. All o f the above
Explanation: Induction o f emesis is contraindicated in Patients who have ingested a strong alkali
or strong acid ;Patients with compromised airway protective (coma and convulsions); Patients
with centra] nervous system depression ;and Patients who have ingested some type o f
hydrocarbon or petroleum distillates.
13. Answer: C. There is evidence that syrup o f ipecac is beneficial even after delayed
administration
Explanation: Data suggest that there are no benefits following delayed administration after one
hour o f poisoning.
14.Answer: E. A and B
Explanation: Gastric lavage is used in patients who have ingested acids, alkalis, or hydrocarbons.
It should not also be used in patients who are at risk o f GI perforation (the toxic substance may be
absorbed through the perforation).
15. Answer: B. Protect the airways from the ingested poison.
Explanation: In gastric lavage a cuffed endotracheal tube is in place to protect the airways from
the ingested poison
16. Answer: A. Protection o f the airway-Aspiration o f GIT contents- instillation and aspiration o f
250 ml o f water or saline
Explanation: Lavage is performed after a Cuffed endotracheal tube is in place to protect the
airway. After aspiration o f the gastric contents. 250-300ml o f tap water or saline is instilled and
then aspirated. The sequence is repeated until the return is continuously clear.
17.Answer: E. A and B
Explanation: Activated charcoal is available as a colloidal dispersion with water or sorbitol.
18.Answer: A. Ethanol, iron, lithium, methanol, strong acids are strongly adsorbed on activated
charcoal
Explanation: Ethanol, iron, lithium, methanol, strong acids are not adsorbed onto activated
charcoal.
19. Answer: A. Prevent reabsorption during recirculation
Explanation: Toxic ingestions with drugs having an enterohepatic circulation generally require
that charcoal be readministered every 6 hours in order to prevent reabsorption during
recirculation.
20.Answer: C. Whole bowel irrigation
Explanation: A procedure, which employs an isoosmotic cathartic solution and shown to be
effective under certain conditions particularly when, activated charcoal lacks efficacy is whole
bowel irrigation.
21 .Answer: C. They may cause electrolyte imbalance/and dehydration
Explanation: Multiple doses o f any cathartics should be avoided because they may cause
electrolyte imbalance/and dehydration.
22. Answer: D. Alkaline diuresis facilitates the excretion o f weak bases
Explanation: Alkaline diuresis promotes the ionization o f the weak acids, thereby preventing
reabsorption by the kidney, which facilitates the excretion o f these weak acids.
23.Answer: A. Metabolic acidosis
Explanation: Complications o f alkaline diuresis include metabolic alkalosis, Hypernatremia,
Hyperosmolarity and Fluid overload.
24.Answer: A. Substances that are removed by hemodialysis generally are lipid soluble
Explanation: Substances that are removed by hemodialysis generally are water-soluble, have a
small volume o f distribution ( < 0.5 L/Kg ), have a low molecular weight (< 500 Daltons), and are
not significantly bound to proteins.
It is indicated for life threatening ingestions o f ethylene glycol, methanol or paraquat.
25.Answer: E. C and D
Explanation: Hemoperfusion does not correct electrolyte abnormalities associated with poisoning.
It is less effective in removing ethanol or methanol.
26.
Answer: A. Generation o f a toxic metabolite
Explanation: Acetaminophen can produce fatal hepatotoxicity in untreated patients through
generation o f a toxic metabolite
27. Answer: A.GI decontamination with syrup o f ipecac or gastric lavage
Explanation: Patients with levels greater than 150, 70, or 40mg/mL at 4, 8, 12 hours after
ingestion require antidotal therapy with N-acetylcysteine.
Adult patients who have ingested more than 7 grams or children more than 1OOmg/Kg require
treatment. The recommended treatment is GI decontamination with syrup o f ipecac or gastric
lavage for patients presenting within 2 hours o f ingestion.
28.Answer: B. Phase II
Explanation: Phase I ( 12-24 hours post ingestion )-nausea, vomiting, anorexia, and, diaphoresis
Phase II (1-4 days post ingestion) - asymptomatic
Phase III (2-3 days in untreated patients)- nausea, abdominal pain, coma, death
29.Answer. A and B
Explanation: During antidotal therapy in acetaminophen poisoning, the purpose o f including
metaclopramide is to increase the rate o f N-acetylcysteine absorption and to counteract severe
nausea secondary to N-acetylcysteine therapy.
30.Answer: C. Hypercalcemia
Explanation: Calcium reacts with oxalic acid (metabolic product o f ethylene glycol) to form
Calcium oxalate crystals. The calcium in our body gets depleted and this results in
hypocalcaemia.
31 .Answer: A. Ethylene glycol -Glycoaldehyde-glycolic acid -Glycoxylic acid -O xalic acid
Explanation: The correct sequence in the hepatic metabolism o f ethylene glycol is:
Ethylene glycol -Glycoaldehyde-glycolic acid -G lyoxylic acid -O xalic acid
32.Answer: D. All except A
Explanation: The symptoms which occur in 12-24 hours post ingestion include tachycardia,
pulmonary edema, Pneumonitis.
33.Answer: A.Gastric lavage within 30 minutes
Explanation: IV ethanol is indicated if the serum level o f ethylene glycol is greater than 20
mg/dl. Activated charcoal does not adsorb ethylene glycol.
34.Answer: B. It saturates alcohol dehydrogenase thus it inhibits the formation o f toxic
metabolites from ethylene glycol.
Explanation: Intravenous ethanol is used in the treatment o f ethylene glycol poisoning because it
saturates alcohol dehydrogenase thus it inhibits the formation o f toxic metabolites from ethylene
glycol.
35.Answer: C. Oxalic acid
Explanation: The most toxic metabolite o f glycolic acid is Oxalic acid.
Carbonic acid, Sulphuric acid, and Glycoaldehyde are not metabolites o f glycolic acid.
36.Answer: C. Fomepizole
Explanation: Fomepizole is a potent inhibitor o f alcohol dehydrogenase that can prevent the
formation o f toxic metabolite from methanol or ethylene glycol.
37.Answer: A. They convert glyoxylic acid to nonoxalate metabolites
Explanation: Pyridoxine and thiamine are used in the management o f ethylene glycol poisoning
because they convert glyoxylic acid to nonoxalate metabolites
38.
Answer: E. All o f the above
Explanation: Indications for hemodialysis include ethylene glycol levels are more than 50mg/dl,
Congestive heart failure, renal failure or severe acidosis.
39.Answer: A. Metabolic alkalosis
Explanation: It is not Metabolic alkalosis but Metabolic acidosis. The formic acid is the cause of
the metabolic acidosis.
40. Answer: A. It increases the metabolism o f formate
Explanation: The possible mechanism o f folic acid in the management of methanol poisoning is
by increasing the metabolism o f formate.
41.Answer: B. Hemodialysis
Explanation: Hemodialysis is used for methanol levels o f greater than 50 mg/dL, severe resistant
acidosis, renal failure, or visual symptoms.
42.Answer: A. Stopping heparin administration and restarting therapy at a reduced dose after 1-2
hours
Explanation: The treatment recommended for mild over-anticoagulation is stopping heparin
administration and restarting therapy at a reduced dose after 1-2 hours. Severe overdoses may
require the administration o f protamine. The maximum dose o f protamine is 50 mg in any 10minute period.
43.Answer: B. Ill is correct
Explanation: Warfarin is well absorbed when administered through the oral route
44.
Answer: A.Protamine combines with heparin and neutralizes it
Explanation: The mechanism by which protamine counteracts the action o f heparin is protamine
combines with heparin and neutralizes it.
45. Answer: D. Protamine is an acidic drug.
Explanation: Protamine is a basic drug not an acidic drug.
46. Answer: D. All o f the above
Explanation:
Blood level monitoring o f tricyclic antidepressants does not correlate well with clinical sings and
symptoms o f toxicity. Electrocardiographic monitoring is a better guide for assessing the severity
o f ingestion in tricyclic antidepressants. They undergo enterohepatic recirculation.
47. Answer: A. Phenytoin has a hypotensive adverse effect when given in doses exceeding
25mg/min, but fosphenytoin has less hypotensive effect
Explanation: Phenytoin has a hypotensive adverse effect when given in doses exceeding
25mg/min, but fosphenytoin has less hypotensive effect.
48.Answer: E. A and B
Explanation: Phenytoin and Benzodiazepines are used to control seizures as part o f the
management o f tricyclic antidepressants.
49.Answer: B.It may cause asystole as an adverse effect
Explanation: Physostigmine may be used to reverse the severe anticholinergic toxicity due to
tricyclic antidepressant poisoning, but the use o f this antidote is declining because it may cause
asystole as an adverse effect.
50.
Answer: A .ECG monitoring
Explanation: The laboratory data recommended for selective serotonin reuptake inhibitors
poisoning is ECG monitoring. Blood level monitoring is not recommended (the toxic effect o f the
drug does not correlate with its blood level). WBC and Platelet counts are not recommended.
51 .Answer: E. C and D
Explanation: Diazepam and Florazepam are not selective serotonin reuptake inhibitors. They are
benzodiazepines.
52.Answer: A. Amitriptyline
Explanation:
Amitriptyline is a tricyclic antidepressant. The symptoms o f the patient are same with symptoms
o f tricyclic antidepressant poisoning.
53.
Answer: C. Patients may quickly become comatose and increase the risk o f aspiration.
Explanation:
In the treatment o f tricyclic antidepressant poisoning ipecac syrup is not recommended because
patients may quickly become comatose and increase the risk of aspiration.
54.Answer:A. It maintains an arterial pH of 7.45 to 7.55 and this decreases the fraction of
absorbed toxins
Explanation:
It maintains an arterial pH o f 7.45 to 7.55 and this decreases the fraction o f absorbed toxins.
55. Answer: D. Seizure is one symptom of benzodiazepine poisonining
Explanation: Seizure is not a symptom o f benzodiazepine poisonining.
56.Answer: E. C&D
Explanation:
Flumazenil is known for its short elimination half-life. It is contraindicated in mixed overdose
patients (particularly involving tricyclic antidepressants) in whom seizures are likely.
i
57.Answer: A.Unopposed a-Receptor stimulation may lead to profound hypertension
Explanation:
Epinephrine should be used cautiously in [i-blocker Overdoses. Unopposed a-Receptor
stimulation in the face o f complete (3-blocker may lead to profound hypertension.
58.Answer: B. Hypotension
Explanation:
Hypotension is a common clinical symptom that occurs in overdoses o f all classes o f calcium
channel blockers.
59.
Answer: E. A and C
Explanation:
Bradycardia and Atrioventricular block are commonly seen with ingestions o f Verapamil or
Diltiazem.
60. Answer: D. All o f the above
Explanation:
In the treatment of calcium channel blocker poisoning calcium chloride is given for the
management o f Hypotension, Bradycardia, or Heart block.
61 .Answer: C. Erthroxylon coca
62. Answer: C. Cocaine has poor absorption following inhalational administration
Explanation: Cocaine is well absorbed following oral, inhalational, intranasal, and IV
administration.
63.Answer: B. Labetolol
Explanation:
Labetolol is an antihypertensive drug.Diazepam is a benzodiazepine used in the management of
pain. Fluoxetine is a non-selective serotonin reuptake inhibitor.
64.
Answer: D. all o f he above
65. Answer: D. All o f the above
Explanation:
A cyanide antidote kit contains the following:
Amyl nitrite- pearls are crushed and held under a patient’s nostrils.
Sodium nitrite- converts hemoglobin to methemoglobin, which binds the cyanide ion.
Sodium thiosulfate- 50ml o f a 25% solution IV push-may be repeated if there is no response.
Oxygen, and sodium bicarbonate-as needed for severe acidosis.
66.Answer: A. Converts hemoglobin to methemoglobin
Explanation:
Sodium nitrite is included in a cyanide antidote kit because it converts hemoglobin to
methemoglobin (the cyanide binds to methemoglobin and gets excreted from the poisoned
patient).
67.Answer: C. 6-8 hrs Explanation: It takes 6-8 hrs before there is equilibrium between digoxin serum level and its
myocardial binding.(i.e. its site o f action).
68.Answer: C. Cardiac dysrhythmias
Explanation: In more severe cases of digoxin poisoning, cardiac dysrhythmias is a common
symptom.
69.Answer: D. A and B
Explanation:
Removal by emesis is not a supportive therapy. It is a decontamination procedure (i.e. it is helpful
in removal o f the poison only), but managing the hyperkalemia (high potassium level) or
hypokalemia (low potassium level) and inotropic support are supportive therapies.
70.Answer: B. Dose= {ingested digoxin (mg) X 0.8 }/0.6
Explanation: Dose (vial) = {ingested digoxin (mg) X 0.8 }
0.6
Each vial contains 40 mg of digoxin antibodies (Digibind) and should be reconstituted with 4 mL
of sterile water.
71 .Answer: D. Magnesium poisoning is classified as mild if the it’s plasma concentration is
more than 1OmEq/L
Explanation:
Magnesium poisoning is classified as mild if the concentration is more than 4mEq/L. and severe
if more than 10 mEq/L.
72. Answer: B. temporarily antagonize the cardiac effects o f magnesium
Explanation: In the treatment o f magnesium poisoning 10 % calcium chloride is given in order to
temporarily antagonize the cardiac effects o f magnesium. It doesn’t enhance the metabolism of
magnesium.
73.Answer: B. Potassium
Explanation: Potassium is an intracellular cation, whose serum values depends on the pH of
serum and over dosage o f this cation may result in cardiac irritabilities, and peripheral weakness.
74. Answer: A. To increase serum pH and cause an intracellular shift o f potassium
Explanation:
The plasma concentration o f potassium depends up on the pH o f blood. The purpose o f using
sodium carbonate in the treatment o f potassium over dosage is to increase serum pH and cause an
intracellular shift o f potassium. Potassium is simply a cation so it is not metabolized.
75. Answer: B. It shifts potassium from the extra cellular fluids into cells
Explanation:
50 ml o f 50 % dextrose and 5-10 units o f regular insulin are administered via IV push to shift
potassium from the extra cellular fluids in to cells. The movement o f potassium from extra
cellular fluids into cells decreases the amount o f potassium in the blood and the toxic effects o f
potassium decrease accordingly.
;
76.Answer:A. They bind potassium in exchange for another cation
Explanation:
Cation exchange resins bind potassium in exchange for another cation (sodium).
77.Answer:
D. 23.5 % sorbitol
Explanation:
Sodium polystyrene sulfonate (Kayexelate) is given in a dose o f 15 g/60 mL with 23.5 % sorbitol.
Altematively.it can be given rectally in 200ml o f sodium polystyrene sulfonate.
78. Answer: B. Fumarate salt-13% elemental iron
Explanation: Numerous OTC products o f iron products are available. Toxicity on the amount of
elemental iron ingested: Sulfate salt 20 % elemental Fe; Fumarate salt 33% elemental Fe; and
Gluconate salt 12% elemental Fe.
79.Answer: D. A and B
Explanation:
Iron is absorbed in the Duodenum and Jejunum.
80.Answer: A. Phase 1
Explanation: Phase 1 - nausea, vomiting, diarrhea, GI bleeding, hypotension.
Phase II - clinical improvement seen 6-24 hours post ingestion
Phase III - metabolic acidosis, renal and hepatic failure, sepsis, pulmonary edema, and death.
81.
Answer: C. Deferoxime
Explanation: Dimercaprol and Deferoxime are chelating agents i.e. they have the capacity to form
complexes with metal ions. Deferoxime is a chelator used in the treatment o f iron poisoning.
Pyridoxine and Sodium bicarbonate are not chelating agents.
82. Answer: E. All o f the above
Explanation: Serum Fe levels, Liver function tests (because liver is involved in metabolism and
storage o f iron), Hemoglobin, and Hematocrit (the red blood cell portion o f the blood cells).
83.Answer: B. Gastric lavage using sodium bicarbonate is very effective procedure
Explanation:
Gastric lavage using sodium bicarbonate has not been shown to be effective procedure.
84.Answ'er: A. 6 g/day
Explanation: Deferoxime is used to chelate iron. It is administered 25-50mg/Kg up to a dose of
lg, and observe for a red color in the urine. Then administer at a rate o f 15mg/kg/hr up to a
maximum dose of 6 g/day.
85.Answer: C. Pyridoxine
Explanation: Pyridoxine is a coafator that reverses Isoniazid-induced seizures.
86. Answer: B. Patients at high risk o f developing seizures
Explanation: Emesis should not be used in the treatment o f isoniazid poisoning because patients
at high risk o f developing seizures (the poisoning may result in seizures). If emesis is induced in
patients with seizure the GI contents will enter the airways (they will get aspirated).
87. Answer: A. Alkalosis
Explanation: The laboratory data in isoniazid poisoning shows severe lactic acidosis,
Hypoglycemia, Mild hyperkalemia, and Leukocytosis.
88.Answer: B. Lead
Explanation: Lead is found in lead based paints and gasoline fume inhalation. The clinical
presentation o f lead poisoning includes nausea, vomiting, abdominal pain, peripheral
neuropathies, convulsions, and coma.
89.Answer: A. 2 months
Explanation: Lead has a half-life o f approximately 2 months in the human body.
90. Answer: E. A and B
Explanation: The treatment for lead poisoning is Edetate calcium disodium or D im ercaprol.
91 .Answer: B. 1.5- 2.5 mEq/L
Explanation: The following are concentration ranges o f lithium
Therapeutic range: 0.6-1.2 mEq/L
Mild toxicity toxicity: 1.5 mEq/L-2.5 mEq/L
Moderate toxicity: 2.5-3 mEq/L ,and severe toxicity is more than 3 mEq/L.
92.Answer: E. AH except B
Explanation: The plasma concentration o f lithium was 4 mEq/L, which is classified as severe
toxicity.
Mild intoxication: polyuria, slurred speech, blurred vision, weakness, ataxia, tremor and
myoclonic jerks.
Severe intoxication: delirium, coma, seizures, and Hypertherima.
93.Answer: A. Rebound effect
Explanation:In the treatment o f lithium poisoning by hemodialysis, lithium levels may rise after
dialysis due to a rebound effect.
94.
Answer: D.A and B
Explanation: Naloxone (given as a treatment in opiod over dosage) has a very short half-life, and
resedation is a problem in patients overdosing on long acting opiods or sustained release dosage
forms.
95.Answer: D. A and B
Explanation: Organophosphates are usually used as Pesticides or Chemical warfare agents.
Theyare not used as drugs for humans.
96.Answer: B. Excessive cholinergic stimulation
Explanation: The clinical presentation o f organophosphate poisoning includes excessive
cholinergic stimulation. There is excessive action o f the neurotransmitter acetlycholine because
organophosphates inhibit the enzyme, which metabolizes acetlycholine.
97.Answer: B. Atropine
Explanation: Naloxone and nalmefene are narcotic analgesics. Dimercaprol is a chelator used in
the treatment o f metal poisoning. Atropine reverses the peripheral muscarinic (cholinergic)effects
o f organophosphates.
98.
Answer: A. Salicylates have poor absorption when given by the oral route, so they should be
given parentally
Explanation: Salicylates have good absorption when given by the oral route. They are not given
parentally probably due to their ability to disturb the pH o f blood.
99.Answer: A. Alkaline diuresis
Explanation:Alkaline diuresis is given to enhance salicylate excretion. This is indicated for levels
greater than 40mg/dL.
Hemodialysis is indicated when the serum levels are greater than 100 mg/dL
Induction oTEmesis with syrup o f ipecac is effective if given within 30 minutes o f exposure.
] 00.
Answer: C. Bradycardia is one o f the most common clinical symptoms
Explanation:Clinical presentation includes nausea, vomiting, syncope, tachycardia, and cold
clammy skin. Bradycardia does not occur in cases o f snakebite.
Onset o f symptomatolgy depends on the species o f snake (if the snake is very poisonous type the
symptoms may occur rapidly) and the patient’s underlying medical conditions.
101.
Answer: D. all o f the above
Explanation: All o f the above are true about the supportive treatment o f snakebites.
102.
Answer: A. Antivenin polyvalent
Explanation: Antivenin polyvalent is horse-derived antivenom that has been reported to produce
allergic reaction.Crotalidae polyvalent immune Fab is a polyvalent antivenin made from sheep
sources.Tetanus antitoxin is given to protect from tetanus; it is not an antivenom.
103.
Answer: C. Charcoal hemoperfusion
Explanation: Hemoperfusion is a technique in which anti coagulated blood is passed through
(perfused) a column containing activated charcoal or resin particles.
Charcoal hemoperfusion is utilized in patients who in status epilepticus (one type o f seizure).
Coronary Artery Disease
“Your vision will become clear only when you can look into your own heart. Who
looks outside, dreams; who looks inside, awakens”.
Carl Jung
1. The most common cause o f ischemic
heart disease due to its ability to decrease
coronary blood flow is:
A.
B.
C.
D.
E.
atherosclerosis
coronary artery spasm
traumatic injury
embolic therapy
none o f the above
6. In a cardiac muscle the phase o f
contraction is known as:
A. systole
B. diastole
C. asystole
D. C and D
E. none o f the above
7. The two phases o f systole are:
2. All o f the following may result in
coronary artery spasm (sustained
contraction o f one or more coronary
arteries) EXCEPT:
A.
B.
C.
D.
E.
coronary catheterization
intimal hemorrhage
exposure to heat
ergot -derivative drugs
none o f the above
3. AH o f the following factors result in
increased heart rate EXCEPT:
A.
B.
C.
D.
E.
cold
smoking
p-blockers
exercise
nitroglycerin
4. Which o f the following may occur in
ischemic heart disease?
A.
B.
C.
D.
E.
decreased blood flow
increased blood flow
increased oxygen demand
decreased oxygen demand
A and C
5. Which o f the following result in
increased myocardial oxygen demand:
A.
B.
C.
D.
E.
exercise
emotional stress
shoveling snow
Inotropic state o f the heart
all o f the above
A.
B.
C.
D.
E.
contraction
ejection
relaxation
retention
A and B
8. Which o f the following result in
increased oxygen demand?
A. increased force o f myocardial
contraction
B. increases in systolic wall tension.
C. shortening o f ejection time.
D. decrease in heart rate
E. A and B
9. Which o f the following statements is
FALSE about angina pectoris
A. it includes varying forms of
transient chest discomfort that are
attributable to insufficient
myocardial oxygen.
B. it is characterized by discomfort in
the c h e st, jaw and shoulder.
C. the discomfort associated with
angina pectoris is usually
aggravated by nitroglycerin.
D. angina can occur in patients with
valvular disease.
E. none o f the above
10. Which o f the following diseases cause
oxygen imbalance?
A.
B.
C.
D.
E.
tachycardia
anemia
hypertension
hypotension
all o f the above
B.
C.
D.
E.
unstable angina
angina decubitis
vasospastic angina
none o f the above
15.Prinzmetal's angina occurs due to :
11 .Which o f the following statements is
incorrect about stable angina?
A. it is usually precipitated by exertion
, emotional stress or a heavy meal.
B. it usually lasts for hours.
C. the anginal episode is usually
substemal but has a tendency to
radiate to the neck, jaw, epigastrium
or arms.
D. it is characteristically due to a fixed
obstruction in a coronary artery.
£ . none o f the above
12. Which o f the following statements are
true about unstable angina ?
A. it has decreased response to rest or
nitroglycerin
B. it is characterized by rest angina ,
which usually is prolonged greater
20 minutes occurring within a week
o f presentation.
C. it represents a progressive clinical
entity.
D. it may signal incipient myocardial
infraction.
E. all o f the above
13.Angina decubitus is also known as:
A.
B.
C.
D.
E.
acute coronary syndrome
nocturnal angina
acute coronary syndrome.
Hyperlipidemia
none o f the above
14. Which o f the following types o f angina
occurs in the recumbent position ?
A. stable angina
A. reduction o f coronary blood flow
secondary to coronary artery spasm.
B. vasodilatation o f coronary blood
vessels.
C. increased myocardial force o f
contraction.
D. an overdose o f calcium channels
blockers.
E. none o f the above
16. Which o f the following types o f angina
respond well to nitroglycerin therapy?
A.
B.
C.
D.
E.
F.
classic angina
unstable angina
angina decubitis
vasospastic angina
A and C
B and D
17. Which o f the following statements is
Incorrect?
A. vasospastic angina usually occurs at
rest ( i.e. pain may disrupt sleep )
rather than with exertion emotional
stress
B. an ECG taken during a vasospastic
anginal attack characteristically
shows an inverted T wave
C. calcium channel blockers, rather
than B- blockers are more effective
for the treatment o f Prizementals
angina
D. diuretics alone or in combination
effectively reduce left ventricular
volume and thus, they may help
relief pain in patients with angina
decubitus
E. none o f the above
18. Which o f the following statements are
incorrect about exercise stress?
A. it is preferable to other variations of
stress test such as pharmacological
stress testing in patients who are
able to exercise
B. it is useful in diagnosis o f all patents
with angina pectoris
C. it aids in the diagnosis o f patients
who have normal testing ECG
D. it can be done with out ECG
E. B and D
19. Which o f the following drugs are used
in the phannacological stress testing (in the
diagnosis o f angina pectoris)
A.
B.
C.
D.
E.
Dipyridamole
Adenosine
Furosemide
Dobutamine
A,B and D
20. Which o f the following radioactive
elements are used as stress perfusion
imaging agents that can diagnose
multivessel diseases, localized ischemia,
and may be able to determine myocardial
viability?
A.
B.
C.
D.
E.
R ubidium 82
Technetium 99m
Thallium 201
X en o n '33
B and C
21 .Various drugs can have an effect on the
ECG and should be considered prior to,
during, and after an exercise test is carried
out. Which one o f the following drugs
produces abnormal exercise induced ST
depression in 25%-40% o f the apparently
healthy normal subjects with ischemia?
A. Digoxin
B. Lidocain
C. Flecainide
D. Verapamile
E. none o f the above
22. The goals o f treatment in angina
pectoris are:
A. to prevent myocardial infarction and
death
B. to reduce symptoms o f angina and
occurrence o f ischemia
C. to remove or reduce risk factors
D. B & C only
E. all o f the above
23.In the management o f hyperlipidemia,
the primary target treatment is to reduce:
A. LDL cholesterol ( low density
lipoprotein)
B. HDL cholesterol ( high density
lipoprotein)
C. triglycerides
D. A & C
E. none of the above
24. Which of the following statements is
False about the management of
hyperlipedemia in order to reverse cardiac
risk factors which may contribute to the
development o f ischemic heart diseases?
A. if LDL is less than 100 m g/dl,
patients with IHD should be given
instructions on diet and exercise and
have levels monitored annually
B. if the LDL cholesterol level is 101 129 mg/dl either at baseline or with
LDL lowering therapy, initiate or
intensify life style and /or therapies
to lower LDL to less than 100 mg/dl
C. if triglycerides are 200- 499 mg/dl ;
only exercise is recommended with
LDL lowering therapy
D. if triglycerides are >_500mg,
consider fibrate or niacin before
LDL lowering therapy.
E. None o f the above
25. Which o f the following indicate the
presence o f metabolic syndrome ?
A. abdominal obesity
B. triglycerides > 150 mg/dL
C. blood pressure readings > 135/85
mm Hg
D. fasting serum glucose level
morethan or equal to 11 Omg/dl
E. All o f the above
26. The mechanism o f action o f bile acid
sequestrant resins against hyperlipidemia is
that they
A. bind to bile acids within the
intestines.
B. inhibit an enzyme involved in the
synthesis o f fatty acids.
C. inhibit the excretion o f lipids
D. enhance elimination o f dietary fatty
acids
E. none o f the above
27. Statins reduce cholesterol production by
inhibiting the enzyme;
A.
B.
C.
D.
E.
Cholesterol synthetase
HMG-CoA reducase
Cholesterol esterase
Cholesterol epoxidase
none o f the above
28.The biochemical effects o f HMG-CoA
reducase inhibitors is to :
A.
B.
C.
D.
E.
lower LDL levels.
increase HDL levels
increased triglyceride levels.
A and B only
All o f the above
29. Which o f the following Statins results in
long lasting inhibition o f HMG-CoA
reducase?
A.
B.
C.
D.
E.
Simvastatin
Pravastatin
Atorvastatin
Lovastatin
none o f the above
30. Which o f the following drugs may
increase the risk o f myopathy if they are
given concurrently with Statins?
A.
B.
C.
D.
E.
cyclosporine
macrolide antibiotics
azole antifungals
A & B only
all o f the above
31 .When fibric acid derivatives are given
concurrently with Statins , patients should
be monitored to identify severe adverse
effects such as:
A.
B.
C.
D.
E.
myopathy
rhabdomyolysis
constipation
gastrointestinal distress
A and B
32. All o f the following are actions o f niacin
in the lowering o f cholesterol and
triglycerides EXCEPT:
A. decreases hepatic LDL and VLDL
production
B. inhibition o f adipose tissue lipolysis
C. decreases lipoprotein lipase activity'
D. deceases hepatic triglyceride
esterification
E. none o f the above
33.Patients taking niacin may experience
flushing and itching skin. This can be
reduced by administration o f 325 mg o f :
A. Acetaminophen
B.
C.
D.
E.
Aspirin
Naproxen
Ibuprofen
none o f the above
34. All of the following drugs are bile acid
sequestrants EXCEPT:
A.
B.
C.
D.
E.
Cholestyramine
Colestipol
Colesevelam
Cerivastatin
none o f the above
38. Which o f the following statements is
FALSE about ezetimibe?
A. it reduces total cholesterol.
B. it is associated with elevation o f
liver transaminases when given with
HMG-CoA reductase inhibitors.
C. it increases triglyceride levels.
D. the normal recommended dose o f
ezetimibe is lOmg given once daily.
E. none o f the above
39. All o f the following are transdermal
nicotine containing patches EXCEPT:
35. Which one o f the following classes of
anti-hyperlipidemia agents doesn’t decrease
the level o f triglycerides?
A.
B.
C.
D.
E.
HMG-CoA reducase inhibitors
Fibric acids
Nicotinic acid
Bile acid sequestrants
None o f the above
36.The class o f anti-hyperlipidemia
associated with unexplained non-coronary
disease in a WHO study is :
A.
B.
C.
D.
E.
nicotinic acid derivatives
bile acid sequestrants
HMG-CoA reductase inhibitors
fibric acid derivatives
none o f the above
37.The mechanism of action of ezetimibe is
A. it selectively inhibits the intestinal
absorption of cholesterol .
B. it decreases the elimination of
cholesterol
C. it inhibits HMG-CoA
D. it induces the synthesis of
cholesterol
E. none of the above
A.
B.
C.
D.
E.
Nicotrol
Habitrol
Nicoderm
Nicorette
none
40.A prescription antidepressant, marketed
under the brand name zyban as an aid to
smoking cessation is:
A.
B.
C.
D.
E.
Trazodone
Bupropion
Amoxapine
Maprotiline
none o f the above
41 .Which of the following represent a
wrong match o f a class recommendation of
drugs used in the treatment o f stable angina
and the reason for their inclusion in that
class ?
A. Class Il-conflicting evidence or a
divergence o f opinion about the
usefulness/efficacy o f a treatment.
B. Class I-evidence and /or general
agreement that a treatment is
ineffective.
C. Class III- evidence and /or general
agreement that a treatment is not
useful/effective.
D. Class 11-evidence and/ general
agreement that the treatment is
harmful.
E. B and D
42.All o f the following are true about the
actions o f nitrates EXCEPT:
A. they result in venous dilatation
B. they increase left ventricular
volume.
C. they reduce arteriolar resistance.
D. they decrease oxygen requirements
E. reduce myocardial wall tension
43.Which o f the following are WRONG
about nitrates?
A. acute attacks o f angina pectoris can
be managed with intravenous
nitrates only.
B. sublingual nitrates should be taken
after food or after sexual activity in
order to be effective.
C. they may not be effective as single
agents for the treatment of
Prinzm etal's angina.
D. nitrates should be used in
combination with p-adrenergic
blockers have been shown to be
effective than nitrates or padrenergic blockers alone.
E. A and B
The most common side effect o f nitrates
A.
B.
C.
D.
E.
an increase in blood pressure
headache
angina pectoris
constipation
none o f the above
A.
B.
C.
D.
E.
Felodipine
Nicardipine
Isradipine
Verapamil
none o f the above
46. Which o f the following statements are
false about B-blockers in the treatment o f
angina pectoris?
A. they reduce the frequency and
seventy o f exertional angina that is
not controlled by nitrates
B. they reduce oxygen demand both at
rest and during exercise
C. they decrease heart rate
D. they increase myocardial
contractility
E. none o f the above
47.6-blockers should be avoided in
vasospastic angina because:
A. they do not relieve the anginal pain.
B. they increase coronary resistance
and may induce vasospasm.
C. they dilate coronary blood vessels.
D. they do not have any effect on
coronary blood vessels.
E. none o f the above
48. All o f the following nitrates are shortacting EXCEPT:
A. isosorbide dinitrate oral tablets.
B. pentaerythritol tetranitrate
sublingual tablets.
C. erythritol tetranitrate sublingual
tablets
D. nitroglycerin sublingual tablets
E. none o f the above
49. Which o f the following statements is
FALSE about calcium channel blockers?
45.All o f the following are dihydropyridine
derivative calcium channel blockers
EXCEPT:
A. they are used in stable or exertional
angina that is not controlled by
nitrates and P-blockers and in
B.
C.
D.
E.
patients in which fi-blocker therapy
is inadvisable.
they decrease coronary vascular
resistance
they result in coronary spasm by
inhibiting calcium influx into
vascular smooth muscle.
they reverse coronary spasm
resulting in increased myocardial
oxygen supply.
none of the above
50. Which one o f the following calcium
channel blockers does not have a strong
negative inotropic effect?
A.
B.
C.
D.
E.
diltiazem
verapamil
nifedpine
bepridil
none o f the above
51 .Which o f the following statements is
FALSE about nifedipine?
A. it decreases myocardial oxygen
demand
B. it can produce tachycardia
C. its potent peripheral dilatory effects
can increase coronary perfusion and
produce excessive hypotension ,
which can aggravate myocardial
ischemia.
D. co-administration o f a p-blocker
with nifedpine prevents the reflex
tachycardia.
E. none o f the above
52. Which o f the following second
generation dihydropyridine derivative
calcium channel blockers, has been shown
to have less negative inotropic potential in
patients with CHF than other members of
the class?
A. Felodipine
B. Nicardipine
C. Amlodipine
D. Isradipine
E. Nisoldipine
53.The daily dose o f aspirin which should
be used in all patients without acute or
chronic ischemic heart disease is:
A.
B.
C.
D.
E.
500-750 mg
450-550 mg
75-325 mg
500-1000mg
none o f the above
54.Ticlopidine and clopidogrel are
chemically:
A.
B.
C.
D.
E.
thienopyridine derivatives
tetrazole derivatives
thiazole derivatives
pyrimidine derivatives
None
55. Which o f the following statements is
FALSE?
A. ticlopidine inhibits platelet
activation induced by adenosine
diphosphate
B. ticlopidine has been shown to
decrease adverse cardiovascular
events in patients with stable angina.
C. clopidogrel possesses
antithrombotic effects that are
greater than that o f ticlopidine.
D. clopidogrel is a therapeutic option in
those patients who can not take
aspirin due to contraindications.
E. none o f the above
56.Angiotensin converting enzyme
inhibitors are recommended as whcih class
o f agents for their use in patients with
ischemic heart disease and other vascular
disorders.
A. class 1A
B. class IB
C. class 11 a
D. class 11 b
E. none o f the above
57.An ACE inhibitor studied in the heart
outcomes prevention trail, and reduced
cardiovascular death, myocardial infarction
and stroke in patients who were at high risk
for or had vascular disease in the absence of
heart failure is:
A.
B.
C.
D.
E.
Ramipril
Lisinopril
Perindopril
Trandopril
none o f the above
58.In acute coronary syndromes due to
STEMI and NSTEMI, a portion of the
cardiac muscle suffers a severe and
prolonged restriction o f oxygenated
coronary blood. In most patients the cause
of this is:
A.
B.
C.
D.
E.
occlusive thrombus
vasospasm
vasodilatation
B and C
None o f the above
59. Which of the following statements is
FALSE?
A. Reperfusion therapy routinely
reverses the damage to myocardial
tissues in patients with STEMI.
B. Introduction o f thrombolysis or
percutaneous coronary intervention
for the management o f STEMI has
demonstrated the ability to remove
the offending thrombus from the
affected coronary artery.
C. Patients with NSTEMI do not
benefit from reperfusion therapy.
D. The development o f unstable angina
carries a 10%-20% risk o f
progression to an MI in untreated
patients.
E.
none o f the above
60. Which o f the following statements is
FALSE about creatnine kinase (CK-MB) in
relation with acute coronary syndrome?
A. it is first elevated 3-12 hours after
the onset o f pain.
B. its level peaks in 24 hours.
C. its level may be elevated due to
some other conditions (other than
myocardial infarction).
D. noncardiac causes o f change in
levels o f creatnine kinase
demonstrate the typical pattern o f
rise and fall seen in a myocardial
infarction.
E. none o f the above
61 .Which o f the following statements is
FALSE about cardiac troponins?
A. cardiac troponin I and troponin T
are even more sensitive than MBCK.
B. they represent a powerful tool for
risk stratification and have greater
sensitivity than Creatnine kinase
heart (CK-MB).
C. they do provide a high sensitivity in
the early phases o f myocardial
infarction.
D. they increase 3-12 hours after the
onset o f pain
E. none o f the above
62.Overall treatment goals in acute
coronary syndrome include all o f the
following EXCEPT:
A. to relieve chest pain anxiety
B. to reverse myocardial damage
C. to prevent or arrest complications,
such as lethal arrhythmias, CHF or
sudden death.
D. to reopen (or reperfuse) closed
coronary vessels with thrombolytic
drugs and /or percutaneous coronary
intervention
E. none o f the above
63. Which o f the following statements are
true about class I recommendation
therapeutic interventions against unstable
angina/NSTEM I?
A. bed rest with continuous ECG
monitoring for ischemia and
arrhythmia detection in patients
with on going rest pain.
B. supplemental oxygen for patients
with cyanosis or respiratory distress
and continued need for
supplemental oxygen in the
presence o f hypoxemia.
C. in patients with continuing or
frequently recurring ischemia when
j3-adrenergic blockers are
contraindicated, a non­
dihydropyridine calcium
antagonists are recommended as an
intial therapy in the absence of
severe left ventricular dysfunciton
D. morphine sulfate is useful in
patients with severe agitation.
E. All o f the above
64.Morphine can produce orthostatic
hypotension and fainting in patients with
ACS because:
A. it increases peripheral
vasodilatation.
B. It decreases peripheral resistance.
C. It has vasospastic effect.
D. A and B
E. C and D
65.Morphine has a vagomimetic effect that
can produce:
A.
B.
C.
D.
E.
brady arrhythmias
tachy dysarrhythmi as
dysarrhythmias
tachycardia
none o f the above
66.Patients taking morphine must be
protected against aspiration o f stomach
contents because:
A. nausea and vomiting may occur.
B. it results in brochospasm.
C. it decreases myocardial oxygen
consumption.
D. it reduces pre-load.
E. none o f the above
67. All o f the following are gastrointestinal
effects o f morphine EXCEPT:
A.
B.
C.
D.
E.
nausea
vomiting
diarrhea
constipation
none o f the above
68. Which o f the following is NOT TRUE
about thrombolytic agents in the treatment
o f acute coronary syndrome?
A. they have not demonstrated
beneficial clinical outcomes in the
absence o f STEMI.
B. they have failed to show benefit
against UA versus standard therapy
to prevent MI.
C. they are recommended in the
management o f acute coronary
syndrome without ST elevation.
D. they may increase the risk o f MI in
some patients
E. none o f the above
69.Clopidogrel should be administered to
hospitalized patients (with ACS):
A. who have gastrointestinal
intolerance
B. who have hypersensitivity reactions
to aspirin
C. all patients
D. A & B
E. All of the above
70. All o f the following are heparins used as
antithrombotic agents in the treatment of
ischemic heart disease EXCEPT:
A.
B.
C.
D.
E.
Dalteparin
Enoxaparin
Heparin
Enalapril
None
71 .A drug which should be administered to
patients already receiving heparin, aspirin
and clopidogrel in whom catheterization
and percutaneous coronary intervention are
planned is:
A.
B.
C.
D.
E.
Dalteparin
Glycoprotein llb/lla antagonist
Ticlopidine
Tirofiban
none o f the above
B.
C.
D.
E.
be lysed when administered early
after symptom onset (<6-12 hours ).
they do not help restore blood flow
they may be helpful in patients as
late as 12 hours after pain starts.
they shoud be administred in less
than 6 hours after after onset o f
symptoms in order to be efeftive.
none o f the above
75. Which o f the following thrombolytic
agents may restore blood flow in an
occluded artery if administred
intravenously within 12 hours o f an acute
MI?
A. streptokinase
B. recombinant tissue-type
plasminogen activator alteplase
C. anisoylated plasminogen
streptokinase activator complex
D. reteplase
E. all o f the above
72. Atherosclerotic plaques are made up of:
A.
B.
C.
D.
E.
lipid
'
fibrous proteins
carbohydrates
vitamin B
A and B
73. Which o f the following is the substance
released from injured blood vessels that
initiates the clotting cascade?
A.
B.
C.
D.
E.
serotonin
thromboxane A2
thromboplastin
fibrin
none o f the above
74. Which o f the folllowing statements is
FALSE about thrombolytic agents ?
A. administration o f thrombolytic
agents causes the thrombus clot to
76. Which one o f the fol lowing
thrombolytic agents causes greater degree
o f systemic bleeding as compared with the
others?
A. recombinant tissue-type
plasminogen activator alteplase
B. reteplase
C. tenecteplase
D. streptokinase
E. none o f the above
77.Recombinant t-PA is absolutely
contraindicated in which o f the following
conditions?
A.
B.
C.
D.
E.
internal bleeding
recent cardiovascular accident
intracranial surgery
pregnancy
all o f the above
78.Many patients develop arrhythmias,
within 30-45 minutes o f streptokinase
administration,which do not require
treatment.These arrhythmias are called:
A.
B.
C.
D.
E.
79.As
ventricular arrhythmia
reperfusion arrhythmias
supraventricular arrhythmias
torsades de pointes
none o f the above
compared to t-PA, tenecteplase has:
A.
B.
C.
D.
fewer bleeding complications.
less fibrin specificity.
slower rate o f administration.
more effective in late-treated
patients.
E. A and D
80. Which of the following decreases
mortality in patients with MI even if they
have not received thrombolytic therapy?
A.
B.
C.
D.
E.
Aspirin
Heparin
Ticlopidine
Clopidogrel
none o f the above
81 .Unless chosen for a specific clinical
indication, heparin use with which o f the
following is not recommended because o f
the risk o f hemorrhage.
A.
B.
C.
D.
E.
Reteplase
Tenecteplase
Streptokinase
t-PA
none o f the above
82. All o f the following prevent ischemia in
patients with STEMI EXCEPT:
A. antiplatelets
B. p-blockers
C. anticoagulants
D. statins
E. none o f the above
83. All o f the following drugs act by
inhibiting glycoprotein Ilb/IIIa receptors
EXCEPT:
A.
B.
C.
D.
E.
Abciximab
Eptifibatide
Enoxaparin
Tirofiban
none o f the above
84.p-blockers have all o f the following
actions in STEMI patients EXCEPT:
A. prevent reocclusion o f coronary
artery.
B. reduce ischemia
C. decrease oxygen demand
D. decrease cardiac work load
E. none o f the above
ANSWERS
Coronary Artery Disease
1. Answer: A. Atherosclerosis
Explanation:
Atherosclerosis is the most common cause o f ischemic heart disease. In Atherosclerosis the
coronary arteries are progressively narrowed by smooth-muscle cell proliferation and the
accumulation o f lipid deposits (plaque) along the inner lining (intima) o f the arteries.
2. Answer: C. Exposure to heat.
Explanation:
_
Coronary artery spasm is sustained contraction o f one or more coronary arteries. It can occur
spontaneously or be induced by irritation {e.g Coronary catheterization,(for diagnostic purposes),
or intimal hemorrhage (bleeding o f inner wall o f arteries), exposure to cold and ergot derivatives.
Exposure to heat has not been shown to cause coronary artery spasm.
3. Answer: C. (3-blockers
Explanation:
Cold, smoking, and exercise result in increased heart rate, while p-blockers decrease heart rate.
4. Answer: E. A and C
Explanation:
In ischemic heart rate disease, there is imbalance between myocardial oxygen demand and
coronary blood flow. There is increased oxygen demand, while there is decreased blood flow and
there may be reduced blood oxygenation (as in various anemias)
5. Answer: E.all o f the above
Explanation: Increased myocardial oxygen demand occurs with exertion suchas exercise,
shoveling and emotional stress.lnotropic state of heart also causes the need for increased oxygen
requirement by the myocardial tissue.
6. Answer: A. systole
Explanation:
In a normal heart beat, the two atria contract while the two ventricles relax. The term systole
refers to the phase o f contraction whereas diastole refers to the phase o f relaxation.
7. Answer:E. A and B
Explanation:
The two phases o f systole are contraction and ejection.
8. Answer: E. A and B
Explanation: The contractile (inotropic) state o f the heart, increases in systolic wall tension and
lengthening of ejection time and increases in heart rate demand oxygen supply.
9. Answer: C. The discomfort associated with angina pectoris is usually aggravated by
nitroglycerin.
Explanation; The term angina pectoris is applied to varying forms o f transient chest discomfort
that are attributable to insufficient myocardial oxygen. Angina is a clinical syndrome
characterized by discomfort in the chest, jaw and shoulder. Nitroglycerin relieves the discomfort
associated with angina.
10. Answer: E. all o f the above
Explanation:
Atherosclerotic lesions that produce a narrowing o f the coronary arteries are the major cause of
angina. However, tachycardia, anemia, hyperthyroidism, hypotension, and arterial hypoxemia can
all cause an oxygen imbalance.
11 .Answer: B. It usually lasts for hours.
Explanation:
In stable angina, episode typically lasts for minutes. The angina is normally related to physical
exertion, and the discomfort usually subsides quickly (i.e. in 3-5 minutes) with rest, if precipitated
by emotional stress, the episode lasts longer(i.e. about 10 minutes ).
12. Answer: E. all o f the abeVe*
Explanation: Unstable angina has decreased response to rest or nitroglycerin, it is characterized
by rest angina, which usually is prolonged greater 20 minutes occurring within a week of
presentation. It represents a progressive clinical entity. It may signal incipient myocardial
infraction.
13.Answer: B. Nocturnal angina
Explanation: Nocturnal angina is the second name o f angina decubitis. Unstable angina is referred
to as acute coronary syndrome.
14.Answer: :C. Angina decubitis
Explanation:
Angina decubitis occurs in the recumbent position and is not specifically related to either rest
or exertion.
] 5. Answer: A. Reduction o f coronary blood flow secondary to coronary artery spasm.
Explanation:
Coronary artery spasm that reduces blood flow precipitates Prinzm etal's angina (it is also
known as vasospastic or variant angina)
]6.Answer:!E. A and C
Explanation:
Stable (classic angina) angina and angina decubitis respond well to nitroglycerin therapy.
17. Answer: B. An ECG taken during a vasospastic anginal attack characteristically shows an
inverted T wave
Explanation:
In vasospastic angina an ECG taken during an attack o f vasospastic angina reveals an ST
segment elevation.All the other choices are correct.
18.Answer: E. B and D
Explanation:
It is a well established procedure, which aids the diagnosis in patients who have normal
resting ECGs. Exercise stress testing is preferable to other variations o f stress tests
(pharmacological) in patients who are able to exercise.
19.
Answer: E.A,B and D
Explanation:
The pharmacological testing is useful in patients with suspected IHD who are unable to
exercise. IV dipyridamole ( coronary vasodilator), adenosine ( coronary vasodilator),by
inhibiting cellular uptake and degradation o f adenosine increase coronary blood flow, and high
dose Dobutamine ( 20-40 (_ig/kg (m in )) which increases oxygen demand through increase in
myocardial blood flow are all able to induce detectable cardiac ischemia in conjunction with
ECG testing.
20.Answer: E. B and C
Explanation:
Stress perfusion with Thallium 20L or Technetium 99mcan diagnose multivessel diseases, localized
ischemia, and may be able to determine myocardial viability because these techniques are
expensive, they are reserved for patients who have ECG abnormality at rest.
21 .Answer: A. Digoxin
Explanation:
Digoxin produces abnormal exercise induced ST depression in 25%- 40 % o f apparently healthy,
normal subjects without ischemia.
22. Answer: E. All o f the above
Explanation:
The goals o f treatment in angina pectoris are to prevent myocardial infarction and death, to
reduce symptoms o f angina and occurrence o f ischemia,and to remove or reduce risk
factors.Treatment includes therapies aimed at reversing cardiac risk factors.
23.Answer: A. LDL cholesterol (low density lipoprotein)
Explanation:
Total cholesterol is no longer primary. Target o f treatment in patients with hyperlipidemia; LDL
cholesterol is now the primary target. Lipids and cholesterols are transported through the blood
stream as macromolecular complex o f lipid and protein known as lipoproteins. There are four
main classes o f lipoproteins differing in the relative proportion of lipids and in the type o f
apoprotein. They also differ in size and density,-and this later property, as measured by ultra
configuration, is the basis for their classification into:
a. High density lipoprotein ( HDL)
b. Low density lipoprotein (LDL)
c. Very low density lipoproteins(VLDL)
d. Chylomicrons
Cholesterol is esterified with long chain fatty acid in HDL particles, and the resulting cholestryl
ester are subsequently transferred to VLDL or LDL, Lipoproteins is associated with
atherosclerosis ( and localized in atherosclerosis ).
24.
Answer: C. If triglycerides are 200- 499 m g /d l; only exercise is recommended with LDL
lowering therapy
Explanation:
If triglycerides are 200-499 mg/dl; consider administration of fibrate or niacin before LDLlowering therapy.
25. Answer: E. All o f the above
Explanation: The metabolic syndrome is closely linked to insulin resistance, where the normal
actions o f insulin are impaired. Excess body fat and physical inactivity promote the development
o f the syndrome, however; some individuals may be predisposed genetically. Patients with three
or more o f the following characteristics are referred to as having the metabolic syndrome, and
should be treated accordingly ; abdominal obesity, triglycerides >150mg/dL , HDL levels o f < 40
mg/dL for men and 50mg/dL for women , blood pressure readings > J 30/85 mm Hg and a fasting
serum glucose le v e ls 110 mg/dL .
26. Answer: : A. They bind to bile acids within the intestines
Explanation:
Bile acid sequestrant resins bind to bile acids within the intestines and the complex formed is
eliminated via the feces. When taken by mouth, bile acid sequestrant resins sequester bile acids in
the intestine and prevent their absorption and enterohepatic metabolism. The result is decreased
absorption o f exogenous cholesterol and increased metabolism o f endogenous cholesterol into
bile acids in the liver. This leads to increased expression o f LDL receptors on the liver cells and a
reduced concentration o f LDL- cholesterol in plasma.
27. Answer: B. HMG-CoA reducase
Explanation:
Statins or HMG-CoA reducase inhibitors inhibit the enzyme which catalyzes the conversion of
HMG-CoA to mevalonic acid. ( an important step in the synthesis o f cholesterol) and reduce
cholesterol production. The resulting decrease in hepatic cholesterol synthesis leads to increased
synthesis o f LDL receptors and increased clearance of LDL. The main biochemical effect of
Statins is, therefore, to reduce plasma LDL- cholesterol concentration.
28.Answer: D. A and B only
Explanation:
Statins (HMG-CoA reducase inhibitors) are effective in lowering LDL levels, while increasing
HDL levels and lowering triglyceride levels . They are primarily used to lower LDL levels.
29.
Answer: C. Atorvastatin
Explanation:
Simvastatin, Pravastatin, and Lovastatin are competitive reversible inhibitors of HMG-CoA
reducase. Atorvastatin causes long lasting inhibition o f HMG-CoA reducase.
30. Answer: E. All o f the above
Explanation:
Concurrent therapy o f Statins with other agents including cyclosporine, macrolide antibiotics,
azole antifungals, niacin, or fibrates may increase the risk o f myopathy associated with Statins.
31 .Answer: E. A and B only
Explanation:
Use o f Statins with fibric acid derivatives can lead to elevated creatinine kinase, and monitoring
is necessary to identify Myopathy and Rhabdomyolysis.
32.Answer: C. decreases lipoprotein lipase activity
Explanation:
Niacin lowers o f cholesterol and triglycerides through various mechanisms such as participation
in tissue respiration oxidation , reduction, which decreases hepatic HDL and very low density
lipoprotein (VLDL) production ; inhibition o f adipose tissue lipolysis, decreased hepatic
triglyceride esterification, and increases in lipoprotein lipase activity.
33.Answer: B. Aspirin
Explanation:
Patients taking niacin may experience flushing and itching skin. This can be reduced by
administration o f 325 mg o f Aspirin about 30 minutes before the dose.
34.Answer: D. Cerivastatin
Explanation:
Cholestyramine, Colestipol, Colesevelam are bile acid sequestrants while Cerivastatin is an
HMG-CoA reducase inhibitor..
35.Answer: D. Bile acid sequest rants
Explanation:
Bile acid sequestrants do not change the level o f triglycerides.
36.Answer: D. Fibric acid derivatives
Explanation:
Fibric acid derivatives (e.g. gemfibrozil, fenobirate and clofibrate) were associated with
unexplained non-CHD deaths in WHO study.
37.Answer:A. It selectively inhibits the intestinal absorption o f cholesterol .
Explanation:
Ezetimibe works by selectively inhibiting the intestinal absorption of cholesterol and related
phytosterols, with a resultant decrease in intestinal cholesterol delivered to the liver, decreased
hepatic cholesterol stores and an increase in the clearance of cholesterol from the blood.
38.Answer:
Explanation:
C. It increases triglyceride levels.
Ezetimibe has demonstrated the ability to reduce total cholesterol, LDL, apo-lipoprotein B, and
triglyceride levels , while increasing HDL levels in patients with hypercholesterolemia.
39.Answer: D.nicorette
Explanation:
Nicorette is an oral nicotine polacrilex chewing gum, it is not transdermal nicotine containing
patch.
40.Answer: B. Bupropion
Explanation:
Bupropion is a prescription antidepressant, marketed under the brand name zyban as an aid to
smoking cessation.
41 .Answer: E. B and D
Explanation:
Recent evidence based guidelines have provided recommendations for the treatment o f patients
with stable angina.
Recommendations utilize 3 classes guidelines based on the levels o f evidence, class I { there is
evidence or general agreement that a treatment is useful or effective}, class II {conflicting
evidence or a divergence o f opinion about the usefulness/efficacy o f a treatment }, class III {
there is evidence and/or general agreement that a treatment is not useful/effective and in some
cases may be harmful}.
42.Answer: B. They increase left ventricular volume.
Explanation:
Organic nitrates relax vascular smooth muscles. They cause marked vasodilatation with a
subsequent reduction in central venous pressure (reduced pre-load), and myocardial wall tension,
decreasing oxygen requirements. Due to their effect on larger muscular arteries, there is reduction
in central (aortic) pressure and coronary after load.
43.Answer: A and B
Explanation:
Acute attacks o f angina pectoris can be managed with sublingual nitrates, transmucosal (spray or
buccal tablets), or intravenous delivery. Sublingual nitrates can be used before eating, sexual
activity (since they are vasodilators they may interfere with erection), or any stressful event.
44.Answer: B. headache
Explanation:
The most common side effect o f nitrates is headache. Patients should be warned o f the nature,
suddenness, and potential strength o f these headaches to minimize the anxiety that might
otherwise occur. Acetaminophen ingested 15-30 minutes before nitrate administration may
prevent the headache.
45.Answer: D. Verapamil
Explanation:
Felodipine, isradipine, and nicardipine are dihydropyridine derivatives. Verapamil is not a
dihydropyridine derivative.
46.Answer: D. They increase myocardial contractility
Explanation:
6-blockers reduce oxygen demand, both at rest and during exercise by decreasing the heart rate
and myocardial contractility, which also decrease arterial blood pressure.
47.Answer: B. They increase coronary resistance and may induce vasospasm
Explanation:
6-blockers should be avoided in vasospastic angina because they increase coronary resistance
and may induce vasospasm.
48.Answer: A. Isosorbide dinitrate oral tablets.
Explanation:
Isosorbide dinitrate oral tablets have long duration o f action (up to 8 hours).The others are short
acting (the same as nitroglycerin sublingual tablets or spray which has short term effects o f 1-7
minutes)
49.
muscle
Answer: C. They result in coronary spasm by inhibiting calcium influx into vascular smooth
Explanation:
Calcium channel blockers prevent and reverse coronary spasm by inhibiting calcium influx into
vascular smooth muscles and myocardial muscles. This results in increased blood flow, which
enhances myocardial oxygen supply.
Calcium channel blockers decrease coronary vascular resistance and increase blood flow,
resulting in increased oxygen supply. Calcium channel blockers decrease systemic vascular
resistance and arterial pressure; in addition, they decrease inotropic effects, resulting in decreased
myocardial oxygen demand.
50.Answer: C. nifedpine
Explanation:
Diltiazem, verapamil, and bepridil produce strong negative inotropic effect, and patients must be
monitored closely for signs o f developing cardiac decompensation (i.e. fatigue, shortness of
breath, edema), when co-administered with p-blockers or other agents that produce negative
inotropic effects (e.g. disopyramide, quinidine, procainamide, flecainide), the negative
chronotropic effects are additive. Nifedipine does not seem to have a strongly inotropic effect;
therefore, it is preferred for combination therapy with agents that do.
51.Answer: A. It decreases myocardial oxygen demand
Explanation:
Because nifedipine increases heart rate, it can produce tachycardia, which would increase oxygen
demand.
52. Answer: C. Amlodipine
Explanation:
Second generation dihydropyridine derivative calcium channel blockers should not be used in
patients with CHF because they have potent negative inotropic potential.
Amlodipine has less negative inotropic potential as compared to other members o f the class.
53.Answer: C. 75-325 mg
Explanation:
Aspirin in dose o f 75-325 mg daily should be routinely used in all patients with acute or chronic
IHD with or with out symptoms in the absence o f any contraindications.
54.Answer: A. thienopyridine derivatives
55.Answer: B. Ticlopidine has been shown to decrease adverse cardiovascular events in patients
with stable angina.
Explanation:
Ticlopidine has not been shown to decrease adverse cardiovascular events in patients with stable
angina and is associated with thrombotic thrombolytic purpura.
56.Answer: C. class Ha
Explanation:
ACE inhibitors have attracted continued attention as additional therapy in patients with ischemic
heart disease, as evidenced by the most recent guidelines, which provide a class Ila
recommendation for their use in patients with IHD or other vascular disease.
57.Answer: A. Ramipril
Explanation:
In the heart outcomes prevention trail (HOPE) trial, Ramipril reduced cardiovascular death,
myocardial infarction and stroke in patients who were at high risk for or had vascular disease in
the absence o f heart failure.
58.Answer: A. Occlusive thrombus
Explanation:
In acute coronary syndromes due to STEMI and NSTEMI, a portion o f the cardiac muscle suffers
a severe and prolonged restriction of oxygenated coronary and in most patients it is due to
occlusive thrombus.
59. Answer: A. Reperfusion therapy routinely reverses the damage to myocardial tissues in
patients with STEMI.
Explanation:
Damage to myocardial tissues is not routinely reversible in patients with STEMI; due to the
potential death o f myocardial tissue if perfusion does not take place early enough.
60.Answer: D. Noncardiac causes o f change in levels of creatnine kinase demonstrate the typical
pattern o f rise and fall seen in a myocardial infarction.
Explanation:
Creatnine kinase (CK-MB) is first elevated 3-12 hours after the onset o f pain, peaks in 24 hours
and returns to baseline in 48-72 hours, other causes can result in elevated CK-MB levels but do
not demonstrate the typical pattern o f rise and fall as seen in myocardial infarction. Until,
recently, CK-MB had been the principal serum cardiac marker used in the evaluation o f acute
coronary syndrome.
61 .Answer: C. They do provide a high sensitivity in the early phases o f myocardial infarction
Explanation:
Cardiac troponin I and T are even more sensitive than MB-CK, do provide a low sensitivity in the
early phases o f MI (<6 hours after symptom on set) and require repeat requirements at 8-12
hours, if negative.
62.Answer: B. to reverse myocardial damage
Explanation:
Reversing myocardial damage is not the objective o f overall treatment goals in acute coronary
syndrome, rather the treatment aims to prevent/reduce myocardial damage by limiting the area
affected and preserving pump function.
63.
Answer: E. All o f the above
Explanation:
All the given choices are true.
64.Answer: D.Aand B
Explanation:
Morphine can produce orthostatic hypotension in patients with ACS because it increases
peripheral vasodilatation and decreases peripheral resistance.
65.Answer: A. Brady arrhythmias
Explanation:
Morphine has a vagomimetic effect (the same action as the vagus nerve, which has a slowing
effect on the heart) that can produce Brady arrhythmias.
66.
Answer: A. "Nausea and vomiting may occur.
Explanation:
Nausea and vomiting may occur, especially with initial doses, and patients must be protected
against aspiration o f stomach contents.
67.Answer: C. Diarrhea
Explanation:
Diarrhea doesn’t occur at therapeutic or toxic doses o f morphine.
68.Answer: C. They are recommended in the management o f acute coronary syndrome without
ST elevation.
Explanation:
Thrombolytic agents have not demonstrated beneficial clinical outcomes in the absence of
STEMI. Studies carried out to date have failed to show benefit with using thrombolytic agents
against UA versus standard therapy to prevent ML In fact,thrombolytic agents increased the risk
o f MI in such patients. Therefore, based on current evidence based guidelines, thrombolytic
agents are not recommended in the management o f ACS without ST-segment elevation.
69.Answer: D. A and B
Explanation:
As part o f the anti-platelet and anticoagulant therapy in acute coronary syndrome clopidogrel
should be administered to hospitalized patients who are unable to take aspirin because o f
hypersensitivity or gastrointestinal intolerance.
70.Answer: D. Enalapril
Explanation:
Enalapril is not a heparin but an ACE inhibitor.
71 .Answer: B. Glycoprotein Ilb/lla antagonist
Explanation:
A platelet glycoprotein llb/IIa antagonist should be administered to patients already receiving
heparin, aspirin and clopidogrel in whom catheterization and percutaneous coronary intervention
are planned.
72.Answer: E. A and B
Explanation:
Atherosclerotic plaques are made up o f Lipid and fibrous proteins.
73.Answer: C. thromboplastin
Explanation:
Atherosclerotic plaques are made up o f Lipid and fibrous proteins. When lesions rupture , the
release o f adenosine diphosphate alteplase(ADP), serotonins, and thromboxane A2 is triggered ,
leading to platelet aggreagtion and the formation o f the primary clot. Thromboplastin relased
from injured blood vessels initiates the clotting cascade. The resulting fibrin traps red blood cells
(RBCs), platelets, and plasma protein to form an intraluminal thrombus.
74.
Answer: B. They do not help restore blood flow
Explanation:
Administration o f thrombolytic agents causes the thrombus clot to be lysed when administered
early after early symptom onset (<6-12 hours) and to restore blood flow.
75. Answer: E.all of the above
Explanation:
IV administration o f streptokinase, recombinant tissue-type plasminogen activator alteplase,
anisoylated plasminogen streptokinase activator, reteplase and tenecteplase may restore blood
flow in an occluded artery if adminisered within 12 hrs o f an acute MI.
76.Answer: D. streptokinase
Explanation:
SK activates the fibrinolytic system and has a greater likelihood o f causing systemic bleeding as
compared with recombinant tissue-type plasminogen activator alteplase, reteplase, and
tenecteplase.
77. Answer; E. All o f the above
Explanation;
Absolute contraindications to Recombinant t-PA include active internal bleeding, recent
cardiovascular accident, intracranial surgery, spinal surgery, or trauma; severe uncontrolled
hypertension etc.
Recombinant t-PA is used in the management o f STEMI.
78.Answer: B. reperfusion arrhythmias
Explanation:
Patients taking streptokinase must be monitored for bleeding, arrhythmias, anaphylactoid
reactions, and hypotension. Many patients develop arrhythmias, within 30-45 minutes o f
streptokinase administration; these arrhythmias are called reperfusion arrhythmias.
79.Answer: E. A and D
Explanation:
Rapid rate o f administration, fibrin specificity, fewer bleeding complications, and superior
activity in late treated patients as compared to t-PA, make tenecteplase a very likely candidate to
replace t-PA as an agent o f choice in STEMI.
80.Answer: B. Heparin
Explanation:
Heparin has been administered along with the thrombolytics to prevent reocclusion once a
coronary artery has been opened. It also appears to decrease mortality in patients with Ml even if
they have not received thrombolytic therapy.
81 .Answer: C. Streptokinase
Explanation:
Unless chosen for a specific clinical indication, heparin use with streptokinase is not
recommended because o f the risk o f hemorrhage.
82.Answer: D. Statins
Explanation;
Statins have not been shown to prevent ischemia in STEMI patients.
83.Answer: C. Enoxaparin
Explanation:
Drug Information Resources
“Knowing is not enough; we must apply. Willing is not enough; we must do. ”
Johann von Goethe
]. Drug information should fulfill all of
the following criteria EXCEPT:
A. It should use the most recent, up-todate sources.
B. It should be critically examined
information.
C. It should be relevant.
D. It should only be information
published in the USA.
E. None
2. A Critically examined drug information
should fulfill which o f the following
criteria?
A. More than one source should be
used when appropriate.
B. The extent o f agreement of sources
should be determined; if sources dc
not agree, good judgment should b
used.
C. The plausibility o f information,
based on clinical circumstances
should be determined.
D. A,B&C
E. A and B
3. Which of the following sources o f dru
information are primary resources?
A. British medical journal
B. Journal o f pharmaceutical research
C. International pharmaceutical
abstracts.
D. Iowa drug information system
E. A and B
4. Primary drug information resources
enable the pharmacist to:
A. Keep abreast of professional news;.
B. Learn how a second clinician
handles a particular problem.
C. To keep up with new developments
in pathophysiology, diagnostic
agents, and therapeutic regimens.
D. To decide the medical intervention
required for a particular patient.
5. The main limitation o f primary drug
information resources is:
A. There is no guarantee that the
articles are accurate.
B. They do not provide any reliable
information about drugs.
C. They provide information limited to
clinical application o f drugs only.
D. The information published can be
easily found in textbooks.
E. None
6. The lag-time o f secondary drug
information resources is:
A. The interval of time between an
article is submitted for publication
and the time it is published.
B. The interval o f time between
publication o f an article and citation
o f the article in an index.
C. The interval of time between
submission o f a journal to printing
press and its distribution to readers.
D. The time required for editing a
journal.
E. None
7. Which o f the following statements is
WRONG about secondary drug information
resources?
A. They are valuable tools for quick
and selective screening of the
primary literature for specific
information, data, citation, and
articles.
B. In some cases, the sources provide
sufficient information to serve as
references for answering drug
information requests.
C. The lag time for all indexing
/abstracting services is the same.
D. Each indexing or abstracting service
reviews a finite number o f journals;
therefore relying on only one
service can greatly hinder the
thoroughness o f a literature search.
E. None
8. In general abstracts should not be used
as primary sources of information because:
A. They are not easily available.
B. They are generally interpretations o f
a study and may be a
misinterpretation o f important
information.
C. They do not have any drug related
information.
D. They are detailed, thus they may
contain irrelevant information.
E. None
9. Which o f the following statements is
WRONG about tertiary information
resources?
A. They can provide easy and
convenient access to a broad
spectrum of related topics.
B. The Information might not include
the most recent developments in the
field.
C. They may be misinterpretations o f a
primary or secondary literature.
D. They are most reliable o f all
information resources.
E. None
10. Once should consider all o f the
following when examining and using
textbooks as sources o f drug information
EXCEPT:
A. The year o f publication.
B. The country where the book was
published.
C. The edition o f the text book.
D. What are the author’s and
publishers track records?
E. None
11 .Which of the following statements is
TRUE about internet information
resources?
A. Information obtained from the
internet may not be peer reviewed or
edited prior to release.
B. A website should be evaluated by its
source (author) o f information.
C. Pharmacists should use traditional
literature
evaluation
skills
to
determine whether the information
given in the internet is clear, concise,
unbiased, relevant and referenced.
D. Disclosing name, location, and
sponsorship o f the internet resource
is an important in assessing the
credibility o f the information.
E. All o f the above
12. All o f the following drug information
resources are updated annually EXCEPT:
A.
B.
C.
D.
The American drug index
Drug facts and comparisons
The physician5s Desk Reference
Martindale: The complete drug
reference
E. None
13. All of the following provide
information about investigational drugs
EXCEPT:
A. Martindale: The complete
reference.
B. Drug facts and comparisons.
C. Unlisted drugs
D. United states pharmacopoeia
E. The NDA pipeline
drug
14.Orphan drugs are:
A. Drugs that are used to prevent or
treat a rare disease
B. Drugs that are used to prevent or
treat a disease common in orphan
children.
C. Drugs are that are imported from
foreign countries.
D. Drugs that do not have adverse
effects.
E. None
15. Which o f the following provide
information regarding orphan drugs?
A. Drug facts and comparisons
B. The national information center for
orphan drugs and rare diseases.
C. The physician’s desk reference
D. British pharmacopoeia
E. A and B
16. Which o f the following
abstracting/indexing services is known for
the information it provides about orphan
drugs?
A. Pharmaceutical news index
B. International pharmaceutical
abstracts
C. Science citation index
D. Drugdex
E. None
17. Which o f the following sources are
helpful for identification o f an unknown
drug (i.e. one that is in hand but not
identified)?
A.
B.
C.
D.
E.
Identidex
The manufacturer
Ident-A-Drug reference
A, B and C
A and B
18. All o f the following resources provide
information both on approved and
unapproved uses o f drugs EXCEPT:
A.
B.
C.
D.
E.
Drugs facts and comparisons
AFHS drug information
Drugdex
Clinical pharmacology
None
19. Which o f the following questions are
important to be asked if a patient
experiences any signs or symptoms o f a
possible adverse reaction?
A. How severe was the reaction.
B. When did the reaction appear?
C. Has the patient (or any member o f
the patient’s family) experienced
any allergic or adverse reactions to
medications in the past?
D. A, B and C
E. None
20. All o f the following references provide
information about stability o f a drug and its
compatibility with other drugs Except:
A. Trissel’s Stability o f compounded
formulations.
B. King’s Guide to parenteral
admixtures.
C. Trissel’s handbook on injectable
drugs.
D. Medline
E. None
21 .After identification o f a drug
information resource the step which follows
is:
A. Giving the final appropriate
response to the information inquirer.
B. Critical assessment o f the available
information.
C. To check whether the information
included in the source is also found
in other information resources.
D. To check the background o f the
author.
E. None
22. When evaluating a clinical study
involving patients which o f the following
questions help determine the profile o f the
study population?
A. Were healthy subjects or affected
patients used in the study?
B. Were the subjects volunteers?
C. What were the criteria for selecting
the subjects?
D. How many subjects were included,
and what is the breakdown o f age,
sex, and race?
E. All o f the above
23.If studying a group o f patients that
exhibits significant intrapatient variability,
researchers may divide the patients into
groups according to the variables likely to
be associated with responsiveness to
therapy. This is known as:
A.
B.
C.
D.
E.
Stratification
Segregation
Selection
Aggregation
None
24. Which o f the following statements is
FALSE about patient selection o f a clinical
study being evaluated?
A. Patient selection does not affect the
outcomes o f a clinical study.
B. If a disease state is being studied in
a clinical study, patients should
exhibit similar severity o f
symptoms.
C. By selecting patients with similar
characteristics, researchers can
avoid results that are caused by
individual differences among
patients.
D. Strong inter-individual differences
can obscure the results of the
experiment.
E. None
25. Details o f treatment for a drug used in a
clinical study may include which o f the
following:
A.
B.
C.
D.
E.
Daily dose
Frequency o f administration.
Route o f administration.
Dosage form.
All o f the above
26. All o f the following statements are true
about the characteristics o f retrospective
studies?
A. They look at events that have
already occurred to find some
common link between them.
B. They require reliance on patient
memories and require accurate
medical record.
C. They are useful for studying rare
diseases.
D. They are able to show cause and
effect.
E. None
27. Which o f the following are true about
prospective studies?
A. they look forward in time at a
question the study seeks to Answer:
choice
B. they can be observational
C. they can be experimental
D. A, B and C
E. B and C only
28. Which o f the following statements is
WRONG about crossover study design?
A. It may be used as an additional
control for interpatient and
intrapatient variability.
B. In this study a patient undergoes
each type o f treatment, and the
sequence in which the subjects
undergo treatment is reversed for
one group.
C. It reduces the possibility that the
results were strongly influenced by
the order in which therapy was
given.
D. It is not helpful in uncovering any
differences in responsiveness
between the groups due to patient
selection.
E. None
32. If statistical tests show no significant
difference between test groups, which o f
the following should be checked?
29. Which o f the following best describes
double blind study?
A. It means that the patients do not
know whether they received the
substance being studied or a placebo
and the people observing the
patients do not know who is a
subject and who is a control.
B. Only the people observing the
patients do not know who is a
subject and who is a control.
C. The publisher and the editor o f the
journal do not know who was a
subject and who was a control in a
clinical study.
D. Only the patients do not know
whether they received the substance
being examined or a placebo.
E. None
30. Placebos are:
i
A. Products containing less amount df
the active ingredient as compared tj>
the product under study.
B. products that are physically identical
to the active dosage form bein^
studied, but does not contain the
drug
I
C. Products containing more amount o f
the active ingredient as compared to
the product under study.
D. Products containing less amount o f
the active ingredient as compared tc
the product under study.
E. None
31 .Which o f the following measures helps
eliminate carry over effects when
comparing between drug therapies?
A.
B.
C.
D.
E.
Use o f parallel study design
Use o f controls.
Scheduling a run in period
Use o f more efficient instruments.
None
A. The number o f patients involved in
the study.
B. Conclusion o f the study.
C. Reputation o f members o f the
research team.
D. The aim o f the study.
E. None
33. In which o f the following situations
should a pharmacist be careful in giving
information to an information inquirer?
A. If a patient asks a pharmacist to
identify a tablet that is prescription
product known for a high rate o f
abuse.
B. If a patient asks a pharmacist to how
much dose o f the drug can be
increased.
C. If a patient asks a pharmacist about
the cost o f an OTC drug.
D. All o f the above
E. A and B only
34. Which o f the following statements is
INCORRECT?
A. Abstracts can give answers to all
drug related questions.
B. The inquirer o f drug related
information should be alerted o f a
possible delay when it takes longer
than anticipated to answer the
question.
C. Drug related information should be
organized before attempting to
communicate the response to the
inquirer.
D. When evaluating a clinical study,
description o f the physical setting in
which the study was conducted is
important.
E. None
Answers
Drug Information Resources
1. Answer: D. It should only be an information published in the USA.
Explanation:
Drug information is current, critically examined, relevant data, about drugs and drug use in a
given patient or situation.
2. Answer: D. A, B &C
Explanation:
Critically examined information should meet the following criteria:
-more than one source should be used when appropriate.
-the extent o f agreement o f sources should be determined
-the plausibility o f information, based on clinical circumstances should be determined.
3. Answer: E. A and B
Explanation:
There are three sources o f drug information: journals, (primary sources), indexing and abstracting
services (secondary sources), and textbooks (tertiary sources). British medical journal and Journal
o f pharmaceutical research are primary resources.
International Pharmaceutical abstracts and Iowa drug information system belong to the indexing
and abstracting services which are categorized under secondary sources.
4. Answer: E. A, B, and C
Explanation:
Primary drug information resources do not help the pharmacist decide the medical intervention
required for a particular patient (in fact this is not the job o f a pharmacist). Journals enable the
pharmacist to:
-keep up with new developments in pathophysiology, diagnostic agents, and therapeutic
regimens.
- Distinguish useful from useless or even harmful therapy.
-Enhance communication with other health-care professionals and consumers.
-Obtain continuing education credits.
- Keep abreast of professional news.
- prepare for board certification examination in pharmacotherapy, nutrition support etc.
5. Answer: A. There is no guarantee that the articles are accurate.
Explanation:
Although publication o f an article in a well-known, respected journal enhances the credibility o f
information contained in an article, this does not guarantee that the articles are accurate.
6. Answer: B. The interval o f time between publication o f an article and citation o f the article
'in an index.
Explanation:
Lag-time is the interval o f time between publication o f an article and citation o f that article in an
index.
7. Answer: C. The lag time for all indexirg /abstracting services is the same.
Explanation:
There is substantial difference in lag time anliong various indexing /abstracting services.
8. Answer: B. They are generally interpretations o f a study and may be a misinterpretation of
important information.
Explanation:
Indexing and abstracting services are primari ly used to locate journal articles. In general,
abstracts should not be used as primary sourc es o f information because they are generally
interpretations o f a study and may be a misi:rtterpretation o f important information. Pharmacists
should obtain and evaluate the original articl s because abstracts might not tell the whole story.
9. Answer: D. They are most reliable o f all information resources.
Explanation:
General reference textbooks can provide e asy and convenient access to a broad spectrum of
related topics. Background information on drugs and diseases is often available. Although a
textbook might answer many drug-related questions, the limitations o f these resources should not
be overlooked.
It could take several years to publish a text, so information available in textbooks might not
include the most recent developments in fhe field. Other resources should be to update or
supplement information obtained from textbooks.
The author o f a textbook might not have done a thorough search o f the literature, so pertinent data
could have been omitted. An author also rhight have misinterpreted the primary or secondary
literature. Reference citations should be available to verify the validity and accuracy o f the data.
10. Answer: B. The country where the book was published.
Explanation:
General considerations when examining ar d using textbooks as sources o f drug information
include:
- The year of publication (copyright date)
- The edition o f the text: is it the most current edition?
- The author, publisher, or both: what are the author’s and publisher’s track records?
- The presence or absence o f a bibliography: if a bibliography is included, are important
statements accurately referenced? When were the references published?
- The scope o f the textbook: how accessible is the information?
- Alternative resources that are available (e.g. primary and secondary sources, other relevant
texts).
The country o f publication o f the book is not important. (Examining the author’s and publisher’s
track records is more than enough)
]] . Answer: E. all o f the above
j
Explanation:
I
Information received from the internet may be as reliable as the person who posted it and the
users who read and comment on its content. A web site should be evaluated by its source (author)
o f information. The name, location, and sponsorship should be disclosed. Also, a reputable site
will provide an ease o f access to information and the ability to give feed back. Pharmacists should
use traditional literature evaluation skills to determine whether the information given in the
internet is clear, concise, unbiased, relevant and referenced.
12.Answer: D. Martindale: The complete drug reference
Explanation: Martindale: The complete drug reference is updated every 3 years.
13.Answer: D. United states pharmacopoeia
Explanation:
j
For investigational drugs the resources available are:
- Martindale: the complete Drug reference
- Drug facts and comparisons
;
- Unlisted drugs
|
- The NDA(new drug application) pipeline
The United States pharmacopoeia doe^ not provide information about new investigational drugs.
14.Answer: A. Drugs that are used t6 prevent or treat a rare disease
Explanation:
Orphan drugs are drugs used to prevent or treat a rare disease.
15.Answer: E. A and B
i
j
|
Explanation:
j
For orphan drugs the resources available are:
-Drug facts and comparisons
J
-The national information center for orphan drugs and rare diseases.
-Drugdex
The physician’s desk reference and the British pharmacopoeia do not exclusively provide
information regarding orphan drugs. |
16.Answer: D. Drugdex
Explanation:
j
Drugdex provides information aboilt orphan drugs.
17.Answer: D. A, B and C
Explanation:
For an unknown drug (i.e. one that is in hand but not identified),the following sources can be
consulted for help:
- The PDR, drug facts and comparisons! Drug topics Red book, Ident-A-Drug reference
- Identidex
- The manufacturer
Lexi-Comp’s clinical reference library-dru; y identification.
] 8.Answer: D. Clinical pharmacology
Explanation:
Clinical pharmacology studies the clinical use o f drugs. It is not concerned with the unapproved
uses o f drugs.
19. Answer: D. A, B and C
Explanation:
All o f the above are important questions if a patient experiences any signs or symptoms o f a
possible adverse reaction.
j
20.Answer: D. Medline
Explanation:
Medline is an abstracting/abstracting service which provides health related information. It does
not specifically provide information about stability and compatibility o f drugs.
I f the stability o f a drug, compatibility With other drugs, the administration technique, and the
equipment that holds it is required, the resources which might be referred to are:
-T rissel’s Stability o f compounded formulations.
- King’s Guide to parenteral admixtures.
- Trissel’s handbook on injectable drugs.
21 .Answer: B. Critical assessment o f th i available information.
Explanation:
After an information resource has been identified for required information; it is followed by
Critical assessment o f the available information. This step is critical in developing an appropriate
response.
22. Answer: E. All o f the above
Explanation:
When evaluating the subjects o f the study determining the profile o f the study population is by
looking for the following information:
- Were healthy subjects or affected patients used in the study?
- Were the subjects volunteers?
- What were criteria for selecting the subjects?
- How many subjects were included and kvhat is the breakdown o f age, sex, and race?
-What was the patient selection method, and who was excluded from the study?
23.Answer: A. Stratification
Explanation:
If studying a group o f patients that exhibits significant intrapatient variability, researchers may
divide the patients into groups according to the variables likely to be associated with
responsiveness to therapy. This is known as stratification.
24.
Answer: A. Patient selection does not affect the outcomes o f a clinical study.
Explanation:
Patient selection is one o f the important factors which affect the outcomes o f a clinical study.
25. Answer: E. All o f the above
Explanation:
For each drug being investigated, determine the following information:
1. Details o f treatment with the drug being studied
- Daily dose, Frequency o f administration, route o f administration, hours o f a day when
administered, source o f drug (i.e. supplier), dosage form, total duration o f treatment.
2. Other therapeutic measures in addition to the agent being studied
26. Answer: D. They are able to show cause and effect.
Explanation:
Retrospective studies look at events that have already occurred to find some common link
between, require reliance on patient memories and accurate medical records , and are unable to
show cause and effect. Retrospective studies are useful for studying rare diseases (or effects) and
can help to decide if enough information exists to warrant prospective examination o f a problem.
27. Answer: D. A, B and C
Explanation:
Prospective studies look forward in time at a question the study seeks to answer. They can be
observational or experimental (i.e. clinical trials).
28. Answer: D. It is not helpful in uncovering any differences in responsiveness between the
groups due to patient selection.
Explanation:
Crossover design may be used as an additional control for interpatient and intrapatient variability.
In this type o f study design, each patient group undergoes each type o f treatment. However, the
sequence in which the subjects undergo treatment is reversed for one group. Crossover design
reduces the possibility that the results were strongly influenced by the order in which therapy was
given. And because both groups o f patients receive both types o f treatment, any difference in
responsiveness between the groups due to patient selection will be uncovered.
29. Answer: A. It means that the patients do not know whether they received the substance
being studied or a placebo and the people Observing the patients do not know who is a subject
and who is a control.
Explanation:
In a double blinded clinical study both t le patients (the patients do not know whether they
received the substance being studied or i placebo) and the people are blinded (the people
observing the patients do not know who is a subject and who is a control).
30.Answer: B. products that are physical y identical to the active dosage form being studied,
but does not contain the drug.
Explanation:
Placebos are products that are physically idfentical to the active agent being studied. They do not
contain any therapeutic substance. (A drug plroduct minus the active ingredient).
31 .Answer: C. Scheduling a run in period
j
Explanation:
A run in period (wash out) is a period where the effects o f previous drug therapy are minimized,
so that its effects are not carried over to and nterfere with effects o f next drug given.
32.Answer: A. The number o f patients inv jived in the study.
Explanation:
I f statistical test results do not show signific ant difference between test groups, it is advisable to
check the whether there were enough patients or not. ( i.e statistical power).
33.Answer: E. A and B only
Explanation:
Response is not necessary if the inquirer intends to misuse or abuse information that is provided.
The inquirer often admits intent or offers clues to potential abuse, such as in the following
examples:
- A patient asks how a certain drug is dosed (i.e. how much the drug can be increased, when it
can be increased, what the maximum daily dose is). This kind o f inquiry signals that the
patient might be adjusting his or her owni therapy.
A patient asks a pharmacist to identify a tablet that is a prescription product known for a high
rate o f abuse.
34.Answer: A. Abstracts can give Answer bhoices to all drug related questions.
Explanation:
j
The pharmacist should use more than abstracts to answer drug information questions because
they might be taken out o f context and do not include all of the data available in the original
article. ~
Drug Interactions
“ Most of the important things in the world have been accomplished by people who have
kept on trying when there seemed to be no hope at all. “
Dale Carnegie
1. Which o f the following is/are true about
drug interaction?
A. It refers to the altered response o f a
drug as a result o f administration o f
another substance
B. It may be employed to improve
therapeutic response
C. it may be used to decrease adverse
drug effects
D. It may be harmful to the patient
E. all o f the above
2. A precipitant drug is
A. The drug affected by the
B. The substance which
interaction negatively
C. The substance which
interaction positively
D. The substance which
interaction
E. A and C
interaction
affects the
affects the
Drug-blood protein interaction
Food-drug interaction
Chemical-drug interaction
Drug-laboratory interaction
Drug-drug interaction
4. The interaction caused by a chemical or
physical incompatibility when two or more
drugs are mixed together is called
A.
B.
C.
D.
E.
Pharmacodynamic interaction
Pharmacokinetic interaction
Pharmaceutical interaction
Pharmacodynamic interaction
B and D
6. Which o f the following is not true about
the effect o f drug-interaction up on the
absorption o f drugs?
A. Drug interaction always results in
decreased rate o f absorption
B. Drug interaction always decreases
bioavailability o f drugs
C. The extent o f drug absorption is not
affected by drug-interaction
D. Only drug absorption from the GIT
is affected by drug-interaction
E. All o f the above
causes the
3. Drug interaction includes all o f the
following except
A.
B.
C.
D.
E.
A.
B.
C.
D.
E.
Pharmacokinetic interaction
Biopharmaceutical interaction
Pharmacodynamic interaction
Pharmaceutical interaction
Chemical- drug interaction
5. The precipitation o f phenytoin sodium
from a solution that has an acidic pH, such
as dextrose 5% is classified as
7. Which o f the following is a wrong
match between a precipitant drug and the
kind o f drug interaction it is involved?
A. Cholestyramine; adsorption
B. Anticholinergic drugs; decreased GI
motility
C. Antacids; alteration o f gastric pH
D. Antibiotics; alteration o f intestinal
flora
E. None o f the above
8. Activated charcoal decreases the
bioavailability o f many drugs because
A.
B.
C.
D.
It increases the intestinal motility
It decreases the pH o f the GI tract
It has the ability to adsorb drugs
It has the ability to form chelation
with drugs
E. All o f the above
9. The type o f drugs that are more likely to
be affected by laxatives and cathartics
include
A. Drugs that are absorbed slowly
B. Controlled release drugs
C. Drugs that are metabolized in the
small intestine
D. Drugs that are degraded in the
stomach
E. A and B
10.Digoxin has better bioavailability if
administered after erythromycin. This is
because,
A. Erythromycin decreases the gastric
pH
B. Erythromycin decreases the GI
motility
C. Erythromycin reduces the bacterial
inactivation o f digoxin
D. Erythromycin decreases the stomach
degradation o f digoxin
E. All o f the above
11 .Digoxin administration often increases
the bioavailability o f many object drugs in
case o f CHF. This is because
A. Digoxin increases blood flow into
GI
B. Digoxin decreases the rate renal
excretion o
C. Digoxin
decreases
hepatic
metabolism
D. Digoxin decreases acid secretion
from stomach
E. All o f the above
12.Calcium, magnesium or aluminum and
iron salts are known to cause the following
that can lead to drug interaction.
A.
B.
C.
D.
Inhibition o f drug metabolism
Alteration of gastric pH
Complexation/chelation
Competition for carrier mediated
drug absorption
E. B and C
13.Digoxin toxicity can be enhanced by
concurrent administration o f quinidine.
This is because
A. Quinidine inhibits the metabolism o f
digoxin
B. Quinidine displaces digoxin from
plasma protein binding site
C. Quinidine displaces digoxin from
tissue binding site
D. Quinidine binds with digoxin
inhibiting protein binding o f digoxin
E. A and C
14. Which o f the following affect hepatic
drug metabolism,
A. Enzyme induction
B. Enzyme inhibition
C. Substrates competition for the same
metabolizing enzymes
D. Change in hepatic blood flow
E. All o f the above
15. A patient taking the drug cyclosporine is
advised not to take St.John’s wort since
A. St. John’s wort induces the enzyme
that metabolize cyclosporine so that
there is accumulation o f the toxic
metabolite o f the drug
B. St. John’s wort inhibits the enzyme
responsible for the metabolism o f
cyclosporine thus leading to toxic
accumulation o f the drug
C. St. John’s wort induces the enzyme
that
metabolizes cyclosporine
resulting in sub-therapeutic level o f
the drug
D. St.John’s wort inhibits the
clearance o f cyclosporine as a result
o f which there increased level o f the
drug
E. B and D ,
16.Grape juice should be avoided when
taking one o f the following drugs
A.
B.
C.
D.
E.
Cimetidine
Cyclosporine
Isoniazid
Saquinavir
All o f the above
17.The effect o f methylxanthines upon
many drugs is
A.
B.
C.
D.
E.
To increase the blood level
To increase the metabolism
To increase renal excretion
To increase extrarenal excretion
All o f the above
18. Which o f the following is/are the
effect(s) o f antacids up on salicylates
A. They increase the ionization o f
salicylates
B. They
decrease
the
tubular
reabsorption o f salicylates
C. They increase the clearance o f
salicylates
D. B and C
E. A, B and C
19.The fact that probenecid can increase
the blood levels o f penicillin and some
cephalosporin antibiotics is attributed to
A.
B.
Its ability to increase renal perfusion
Its ability to decrease glomerular
filtration rate
C. Its ability to increase the urine pH
D. Its ability to increase tubular
reabsorption o f these drugs
E. Its ability to block active tubular
secretion o f these drugs
20. Which o f the following herbal
preparations should be avoided in patients
taking warfarin?
A. ginger
B. wheat grass
C. feverfew
D. garlic
E. all the above
21 .The type and extent o f interaction
between herbs and drugs is directly
influenced by
A. The stage o f growth during which
the herb was harvested
B. The solvents used in extraction o f
the herb
C. The shelf life o f the herbal extract
D. The relative potency o f each
constituents in the herb
E. All o f the above
22. Which o f the following is not true about
food-drug interaction?
A. Food can increase, decrease or not
affect the absorption o f drugs
B. The effect o f food upon the
bioavailability o f drugs is more
pronounced for modified release
dosage forms than for immediate
release ones
C. Foods do not antagonize drugs
pharmacologically.
D. Food can compete for metabolizing
enzyme with other drugs
E. None o f the above
23. The metabolism o f one o f the following
drugs is not affected by smoking.
A.
B.
C.
D.
E.
Theophylline
Penicillin
Diazepam
Amitriptlylin
None o f the above
24. Which o f the following is not true about
the effect o f alcohol upon the metabolism
o f drugs?
I .Alcohol increases the activity of
hepatic drug metabolizing enzymes
II Alcohol decreases the activity of
hepatic drug metabolizing enzymes
III Acute alcohol intoxication can inhibit
hepatic enzymes in nonalcoholic
individuals
A.
B.
C.
D.
E.
I only
I and III
II and III
II only
I, II and III
25. Which o f the following are examples of
pharmacodynamic type o f drug-drug
interactions?
A.
B.
C.
D.
E.
Alcohol and antihistamines
Thiazide derivatives and digoxin
Aspirin and warfarin
Promethazine
All o f the above
26.One o f the following would be expected
to trigger drug interaction
A.
B.
C.
D.
E.
Multiple-drug therapy
Multiple prescribers
Patient compliance
Patient age
all o f the above
27. Which o f the following is not true about
the clinical significance o f drug-drug
interaction?
A. All drug interactions are clinically
significant
B. Not all drug interactions cause
adverse effects
C. Sometimes it is possible to prescribe
interacting drugs
D. Drug interactions could be exploited
to reduce adverse effects
E. Therapeutic efficiency could be
improved by administrating
interacting drugs
28. Which o f the following combination o f
drugs does not have beneficial effects?
A. Trimethoprim and sulfamethoxazole
B. Amoxicillin
and
clavulanate
potassium
C. Phenobarbital and Warfarin
D. Hydrochlorothiazide
and
triamterene
E. None
29. Which o f the following is a wrong
match between a class o f the likelihood o f a
drug interaction and its definition?
A. Established - a drug interaction
supported by well-proven clinical
studies
B. Probable - a drug interaction that
could occur; limited date available
C. Suspected - a drug interaction that
might occur; some date might be
available
D. Unlikely - a drug interaction that is
doubtful; no good evidence o f an
altered clinical effect is available.
E. None o f the above
30. One o f the following is not needed to be
considered in the clinical relevance o f a
potential drug interaction.
A.
B.
C.
D.
E.
Size o f the dose
Dosage form
Extrapolation to related drugs
Onset o f the potential interaction
Duration o f the therapy.
ANSWERS
Drug interactions
1. Answer: E.all of the above
Explanation:
Drug interaction refers to an altered drug response produced by the administration o f a drug or
co-exposure of the drug with another substance, which modifies the patient’s response to the
drug. Some drug interactions are intentional in order to provide improved therapeutic response or
to decrease adverse drug effects.
2. Answer: D. The substance which causes the interaction.
Explanation:
A precipitant drug is the drug, chemical, or food element causing the interaction. The drug
affected by the interaction is known as an object drug.
3. Answer: A. Drug-blood protein interaction.
Explanation:
Drug interactions include drug-drug interaction, drug-herbal interaction, food-drug interaction,
chemical drug interaction, and drug-laboratory interaction. The interaction between drugs and
blood proteins is not considered as a type o f drug interaction since by definition drug-interaction
is between drugs and other drugs or substances and not with body components/molecules.
4. Answer: D. Pharmaceutical interaction.
Explanation:
The interaction which occurs when the absorption, distribution, (protein and tissue binding), or
elimination (excretion and/or metabolism) o f the drug us affected by another drug, chemical or
food element is called pharmacokinetic or biopharmaceutical interaction. Pharmacodynamic
interactions occur when the pharmacodynamic effect o f the drug is altered by another drug,
chemical or food element producing an antagonistic, synergistic, or additive effect.
Pharmaceutical interactions are those caused by a chemical or physical incompatibility when two
or more drugs are mixed together.
5. Answer: C. Pharmaceutical interaction.
Explanation:
Pharmaceutical interactions can occur during the extemporaneous preparation o f drugs, including
preparation o f IV solutions. For example, the interaction between phenytoin sodium and the
acidic dextrose 5% solution can lead to the precipitation o f the former. This is typical example of
pharmaceutical interaction.
6. Answer: E. All o f the above.
Explanation:
Drug-interactions can affect the rate and the extent o f drug absorption (bioavailability) from the
absorption site, resulting in increased or decreased drug bioavailability. The most common drug
absorption site is in the GI tract. However, drug bioavailability from other absorption sites, such
as the skin, can be affected by drug interactions. For example, epinephrine, a vasoconstrictor, will
decrease the percutaneous absorption o f lidocaine, a local anesthetic agent.
7. Answer: E. None o f the above
Explanation:
All the given choices are correct.
8. Answer; C. It has the ability to adsorb drugs.
Explanation:
Activated charcoal has the ability to adsorb many drugs thus decreasing the amount o f drugs
available for absorption and therefore, decrease their bioavailability. Other precipitant drugs with
similar properties are cholestyramine and kaolin.
9. Answer: E. A and B.
Explanation:
The effect o f laxatives and cathartics is to increase the GI motility. GI motility decreases the
bioavailability o f drugs that are absorbed slowly. It may also affect the bioavailability o f drugs
from controlled-release drugs.
10. Answer: C. Erythromycin reduces the bacterial inactivation o f digoxin
Explanation:
Antibiotics like erythromycin have the ability to decrease the microbial flora o f the GI tract. Since
digoxin is one o f the drugs that are degraded by the intestinal bacteria, it’s bioavailability will be
increased if these bacteria are reduced by administering drugs like erythromycin.
11 .Answer: A. Digoxin increases blood flow into GI.
Explanation:
In congestive heart failure, the blood flow to the GJ tract is poor and an orally administered drug
can have a slower rate o f bioavailability. After digoxin therapy, the perfusion o f the GI tract is
improved along with bioavailability o f the object drug.
12.Answer: E. B and C.
Explanation:
Levofloxacin complexes with divalent cations (Ca, Mg, Al, Fe) causing a decreased
bioavailability. Antacids increase gastric pH, which can lead to reduced dissolution o f drugs like
ketoconazole and omeprazole.
13.Answer: C. Quinidine displaces digoxin from tissue binding site.
Explanation:
The distribution o f the drug may be affected by plasma protein binding and displacement
interactions or tissue and cellular interactions. For example, Valproic acid displaces phenytoin
from plasma protein-binding sites and reduces hepatic phenytoin clearances by inhibiting the
liver’s metabolism of phenytoin. Aspirin decreases protein binding and inhibits the metabolism of
valproate. Quinidine reduces digoxin clearance and displaces digoxin from tissue-binding sites,
leading to a higher plasma digoxin concentration and reduces distribution volume. This can result
in enhanced digoxin toxicity by concurrent administration o f quinidine.
14.
Answer: E. All o f the above
Explanation:
The metabolism o f drugs by liver is affected by such factors as the induction or inhibition of
enzymes involved. Many drugs that share the same drug-metabolizing enzymes have also the
potential for a drug interaction. A decrease in the hepatic blood flow can decrease the hepatic
clearance for high extraction drugs, such as propranolol and morphine.
15.Answer: C. St. John’s wort induces the enzyme that metabolizes cyclosporine resulting in
sub-therapeutic level o f the drug
Explanation:
Over the counter (OTC) drugs and herbal preparations can also be involved in CYP450
isoenzyme metabolism and can cause serious drug-herbal interactions. For example, St. John’s
wort may induce CYP3A4 isoenzymes and decrease cyclosporine to sub-therapeutic levels.
16.Answer: D. Saquinavir.
Explanation:
Foods may interfere with hepatic drug metabolism. For example, grape juice is a powerful
inhibitor of the CYP3A4 isoenzyme, and will increase blood levels o f saquinavir if taken
together.
17.Answer: C. To increase renal excretion.
Explanation:
Renal drug clearance can be affected by changes in glomerular filtration, tubular reabsorption,
active drug secretion, and renal blood flow and nephrotoxicity. For example, methylxanthines
(e.g., caffeine, theobromine) increase renal blood flow and GRF will decrease time for absorption
o f various drugs, leading to more rapid urinary drug excretion.
18.Answer: E. A,B and C
Explanation:
Antacids (and sodium bicarbonate) increase the pH of urine. This alkalization o f urine pH
results in increased ionization o f the salicylates, decreased reabsorption, and thus increases the
clearance o f salicylates. Other drug affected by antacids and sodium bicarbonate is amphetamine.
Alkalization o f the urine due to the antacids/sodium bicarbonate increases the reabsorption o f
amphetamine and decreases its clearance.
19.
Answer: E. Its ability to block active tubular secretion of these drugs.
Explanation:
Probenecid has the ability to block the active tubular secretion o f these drugs, thus decreasing
their renal clearance and thereby increase the blood levels of these drugs.
20. Answer: E. all the above.
Explanation:
Ginger, wheat grass, feverfew, and garlic are known to increase the bleeding time in patients
taking warfarin. Therefore, patients on warfarin treatment should avoid these herbal
preparations.
21 .Answer: D. The relative potency o f each constituents in the herb.
Explanation:
In herbal-drug interactions, the predominant effect or interaction depends upon the relative
potency o f each constituent in the herb. Potency is affected by a variety o f factors which include,
the stage o f growth during which the herb was harvested, the solvents used in extraction o f the
herb, the shelf life and storage condition o f the herbal extract, and drying time.
22. Answer: C. foods do not antagonize drugs pharmacologically
Explanation:
There are examples in which food pharmacologically antagonize the effect of drugs. Spinach and
broccoli provide dietary sources o f vitamin K, which antagonize the effect o f warfarin.
23.Answer: B. Penicillin.
Explanation:
Smoking by inhaling aromatic polycyclic hydrocarbons can increase the intrinsic clearance
(enzyme induction) o f drugs such as theophylline, diazepam, and tricyclic antidepressants (e.g.,
amitriptlyn).
24.Answer: E. I, II and III.
Explanation:
Alcohol can increase or decrease the activity o f hepatic drug metabolizing enzymes. Chronic
alcoholism can increase the rate o f metabolism o f tolbutamide, warfarin, and phenytoin. Acute
alcohol intoxication can inhibit hepatic enzymes in nonalcoholic individuals.
25.
Answer: E. All o f the above
Explanation:
Drugs that have similar pharmacodynamic actions may produce an excessive pharmacological or
toxic responses. For example, central nervous system depressants, such as the combination o f
alcohol and anthistamines (e.g., chlorpheniramine) can produce increased drowsiness in the
patient. The alteration o f electrolyte concentrations produced by a diuretic, such as a thiazide
derivative, will deplete potassium, resulting in sensitization o f the heart to digoxin therapy. By
inhibiting platelet aggregation, aspirin increases the risk o f bleeding in patients on anticoagulant
(e.g., warfarin, dicoumarol, clopidogrel) therapy.
26. Answer: E. All of the following
Explanation:
Multiple drug therapy, including both prescription and nonprescription (OTC) medication, can
potentially lead to drug interaction. The more drugs used by a patient, the greater the potential for
a drug interaction in the patient. Patients can be seen by different prescribes who prescribe
interacting medication. Patients need to follow proper instruction for taking medications. For
example, a patient might take tetracycline with food rather than before meals. Older patients are
at more risk for drug interactions than younger patients. Older patients might have changes in
their physiological and pathophysiological condition that lead to altered body composition,
altered GI transit time and drug absorption, decreased protein binding, altered distribution, and
decreased drug clearance. Patients with predisposing illness (diabetes, AIDS, asthma and
alcoholism) and patients who are clinically hypersensitive (atopic) are more at risk for drug
interaction than non-atopic patients.
27. Answer: A. All drug interactions are clinically significant.
Explanation:
Not all drug interactions are clinically significant and not all drug interactions could cause
adverse effects. In some cases, interacting drugs can be prescribed for patients as long as the
patient is given proper instructions and is complaint. For example, cimetidine and antacid might
be prescribed to the patient, but the patient should be instructed not to take both medications at
the same time. Combination o f interacting drugs may be used to improve the therapeutic
objective or to decrease adverse effects.
28.Answer: C. Phenobarbital and Warfarin.
Explanation:
Phenobarbital and Warfarin should not be administered simultaneously, since phenobarbital
increases the metabolism o f Warfarin making its blood concentration below the therapeutic level.
Trimethoprim and sulfamethoxazole are combination antibiotics that may be used for increased
efficacy in urinary tract infection. The combination o f amoxicillin and clavulanate potassium is a
combination in which a P-lactamase inhibitor (clavulanate) is used to inhibit the break down of
amoxicillin. Hydrochlorothiazide and triamterene constitute a combination o f a diuretic and
antihypertensive to minimize potassium excretion.
29. Answer: B. Probable - a drug interaction that could occur; limited date available.
Explanation:
A probable likelihood o f drug interaction is one in which a drug interactions is very likely but
might not be proven clinically. If the situation is such that, a drug interaction could occur but only
limited data is available, the likelihood is called possible.
30.Answer: B. Dosage form
Explanation:
The clinical relevance o f a potential drug interaction should also consider size o f the dose and the
duration o f therapy; onset (rapid, delayed) and severity (major, moderate, minor) o f the potential
interaction; and extrapolation to related drugs. The dosage form is less important in drug
interaction.
Endocrinology & Related Drugs
pv
The minute you settle for less than you deserve, you get even less than you settled
for.
Maureen Dowd
1. Which one o f the following is
posterior pituitary hormone?
A. growth hormone
B. human chorionic gonadotropin
C. vasopressin
D. thyrotropin
E. none o f the above
2. Which one o f the following anterior
pituitary hormones is used
therapeutically?
A.
B.
C.
D.
E.
thyrotropin
menotropin
human chorionic gonadotropin
leuteinizing hormone
all
6. A hormone that plays an important
role in the induction o f labor is
A.
B.
C.
D.
E.
vasopressin
oxytocin
menotropin
corticotropin
urofollitropin
7. Which one o f the following
hormones is present in the urine o f
pregnant woman?
A.
B.
C.
D.
urofollitropin
corticotropin
thyroid-stimulating hormone
human chorionic
gonadotropin(HCG)
E. all o f the above
3. Thyrotropin is
A. adrenocorticotropic hormone
B. somatotropin
C. thyroid-stimulating hormone
D. follicle-stimulating hormone
E. none o f the above
4. One o f the following hormones has
high FSH-like activity
menotropin
urofollitropin
human chorionic gonadotropin
human menopausal
gonadotropin
E. luteneinizing hormone
A.
B.
C.
D.
5. All o f the following are
therapeutically important pituitary
hormones .EXCEPT
A. growth hormones
B. corticotropin
C. urofollitropin
D. oxytocin
E. none o f the above
8. Corticotropin is used
A. to treat post operative
abdominal distention
B. to control postpartum bleeding
and hemorrhage
C. to induce spermatogenesis
D. for the diagnosis and
differentiation o f primary and
secondary adrenal
insufficiency
E.
none o f the above
9. One o f the following hormones is
used to treat neurogenic diabetes
insipidus
A.
B.
C.
D.
E.
vasopressin
menotropins
oxytocin
corticotropin
none o f the above
10.All are adverse effects associated
with the use of oxytocin, EXCEPT
A.
B.
C.
D.
E.
Gynecomastia
uterine hypertonicity
water intoxication
neonatal jaundice
post partum haemorrhage
11 .Most o f the natural and synthetic
gonadal hormones are derivatives of
A. cyclopentanoperhydrophenanthr
ene
B. bipyridine
C. sulfamoylbenzamide
D. phenylcyclopropylamine
E. aromatic amino acids
A. clomiphene
B. chlorotrianisene
C. tamoxifen citrate
D. toremifene citrate
E. fulvestrant
16.Estrogen receptors are found in
A. hypothalamus
B. mammary glands
C. anterior pituitary
D. uterus
E. all o f the above
17. All are therapeutic uses o f estrogens,
EXCEPT
12. Steroid hormones that have aromatic
A ring is
A.
B.
C.
D.
E.
progestin
estrogen
androgen
gonadotropin
none o f the above
13.The two estradiol derivatives that are
used as oral contraceptives are
A. ethinyl estradiol and mestranol
B. estradiol cypionate and estradiol
valerate
C. estrone and estriol
D. diethylstilbestrol and quinestrol
E. estrone and quinestrol
14.All are nonsteroidal synthetic
estrogens EXCEPT
A. dienestrol
B. chlorotrianisene
C. quinestrol
D. diethylstilbestrol
E. none o f the above
15.One o f the following is not estrogen
antagonist
A .acne
B.
osteoporosis
C. anemia
D. urogenital atrophy
E. vasomotor disorders
18. One o f the following is estrogen
antagonist that is used to treat estrogen
dependent breast cancer
A. clomiphene
B. tamoxifen
C. quinestrol
D. none
19. Which one o f the following is
steroidal irreversible inhibitor of
aromatase?
A. anastrozole
B. exemestane
C. letrozole
D. raloxifene
E. none o f the above
20. Which one o f the following is
selective estrogen receptor modulator?
A. raloxifene
B. anastrozole
C. clomiphene
D. fulvestrant
E. letrozole
21 .Selective estrogen receptor
modulators( SERMs) are used for the
prevention of
A. breast cancer
B. hepatic adenomas
C. osteoporosis
D. endometrial cancer
E. all o f the above
22. Which class o f drugs is used to treat
advanced breast cancer?
A. estrogens
B. selective estrogen receptor
modulator
C. antiestrogens
D. aromatase inhibitors
E. progestins
25. One o f the following is structurally
classified as androgen but contains
progestational activity
A. norethindrone
B. fluoxymesterone
C. dromostanolone
D. oxandrolone
E. none o f the above
26.Progestins are used therapeutically
for all, EXCEPT
A. oral contraceptives
B. breast cancer
C. endometriosis
D. uterine bleeding
E. none o f the above
27. Which o f the following is the adverse
effect o f progestin?
A. irregular menses
B. amenorrhea
C. exacerbation o f breast carcinoma
D. weight gain and oedema
E. all o f the above
23. Which one o f the following is a
naturally occurring progestin?
A. megestrol
B. progesterone
C. medroxyprogesterone
D. norethindrone
E. norethynodrel
28.One o f the following is a naturally
occurring androgen
A. fluoxymesterone
B. oxandrolone
C. testosterone
D. progesterone
E. A and C
24. Which one o f the following is a 17 ahydroxyprogesterone derivative?
A.
B.
C.
D.
E.
norethindrone
ethynodiol diacetate
norgestrel
megestrol acetate
mestranol
29.Drug that have enhanced anabolic
effect than androgenic effect is
A. testosterone
B. fluoxymesterone
C. dromostanolone
D. nilutamide
E. none o f the above
30.The enzyme that converts
testosterone to dihydrotestosterone is
A. 5 a-reductase
B. aromatase
C. esterase
D. 5-p-reductase
E. none o f the above
31. Which one o f the following
compounds is incorrectly matched with
its therapeutic use?
A. flutamide - treatment o f
prostate cancer
B. oxandrolone - anemia
C. dromostanolone - oral
contraceptive
D. finasteride - benign prostatic
hyperplasia
E. finasteride —androgenic
alopecia
32. Which o f the following is the adverse
effect o f androgens
A.
B.
C.
D.
psychological changes
liver disorders
decreased fertility in male
development o f masculine
features in females
E. all o f the above
33. All are antiandrogens, EXCEPT
A. flutamide
B. bicalutamide
C. finasteride
D. nilutamide
E. none o f the above
B. flutamide - antiandrogens
C. nilutamide - inhibit the action
o f androgens by competitively
binding to androgen receptors in
the target tissue
D. bicalutamide - inhibits the
conversion o f testosterone to 5
a-dihydrotestosterone
E. none o f the above
35.The therapeutic use o f 5 a-reductase
inhibitors is
A. androgenic alopecia
B. anabolic therapy
C. breast cancer
D. endometriosis
E. oral contraception
36.Antiandrogens are therapeutically
used for
A. anabolic therapy
B. treatment o f prostate cancer
C. menstrual disorder
D. oral contraceptive
E. none of the above
37.
A drug which has increased
glucocorticoid activity without an
increase in the mineralocorticoid
activity is
A. hydrocortisone
B. prednisolone
C. dexamethasone
D. fludrocortisone
E. cortisone
38.Fludrocortisone has
34.All the following compounds are
matched to the correct mechanism of
action, EXCEPT
A. finasteride - 5 a-reductase
inhibitor
A. increased glucocorticoid and
decreased mineralocorticoid
activity
B. increased mineralocorticoid and
decreased glucocorticoid
activity
C. increased mineralocorticoid and
glucocorticoid activity
D. decreased mineralocorticoid and
glucocorticoid activity
E. none o f the above
39.Fluorination o f hydrocortisone and
cortisone at position C-6
A. increases both mineralocorticoid
and glucocorticoid activity
B. increases mineralocorticoid and
decreases glucocorticoid
activity
C. increases glucocorticoid activity
and decreases mineralocorticoid
activity
D. increases glucocorticoid activity
with less effect on
mineralocorticoid activity
E. decreases both glucocorticoid
and mineralocorticoid activity
40.
Which one o f the following is
prototypical glucocorticoid?
A. hydrocortisone
B. prednisolone
C. aldosterone
D. fludrocortisone
E. prednisone
41 .The prototypes cortisone and
hydrocortisone are modified to
A. increase the glucocorticoid
activity only
B. increase both glucocorticoid and
mineralocorticoid activity
C. increase the glucocorticoid
activity and decrease the
mineralocorticoid activity
D. decrease both glucocorticoid
and mineralocorticoid activity
E. decrease glucocorticoid and
increase mineralocorticoid
activity
42. Which one o f the following drugs
has enhanced topical absorption?
A. fluprednisolone
B. fluocinonide
C. prednisolone
D. dexamethasone
E. none o f the above
43.Aldosterone is formed in
A. middle layer o f the adrenal
cortex
B. outer layer o f the adrenal cortex
C. fascicular o f the adrenal cortex
D. B and C
E. none o f the above
44. Which one of the following drugs are
clinically useful mineralocorticoids?
A. triamcinolone and fluocinonide
B. desoxycorticosterone acetate
and dexamethasone
C. fludrocortisone acetate and
fluprednisolone
D. desoxycorticosterone acetate
and fludrocortisone acetate
E. desoxycorticosterone acetate
and fluprednisolone
45. Which o f the following
glucocorticoid has the least
mineralocorticoid activity?
A.
B.
C.
D.
E.
cortisone
dexamethasone
fludrocortisone
prednisolone
hydrocortisone
46.Adrenocorticosteroids are
therapeutically used for
A. treatment o f collagen vascular
diseases
B. inflammatory ocular disorders
C. treatment o f rheumatic carditis
D. nephritic syndrome
E. all o f the above
47.All are adverse effects associated
with the use o f adrenocorticosteroid ,
EXCEPT
A. suppression o f pituitary-adrenal
integrity
B. cholestatic jaundice
C. increased intraocular and
intracranial pressures
D. cushingoid “moon face” and
“buffalo hump”
E. ulcerative esophagitis
4 8.The enzyme that converts
levothyroxine T4 to liothyronine T3 is
A.
B.
C.
D.
E.
5 a-reductase
iodoperoxidase
5'-deiodinase
5’-iodinase
none
49. Which one o f the following is the
hormone that stimulates the production
o f T4 and T3 by the thyroid gland?
I. thyroid stimulating hormone
II. thyrotropin - releasing hormone
III. thyrotropin
A.
B.
C.
D.
E.
I only
II only
I & II
II and III
I & III
50.A thyroid preparation which is
highly purified and lyophilized
thyrotropic hormone isolated from
bovine anterior pituitary gland is
A. thyroid
B.
C.
D.
E.
liotrix
thyroglobulin
thyrotropin
none o f the above
51 .One o f the following thyroid
hormones is less potent but has a longer
duration o f action
A.
B.
C.
D.
E.
thyrotropin
levothyroxine
thyroglobulin
liothyronine
none o f the above
52.The administration o f levothyroxine
sodium can produce the natural ratio o f
A.
B.
C.
D.
E.
4 to
4 to
3 to
3 to
2 to
1 o f T4 to T3
I o f T3 to T4
1 o f T3 to T4
1 o f T4 to T3
1 o f T4 to T3
53. Which one of the following is NOT a
true statement?
A. levothyroxine and liothyronine
are naturally occurring thyroid
hormones
B. levothyroxine can be converted
to liothyronine in the peripheral
circulation
C. levothyroxine is more potent
than liothyronine
D. the plasma concentration of
liothyronine is less than that of
levothyroxine
E. levothyroxine is less potent than
liothyronine
54.All are thyroid function inhibitors,
EXCEPT
A. propylthiouracil
B. liotrix
C. methimazole
B.
C.
D.
E.
D. lugol’s solution
E. none o f the above
radio active iodine
ionic inhibitors
lugol’s solution
methimazole
55.A drug that inhibits the conversion o f
T4 to T3 is
60. One o f the following drugs decreases
the absorption o f thyroid hormones?
A. lugol’s solution
B. radioactive iodine
C. methimazole
D. propylthiouracil
E. none o f the above
A.
B.
C.
D.
E.
56. A thyroid inhibitor that interferes
with the concentration o f iodide ion by
the thyroid gland is
A.
B.
C.
D.
E.
thiourylenes
radioactive iodine
ionic inhibitors
iodides in high concentrations
all o f the above
57.Thyroid hormone preparations are
therapeutically indicated for
A.
B.
C.
D.
E.
hypothyroidism
myxedema coma
cretinism
simple goiter
all
'
phenytoin
carbamazepine
ferrous sulfate
rifampin
isoniazid
61 .Over dosage o f thyroid hormones
can cause
A.
B.
C.
D.
E.
hypothyroidism
palpitation
agranulocytosis
Bradycardia
all
62.A thyroid inhibitor with possible
effects on the future offspring o f young
adults is
A.
B.
C.
D.
E.
ionic inhibitor
iodides
radioactive iodine
methimazole
none
58.A drug that is used in the detection
and treatment o f thyroid cancer is
A.
B.
C.
D.
E.
levothyroxine
liothyronine
thyrotropin
methimazole
all o f the above
59.A thyroid inhibitor that is
particularly used in treating
hyperthyroidism in older patients and in
patients with heart disease is
A. thiourylenes
63.A drug which accelerates thyroid
metabolism is
A.
B.
C.
D.
E.
carbamazepine
iron
sucralfate
calcium
none o f the above
64. A class o f thyroid inhibitors that has
the following adverse effect- urticarial
papular rash, dermatitis,
agranulocytosis, thrombocytopcnia,
granulocytopenia, pain, stiffness in the
joints, headache and paresthesias is
A.
B.
C.
D.
E.
thyrotropin
thiourylenes
iodides
ionic inhibitors
propylthiouracil
65.How many polypeptide chains are
present in insulin?
A.
B.
C.
D.
E.
3
2
4
1
5
66.Human insulin are prepared by
] - mixing both bovine and porcine
insulin
II- enzymatic conversion o f the
terminal amino acid o f porcine
insulin
III- recombinant DNA technology
A.
B.
C.
D.
E.
I & II
1 & III
II & III
III only
II only
67.The solubility o f insulin at the
injection site depends on
A.
B.
C.
D.
E.
the zinc content
the nature o f the buffer
the physical state
protein content
all
68.Insulin that can be given
intravenously is
D. regular insulin
E. all o f the above
69.Regular insulin can be mixed with all
other insulin, EXCEPT with
A. PZI (protamine zinc insulin)
B. semilente insulin
C. insulin glargine
D. ultralente insulin
E. none o f the above
70. Which one o f the following is long
acting insulin?
A.
B.
C.
D.
E.
lispro insulin
insulin glargine
insulin aspart
lente insulin
all o f the above
71 .Which insulin is a mixture o f 70%
ultralente crystals and 30% semilente
powder?
A.
B.
C.
D.
E.
NPH( isophane insulin)
PZI(protamine zinc insulin)
Insulin aspart
insulin zinc suspension
none o f the above
72.Which one o f the following is a
second generation sulfonylurea oral
hypoglycemic agent?
A.
B.
C.
D.
E.
tolazamide
glimepride
chlorpropamide
tolbutamide
none
73.Lente insulin cannot be mixed with
A. insulin aspart
B. lispro insulin
A. insulin aspart
B. insulin glargine
C. semilente insulin
C. protamine zinc insulin
D. lispro insulin
E. al o f the above
74.Which is a biguanide oral
hypoglycemic agent that is still available
in the market?
A.
B.
C.
D.
E.
metformin
phenformin
nateglinide
precose
none o f the above
C. sulfonylureas
D. inhibitors o f a-glucosidase
E. biguanides
79. Which one o f the following is a
tetrasaccharide inhibitor of aglucosidase?
A.
B.
C.
D.
E.
miglitol
metformin
acarbose
glibenclamide
all
75.Oral hypoglycemic agent that is a
basic compound is
A.
B.
C.
D.
E.
sulfonylureas
biguanide
thiazolidinediones
meglitinide
none o f the above
76.Repaglinide and nateglinide belong
to which class o f oral hypoglycemic
agent?
A.
B.
C.
D.
E.
biguanide
sulfonylurea
meglitinides
thiazolidinediones
none
77. An oral hypoglycemic agent that is
withdrawn form the market because of
rare but severe hepatic toxicity is
A.
B.
C.
D.
E.
rosiglitazone
troglitizone
pioglitazone
repaglinide
phenformin
78.Repaglinide belongs to which class
o f oral hypoglycemic agent?
A. meglitinides
B. biguanides
80. A class o f oral hypoglycemic agent
that is also classified as potassium
channel blocker is
A.
B.
C.
D.
E.
biguanide
sulfonylureas
meglitinides
a-glucosidase inhibitors
thiazolidinediones
81 .Which one o f the following interacts
with a specific cell surface receptor to
facilitate the transport o f glucose and
amino acids?
A.
B.
C.
D.
E.
metformin
insulin
glyburide
tolbutamide
glipizide
82. Which one o f the following
hypoglycemic agent is best described as
antihyperglycemic agent?
A.
B.
C.
D.
E.
metformin
glyburide
insulin
acarbose
glibenclamide
83. Which one o f the following
compounds is incorrectly matched with
its mechanism o f action?
A. sulfonylureas - block ATP
sensitive potassium channels
B. acarbose - inhibits the digestion
o f carbohydrates
C. rosiglitazone - inhibits
gluconeogenesis
D. metformin - increases insulin
action in peripheral tissue
E. meglitinides- stimulate insulin
release
84. One o f the following drugs
stimulates the release o f insulin from
pancreatic p cell?
A.
B.
C.
D.
E.
metformin
miglitol
tolazamide
pioglitazone
phenformin
D. local irritation
E. none o f the above
87. Which sulfonylurea antidiabetic
agent primarily causes hyponatremia?
A.
B.
C.
D.
E.
tolbutamide
chlorpropamide
tolazamide
glipizide
metformin
88. Which one o f the following classes
o f compounds does NOT cause
hypoglycemia?
A.
B.
C.
D.
E.
biguanides
sulfonylureas
insulin preparation
meglitinides
none o f the above
89.All are adverse effects associated
with the use o f biguanides , EXCEPT
85.Insulin preparations can be used to
treat
I. insulin dependent diabetes
mellitus
II. non-insulin dependent diabetes
mellitus
III. patients w'hose glucose is not
adequately controlled by diet or oral
antidiabetic agent
A.
B.
C.
D.
E.
1 only
11 only
II and III
I and III
1 and II
86. All are the adverse effect of insulin
preparation, EXCEPT
A. cholestatic jaundice
B. hypoglycemia
C. hypersensitivity
A.
B.
C.
D.
E.
fatal lactic acidosis
metallic taste
GI effect
hypoglycemia
none o f the above
90. The use o f thiazides with an oral
antidiabetic agent can
A. increase the blood glucose level
B. has no effect on blood glucose
level
C. can decrease the blood glucose
level
D. decreases the blood glucose
level in some patients and
increases the blood glucose
level in others
E. none o f the above
91 .Varying effects on glucose levels is
observed when oral antidiabetic agents
interact with
A. monoamine oxidase inhibitors
B. p-blockers
C. thiazide diuretics
D. oral contraceptives
E. ACE-inhibitors
92. Sulfonylureas interact with
A.
B.
C.
D.
E.
digoxin
ranitidine
quinine
minoxidil
none o f the abovel
96.A drug that has no drug interaction
involving CYP450 enzyme is
A.
B.
C.
D.
E.
pioglitazone
nateglinide
metformin
rosiglitazone
glibenclamide
97.An antidiabetic drug that decreases
the bioavailability o f oral contraceptives
is
A.
B.
C.
D.
E.
metformin
pioglitazone
nateglinide
repaglinide
none o f the above
93.A drug metabolized by CYP2C9 is
A.
B.
C.
D.
E.
pioglitazone
repaglinide
glimepride
rosiglitazone
tolbutamide
•
94. Which o f the following drugs can
interfere with the renal tubular secretion
o f metformin?
A.
B.
C.
D.
E.
amiloride
morphine
ranitidine
quinidine
all
95.Which class o f antidiabetic agent
impairs the oral absorption o f digoxin?
A. sulfonylureas
B. a-glucosidase inhibitors
C . biguanides
D. meglitinides
E. none o f the above
98. Which o f the following is not
correctly paired with the correct
isozyme?
A. glimepride - CYP2C9
B. nateglinide-C Y P2C 8
C. pioglitazone - CYP3A4
D. rosiglitazone - CYP2C8
E. repaglinide - CYP3A4
ANSW ERS
Endocrinology & Related Drugs
1. Answer: C. vasopressin
Explanation:
Oxytocin and vasopressin are posterior pituitary hormones. Corticotrophin, thyrotropin,
thyrotropin-releasing hormone, growth hormone, menotropins, urofollitropin and human
chorionic gonadotropin are anterior pituitary hormones.
2. Answer: A. thyrotropin
Explanation:
Corticotrophin, thyrotropin, thyrotropin-releasing hormone and growth hormone are the anterior
pituitary hormones that are used therapeutically.
3. Answer: C. thyroid-stimulating hormone
Explanation:
Thyrotropin is a glycoprotein with a molecular weight o f 28000, known as thyroid stimulating
hormone.
4. Answer: B. urofollitropin
Explanation:.
Urofollitropin has high FSH-like activity. Menotropins also known as human menopausal
gonadotropin have a high FSH-like and LH-activity. Human chorionic gonadotropin has LH-like
activity.
5. Answer: C. urofollitropin
Explanation:
The therapeutically important anterior pituitary hormones are corticotrophin, growth hormone
(somatotropin) and menotropins (gonadotropin) and the posterior pituitary agents (vasopressin
and oxytocin).
6. Answer: B. oxytocin
Explanation:
Oxytocin plays an important role in the induction o f labor.
7. Answer: D. human chorionic gonadotropin(HCG)
Explanation:
HCG is secreted by chorionic tissue and is present in the urine only after conception has occurred.
8. Answer: D. for the diagnosis and differentiation o f primary and secondary adrenal
insufficiency
Explanation:
Corticotropin is used mainly for the diagnosis and differentiation o f primary and secondary
adrenal insufficiency.
9. Answer: A. vasopressin
Explanation:
Since vasopressin has vasopressor and antidiuretic hormone activity which promotes the
reabsorption o f water from the distal renal tubular epithelium, it can be used to treat neurogenic
diabetes insipidus.
10. Answer: A.gynecomastia
Explanation:
The use o f oxytocin is associated with severe water intoxication with convulsions and coma,
uterine hypertonicity with spasm, tetanic contraction or uterine rupture, postpartum hemorrhage
and fetal effects such as bradycardia, neonatal jaundice, cardiac dysrhythmias and premature
ventricular contractions.
11 .Answer: A. cyclopentanoperhydrophenanthrene
Explanation:
Most natural and synthetic gonadal hormones are derived from
cyclopentanoperhydrophenanthrene, the parent structure o f a steroid..
12.Answer: B. estrogen
Explanation:
Unlike other steroid hormones, all estrogens have an aromatic A ring.
0
'O H
HO
Estriol.
Note the two hydroxyl (-OH)
groups attached to the D ring
(rightmost ring).
H Q -
’- c - '
'v .-'
Estradiol. Note one hydroxyl
group attached to the D ring.
The 'di' refers both to this
hydroxyl and the one on the A
ring (leftmost).
Estrone. Note the ketone (= 0 )
group attached to the D ring.
Al
13.Answer: A. ethinyl estradiol and mestranol
Explanation:
The two estradiol derivatives, ethinyl estradiol and its 3-methyl ether mestranol are 17 asubstituted estradiols which have increased resistance to first pass metabolism and are effective
for oral contraceptive.
Ethinyl estradiol
Mestranol
14.Answer: C. quinestrol
Explanation:
Dienestrol, chlorotrianisene and diethylstilbestrol are nonsteroidal stilbene derivatives that appear
to assume and estradiol-like conformation in vivo.
Quinestrol is estrogen derivative that is used principally for estrogen-replacement therapy.
15.Answer: B. chlorotrianisene
Explanation:
The antiestrogens clomiphene, tamoxifen citrate and toremifen are stilbene derivativesthat are
structurally related to chlorotrianesene. Fulvestrant is the newest potent steroidal antiestrgen.
16.
Answer: E. all o f the above
Explanation:
Estrogen receptors are found in estrogen responsive tissues such as vagina, uterus, mammary
glands, anterior pituitary and hypothalamus.
17.Answer: C. anemia
Explanation:
Estrogens are used as oral contraceptives, treatment o f menopausal symptoms such as vasomotor
disorders, urogenital atrophy, psychological disorder, acne, osteoporosis and prostate cancer.
18.Answer: B. tamoxifen
Explanation:
Tamoxifen, toremifene and fulvestrant are estrogen antagonists that are used to treat estrogen
dependent breast cancer.
19. Answer: B. exemestane
Explanation:
Anastrozol and letrozol are potent and selective nonsteroidal inhibitors o f aromatase. Exemestane
is the only steroidal irreversible inhibitor o f aromatase an enzyme responsible for the conversion
o f androgens to estrogens.
20.Answer: A. raloxifene
Explanation:
Raloxifene is a selective estrogen receptor modulator with biological action similar to that of
estrogens but exhibits estrogen antagonist effects on uterine and breast tissue.
21.Answer: C. osteoporosis
Explanation:
SERMs are used for the prevention o f osteoporosis.
22.Answer: D. aromatase inhibitors
Explanation:
Aromatase inhibitors (anastrozole, letrozole and exemestane) are used to treat advanced breast
cancer.
23 .Answer: B. progesterone
Explanation:
Progesterone is a naturally occurring progestin with a C-21 steroidal skeleton.
24.Answer: D. megestrol acetate
Explanation:
Medroxyprogesterone acetate and megestrol acetate are examples o f 17 a-hydroxyprogesterone
derivatives, which have a methyl group at position C-6 o f progesterone and an acetoxyl group at
position C-17.
25.Answer: A. norethindrone
Explanation:
The 17 a-ethinylandrogens such as norethindrone, norethynodrel, and norgestrel and ethynodiol
diacetate are structurally classified as androgens but contain progestational activities.
26. Answer: B. breast cancer
Explanation:
Progestins are used as oral contraceptives alone or in combination with estrogens, menstrual
disorder such as dysfunctional uterine bleeding and dysmenorrhea and endometriosis.
27. Answer: E. all o f the above
Explanation:
Gynecological effects such as irregular menses, breakthrough bleeding and amenorrhea, weight
gain and edema, exacerbation o f breast carcinoma are the adverse effects o f progestins.
28.Answer: C. testosterone
Explanation:
Testosterone is the primary natural androgen which has androgenic and anabolic effect.
Testosterone
29.Answer: C. dromostanolone
Explanation:
Oxandrolone and dromostanolone are drugs that have more anabolic effect than androgenic
effect.
30. Answer: A. 5 a-reductase
Explanation:
Since testosterone can not bind to the androgen receptor, the enzyme 5 a-reductase converts
testosterone to dihydrotestosterone m the cytoplasm o f androgen-responsive tissue which then
binds to an androgen receptor in the nucleus.
31 .Answer: C. dromostanolone - oral contraceptive
Explanation;
Dromostanolone is an androgen with more anabolic effect and the therapeutic use o f androgens
are androgen-replacement therapy, breast cancer and endometriosis, female hypopituitarism,
anabolic therapy and anemia.
32.Answer: E. all the above
Explanation:
The adverse effect o f androgens are fluid retention, increased low density lipoprotein and
decreased high density lipoprotein cholesterol levels, psychological changes, liver disorders,
development o f masculine features in female and decreased fertility in male.
33.Answer: C. finasteride
Explanation:
Finasteride is a 5 a-reductase inhibitor, an enzyme that converts testosterone to 5 a-
dihydrotestosterone.
34.
Answer: D. bicalutamide - inhibits the conversion o f testosterone to 5 a-dihydrotestosterone
Explanation:
Bicalutamide is an antiandrogen that inhibits the action o f androgens by competitively binding to
androgen receptors in the target tissue.
35.Answer: A. androgenic alopecia
Explanation:
5 a-reductase inhibitors are therapeutically used for benign prostatic hyperplasia and
androgenic alopecia.
36. Answer: B. treatment o f prostate cancer
Explanation:
Antiandrogens are used in the treatment o f prostate cancer, in combination with luteinizing
hormone-releasing hormone (LH-RH) antagonists.
37.Answer: B. prednisolone
Explanation:
In prednisolone, there is a double bond between positions C -l and C-2. This double bond
increases glucocorticoid activity without increasing mineralocorticoid activity.
iC H ,O H
38.Answer: C. increased mineralocorticoid and glucocorticoid activity
Explanation:
Fludrocortisone has a fluorine at position C-9 which greatly increases both mineralocorticoid and
glucocorticoid activity.
CHgOCOCH,
CO
— OH
39.Answer: D. increases glucocorticoid activity with less effect on mineralocorticoid activity
Explanation:
Unlike fluorination at C-9, this increases mineralocorticoid and glucocorticoid activity,
fluorination at C-6 increases glucocorticoid activity with less effect mineralocorticoid activity.
40.Answer: A. hydrocortisone
Explanation:
The two prototypical glucocorticoids that are formed in the middle layer o f the adrenal cortex are
cortisone and hydrocortisone.
41 .Answer: C. increase the glucocorticoid activity and decrease the mineralocorticoid activity
Explanation:
Cortisone and hydrocortisone are modified to increase glucocorticoid activity while decreasing
the mineralocorticoid activity.
42.Answer: B. fluocinonide
O
n
c h 2o c c h 3
F
Explanation:
Fluocinonide has an acetate ester at position C-21 that enhances its topical absorption.
43.Answer: B. outer layer o f the adrenal cortex
Explanation:
Aldosterone is formed in the outer (glomerular) layer o f the adrenal cortex.
44.Answer: D. desoxycorticosterone acetate and fludrocortisone acetate
Explanation:
Desoxycorticosterone acetate and fludrocortisone acetate are the two clinically useful
mineralocorticoids.
45.Answer: B. dexamethasone
ch2oh
CO
Explanation;
Dexamethasone has a methyl group at position C-16 that enhances glucocorticoid activity and
abolishes mineralocorticoid activity.
46. Answer: E. all o f the above
Explanation:
Adrenocorticosteroids are used as replacement therapy to treat acute and chronic adrenal
insufficiency, for the treatment o f severe allergic reactions, chronic ulcerative colitis, rheumatic
carditis, renal diseases including nephritic syndrome collagen vascular disease and cerebral
edema. It is also used as therapy at last resort, to treat severe, disabling arthritis. The topical
agents are used to treat skin disorders and inflammatory.
47. Answer: B. cholestatic jaundice
Explanation:
The adverse effects associated with the use o f adrenocorticosteroids are suppression of pituitaryadrenal integrity, GI effects, CNS effects and other effects such as weight gain, osteoporosis,
hyperglycemia, flushed face and neck, acne, hirsutism, cushingoid “moon face” and “buffalo
hump” and increased susceptibility to infection.
48.Answer: C. 5’-deiodinase
Explanation:
Peripheral deiodination converts T4to T3by the enzyme 5'-deiodinase.
49.Answer: E. I & III
Explanation:
The production o f thyroid hormone is regulated by hypothalamic-pituitary-thyroid feed back
system. The hypothalamus secrets thyrotropin-releasing hormone (TRH) which stimulates the
release o f thyroid-stimulating hormone (TSH, thyrotropin) from the anterior pituitary. The
thyroid gland is stimulated by thyrotropin which produces T4 and T3.
50. Answer: D. thyrotropin
Explanation:
Thyrotropin is a thyroid preparation isolated from bovine anterior pituitary gland. It is highly
purified and lyophilized thyrotropic hormone.
51 .Answer: B. levothyroxine
Explanation:
Levothyroxine is less potent but has longer duration o f action 6-7 days compared to liothyronine
which lasts for 1-2 days.
52. Answer: A. 4 to 1 o f T4 to T3
Explanation:
The sodium salts o f both levothyroxine and liothyronine can be used therapeutically. Since
levothyroxine can he converted to liothyronine peripherally, the administration o f levothyroxine
sodium can yield the natural 4 to 1 ratio o f T4 to T3
53 .Answer: C. levothyroxine is more potent than liothyronine
Explanation:
Liothyronine is more potent when compared to levothyroxine but has short duration o f action 1-2
days.
54.Answer: B. liotrix
Explanation:
Liotrix is a thyroid preparation which contains 4 to 1 mixture o f levothyroxine sodium to
liothyronine sodium.
55.Answer: D. propylthiouracil
Explanation:
The thyroid inhibitor thiourylenes inhibit the enzyme iodoperoxidase which inhibits two crucial
steps in thyroid synthesis; the incorporation o f iodine into tyrosine precursor molecules and the
coupling o f iodinated tyrosines to form T4and T3. Additionally, propylthiouracil inhibits the
conversion o f T4 to T3
56.
Answer: C. ionic inhibitors
Explanation:
Ionic inhibitors such as thiocyanate and perchlorate are inorganic monovalent anions that
interfere with the concentration o f iodide ion by the thyroid gland.
57.Answer: E. all
Explanation:
Thyroid hormone preparations are therapeutically used for hypothyroidism i.e. myxedema,
myxedema coma, cretinism, simple goiter, endemic goiter and thyrotropin-dependent carcinoma.
58.Answer: C. thyrotropin
Explanation:
Thyrotropin is the drug that is used as an adjunct in the detection and treatment o f thyroid cancer.
59.Answer: B. radio active iodine
Explanation:
Radio active iodine (3jll ) is used particularly in treating hyperthyroidism in older patients and in
patients with heart disease.
60.Answer: C. ferrous sulfate
Explanation:
The absorption o f thyroid hormones can be decreased by aluminum hydroxide antacids, ferrous
sulfate, calcium, bile acid sequestrants (BAS), sucralfate and iron. Adequate spacing during
administration o f these agents is required.
61.Answer: B. palpitation
Explanation:
The use o f thyroid hormones is rarely associated with side effects but over dosage o f these agents
can cause palpitation, nervousness, insomnia and weight loss.
62.Answer: C. radioactive iodine
Explanation:
The adverse effects associated with the use o f radio active iodides are delayed hypothyroidism
and there is a possible effect on the future offspring o f young adults.
63.Answer: A. carbamazepine
Explanation:
Phenytoin, carbamazepine and rifampin accelerate thyroid metabolism and the dose o f thyroid
hormone should be increased in patients taking these agents.
64.Answer: B. thiourylenes
Explanation:
The adverse effects associated with the use o f thiourylenes is dermatological effects such as
urticarial papular rash and dermatitis, hematological effects such as agranulocytosis,
thrombocytopenia, and granulocytopenia, GI effects such as vomiting, nausea and GI distress,
pain, stiffness in joints, headache and paresthesias.
65.Answer: B. 2
Explanation:
Insulin is an endocrine hormone secreted by the P-cells o f the pancreas. It has 51 amino acids
composed o f two polypeptide chains an A chain o f 21 amino acids and a B chain o f 30 amino
acids.
66.Answer: C. II & III
Explanation:
Human insulin is prepared either by enzymatic conversion o f the terminal amino acid o f porcine
insulin or by means o f recombinant DNA technology.
67.Answer: E. all
Explanation:
The solubility o f insulin at the injection site depends on the physical state, the zinc content, the
nature o f the buffer and the protein content.
68.Answer: D. regular insulin
Explanation:
Most insulin preparations are suspensions and they contain particulate matter. Since only clear
solutions can be administered intravenously, regular insulin which contains water-soluble
crystalline zinc insulin can be administered intravenously.
69.
Answer: C. insulin glargine
Explanation:
Regular insulin is the only preparation that has a rapid onset o f action and can be given IV
because it is a clear solution. All others are suspensions.
70.Answer: B. insulin glargine
Explanation:
Insulin glargine is long acting insulin. It differs from normal insulin in that Gly replaces the
ASN2j residue o f the a-chain and a basic Arg-Arg dipeptide replaces the Thr30 o f the p-chain.
Because o f this structural alterations; the solubility at physiological pH is decreased, precipitation
occurs and the absorption is delayed following subcutaneous injection. This increases the
duration o f action.
71 .Answer: D. insulin zinc suspension
Explanation:
Lente insulin which is also called insulin zinc suspension an intermediate-acting insulin. It is a
mixture o f 70% ultralente crystals and 30% semilente powder.
72.Answer: B. glimepride
Explanation:
Glimepride, glyburide and glipizide are second generation sulfonylurea ora] hypoglycemic
agents. They differ from the first generation sulfonylureas by the larger group attached to the
aromatic ring which makes it more lipid soluble and more potent than the first-generation agents.
73.Answer: C. protamine zinc insulin
Explanation:
Lente insulin does not contain modifying protein and are prepared with an acetate buffer.
Isophane insulin and protamine zinc insulin are prepared with a phosphate buffer which is
incompatible with the acetate buffer o f the lente insulins.
74.Answer: A. metformin
Explanation:
The only biguanide that is still used as oral hypoglycemic agent is metformin. Phenformin was
withdrawn from the market because o f high incidence o f fatal lactic acidosis. Nateglinide is a
meglitinide and precose is a-glucosidase inhibitor.
75.Answer: B. biguanide
Explanation:
Biguanides and inhibitors o f a-glucosidase are class o f oral hypoglycemic agents that are basic
compound. All the other class or oral hypoglycemic agents are acidic compounds.
76.Answer: C. meglitinides
Explanation:
Repaglinide and nateglinide are acidic compounds and belong to meglitinides.
77.Answer: B. troglitizone
Explanation:
Rosiglitazone. pioglitazone and troglitizone belong to thiazolidinediones oral hypoglycemic
agent. Troglitizone is no longer available in the market because of rare but severe hepatic
toxicity.
78.Answer: A. meglitinides
Explanation:
Repaglinide and nateglinide are chemically classified as meglitinides.
79.Answer: C. acarbose
Explanation:
Acarbose (precose) is a basic analogue with 1-4 linked tetrasaccharide. It is a-glucosidase
inhibitor with less oral absorption than the monosaccharide miglitol.
80.Answer: B. sulfonylureas
Explanation:
Sulfonylureas block adenosine triphosphate(ATP) sensitive potassium channels. This ATP
sensitive potassium channels stimulate the release of insulin form pancreatic (3-cells. That is why
sulfonylureas are also classified as potassium channel blockers.
81.Answer: B. insulin
Explanation:
Insulin preparations mimic the activity o f endogenous insulin, which is required for the proper
utilization o f glucose in normal metabolism. To facilitate the transport o f glucose and amino
acids, insulin interacts with a specific cell surface receptor.
82.Answer: A. metformin
Explanation:
Biguanides are best described as antihyperglycemic agent because they do not stimulate the
release o f insulin and thus do not cause hypoglycemia. They reduce glucose levels by causing an
increase in insulin action in peripheral tissues as well as inhibition o f gluconeogenesis. They
increase glucose transport across skeletal muscle cell membranes. All the other classes o f
hypoglycemic agents cause hypoglycemia.
83.Answer: C. rosiglitazone - inhibits gluconeogenesis
Explanation:
Thiazolidinediones (rosiglitazone and pioglitazone) bind to nuclear peroxisome proliferatoractivated receptors which is involved in the transcription o f insulin-responsive genes and
regulation o f adipocyte differentiation and lipid metabolism which decreases insulin resistance
and improves target cell response to insulin.
84.Answer: C. tolazamide
Explanation:
O f the five class o f oral hypoglycemic agents, sulfonylureas (tolazamide) and meglitinides
stimulate the secretion o f insulin from pancreatic p cells. The other three classes have different
mechanism o f action. Biguanides (metformin) increase the peripheral use o f insulin. They also
suppress gluconeogenesis. a-Glucosidase inhibitors decrease the digestion o f carbohydrates in
small intestine and decrease the absorption o f glucose. Thiazolidinediones decrease insulin
resistance by binding to nuclear peroxisome proliferator-activated receptors which are involved in
transcription of insulin-responsive genes and in regulation o f adipocyte differentiation and lipid
metabolism. This improves target cell response to insulin.
85.Answer: D. I and III
Explanation:
Insulin preparations can be used to treat insulin dependent diabetes mellitus that cannot be
controlled by diet alone. It can also be used non-insulin diabetes mellitus in patients whose
glucose levels cannot be controlled by diet and oral antidiabetic agents.
86.
Answer: A. cholestatic jaundice
Explanation:
The adverse effects associated with insulin preparation are hypoglycemia which causes sweating,
tachycardia and hunger with a possibility o f progressing to insulin shock with hypoglycemic
convulsions. Hypersensitivity reaction and local irritation at the injection site are also the adverse
effects o f insulin.
87. Answer: B. chlorpropamide
Explanation:
Chlorpropamide primarily causes hyponatremia due to the potentiation o f the effects o f
antidiuretic hormone.
88.Answer: A. biguanides
Explanation:
Biguanides do not stimulate the release of insulin and they do not cause hypoglycemia. They act
by increasing the action o f insulin in peripheral tissue. They also suppress gluconeogenesis. All
other classes o f antidiabetic agents can cause hypoglycemia.
89.Answer: D. hypoglycemia
Explanation:
Biguanides are described as antihyperglycemic agents because they do not cause hypoglycemia as
they act by increasing the action o f insulin in the peripheral tissue and they inhibit
gluconeogenesis. The adverse effects o f biguanides are fatal lactic acidosis, metallic taste and GI
effects such as epigastric distress, nausea, vomiting, diarrhea and anorexia.
90.Answer: A. increase the blood glucose level
Explanation:
Thiazides can cause an increase in blood glucose by altering the metabolism o f carbohydrates.
91 .Answer: B. P-blockers
Explanation:
p-Blockers have varying effects on glucose levels. They inhibit the effects o f catecholamine on
glycogenolysis and glucagon release and potentiate hypoglycemia. They promote hyperglycemia
by inhibiting insulin secretion and decreasing tissue sensitivity to insulin, p-blockers can mask
hypoglycemia by blunting the reflux tachycardia. Thiazide diuretics can cause an increase in
blood glucose level by altering carbohydrate metabolism. Monoamine oxidase inhibitors cause
hypoglycemia by stimulating insulin secretion. Oral contraceptives decrease the efficacy of
antidiabetic agents by promoting insulin resistance.
92. Answer: D. minoxidil
Explanation:
Minoxidil and diazoxide are potassium channel openers and sulfonylureas act by causing the
release o f insulin by blocking potassium channels in pancreatic cells.
93.Answer: C. glimepride
Explanation:
All sulfonylureas except acetohexamide are oxidatively metabolized by the CYP450 enzymes.
Glimepride is metabolized by the CYP2C9 isoform. Pioglitazone and repaglinide are metabolized
by CYP3A4. Rosiglitazone requires CYP2C8 to metabolize. Drug interactions involving
metabolism would be limited to those capable o f inducing or inhibiting these isozymes.
94.Answer: E. all
Explanation:
Cationic drugs which are eliminated by renal tubular secretion such as amiloride, cimetidine,
dofetilide, midodrine, morphine, procainamide, quinidine, quinine, ranitidine, triamterene,
trimethoprim and vancomycin can interfere with the renal tubular secretion o f metformin. If
metformin is co-administered with any o f these agents, there is an increased risk o f lactic acidosis
and acute renal failure.
95.Answer: B. a-glucosidase inhibitors
Explanation:
a-glucosidase inhibitors impair the oral absorption o f digoxin.
96.Answer: D. rosiglitazone
Explanation:
Rosiglitazone is metabolized by CYP2C8 and has no drug interaction involving CYP450 enzyme.
97.Answer: B. pioglitazone
Explanation:
Pioglitazone requires CYP3A4 for oxidative metabolism. It induces CYP3A4 isozyme and
decrease the bioavailability o f oral contraceptives.
98.
Answer: B. nateglinide - CYP2C8
Explanation:
Nateglinide is oxidatively metabolized by cytochrome P450 enzymes, specifically by CYP2C9
and CYP3A4 isozymes.
'
“Optimism is a kind of heart stimulant- the digitalis of failure”
Elbert Hubbard
Heart Failure
A. low-out put failure
10. Which of the following are treatment
approaches for HF:
A.
B.
C.
D.
E.
elimination o f substances that
exacerbate HF
reducing metabolic demands
administration o f combination of
diuretics,
ACE
inhibitors,
(3adrenergic blockers and digitalis
reducing fluid volume excess
all o f the above
11 .Which one o f the following is/are
included in the compensatory mechanisms
in HF?
A.
B.
C.
D.
E.
sympathetic response
hormonal stimulation
concentric cardiac hypertrophy
frank-starling mechanism
all o f the above
12.In cardiac cycle, the term / After load’
indicates
A. the tension in ventricular muscles
during contraction
B. ventricular end diastolic pressure
C. the force exerted on the ventricular
muscle at the end o f diastole
D. B & C
- '
E. None
13. What produces the signs and symptoms
o f HF?
A. increased TPR
B. decreased percentage o f blood
ejected
C. pressure in the pulmonary artery
D. the fluid back up either in lungs or
peripheral circulation
E. increased degree o f muscle fiber
stretch
Heart Failure
14. All o f the following are sings and
symptoms of fluid accumulation behind the
left ventricle, EXCEPT
A.
B.
C.
D.
dyspnea
dry wheezing cough
nocturia
complaints by the
tightness and swelling
E. none o f the above
patient
of
15.In which stage o f HF is digitalis
included as part o f therapy
A.
B.
C.
D.
E.
stage A
stage B
stage C
stage D
A and B
16. Which one of the following is NOT
correct about the physical findings in HF?
A. crackles indicate the movement o f
air through fluid filled passages
B. tachycardia
is
an
early
compensatory response detected
through an increased pulse rate
C. S4 atrial gallop is a vibration
produced by rapid filling o f the left
ventricle early in diastole
D. A & B
E. none o f the above
17. Which one o f the following is NOT one
o f diagnostic test results o f HF?
A.
B.
C.
D.
cardiomegaly
transudative pleural effusion
venous stasis
arm-to-tongue circulation time is
prolonged
E. none o f the above
18. An early sign o f right-sided HF is:
248
A. jugular vein distention
B. hepatomegaly
C. bilateral leg edema
D. pitting ankle edema
E. none o f the above
19. Which one o f the following is NOT an
advantage o f bed rest in HF patients?
A.
B.
C.
D.
E.
decreased cardiac work load
decreased excess fluid volume
promoted diuresis
decreased risk o f venous stasis
none
20. Which one o f the following is a correct
dietary control in HF patients?
A. consuming small but frequent
low calorie meals
B. consuming diary food products
C. using water softeners in the
water
D. all except C
E. all
21 .Which one o f the following is/are part o f
the basic core o f treatment for HF?
A.
B.
C.
D.
E.
ACE inhibitors
diuretics
P-adrenergic blockers
digitalis
all of the above
22. Which o f the following acts by
furthering the activation o f neurohormonal
systems rather than as a positive inotropic
agent
A.
B.
C.
D.
E.
dopamine
digitalis
milrinone
A&B
All
23.The dosage forms in which digoxin is
available is/are:
A.
B.
C.
D.
E.
tablet
injection
elixir
capsule
all o f the above
24.0.125 mg o f digoxin tablet is equivalent
to how many milligrams capsule
A.
B.
C.
D.
E.
0.5 mg
0.25 mg
0.125 mg
0.1 mg
none o f the above
25. Which one o f the following statements
is true?
A. 0.8-2.0 ng/mL of serum digoxin
is associated with therapeutic
response with minimal toxicity
B. rapid digitalization is achieved
within 24 hours
C. In
a patient with
renal
dysfunction, digitalization takes
7 -8 days
D. all except B
E. all except C
26.Digoxin effect decreases with increased
level o f which o f the following ions?
A.
B.
C.
D.
E.
potassium
calcium
magnesium
A&B
A&C
27.Risk o f digoxin toxicity increases with
coadministration o f which o f the following?
A. verapamil
B. quinidine
C. spironolactone
D. amiodarone
E. all o f the above
A.
B.
C.
D.
E.
28. Which o f the following are signs of
digoxin toxicity?
A.
B.
C.
D.
E.
anorexia
mental confusion
alteration in visual perception
Nausea and vomiting
all o f the above
29. Which one o f the following agents is/are
used in the treatment o f toxicity?
A. lidocaine
B. cholestyramine
C. purified digoxin-specific
fragment antibodies
D. A & C
E. All of the above
Fab
30.HF patients who experience diuretic
resistance need
A. a combination o f two agents
with differing mechanisms
B. addition
o f agents
which
increase renal blood flow
C. intravenous administration of
the diuretic
D. addition o f an agent that
increase renal blood flow
E. All o f the above
diuretics
cardiac glycosides
vasodilators
B&C
None o f the above
33. Which o f the following agents
decreases after load and increases cardiac
output in patients with HF
A.
B.
C.
D.
E.
nitroprusside
hydralazine
prazosin
nitrates
none o f the above
34.In chronic HF, which combination is
used to reduce preload
A. hydralazine - nitroglycerine
B. hydralazine
isosorbide
dinitrate
C. hydralazine - prazosin
D. hydralazine - furosemide
E. none of the above
35.Currently, which o f the following are
considered the first line agents in the
treatment o f HF?
A.
B.
C.
D.
E.
vasodilators
ACE-inhibitors
Diuretics
Digitalis glycosides
None o f the above
31 .Diuretics have been shown to reduce
A.
B.
C.
D.
E.
peripheral edema
jugular venous pressure
pulmonary congestion
body weight
all of the above
32. Which o f the following agents reduce
pulmonary congestion and increase cardiac
output by reducing preload and/or after load
36.ACE inhibitors are contraindicated in
which o f the following conditions?
A. when serum potassium > 5.5
mEq/L
B. symptomatic hypotension
C. severe renal artery stenosis
D. pregnancy
E. all of the above
37. Which o f the following agents is
recommended to treat patients with HF due
to left ventricular dysfunction
A.
B.
C.
D.
E.
ACE inhibitors
calcium channel blockers
p- adrenergic blockers
A&B
A&C
38. Which o f the following can be used in
the emergency treatment o f patients with
HF
A.
B.
C.
D.
E.
ACE inhibitors
p- adrenergic blockers
Calcium channel blockers
inotropic agents
none o f the above
39.Patients with fluid retention should take
P- adrenergic blockers for treatment o f HF
along with which o f the following?
A.
B.
C.
D.
E.
Ace inhibitors
Diuretics
Digoxin
Calcium channel blockers
None o f the above
40. p- adrenergic blockers may be
considered in all the following cases,
EXCEPT
class II HF
class IV HF
for acute management o f HF
in
HF
post
myocardial
infarction
E. none o f the above
A.
B.
C.
D.
D. A & B
E. All o f the above
42.The calcium channel b)ocker? which is
less likely to cause a worsening in
nonischemic HF is
A.
B.
C.
D.
E.
nifedipine
felodipine
amlodipine
diltiazem
none o f the above
4 3.Which inotropic agent is a recombinant
form o f human B type natriuretic peptide?
A.
B.
C.
D.
E.
dopamine
dobutamine
inamrinone
milrinone
nesiritide
44. Which o f the following inotropic agents
possesses both positive inotropic effect and
a vasodilating effect
A.
B.
C.
D.
E.
dopamine
dobutamine
inamrinone
milrinone
C&D
45.Which o f the following inotropic agents
stimulates specific receptors within the
kidney
A.
B.
C.
D.
E.
dopamine
dobutamine
inamrinone
nesiritide
A&D
41 .Which one o f the following is selective
p- adrenergic blocker used in HF?
A. carvedilol
B. metoprolol
C. bisoprolol
46.At what dose does dopamine increase
cardiac output in HF patients?
A. 2 —5 ^g/kg/min intravenous
B. 5 - 1 0 jig/kg/min intravenous
C. > 1 0 [ig/kg/min intravenous
D. none o f the above
47. Which o f the following can be used in
patients with HF that have been refractory
to treatment with other inotropic agents?
A.
B.
C.
D.
E.
dobutamine
inamrinone
milrinone
nesiritide
none o f the above
48. Which o f the following inotropic agents
is approved to treat patients with acutely
decompensated HF associated with
shortness o f breath at rest or with minimal
activity?
A.
B.
C.
D.
E.
milrinone
inamrinone
nesiritide
A&C
None o f the above
ANSW ERS
Heart Failure
1. Answer: D. all except C
Explanation:
Heart failure (HF) is a complex clinical syndrome that can result from any cardiac disorder that
impairs the ability o f the ventricles to deliver adequate quantities of blood to the metabolizing
tissue during normal activity or at rest. The condition in the past has been referred to as
“congestive heart failure” due to the edematous state commonly produced by the fluid back up
resulting in shortness o f breath, fatigue, limitation o f exercises tolerance and fluid retention. Fluid
retention may lead to pulmonary and peripheral edema. Most recently, due to the fact that all
patients do not necessarily present with fluid over load at the initial or follow up evaluations, the
term “heart failure” more adequately reflects the clinical syndrome.
2. Answer: C. HF is considered an independent diagnosis
Explanation:
There is currently no diagnostic test for HF, and the clinical diagnosis is based on patients history
and physical examination and HF should not be considered an independent diagnosis, as it is
superimposed on an underlying cause.
3. Answer: B. Coronary artery disease
'
Explanation:
HF is superimposed on an underlying cause and in about 2/3 o f the patients with left ventricular
systolic dysfunction. Coronary artery disease is the cause and the remaining V3 o f patients have
non-ischemic cause o f systolic dysfunction due to other causes o f myocardial stress, which
include trauma, disease or other abnormal states( e.g. pulmonary embolism, infection, anemia,
pregnancy, drug use or abuse, fluid over load, arrhythmia, valvular heart disease,
cardiomyopathies and congenital heart disease).
4. Answer: C. Class III
Explanation:
The NYHA has developed a classification system and it is still utilized today to quantify the
functional limitations o f HF patients.
In class I - degree o f effort necessary to elicit HF symptoms equals those that would limit normal
individuals.
Class II - degree o f effort necessary to elicit HF symptoms occurs with ordinary exertion.
Class 111 - degree o f effort necessary to elicit HF symptoms occurs with less than ordinary
exertion.
Class IV - degree o f effort necessary to elicit HF symptoms occurs while at rest.
5.
Answer: A. low-out put failure
Explanation:
Low output failure is the most common type o f HF in which the metabolic demands are within
normal limits but the heart is unable to meet them. When the metabolic demands increase (e.g.
hyperthyroidism, anemia) and the heart is unable to meet them, the failure is designated high
output. In left sided failure, blood cannot be pumped from the left ventricle to peripheral
circulation and it accumulates in the left ventricle. And in the right sided failure blood cannot be
pumped from the right ventricle into the lungs and accumulates with in the right ventricle.
6.
Answer: E. All o f the above
Explanation:
Patients at high risk of developing heart failure (HF) because o f the presence o f conditions that
are strongly associated with the development o f HF are patients with systemic hypertension;
coronary artery disease; diabetes mellitus; history of cardiotoxic drug therapy or alcohol
abuse; personal history o f rheumatic fever or family history o f cardiomyopathy. Such patients
have no identified structural or functional abnormalities o f the pericardium, myocardium or
cardiac valves and have never shown sings and symptoms o f HF. Dyspnea or fatigue due to left
ventricular systolic dysfunction is symptom of HF associated with underlying structural heart
disease.
7. Answer: C. left sided failure produces systemic edema
Explanation:
In left sided failure, given the accumulation, the left ventricle is unable to accept blood from the
left atrium and lung; therefore, the fluid portion o f the blood backs up into the pulmonary alveoli,
producing pulmonary edema. And in the right sided failure, when blood is not pumped from the
right ventricle, the fluid portion o f the blood backs up through out the body (e.g. in the veins,
liver, legs, bowels), producing systemic edema.
8. Answer: B. lithium carbonate
Explanation:
Albumin, glucose, mannitol, saline and urea exacerbate HF by producing osmotic effect but
lithium carbonate promotes sodium retention.
9. Answer: C. diltiazem
Explanation:
Androgen, corticosteroids, diazoxide, estrogen, licorice, lithium carbonate, NSAIDs all promotes
sodium retention. But antiarrhythmic agents, p-adrenergic blockers, select calcium channel
blockers (e.g. diltiazem, nifedipine, and verapamil), direct cardiotoxins (e.g. doxorubicin, ethanol,
cocaine, amphetamines) and tricyclic antidepressants exacerbate HF by decreasing cardiac
contractility.
10. Answer: E. all o f the above
j
j
Explanation:
|
The treatment goals of HF are to remove (or mitigate the underlying causes or risk factors and to
relieve the symptoms and improve pump function and the above statements are all approaches to
the goal.
11 .Answer: E. all o f the above
Explanation:
HF and decreased cardiac output trigger a complex scheme o f compensatory mechanisms
designed to normalize cardiac output! In sympathetic response, inadequate cardiac output
stimulates reflex activation o f the sympathetic nervous system and an increase in circulating
catecholamines and in hormonal stimulation the redistribution o f blood flow results in reduced
renal perfusion which decreases the glotfnerular filtration rate (GFR) which then results in sodium
and water retention and activation o f renin-angiotensin-aldosterone system. While concentric
cardiac hypertrophy describes a mechanism that thickens cardiac walls, providing larger
contractile cells and diminishing the capacity o f the cavity in an attempt to precipitate expulsion
at lower volumes. And the premise o f frank-starling mechanism is that increased fiber dilation
heightens the contractile force, which then increases the energy released.
12. Answer: A.the tension in ventricular muscles during contraction
Explanation:
After load is the tension in ventricular muscles during contraction and it is also known as
intraventricular systolic pressure. But the pre load is the force exerted on the ventricular muscle at
the end o f diastole that determines the degree o f muscle fiber stretch. This concept is also known
as ventricular end-diastolic pressure.
13.Answer: D. the fluid back up either in lings or perpheral circulation.
Explanation:
As the fluid volume expands in the compensation mechanism, so do the demands on an already
exhausted pump allowing increased Volume to remain in the ventricle. The resulting fluid back
up( from the left ventricle into the lungs, from the right ventricle into peripheral circulation)
produces sings and symptoms o f HF thus causing decompensation.
14.Answer: D. complaints by the patient o f tightness and swelling
Explanation:
When fluid accumulates behind the left ventricle signs and symptoms like dyspnea, dry wheezing
cough, exertional fatigue and nocturia are exhibited. But complaints by the patient o f tightness
and swelling including nausea, vortiiting, anorexia, bloating or abdominal pain are signs and
symptoms o f fluid accumulation behind the right side o f the heart.
15.Answer: C. Stage C
Explanation:
In stage A, there is high risk of developing HF but no structural heart disease. The therapy in this
stage includes treating hypertension, encouraging smoking cessation and regular exercise ,
discouraging alcohol intake, treating lipid disorders and taking ACE inhibitors in appropriate
patients.In stage B, there is structural heart disease but with no symptoms o f HF.Therapy includes
all the measures in stage A plus taking ACE inhibitors and p-adrenergic blockers in appropriate
patients. In stage C, there is structural heart disease with prior or current symptoms o f HF.
Therapy includes all the measures under stage A plus taking ACE inhibitors, p-adrenergic
blockers and digitalis and dietary salt restriction. In stage D, there is refractory HF requiring
specialized interventions. Therapy includes all the measures under stages A, B and C, mechanical
assist devices, heart transplantation and continuous intravenous inotropic infusion for palliation
and hospice care.
16.
diastole
Answer: C. S4 atrial gallop is a vibration produced by rapid filling o f the left ventricle early in
Explanation:
A & B are correct about the physical findings in HF but the S4 atrial gallop is a vibration
produced by increased resistance to sudden, forceful ejection of atrial blood in late diastole and it
is S3 ventricular gallop which is the vibration produced by rapid filling o f the left ventricle early
in diastole.
17.Answer: C. venous stasis
Explanation:
The diagnostic test results o f HF include cardiomegaly, left ventricular hypertrophy, pulmonary
congestion (evidenced by chest radiograph, ECG), reduction in left ventricular function
(evidenced via echocardiography and radionuclide ventriculography), prolonged arm-to-tongue
circulation and transudative pleural effusion.
18.Answer: C. Bilateral leg edema
Explanation:
Bilateral leg edema is an early sign o f right sided HF; pitting ankle edema signals more
advanced H F. Since edema is more common in many disorders a concurrent neck vein distention
is required for differential diagnosis. Other physical findings include jugular vein distention, S3
ventricular gallop, S4 atrial gallop and hepatomegaly.
19.
Answer: D. decreased risk of venous stasis
Explanation:
The advantage o f bed rest includes decreased metabolic needs, which reduces cardiac work load
which in turn reduces pulse rate and dyspnea. Bed rest also helps decrease excess fluid volume by
promoting diuresis. The risk o f venous stasis increases with bed rest and can result in
thromboembolism.
20.Answer: A. consuming small but frequent low calorie meals
Explanation:
Consuming small but frequent meals (4 to 6 daily) that are low in calories and residues provides
nourishment without unduly increasing metabolic demands. There should be sodium restriction
(2-4 gm o f dietary sodium/day) and the patient should be advised about medications and common
products that contain sodium and cautioned about their use (e.g. antacids, sodium bicarbonate or
baking soda commercial diet food products, water softeners).
21 .Answer: E.all o f the above
Explanation:
ACE-inhibitors. diuretics, P-adrenergic blockers and usually digitalis form the basic core o f
treatment for HF.
22.Answer: B. digitalis
Explanation:
Dopamine, dobutamine and milrinone act as positive inotropic agents but a recent evidence
suggests that digitalis acts by furthering the activation o f neurohormonal systems rather than as a
positive inotropic agent.
23.
Answer: E. all o f the above
Explanation:
Digoxin is available as tablet injection, elixir and capsule.
24.Answer: D. 0.1 mg
Explanation:
Digoxin solution in capsules is more bioavailable than digoxin tablets; therefore, 0.125 mg tablets
are equivalent to 0.1 mg capsules.
25.
Answer: E. all except C
Explanation:
Digoxin has a narrow range between therapeutic and toxic doses. There is not “magic threshold”
level for digoxin therapy, but serum concentration o f 0.8 - 2.0 ng/mL have been associated with
therapeutic response and minimal toxicity.
Rapid digitalization is achieved within 24 hours but the actual administration rate is usually slow
and delivered in divided doses. In slow digitalization, when urgency is not the driving force, oral
Heart Failure
257
administration o f maintenance does should achieve steady state levels in 7- 8 days for the average
patient ( 3 - 4 weeks in patient with renal dysfunction).
26. Answer: E. A & C
Explanation:
Potassium seems to antagonize digitalis preparations.
Increased potassium levels seems to decrease digoxin binding and decrease its effect( this is
likely in patients taking potassium or a captopril-like agent, which increases reabsorption).
Calcium ions act synergistically with digoxin( an increased level increases the force o f
myocardial contraction). Magnesium levels are inversely related to digoxin activity. As
magnesium levels decrease the predisposition to digitalis toxicity increases and vice versa.
27. Answer: E. all o f the above
Explanation:
Risk o f toxicity o f digoxin, increases with coadministration o f quinidine, verapamil, flecainide,
propafenone, spironolactone and amiodarone.
28.Answer: E. all o f the above
Explanation:
Signs o f digoxin toxicity include anorexia, fatigue, headache, malaise, nausea, vomiting, mental
confusion, disorientation, alteration in visual perception and cardiac effects like premature
ventricular contraction, ventricular tachycardia and fibrillation; SA and atrioventricular(AV)
block, and atrial tachycardia with AV block.
29.
Answer: E. all o f the above
Explanation:
In the treatment o f digoxin toxicity, digitalis is discontinued immediately, if the patient is
hypokalemic, potassium supplements are administered. The arrhythmia is treated with lidocaine
(lOOmg bolus followed by infusion at 2 - 4 mg/ min) or phenytoin (slow IV o f 25- 50 mg/min to
a maximum o f 1.0 g). Cholestyramine, which binds to digitalis glycoside, may help prevent
absorption and reabsorption o f digitalis in the bile.
Patients with very high serum digoxin levels (e.g. from suicidal overdose) may benefit from the
use o f purified digoxin-specific Fab fragment antibodies (one vial, 40 mg, will bind 0.6 mg of
digitalis).
30.Answer: E. all o f the above
Explanation:
Patients who experience diuretic resistance or tolerance to their effect might need intravenous
administration, a combination o f two agents with differing mechanisms (furosemide and
metolazone) or the addition o f agents such as dopamine or dobutamine, which increase renal
blood flow. Additionally, evaluation o f patient drug profiles may identify the addition o f sodium
retaining agents such as NSAIDs.
31 .Answer: E. all of the above
Explanation:
Diuretics have been shown to cause a reduction in jugular venous pressures, pulmonary
congestion, peripheral edema, and body weight in short-term studies, and have been shown to
improve cardiac function and exercise tolerance in intermediate-term studies.
32. Answer: C. vasodilators
Explanation:
Vasodilators reduce pulmonary congestion and increase cardiac output by reducing preload
and/or after load. However, at the current time, there are no large scale trials supporting the use of
vasodilators (nitrates or hydralazine) alone in the treatment o f HF.
33.Answer: B. hydralazine
Explanation:
Nitroprusside is a potent dilator of both arteries and veins and prazosin is a-adrenergic
blocker that acts as a balanced arteriovenous dilator.
Venous dilation by nitrates increases venous pooling, which decreases preload. Their arterial
effects seem to result in decreased after load with continued therapy.And hydralazine is an
arteriole dilator that decreases after load to increase cardiac output in patients with HF.
34.Answer: A. hydralazine - nitroglycerine
Explanation:
Hydralazine has been used with isosorbide dinitrate to reduce after load or with nitroglycerine to
reduce preload for treating chronic HF. These combination therapies should not be used as initial
therapy over ACE inhibitors but should be considered in patients who are intolerant o f ACEinhibitors.
35.Answer: B. ACE-inhibitors
Explanation:
Currently ACE inhibitors are considered the first line agents in the treatment of HF and have
been shown to have a beneficial effect on cardiac remodeling.
36.Answer: E. all o f the above
Explanation:
Relative contraindications in using ACE inhibitors include history o f intolerance or adverse
reactions, serum potassium > 5 . 5 mEq/L, symptomatic hypotension, severe renal artery stenosis
and pregnancy.
37.Answer: E. A & C
Explanation:
Recent guide lines recommend the use o f ACE inhibitors and (3- adrenergic blockers in all
patients with HF due to left ventricular systolic dysfunction unless they have a contraindication to
their use or have demonstrated intolerance to their use. Calcium channel blockers, due to the
lack o f supporting efficacy, should not be used for the treatment o f HF.
38.Answer: D. inotropic agents
Explanation:
Inotropic agents have been used in the emergency treatment o f patients with HF and in patients
refractory to, or unable to take, digitalis.
39.Answer: B. Diuretics
Explanation:
(J- adrenergic blockers are generally used in conjunction with diuretics, ACE inhibitors and
usually digoxin to treat HF. p- adrenergic blockers should not be taken without diuretics in
patients with a current or recent history o f fluid retention to avoid its development and to
maintain sodium balance.
40.Answer: C. for acute management o f HF
Explanation:
Studies support the use o f p- adrenergic blockers in patients with class I - IV HF, and not in the
acute management o f patients, as in an ICU, where other, short term therapies such as digoxin
may be more beneficial. Additionally, p- adrenergic blockers should be considered in patients
who develop HF post-myocardial infarction if they are able to tolerate the negative inotropic
effects.
41 .Answer: E. All o f the above
Explanation:
BisoproJol, carvedilol and metoprolol tartrate are all selective p- adrenergic blockers used in HF
with a target dose o f 10 mg once daily, 25 mg twice daily( wt < 85 kg or 50 mg twice daily for wt
> 85 kg) and 75 mg twice daily respectively.
42.Answer: C. amlodipine
Explanation:
Large scale trials utilizing felodipine and amlodipine have not provided persuasive evidence that
long term treatment can improve the symptoms o f HF or prolong survival. However, current
guidelines suggest that amlodipine seems less likely to cause a worsening in nonischemic HF.
43.Answer: E. nesiritide
Explanation:
Nesiritide is a recombinant form o f human B-type natriuretic peptide, which is naturally
occurring hormone secreted by the ventricles. It is the first o f this drug class to become available
for human use in USA.
44.Answer: E. C & D
Explanation:
Inamrinone is referred to as non-glycoside, nonsympathomimetic inotropic agent and it has both
positive inotropic effect and a vasodilating effect. Milrinone is similar to inamrinone, it possesses
both inotropic and vasodilatory properties.
45.Answer: A. Dopamine
Explanation:
Dopamine stimulates specific dopamine receptors within the kidney to increase renal blood flow
and thus increase urine output. Dobutamine although resembles dopamine chemically, it does not
directly affect renal receptors. It,therefore, does not act as a renal vasodilator.
46.Answer: B. 5 - 10 pg/kg/min intravenous
Explanation:
Dopamine at low doses( 2 -5 pg/kg/min ) stimulates specific receptors within the kidney to
increase urine output; at moderate doses( 5 - 1 0 pg/kg/min ),it increases cardiac output and at
high doses( > 10 pg/kg/min ) alpha peripheral activity increases, resulting in increased total
peripheral resistance and pulmonary pressures and the patient should be monitored for
tachycardia.
47.Answer: B. inamrinone
Explanation:
Inamrinone inhibits phosphodiesterase located specifically in the cardiac cells thus increasing the
amount o f cyclic adenosine monophosphate( cAMP). It is used, in patients that have been
refractory to treatment with other inotropic agents, at a loading dose o f 0.75 mg/kg over 3-4
minutes followed by maintenance infusion o f 5-10 jig/kg/min.
48.Answer: C. nesiritide
Explanation:
Nesiritide binds to natriuretic peptide receptors in blood vessels , resulting in increased
production o f guanosine 3' 5’-cyclic monophosphate( cGMP) in target tissues, which mediate
vasodilation. It reduces pulmonary capillary wedge pressure and systemic vascular resistance. So
it is approved for the intravenous treatment o f patients with acutely decompensated HF associated
with shortness o f breath at rest or with minimal activity.
Hypertension
“One way to break up any kind of tension is good deep breathing.”
Byron Nelson
]. What is hypertension (HTN)?
A. Blood pressure elevated enough to
perfuse tissues and organs
B. A systolic reading greater than or
equal to 140 mmHg
C. A diastolic reading greater than or
equal to 90 mmHg
D. A systolic blood pressure reading o f
120-139 or diastolic blood pressure
o f 80-89 mmHg
E. All except D
2. Hypertension (HTN) could lead to
which o f the following?
A.
B.
C.
D.
E.
Myocardial infarction( MI)
Heart failure
Kidney disease
Stroke
All o f the above
3. When the pressure receptors are
stimulated to constriction, all the following
happen except
A.
B.
C.
D.
E.
Heart rate increases
Peripheral resistance augments
Cardiac output decreases
A&B
None o f the above
A.
B.
C.
D.
E.
Nitric oxide
Endothelin
Bradykinin
Epinephrine
none o f the above
6. Which one o f the following statements
is false?
A. Stage one hypertension has a
systolic blood pressure o f 160
mmHg
B. No antihypertensive is indicated for
pre hypertension
C. Thiazide diuretics are indicated for
most with stage 1 hypertension if
there is no compelling indication
D. Two drug combination is indicated
for stage 2 hypertension
E. None o f the above
7. Which o f the following are indicated for
stage 2 hypertension?
A.
B.
C.
D.
E.
Thiazides + ACE inhibitor
ARB
P-blocker
CCB
all o f the above
8. Which o f the following are major risk
factors for high blood pressure?
4. All the following can increase the blood
pressure except
A.
B.
C.
D.
increased venous system distention
aldosterone release
increased sodium reabsorption
blocking
sympathetic
nervous
system
E. all o f the above lead to an increased
blood pressure
5. Which one o f the following is not
involved in the maintenance o f normal
blood pressure?
A.
B.
C.
D.
E.
cigarette smoking
obesity
dyslipidemia
microalbuminuria
all o f the above
9. Which o f the following are some o f the
findings o f secondary hypertension
A. sudden onset and worsening
hypertension
B. BP elevations not responding
treatment
C. Pheochromacytoma
D. Obesity
E. All o f the above
14.Increased total peripheral resistance in
hypertensive patients is caused due to
I.Primary aldosteronism
II.Renal artery stenosis
Hl.Pheochromocytoma
10. Which o f the following agents may
induce hypertension (HTN)?
A.
B.
C.
D.
E.
steroids
nasal decongestants
appetite suppressants
MAO inhibitors
All o f the above
11 .Which o f following is a correct
laboratory finding that confirms an
underlying cause o f secondary
hypertension?
A. blood urea nitrogen( BUN) confirms renal disease
B. increased urinary excretion o f
catecholamine - confirms cushing’s
syndrome
C. hypokalemia(serum potassium) confirms pheochromocytoma
D. B and C
E. all o f the above
*
12. Which o f the following may suggest an
underlying cause for secondary
hypertension
A.
B.
C.
D.
E.
weight gain
sleep apnea
repeated UT1
muscle cramps
all o f the above
A.
B.
C.
D.
E.
if I only is correct
if III only is correct
i f l and IJ are correct
if II and III are correct
ifl , II and III are correct
15. Which one o f the following is the
objective in treating primary hypertension?
A. ruling out uncommon secondary
causes o f hypertension
B. to determine the presence and extent
o f target-organ damage
C. to determine the presence o f other
cardiovascular risk
factors in
addition to high blood pressure
D. to reduce morbidity and mortality
through multiple strategies that
reduce blood pressure though life
style modifications with or without
pharmacological treatment with
minimal side effects
E. all o f the above
16. Which o f the following are predisposing
factors o f Hypertension?
A.
B.
C.
D.
E.
premature cardiac disease
obesity
stress
dyslipidemia
all o f the above
13.All the following are diagnostic tests o f
secondary HTN except
A.
B.
C.
D.
E.
renal artery stenosis
ventricular hypertrophy
ischemia
ketoacidosis
none o f the above
17.In the examination o f ocular fundi, all of
the following are exhibited in the late
stages o f hypertension, except
A.
B.
C.
D.
cotton-wool patches
shiny deposits
exudates
retinal edema
E. none o f the above
18. Which one o f the following statements
is not true?
A. A single elevated reading o f >
140/90 is sufficient basis for
diagnosis
B. Essential hypertension (primary
hypertension) becomes clinically
evident when vascular changes
affect heart
C. A secondary hypertension requires
treatment o f underlying cause
D. A & B
E. None o f the above
19. All o f the following are the general
principles in the treatment o f Hypertension,
except
A. to cure primary hypertension
B. to lower blood pressure towards
normal
C. to prevent organ damage
D. to reverse organ damage
E. none o f the above
20. Which one o f the following statements
is not true?
A. Patients with diastolic pressure o f
80-89 or a systolic pressure o f 120­
139 mmHg are candidates for drug
treatment
B. Before initiating antihypertensive
drug therapy, controllable risk
factors should be eliminated
C. Patients with hypertension who have
diabetes or renal diseases, the blood
pressure goal recommended by JNC
is 130/80 mmHg
D. Most hypertensive patients will
require
two
or
more
antihypertensive drugs
E. None o f the above
21.The initial choice o f anti hypertensive
therapy is:
A.
B.
C.
D.
E.
Vasodilators
Thiazide diuretics
p-blockers
Calcium channel blockers(CCBs)
ACE inhibitors
22.
ACE inhibitors are especially useful in
hypertensive patients having
A.
B.
C.
D.
E.
systolic dysfunction after MI
diabetic neuropathy
CHF
A&B
All o f the above
23. Which one o f the following is an
incorrect match?
A.
B.
C.
D.
diuretics- ethacrynic acid
vasodilators- diazoxide
calcium channel blockers- diltiazem
angiotensin II receptor antagonists minoxidil
E. p-adrenergic
blocking
agentsatenolol
24. Which one of the following is grouped
as post ganglionic adrenergic neuron
blockers?
A.
B.
C.
D.
E.
Prazosin
Verapamil
Reserpine
Clonidine
Nadolol
25. All o f the following are actions o f
thiazide diuretics except
A. increase urinary excretion o f sodium
and water
B. increase urinary
excretion
of
potassium and bicarbonates
C. increase the effectiveness o f other
agents by preventing re-expansion
o f extra cellular and plasma
volumes
D. stimulation o f renin secretion is
blocked
E. none o f the above
26.One o f the following diminishes the
effectiveness o f thiazide diuretics
A.
B.
C.
D.
E.
ACE inhibitors
NSAIDs
p-adrenergic blockers
angiotensin II receptor antagonists
none o f the above
27.In hypertension patients taking thiazide
diuretics all o f the following happens
except
A.
B.
C.
D.
E.
potassium ion depletion
uric acid retention
blood glucose increase
calcium levels decrease
none o f the above
28.All the following may occur in patients
taking thiazides except
A.
B.
C.
D.
E.
hypertriglyceridemia
cardiac arrhythmias
palpitation
depression
impotence
29. Which one o f the following is an
incorrect match o f thiazides with their daily
dose?
A. Chlorothiazide^ 125-2000mg daily
B. Bendroflumethiazide = 2.5-15 mg
daily
C. Benzthiazide = 50-150 mg daily
D. Chlorthalidone = 12.5 - 50 mg
daily
E. Quinethazone ^ 2 - 4 mg daily
30. All the following are loop diuretics
except
A.
B.
C.
D.
E.
Furosemide
Ethacrynic acid
Amiloride
Bumetanide
Torsemide
31. Which o f the following diuretics is
particularly useful in patients with
hyperaldosteronism
A.
B.
C.
D.
E.
Furosemide
Torsemide
Benzthiazide
Spironolactone
None o f the above
32.Diuretics used in hypertension patients
with impaired renal function
A.
B.
C.
D.
E.
Thiazides
Loop-diuretics
Potassium sparing
Beta blockers
none o f the above
-
33.Transient deafness has been reported
with the usage o f which o f the following
diuretics?
A.
B.
C.
D.
E.
Thiazides
Loop diuretics
Potassium sparing
A&b
None o f the above
34. Which o f the following is an incorrect
match o f loop diuretics with their daily
dose?
A. Bumetanide = 0 . 5 - 2 mg daily
B. Ethacrynic acid = 50 - 200 mg daily
C. Furosemide = 20-80 mg daily
D. Torsemide = 2 5 - 5 0 mg daily
E. none o f the above
35. Which one o f the following is a correct
order o f increasing potency o f the diuretics?
A. loop diuretics - potassium sparingthiazide diuretics
B. potassium sparing- loop diureticsthiazide diuretics
C. thiazide
diureticspotassium
sparing- loop diuretics
D. thiazide diuretics- loop diureticspotassium sparing
E. potassium
sparingthiazide
diuretics- loop diuretics
36.There is an increased risk o f
hyperkalemia when potassium sparing
diuretics are co-administered with which o f
the following?
A.
B.
C.
D.
E.
thiazides
loop diuretics
ACE-inhibitors
A&B
none o f the above
37. Which o f the following diuretics is
never used in patients with kidney stone or
hepatic disease?
A.
B.
C.
D.
E.
amiloride
spironolactone
triamterene
eplerenone
none o f the above
38. All are correct matches o f potassium
sparing diuretics with their usual effective
daily doses for hyertension, EXCEPT.
A.
B.
C.
D.
E.
amiloride = 5- 10 mg daily
spironolactone = 100 -400 mg daily
triamterene = 50- 100 mg daily
eplerenone = 50-100 mg daily
none
39.In the sympatholytic group, one o f the
following agents are particularly effective
in patients with rapid resting heart rates
A.
B.
C.
D.
P-adrenergic blockers
peripheral al-adrenergic blockers
centrally active a-agonists
post ganglionic adrenergic neuron
blockers
E. none o f the above
40.All the following are actions o f pblockers except
A. stimulation o f renin secretion is
blocked
B. cardiac contractility is decreased
C. heart rate is reduced
D. causes vasodilation o f both arteries
and veins
E. none o f the above
41 .A patient with the following
characteristics responds best to p-blocker
therapy
A.
B.
C.
D.
a white patient ,age < 45 years
a patient with high heart rate
a patient with high cardiac output
a patient with normal vascular
resistance
E. all o f the above
42.p-blocker drugs withdrawal syndrome
may produce all the following except
A.
B.
C.
D.
exacerbated angina] attacks
bronchospastic disease
MI
a life threatening rebound o f blood
pressure
E. none o f the above
43.
have
P-blocker is not safe in patients that
A. arterial fibrillation
B. paroxysmal
supraventricular
tachycardia
C. heart failure
D. bronchospastic disease
E. none o f the above
44.Patients on p-blockers therapy, should
be monitored for
A.
B.
C.
D.
E.
cardiac decompensation
ECGS
hypertriglyceridemia
A&B
All o f the above
45.
Which one o f the following statements
is not true?
A. p-blockers have a greater tendency
to occupy p2-receptors
B. p-blockers have the ability to release
catecholamines
C. p-blockers have the ability to
maintain a satisfactory heart rate
D. p-blockers
intrinsic
sympathomimetic
activity
may
prevent bronchoconstriction
E. none o f the above
46. Which o f the following agents block
both pi and p2-receptors?
A.
B.
C.
D.
E.
Propranolol
nadolol
timolol
Metoprolol
A ,B and C
47. Which o f the following has no intrinsic
sympathomimetic activity?
A.
B.
C.
D.
pindolol
acebutolol
carteolol
penbutolol
Hypertension
48.Which o f the following was the first
blocking agent that combined efficacy with
once daily dosing possessing intrinsic
sympathomimetic activity and having
relative cardioselective blocking activity.
A.
B.
C.
D.
E.
metoprolol
nadolol
atenolol
pindolol
acebutolol
49.Which o f the following was the first pblocking agent shown to be effective after
an acute Ml
A.
B.
C.
D.
E.
timolol
esmolol
betaxolol
labetalol
none o f the above
50. Which o f the following agents
possesses both a and p-blocking activity
A.
B.
C.
D.
E.
labetalol
esmolol
carvedilol
A&B
A&C
51. Which o f the following is the first p*
adrenergic blocker to have an ultrashort
duration o f action and is primarily used in
preoperative situations
A.
B.
C.
D.
E.
propranolol
esmolol
betaxolol
labetalol
phentolamine
52.In patients taking peripheral aadrenergic blockers all the following may
be exhibited, except
A.
B.
C.
D.
E.
a syncopal episode
increase in serum lipids
postural hypotension
dizziness
palpitation
53. Which one o f the following is a correct
match o f peripheral al-adrenergic blockers
and their daily doses?
A.
B.
C.
D.
E.
prazosin = 1-16 mg in one dose
terazosin = 1-20 mg in one dose
doxazosin= 2-30 mg in one dose
A&B
All o f the above
54.From the following centrally acting aagonists, which one has different
mechanism o f action?
A.
B.
C.
D.
E.
methyldopa
clonidine
guanabenz
guanfacine
none o f the above
55. Which one of the following is a correct
match o f centrally acting a2-receptors and
their daily dose
A. methyldopa = 500mg - 3g in two
to four doses
B. clonidine = 0.2-1.2 mg in 2 to 3
doses
C. guanabenz = 8 -32 in 2 doses
D. guanfacine = I-3mg in one dose
E. all o f the above
56. Which o f the foil wing is an effective
antihypertnesive in patients with renal
impairment?
A.
B.
C.
D.
E.
methyldopa
clonidine
guanabenz
guanfacine
none o f the above
57.A positive coombs’ test develops in 25
% o f patients with chronic use o f which of
the following?
A.
B.
C.
D.
E.
methyldopa
clonidine
guanabenz
guanfacine
none o f the above
58. Which one of the following is not an
effect seen in patients taking methyldopa?
A.
B.
C.
D.
E.
flu-like symptoms
sleep disturbances
impotence
lactation in either gender
reduced heart rate
59. Which one o f the following statements
is not true?
A. intravenous
administration
of
clonidine causes an initial increase
in pressure
B. guanabenz is the drug o f choice if
there
is
severe
coronary
insufficiency
C. clonidine has a tendency to cause or
worsen depression
D. clonidine heightens the sedating
effects o f alcohol
E. patient compliance is a major issue
for most hypertensive patients
60. Which one o f the following statements
are true about the post ganglionic
adrenergic neuron blocker, reserpine?
A. it acts centrally as
peripherally
by
well as
depleting
B.
C.
D.
E.
catecholamine stores in the brain
and in the peripheral adrenergic
system
a history o f
depression
is
contraindicated
the average daily dose is 0.05 - 0.25
mg in one dose
a
peptic ulcer
is
also
a
contraindication
all o f the above
65. Which one o f the following vasodilators
is closely related to thiazides chemically
but unlike thiazides promotes sodium and
water retention
A.
B.
C.
D.
E.
hydralazine
minoxidil
diazoxide
nitroprusside
none of the above
61 .Which one of the following statements
about vasodilators is not true?
A. it is used as a second line agent
B. they directly relax peripheral
vascular smooth muscle
C. direct vasodilators can be used alone
D. direct vasodilators may increase
heart rate
E. none o f the above
62. Which vasodilator has a potent effect on
both the arterial and venous systems?
A.
B.
C.
D.
E.
hydralazine
minoxidil
nitroprusside
Diazoxide
A&B
63. Which one o f the following is not
usually used in hypertensive crisis?
A.
B.
C.
D.
E.
hydralazine
labetalol
minoxidil
nitroprusside
diazoxide
64. Which vasodilator has the shortest onset
o f action?
A. sodium nitroprusside
B. nitroglycerine
C. Enalaprilat
D. Hydralazine
66. Which o f the following is/are correct
matching o f vasodilators with their adverse
effects?
A. Hydralazine = reflex tachycardia
B. minoxidil =
sodium and water
retention
C. nitroprusside = thiocyanate toxicity
D. diazoxide
=
transient
hyperglycemia
E. all of the above
67.Hydralazine may induce all the
following, except
A.
B.
C.
D.
E.
angina
systemic lupus erythematosus( SLE)
hypertrichosis
peripheral neuropathy
none o f the above
68.ACE inhibitors are indicated in
hypertension patients having the following
cases except
A.
B.
C.
D.
E.
diabetes
post MI
high coronary disease risk
hyperkalemia
chronic kidney disease
69.ACE inhibitors are not recommended to
be taken with
A.
B.
C.
D.
E.
A. patients with angina
B. patients
with
bronchospastic
diseases
C. patients with Raynaud’s disease
D. patients with second or third degree
AV block
E. none o f the above
ibuprofen
spironolactone
hydrochlorothiazide
A&B
B&C
70. Which one o f the following is not an
effect o f ACE inhibitors?
A.
B.
C.
D.
E.
75. Which one o f the following statements
is false?
neutropenia
proteinuria
renal insufficiency
flushing
dry cough
71 .Which o f the following is a long acting
analogue o f enalapril
A.
B.
C.
D.
E.
captopril
lisinopril
quinapril
ramipril
fosinopril
72. Which one o f the following is a prodrug
whose metabolite is used for treating acute
hypertensive crisis.
A.
B.
C.
D.
E.
captopril
enalapril
lisinopril
quinapril
perindopril
76.All o f the following are second
generation CCBs except
A.
B.
C.
D.
E.
73. Which o f the following is the original
ACE inhibitor
A.
B.
C.
D.
E.
A. calcium channel blockers (CCB)
inhibit the influx o f calcium through
slow channels o f vascular smooth
muscle
B. CCBs cause relaxation o f vascular
smooth muscles
C. each agent produces the same
degree o f atrioventricular nodal
depression
D. CCBs, when used with p-blockers,
have an additive effect on inducing
CHF and bradycardia
E. none o f the above
captopril
enalapril
benazepril
quinapril
ramipril
77. Which CCB besides being used for mild
to moderate hypertension has proven
efficacy as an antiarrhythmic and an
antiangina] agent?
A.
B.
C.
D.
E.
Hypertension
ANSW ERS
Hypertension
amlodipine
felodipine
nifedipine
nisoldipine
nicardipine
diltiazem
nifedipine
verapamil
felodipine
none o f the above
78. Which o f the following CCBs has been
associated with a significant degree o f
constipation
A.
B.
C.
D.
E.
diltiazem
nifedipine
verapamil
felodipine
none of the above
79. Which one o f the following statements
is false about angiotensin II type I receptor
antagonists?
A. similar to ACE inhibitors, increase
in serum potassium levels occur
B. they should not be used in special
hypertensive populations such as
diabetics with nephropathy or CHF
C. cough
associated
with
ACE
inhibitors also occurs in these agents
D. in the treatment o f hypertension,
there do not appear to be a
significant difference between ACE
inhibitors and angiotensin receptor
blockers
E. none -
80.In hypertensive emergency, all o f the
following conditions require immediate
reduction, except
A.
B.
C.
D.
E.
hypertensive encephalopathy
acute left ventricular failure
malignant hypertension
dissecting aortic aneurysm
intracranial hemorrhage
ANSWERS
lypertension
1. Answer: E. All except D
Explanation:
The recent recommendations o f the Seventh report o f the joint National Committee on Detection
evaluation and treatment on high blood pressure(JNC-7) has added a “pre hypertension'’
category, which includes individual^ with systolic blood pressure readings o f 120-139 or
diastolic blood pressure readings of 80-89 mmHg and is now included in contemporary
management strategies.
Choices A, B and C are all definitions! o f hypertension.
2. Answer: E. All o f the above
Explanation:
Relationship between elevated blood pressure and cardiovascular disease has been addressed in
the JNC-7 report and formalizes the fact that the higher blood pressure, the greater the chance o f
MI, heart failure, stroke or kidney disc;ase.
3. Answer: C. Cardiac output decreases
Explanation:
Baroreceptors in the carotids and aorti c arch respond to changes in blood pressure and influence
arteriolar dilation and arteriolar constri ction. When stimulated to constriction the contractile force
strengthens, increasing the heart rat and augmenting peripheral resistance, thus increasing
cardiac output.
4. Answer: D. Blocking sympathetic nervous system
Explanation:
Increased fluid volume increases venous system distention and venous return, affecting cardiac
output and tissue perfusion. These changes alter vascular resistance, increasing blood pressure. In
the renin-angiotensin-aldosterone sysem , the renin reacts with circulating angiotensinogen to
produce angiotensin I. This in turn, is hydrolyzed to form angiotensin II( a very potent natural
vasoconstrictor). This vasopressor sti nulates aldosterone release from the adrenal gland (zona
glomerulosa), which results in increase d sodium reabsorption, fluid volume and blood pressure.
But blocking the sympathetic nervous system lowers blood pressure by dilating the peripheral
blood vessels.
5.
Answer: D. Epinephrine
Explanation:
Vasoactive substances that are invol|ed in maintenance o f normal blood pressure have been
identified and these include nitric oxide (vasodilating^ factor), endothelin (vasoconstrictor
peptide), bradykinin (potent vasodilator inactivated by angiotensin converting enzyme (ACE) and
atrial natriuretic peptide (naturally occurring diuretic).
But little evidence suggests that epinephrine and norepinephrine have a clear role in the etiology
o f hypertension.
6. Answer: A. Stage one hypertension has a systolic blood pressure o f 160 mmHg
Explanation:
The systolic blood pressure o f normal hypertension is <120, prehypertension 120-139 mmHg,
stage 1 hypertension 140-159 mmHg and stage 2 hypertension is > 160 mmHg.
7. Answer: E. all of the above
Explanation:
For most stage 2 hypertension, two drug combinations are indicated e.g. thiazide + ACE inhibitor
or ARB or P-blocker or CCB.
8. Answer: E. all o f the above
Explanation:
Major risk factors for high blood pressure include DM, and physical inactivity, cigarette smoking,
obesity, dyslipidemia and microalbuminuria.
9. Answer: E. All o f the above
•
Explanation:
Secondary hypertension results from an identifiable cause, such as renal disease or adrenal
hyperfunction and the blood pressure elevations do not respond to anti hypertensive treatment.
10. Answer: E. All o f the above
Explanation:
Steroid or estrogen intake, including oral contraceptives, NSAIDs, nasal decongestants, tircyclic
antidepressants, appetite suppressants, cyclosporine, erythropoietin and MAO inhibitors, may
induce hypertension.
11 .Answer: A. Blood urea nitrogen( BUN) - confirms renal disease
Explanation:
In the laboratory findings, BUN and creatinine elevations suggest renal disease. Increased urinary
excretion o f catecholamines or its metabolites confirms pheochromacytoma and hypokalemia
suggests primary aldosteronism or Cushing’s syndrome.
12. Answer: E. all o f the above
Explanation:
Weight gain, moon face, truncal obesity, hirsutism and hypokalemia may signal Cushing’s
syndrome. Weight loss, episodic flushing, diaphoresis and increased urinary catecholamines
suggest pheochromocytoma. Repeated UTI, elevated serum creatinine levels may signify rena]
involvement and muscle cramps, excess urination and weakness may suggest primary
aldosteronism. Cushing’s syndrome pheochromocytoma, renal disease and primary
aldosteronism, sleep apneas are all underlying causes o f secondary HTN.
13.Answer: D. Ketoacidosis
Explanation:
Ketoacidosis happens in type 1 DM patients but choices A, B and C are all diagnostic tests of
HTN.
14.Answer: B. Ill only is correct
Explanation:
Pheochromocytoma is a tumor o f the adrenal medulla which stimulates hypersecretion o f
epinephrine and nor epinephrine and directly results in increased total peripheral resistance
(TPR). Primary aldosteronism is hyper secretion o f aldosterone by the adrenal cortex which
increases distal tubular sodium retention, expanding the blood volume, thus indirectly increasing
TPR. And renal artery stenosis results in a decreased renal tissue perfusion activating the reninangiotensin-aldosterone system.
15.
Answer: E. AH o f the above
,
Explanation:
All the above statements are objectives in treating primary hypertension.
16. Answer: E. all o f the above
Explanation:
Major risk factors according to the JNC-7 include smoking, DM, age >55 years(men), > 65 years(
women), a family history o f cardiovascular disease and dyslipidemia. Other predisposing factors
include racial predisposition (African-Americans), high dietary intake o f saturated fats or sodium
and hyperlipidemia.
17. Answer: B. Shiny deposits
Explanation:
Examination o f the ocular fundi is valuable; their condition can indicate the duration and severity
o f hypertension. In the early stages, hard, shiny deposits, tiny hemorrhages and elevated arterial
blood pressure occur. While in the late stages, cotton-wool patches, exudates, retinal edema,
papilledema caused by ischemia, capillary insufficiency, hemorrhages and microaneurysms
become evident.
18. Answer: A. A single elevated reading o f> 140/90 is sufficient basis for diagnosis
Explanation:
Serial blood pressure readings greater than or equal to 140/90 should be obtained on at least two
occasions before specific therapy is begun, unless the initial blood pressure levels are markedly
elevated( i.e. > 2 1 0 mmHg systolic, > 120 mmHg diastolic, or both) or are associated with target
organ damage. A single elevated reading is an insufficient basis for diagnosis. Essential
hypertension usually does not become clinically evident other than through serial blood pressure
elevations until vascular changes affect the heart, brain, kidneys and ocular fundi.
19. Answer: A. To cure primary hypertension
Explanation:
In the general principles, the treatment primarily aims to lower blood pressure toward “normal”
with minimal side effects and to prevent or reverse organ damage. Currently, there is no cure for
primary HTN.
20.Answer: A. Patients with diastolic pressure o f 80-89 or a systolic pressure o f 120-139 mmHg
are candidates for drug treatment
Explanation:
All patients with a diastolic pressure o f > 90 mmHg and a systolic pressure o f greater than 140
mmHg, or a combination o f both should receive antihypertensive drug therapy.
For those patients with a diastolic pressure of 80-89 mmHg or a systolic pressure o f 120-139
mmHg( prehypertension), no drug treatment is indicated unless the patient has a compelling
indication. The goal BP for patients with diabetes or renal disease is 130/80mmHg.
21 .Answer: B. Thiazide diuretics
Explanation:
Thiazide diuretics are the initial choice o f therapy due to the fact that they have demonstrated a
reduction in morbidity and mortality when used as initial monotherapy.
22. Answer: E. All o f the above
Explanation:
ACE inhibitors are used in hypertension patients having systolic dysfunction after myocardial
infarction, a diabetic nephropathy patient who might benefit from a ACE inhibitor in combination
with a diuretic, or a patient with congestive heart failure( CHF).
23.Answer: D. Angiotensin 11 receptor antagonists - minoxidil
Explanation:
Angiotensin II receptor antagonists include candesartan, eprosartan, irbesartan, losartan and
others. But minoxidil is a vasodilator, including others like hydralazine and nitroprusside.
24.Answer: C. Reserpine
Explanation:
All the above drugs are generally grouped as sympatholytics. Prazosin is
a-adrenergic blocking agent( doxazosin, terazosin), verapamil is a calcium channel blocker(
diltiazem, amlodipine, felodipine, nifedipine etc), clonidine is a centrally acting
a-agonists ( guanabenz, guanfacine, methyldopa) and nadolol is a P-adrenergic blocking agent(
betaxolol, carvedilol, metoprolol, propranolol etc).
25.
Answer: D. Stimulation o f renin secretion is blocked
Explanation:
Stimulation o f renin secretion is blocked is the action o f p-adrenergic blockers.
26. Answer: B. NSAIDs
Explanation:
N SAlDs, such as ibuprofen, interact to diminish the antihypertensive effects of the thiazide and
loop diuretics. ACE inhibitors, p-adrenergic blockers and angiotensin II receptor antagonists
work well with thiazide diuretics because a thiazide diuretic increases the effectiveness o f other
antihypertensive agents by preventing the re expansion o f extracellular and plasma volume.
27.Answer: D. Calcium levels decrease
Explanation:
Hypertension patients taking thiazide diuretics face potassium ion ( k+) depletion which may
require supplem entation increased dietary intake or potassium sparing diuretic), uric acid
retention may occur ( this is potentially significant in patients who are predisposed to gout).
Blood glucose level may increase (which may be significant in patients with diabetes) and
calcium levels may increase because o f the potential for retaining calcium ions.
28.Answer: D. Depression
Explanation:
Common effects of thiazides include fatigue, headache, palpitations, rash, vertigo and transitory
impotence. The alterations in fluid and electrolytes (e.g. hypokalemia, hypomagnesemia, and
hypercalcemia) may predispose patients to cardiac irritability, with a resultant increase in cardiac
arrhythmias. Electrocardiograms (ECGs) should be performed routinely to prevent the
development o f life threatening arrhythmias.
29.
Answer: E .Quinethazone = 2 -4 mg daily
Explanation:
Quinethazone dose is 50-200 mg daily but polythiazide and 2-4 mg is the dose of
trichlormethiazide taken daily.
30.Answer: C. Amiloride
Explanation: Furosemide, Ethacrynic acid, Bumetanide and Torsemide act primarily in the
ascending loop o f henle. Hence, they are called “loop” diuretics by acting with in the loop o f
hence, they decrease sodium reabsorption. Their action is more intense but o f shorter duration (1 4 hours) than that o f the thiazides; they may also be more expensive. Amiloride is potassium
sparing diuretic.
31 .Answer: D. Spironolactone
Explanation:
Spironolactone is particularly useful in patients with hyperaldosteronism as it has direct
antagonistic effects on aldosterone (aldosterone-receptor blocker).
32.Answer: B. loop-diuretics
Explanation:
Loop diuretics are indicated when patients are unable to tolerate thiazides, experience loss o f
thiazide effectiveness or have impaired renal function (clearance <30 ml/min). And potassiumsparing diuretics should be avoided in patients with acute renal failure and used with caution in
patients with impaired renal function because they can retain potassium.
33.Answer: B. loop diuretics
Explanation:
In patients taking loop-diuretics, transient deafness has been reported. I f the patient is taking a
potentially ototoxic drug (e.g. aminoglycoside antibiotic), another class o f diuretic ( e.g. a
thiazide diuretic) should be substituted for a loop diuretic.
34.Answer: D.Torsemide-25-50 mg daily
Explanation:
All are correct matches, except Torsemide whose correct daily dose is 2.5 - 10 mg.
35.Answer: E. Potassium sparing- thiazide diuretics- loop diuretics
Explanation:
Loop diuretics action is more intense but o f shorter duration( 1-4 hours) than that o f thiazides.
Potassium sparing diuretics achieve their diuretic effects differently and less potently than the
thiazides and loop diuretics.
36.Answer: C. ACE-inhibitors
Explanation:
~
Co-administration o f potassium sparing diuretics with ACE inhibitors or potassium supplements
significantly increases the risk of hyperkalemia. But they are often used in combination with a
thiazide diuretic because they potentiate the effects o f thiazide while minimizing potassium loss.
37.Answer: C. triamterene
Explanation:
Triamterene( a potassium sparing diuretic) should not be used in patients with a history o f kidney
stones or hepatic disease.
38.Answer: B. spironolactone = 100 -400 mg daily
Explanation:
Spironolactone is taken 100 - 400 mg daily to treat hyperaldosteronism but in the treatment o f
hypertension the dose taken is 25 - 100 mg daily.
39.Answer: A. p-adrenergic blockers
Explanation:
P-blockers are particularly effective in patients with rapid resting heart rates( i.e. artrial
fibrillation, paroxysmal supraventricular tachycardia) or “ compelling indications” such as heart
failure, post-MI, high coronary disease risk, and diabetes.
40.Answer: C. heart rate is reduced
E xplanation:
p -B lock ers action m ay includ e blockade o f stim ulation o f renin secretion, decrease in
cardiac contractility and reduction in heart rate. B ut peripheral a l-a d ren erg ic blockers
b lo ck the peripheral p ostsynaptic a l-a d ren erg ic receptor causing vasodilatation o f both
arteries and vein s.
41 .Answer: E. All o f the above
Explanation:
Young (<45 years) whites with high cardiac output, high heart rate and normal vascular resistance
respond best to p-blocker therapy.
42.Answer: B. bronchospastic disease
Explanation:
Suddenly stopping p-blocker therapy puts the patient at a risk for a withdrawal syndrome that
may produce exacerbated anginal attacks (particularly in patients with coronary artery disease),
MI and a life threatening rebound o f blood pressure to levels exceeding pretreatment readings.
43.Answer: D. bronchospastic disease
Explanation:
P-adrenergic blockers are particularly effective in patients with rapid resting heart rates ( i.e.
artrial fibrillation, paroxysmal supraventricular tachycardia) or “compelling indications” such as
heart failure, post-MI, high coronary disease risk or diabetes. But no P-blocker is totally safe in
patients with bronchospastic disease( e.g. asthma, chronic obstructive pulmonary disease (
COPD).
44.Answer: E. All o f the above
Explanation:
Patients must be monitored for signs and symptoms o f cardiac decompensation ( i.e. increasingly
reduced cardiac output) because decreased contractility can trigger compensatory mechanisms,
leading to CHF. ECGs should be monitored routinely because all p-blockers can decrease
electrical conduction within the heart. Hypertriglyceridemia, reduced HDL cholesterol or
increased LDL cholesterol have been reported as major consequences of p-blockers, which
require routine lipid evaluations with chronic therapy.
45.Answer: A. p-blockers have a greater tendency to occupy p2-receptors
Explanation:
Relative to propranolol, P-blockers have a greater tendency to occupy the pi
Receptor in the heart, rather than the p2-receptors in the lungs( relative cardioselective activity).
P-blockcrs have the ability to release catecholamines and to maintain a satisfactory heart rate(
intrinsic sympathomimetic activity). Intrinsic sympathomimetic activity may also prevent
bronchoconstriction and other direct p-blocking actions.
46.Answer: E. A, B and C
Explanation:
Propranolol, nadolol and timolol block both pi and p2-receptors and metoprolol, atenolol,
betaxolol and bisoprolol are all cardioselective.
47.
Answer: E. bisoprolol
Explanation:
Bisoprolol has no intrinsic sympathomimetic activity. Pindolol was the first
p-blocking agent shown to have high intrinsic sympathomimetic activity while penbutolol has a
weak intrinsic sympathomimetic activity and carteolol has moderate intrinsic sympathomimetic
activity. Acebutolol also possesses intrinsic sympathomimetic activity.
48.Answer: E. acebutolol
Explanation:
Metoprolol was the first P-blocking agent with relative cardioselective blocking activity, the
average daily dose is 50-300 mg and nadolol was the first P-blocking agent that allowed once
daily dosing. It blocks both pi and p2 receptors, the average daily dose is 40-320 mg. while
atenolol was the first p-blocking agent to combine once daily dosing with relative cardioselective
blocking activity, the average daily dose is 25-100 mg and pindolol was the first p-blocking
agent shown to have high intrinsic sympathomimetic activity, the average daily dose is 10-60 mg.
Acebotolol was the first blocking agent that combined efficacy with once daily dosing, possessing
intrinsic sympathomimetic activity and having relative cardio selective blocking activity.
49.Answer: A. Timolol
Explanation:
Timolol was the first p-blocking agent shown to be effective after an acute M] to prevent sudden
death. It blocks both pi and P2 receptors. The average daily dose is 20-60 mg.
50.Answer: E. A and C
Explanation:
Labetalol was the first p-blocking agent shown to possess both a and p-blocking activity. The
average daily dose is 200— 1200 mg. Labetalol is also effective for treating hypertensive crisis.
Carvedilol is a P-blocking agent that has ({-blocking properties as well as a-blocking
properties, with a resultant vasodilatation. The drug is administered twice daily with a starting
dose o f 6-25 mg titrated at 7-14 day intervals to a dose o f 25 mg twice daily( maximum daily
dose is 50 mg daily). But esmolol is a
P-blocking agent with an ultra short acting action.
51 .Answer: B. esmolol
Explanation:
Esmolol was the first p-blocking agent to have an ultrashort duration of action (1-2 minutes).
This agent is not used routinely in treating hypertension owing to its duration o f action and the
need for intravenous administration. The average daily dose is 25-50 fjg/kg/min up to 300
(ig/kg/min intravenously. Propranolol is available both as rapid acting product and a long acting
product, the average daily dose is 40-48 mg. Betaxolol is a new P-blocker with a half life that
allows for once daily dosing. The average daily dose is 5-20 mg.
Labetalol has an onset of action o f 5-10 minutes.
Phentolamine is an a-adrenergic blocker with an onset o f action of 1-2 minutes.
52.Answer: B. increase in serum lipids
Explanation:
In the first dose phenomenon, a syncopal episode may occur with in 30-90 minutes of the first
dose. Similarly associated are postural hypotension, nausea, dizziness, headache, palpitations, and
sweating. To minimize these effects the first dose should be limited to 1 mg o f each agent and
administered just before bed time. These agents have no adverse effects on serum lipids and other
cardiac risk factors.
53.Answer: B. terazosin = 1-20 mg in one dose
Explanation:
Prazosin has a daily dose of 2-30 mg in two doses and doxazosin is taken
1-16 mg in one dose
54.Answer: A. methyldopa
Explanation:
Methyldopa decreases total peripheral resistance by acting on a2-receptors to decrease
sympathetic out flow to the cardiovascular system, while having little effect on cardiac output or
heart rate(except in older patients). While clonidine, guanabenz and guanfacine all stimulate
«2-receptors centrally, decreasing vasomotor tone and heart rate.
55.Answer: E. All o f the above
Explanation:
All the above matches are correct.
56.Answer: B. clonidine
Explanation:
Clonidine is effective as antihypertensive in patients with renal impairment although they may
require a reduced dose or a longer dosing interval. Guanabenz and guanfacine are recommended
as adjunctive therapy with other antihypertensives for additive effects when initial therapy has
failed.
57.Answer: A. methyldopa
Explanation:
'
A positive coombs’ test develops in 25 % o f patients with chronic use o f methyldopa ( longer
than 6 months). Less than 1% o f these patients develop a hemolytic anemia. The anemia is
reversible by discontinuing the drug.
58.Answer: E. reduced heart rate
-
Explanation:
Common untoward effects o f methyldopa include orthostatic hypotension, fluid accumulation (in
the absence o f diuretic) and rebound hypertension upon abrupt withdrawal. Sedation is a common
finding upon initiating therapy and when increasing doses, however, the sedative effect usually
decreases with continued therapy. Other effects include dry mouth, subtly decreased mental
activity, sleep disturbances, depression, impotence and lactation in either gender.
Reduced heart rate is a side effects exhibited by guanabenz and guanfacine, including others like
sedation, dry mouth and dizziness.
59.
Answer: B. guanabenz is the drug o f choice if there is severe coronary insufficiency
Explanation:
Guanabenz and guanfacine should be used cautiously with other sedating medications and in
patients with severe coronary insufficiency, recent MI, cerebrovascular accident (CVA), and
hepatic or renal disease.
60. Answer: E. all o f the above
Explanation:
Because o f the high incidence o f adverse effects with reserpine, other agents are usually chosen
first. When used, Reserpine is given in low doses and in conjunction with other antihypertensive
agents. A history o f depression is contraindicated, even low doses such as 0.25 mg/day, can
trigger a range o f psychic responses, from nightmares to suicide attempts. Drug induced
depression may linger for months after the last dose. Peptic ulcer is also a contraindication for
using reserpine, even single dose tends to increase gastric acid secretion.
61 .Answer: C. direct vasodilators can be used alone
Explanation:
Vasodilators are used as a second-line agents in patients refractory to initial therapy with
diuretics, p-blockers or supplemental agents such as ACE inhibitors or CCBs. Vasodilators
directly relax peripheral vascular smooth muscle arterial, venous or both. The direct vasodilators
should not be used alone owing to increase in plasma renin activity, cardiac output and heart rate.
62.Answer: C. Nitroprusside
Explanation:
Hydralazine directly relaxes arterioles, decreasing systemic vascular resistance. And minoxidil is
a more potent vasodilator than hydralazine; it relaxes arteriolar smooth muscle directly,
decreasing peripheral resistance. It also decreases renal vascular resistance while preventing renal
blood flow. Nitroprusside is a direct acting peripheral dilator, it has potent effects on both the
arterial and venous systems. Diazoxide exerts a direct action on the arterioles but has a little effect
on venous capacity.
63.Answer: C. Minoxidil
Explanation:
Hydralazine is used intravenously or intramuscularly in managing hypertensive crisis.
Nitroprusside is usually used only in short-term emergency treatment o f acute hypertensive crisis,
when a rapid effect is required( it is administered intravenously with continuous blood pressure
monitoring). And diazoxide is used intravenously in the emergency treatment o f acute
hypertensive crisis. But minoxidil is commonly used to treat patients with severe hypertension
that has been refractory to conventional drug regimen. Labetalol is a P-blocking agent that has an
onset o f action o f 5-10 minutes and is effective for treating hypertensive crisis.
64.Answer: A. sodium nitroprusside
Explanation:
Sodium nitroprusside has an onset o f action o f 0.5-1 minute (thus the shortest). Nitroglycerine has
2-5 minutes while diazoxide has 2-4 minutes but hydralazine has 10-20 minutes if it is IV or 20­
30 minutes if it is IM and enalaprilat has onset o f action o f 15-30 minutes.
~
65.Answer: C. diazoxide
Explanation:
Diazoxide is closely related to the thiazides chemically and patients with thiazide sensitivity
cross-react to diazoxide. But unlike the thiazides this agent promotes sodium and water retention,
potentiating edema. Hypotensive reactions may be severe.
66.
Answer: E. all o f the above
Explanation:
When using hydralazine, reflex tachycardia is common and should be considered before initiating
therapy and it triggers compensatory reactions that counteracts its antihypertensive effects, it is
most useful when combined with a p-blocker, central a-agonist, or diuretic. Minoxidil promotes
sodium and water retention, particularly in the presence o f renal impairment so patients should be
monitored for fluid accumulation and signs of cardiac decompensation. And peripheral dilation
results in reflex activation o f the sympathetic nervous system and an increase in heart rate,
cardiac output and renin secretion. Administering along with a sympatholytic agent and a potent
diuretic( e.g. furosemide) minimizes increased sympathetic stimulation and fluid retention.
Nitroprusside with long term treatment may cause thiocyanate toxicity particularly in patients
with reduced renal activity (but can be treated with hemodialysis). Symptoms may include
fatigue, anorexia, disorientation, nausea, psychotic behavior or muscle spasms. Cyanide toxicity
can occur (rarely) with long term, high dose administration. It may present as altered
consciousness, convulsions, tachypnea or even coma. Diazoxide produces transient
hyperglycemia, requiring caution if administered to patients with diabetes.
67.Answer: C. hypertrichosis
Explanation:
Hydralazine may induce angina, especially in patients with coronary artery disease and those not
receiving p-blocker. Drug induced SLE may occur but the risk may be reduced by administering
doses o f less than 200 mg /day( fatigue, malaise, low grade fever and joint aches may signal
SLE). Other effects may include headache, peripheral neuropathy, nausea, vomiting, fluid
retention and postural hypotension. But hypertrichosis( i.e. excessive hair growth) is a common
side effect o f minoxidil particularly if the drug is continued for more than 4 weeks.
68.Answer: D. hyperkalemia
Explanation
Recent JNC-7 recommendations have identified specific patient populations that have “
compelling indications” such as diabetes, post myocardial infarction, high coronary disease risk,
chronic kidney disease, and recurrent stroke prevention as where ACE inhibitors are indicated in
the treatment o f hypertensive or prehypertensive patients. The mechanism o f action o f ACE
inhibitors tends to increase potassium levels,so serum potassium levels should be monitored
regularly for hyperkalemia.
Explanation:
The antihypertensive effect o f ACE inhi^>itors may be diminished by NSAIDs (e.g. ibuprofen)
and potassium sparing diuretics increase serum potassium levels when used with ACE inhibitors,
Hydrochlorothiazide is the diuretic used with various ACE inhibitors in a combination product for
hypertension.
70. Answer: D. Flushing
Explanation:
ACE effects include neutropenia (rare but serious), proteinuria, renal insufficiency (in patients
with predisposing factors) and a dry cc iugh which could disappear within a few days after ACE
inhibitor is discontinued. Other
untoward effects include rashes, altered sense o f taste(dysgeusia), vertigo, headache, fatigue, first
dose hypotension, minor GI disturbance];. Flushing is the adverse effects o f the CCB, nifedipine.
71.Answer: B. lisinopril
Explanation:
Lisinopril is a long acting analogue of nalapril, given initially as a 5-1 Omg daily dose and
adjusted to an average daily dose o f 5-^ 0 mg in one dose.
72.Answer: B. enalapril
Explanation:
Enalapril is a prodrug, which is rapidIV converted to its active metabolite, enalaprilat. Initial doses
are 5 mg daily, with an average daily c ose o f 5-40 mg. The enalaprilat form o f the drug has been
used effectively for treating acute hypertensive crisis.
73.Answer: A. Captopril
Explanation:
Captopril is the original ACE inhibito given initially as 6.25 mg dose three times daily and is
increased to an average daily dose o f 25-150 mg in two or three doses.
74. Answer: D. patients with second or third degree AV block
Explanation:
CCBs are considered alternative dru 1 $ for the initial treatment o f hypertension in select patient
populations that are unable to take f adrenergic-receptor blockers, such as patients with angina
who also have bronchospastic diseases or raynaud’s disease. But CCBs especially diltiazem and
verapamil must be used with extreme caution or not at all in patients with conductive disturbances
involving the SA or AV node, such s second or third degree AV block, sick sinus syndrome and
digitalis toxicity.
75.Answer: C. each agent produces the same degree o f atrioventricular nodal depression
Explanation:
Although the CCBs share a similar mechanism o f action, each agent produces different degrees of
systemic and coronary arterial vasodilation, sinoatrial (SA) and atrioventricular (AV) nodal
depression, and a decrease in myocardial contractility
76.Answer: C. nifedipine
Explanation:
Amlodipine, isradipine, felodipine, nicardipine and nisoldipine are second generation CCBs.
These agents have been developed to produce more sedative effects on specific target tissues than
the first-generation agent’s diltiazem, nifedipine and verapamil. These 2nd generations are
chemically similar to nifedipine and are referred to as dihydropyridine derivatives.
77.Answer: A. diltiazem
Explanation:
Diltiazem in a daily dose o f 120-360 mg in two doses is effective for treating mild to moderate
hypertension. Diltiazem also has proven efficacy as an antiarrhythmic and an antianginal agent.
78.Answer: C. Verapamil
Explanation:
Verapamil use has been associated with a significant degree o f constipation, which must be
treated to prevent stool straining and non compliance. Other effects include dizziness and
hypotension. Nifedipine has been associated with flushing, headache and peripheral edema.
79.Answer: C. Cough associated with ACE inhibitors also occurs in these agents
Explanation:
Cough associated with ACE inhibitors does not appear to occur with this group o f drugs.
80.Answer: C. malignant hypertension
Explanation:
In hypertensive emergency is a severe elevation o f blood pressure( > 200 mmHg/ >140 mmHg)
that demands immediate(within minutes) reduction include hypertensive encephalopathy, acute
left ventricular failure with pulmonary edema, dissecting aortic aneurysm, acute MI an
intracranial hemorrhage. Conditions requiring prompt( within hours) reduction include malignant
or accelerated hypertension.
Immunology
Xbrf<s(D
“M any o f life’s failures are men w ho did not realize how close they were to success
when they gave up.”
Thomas Edison
1. Chemical compounds that bind to
products o f an immune response
A*
B.
C.
D.
Immunogens
Antigens
Haptens
Tolerogens
A.
B.
C.
D.
E.
T-lymphocytes
Macrophages
Natural killer cells
Basophils
Mast cells
6. Which one o f the following statements
is NOT TRUE?
2. Which one o f the following is a
hapten?
A.
B.
C.
D.
E.
pentadecyl catechol
penicillin
pollens
A&B
All o f the above
3. Which one o f the following statements
is NOT TRUE?
A. compounds associated or
secreted by parasitic bacteria
may act as both immunogens
and antigens
B. for a molecule to be
immunogenic it must contain
protein or peptide
C. insulin can act as immunogenantigens
D. the route o f administration o f a
compound may lead to
immunogen-antigen effect
E. none
4. The primary cells o f specific immune
responses are
A.
B.
C.
D.
E.
B-lymphocytes
neutrophils
T-lymphocytes
A&C
B&C
5. These cells recognize and destroy
tumors
A. B-cells have thousands o f
identical antibodies in their
membrane
B. Different B-cells have different
antigen specificities
C. Each B-cell has only one
specificity
D. B-cells that recognize specific
antigens divide to form new Bcells
E. None
7. The memory B-cells membrane
antibodies are immunoglobulin classes of
I. IgA
II.IgD
A.
B.
C.
D.
E.
III. IgM
IV. IgE
I & III
II, III, V
1, III, IV
I,IV ,V
II, IV, V
8. T-cells mature in
A.
B.
C.
D.
bone-marrow
thymus-gland
lymph nodes
none
9. These cells suppress immune
responses through the secretion o f
IL-10 and TGF-(3
A. Tc
B. Tr
C. T„ -
D. CD4+CD25+
E. none
10. All the following are membrane
glycoproteins o f T cells, EXCEPT
A.
B.
C.
D.
E.
CD4
CD8
CD3
CTL
None
11 .T-cells normally recognize peptide
epitopes that are chemically combined
with
A.
B.
C.
D.
antigen presenting cells(APC)
MHC
Memory cells
None
12.These cells activate B-cells to divide
and produce antibody
A.
B.
C.
D.
E.
Plasma cells
TH2 cells
CD8 cells
Virgin T cells
none
15.Eliminating o f an antigen from the
body involves the process
A.
B.
C.
D.
E.
phagocytes
pro inflammatory
cytotoxic
regulatory
all
16.In humoral immune responses,
antigens are recognized by
A.
B.
C.
D.
E.
antigen
antigen
antigen
antigen
A&B
specific
specific
specific
specific
B-cells
TH cells
leukocytes
macrophages
17.The first time a specific antigen is
encountered the antibody secreted in the
primary immune system is
A.
B.
C.
D.
E.
IgD
IgG
IgM
IgA
IgE
18.The most antibody produced with a
second or subsequent encounter with the
same antigen is
13.The best understood APCs are
A.
B.
C.
D.
macrophages
dendritic cells o f lymph nodes
dendritic cells o f spleen
All o f the above
14. Any cell in the body acts as APC for
immune responses involving
A.
B.
C.
D.
CTL cells
Macrophages
TH cells
none
A.
B.
C.
D.
E.
IgA
IgG
IgD
IgM
IgE
19. The function o f an antibody is
A.
B.
C.
D.
E.
to act as antigen receptor
to eliminate antigens
neutralization o f toxins
A&C
All
20. Which one o f the following statements
is false about the structure o f immuno
globulins?
A. immunoglobulin has four
polypeptide
B. each chain is divided into a Cterminal constant region and Nterminal variable region
C. the C-terminal constant region
is responsible for antigen
binding
D. antibody and immunoglobulins
could mean the same thing
E. none
21 .The immunoglobulin that protects the
mucosa from colonization is
I. IgA
II. IgG
24. Which cytokine is responsible for
promotion o f cell mediated immunity and
activation o f TC and NK cells
A.
B.
C.
D.
E.
IL-1
IL-12
IL-13
IL-14
IL-10
25.Immnoglobulins cross-reactivity may
occur through the sharing o f antigens by
two strains of
A.
B.
C.
D.
E.
bacteria
viruses
other microorganisms
A&B
All
III. IgD
26. Which one o f the following is NOT
true about Fab and F (ab')2 fragments
IV. IgE
A.
B.
C.
D.
E.
I only
I& III
IV only
II & IV
II & HI
A. they are enzymatically cleaved
from immunoglobulins
B. they are clinically useful
C. they retain antigen specificity
D. they are class specific
E. none
22.Their serum immunoglobulin content
in a decreasing order is
A.
B.
C.
D.
E.
V, II , I , I V
I I , I , V, III
1, II, III, V
II, V , I , III
1 1 ,1 , V , I V
23. Which cytokine is responsible for
memory cell formation and eosinophil
production?
A.
B.
C.
D.
E.
IL-5
1L-6
1L-7
IL-8
IL-9
27.Complement is responsible for all the
following EXCEPT
A. preparation o f extra cellular
antigen for phagocytosis
B. for increasing inflammatory
response
C. phagocytosis o f antigen
D. lysis o f cells
E. None
28.In which type o f pathway does an
immune complexes o f IgM or IgG
antibodies bind to subunits o f
complement component
A.
B.
C.
D.
E.
classic activation pathway
alternative activation pathway
mannose-binding pathway
B&C
None
29.Proinflammatory cells that rapidly
initiate acute inflammation
A.
B.
C.
D.
E.
basophiles
neutrophils
mast cells
A&B
A&C
30.A11 the following are the primary
effects o f mast cells and basophile
mediators, EXCEPT
A. vascular dilation
B. increased vascular permeability
C. contraction o f respiratory and
gastrointestinal smooth muscles
D. neutrophil and eosinophil
chemotaxis
E. none
33.Non-viral intracellular parasites are
primarily eliminated by
A.
B.
C.
D.
E.
NK cells
CTL cells
T-cell macrophage
A&B
None
34.Which one o f the following statements
is true about a cell infected with a virus?
A. CTL cells recognize infected
cells and directly kill them
B. NK cclls kill infected cells in an
antigen specific manner
C. Antibodies are generally
ineffective against infected cells
D. All except B
E. All except C
35-IFN-y is secreted during the
elimination o f virus from all the following
sources EXCEPT
A.
B.
C.
D.
E.
CTL
NK
Macrophages
TH1 cells
None
31 .In antibody dependent cell mediated
cytotoxicity the cells involved are
36.Tumors are eliminated by
A.
B.
C.
D.
E.
NK cells
Macrophages
Tc cells
All except A
All
A.
B.
C.
D.
E.
NK cells
CTL cells
Macrophages
A&B
All
32.Cell mediated immunity is involved
A.
B.
C.
D.
E.
non-viral intracellular parasite
viruses
tumors
B&C
All
37.Type I hypersensitivity reaction is due
to hyper secretion of
A.
B.
C.
D.
E.
IgM
IgE
IgG
A &C
None
38. A child’s probability o f being a hyper
secretor o f IgE with two hyper secretor
parents is
A.
B.
C.
D.
E.
25%
50%
75%
80%
90%
39.In normosecretors o f IgE
A. 100 ^ g - 1 mg/dl o f IgE is
secreted
B. local mast cells are armed
C. basophiles are armed
D. A & B
E. All
40.Drugs that act as cell or plasma protein
bound haptens are
A.
B.
C.
D.
E.
respiratory allergens
gastrointestinal allergens
skin or mouth aHergens
intravenous allergens
none
41 .Vasodilation and increased capillary
permeability are caused by
A.
B.
C.
D.
E.
histamine
platelet activating factor
chemotactic factors
A&C
All
42.In sensitizes individuals absorption of
peanuts across the mucus membrane can
cause
A.
B.
C.
D.
E.
systemic edemic
hypovolemic shock
asphyxiation
cardiac arrhythmia
all
43. The early reaction o f immediate
hypersensitivity reaction begins with in
A.
B.
C.
D.
15-30m in
1-2 min
1-2 hour
none
44. Which agents are used in the diagnosis
o f type I hypersensitivity reactions
A.
B.
C.
D.
E.
RAST assay
RIST assay
Agglutination test
A&B
All
45. Which one o f the following is not part
o f therapy against type I hypersensitivity
reaction?
A.
B.
C.
D.
E.
competitive Hi antagonists
passive immunization
epinephrine
topical steroids
none
46.Drug that reverses anaphylaxis
through its a-agonist and P-agonist effects
A.
B.
C.
D.
E.
competitive H]-antagoinsts
epinephrine
coromolyn sodium
topical steroids
none
47.Non-IgE mediated type I
hypersensitivity reaction is contributed by
A. hyper reactivity o f mast cells
B. respiratory p2-receptors
unresponsiveness
C. a high concentration o f antigen or
antibody
D. A & B
E. All
D. A & B
E. A & C
48.Type II hypersensitivity reactions are
due to
A.
B.
C.
D.
E.
anaphylaxis
cytotoxicity
immune-complex
A&B
B&C
A.
B.
C.
D.
49. Which one o f the following is not a
common allergen in type II
hypersensitivity reactions?
A.
B.
C.
D.
E.
foreign blood surface antigens
anti sera
drug allergens
self antigens
none
50.The leading cause o f hemolytic anemia
A.
B.
C.
D.
self antigen
drug allergens
foreign blood surface antigens
none
51 .Autoimmune hemolytic anemia is
associated with administration o f
A.
B.
C.
D.
E.
53.Type II hypersensitivity in the first
sensitization inflammation begins in
a-methyl dopa
thiouracil
sulfonamides
B&C
None
3 days
7-10 days
1-2 weeks
none
54.The major clinical symptoms exhibited
in type II hypersensitivity reactions are
A.
B.
C.
D.
E.
hemolytic anemia
lymphadenopathy
thrombocytopnea
A&C
all
55.Transfusion mismatch (type U
hypersensitivity reactions) reactions
begins
A.
B.
C.
D.
E.
1 day after transfusion
12 hours after transfusion
5-7 hours after transfusion
1-2 hours after transfusion
none
56.In type III hypersensitivity reactions,
the immune complexed activate
complement and induce positive
chemotaxis in
A.
B.
C.
D.
E.
macrophages
basophils
neutrophils
eosinophils
none
52. Which one o f the following is a
mpdif^tnr ir>
11
-
Immunology
A.
B.
C.
D.
E.
classic activation pathway
alternative activation pathway
mannose-binding pathway
B&C
None
33.Non-viral intracellular parasites are
primarily eliminated by
A.
B.
C.
D.
E.
NK cells
CTL cells
T-cell macrophage
A&B
None
C. granulomas
D. A & C
E. none
58. Which cells are involved in the
pathogenesis o f type IV
HYPERSENSITIVITY?
A.
B.
C.
D.
E.
mast cells
Th 1 cells
Macrophages
Neutrophils
B&C
59.The inappropriate skin reaction to
haptens in type IV reactions
A.
B.
C.
D.
tuberculin reaction
contact dermatitis
granulomas
erythema
60. Common allergens include all the
following EXCEPT
A.
B.
C.
D.
E.
mycobacterium tuberculosis
lysteria monocytogens
E. coli
Topical neomycin
Candida
61 .This reaction come after the onset o f
chronic immunoresponse and takes the
longer time to show
A.
B.
C.
D.
granulomas
contact sensitivity
tuberculin reactions
none
62. The etiology of autoimmune response
includes all the following effects
EXCEPT
A. aberrant regulation o f TH and Tc
cells
B. cross reactivity with antigens
from microorganisms
C. loss o f tolerance
D. a high concentration o f antibody
E. none
63.All the following reactions are more
common in woman EXCEPT
A.
B.
C.
D.
E.
myasthenia gravis
SLE
Sjogren’s disease
Good pasture’s syndrome
C&D
64. All the following are thought to
contribute to pathogenesis o f
autoimmunity reactions, EXCEPT
A. streptococcus group A
pharyngitis
B. rheumatic fever
C. exposure to organic solvents
D. ultraviolet irradiation
E. Obesity
65.Which one o f the following is NOT an
organ-specific autoimmunity?
A.
B.
C.
D.
E.
rheumatic fever
sj ogren5s syndrome
myasthenia gravis
goodpasture’s syndrome
multiple sclerosis
66.In which subtype o f antithyroid
autoimmunities does the antibodies act as
agonists o f thyroid-stimulating hormone
(TSH)
A.
B.
C.
D.
E.
primary autoimmune myxedema
hashimoto’s disease
graves’ disease
A&B
None
67.The antibodies act as competitive
antagonists o f acetylcholine binding in
A.
B.
C.
D.
E.
rheumatic fever
myasthenia gravis
goodpasture’s syndrome
multiple sclerosis
insulin dependent diabetes
mellitus
68.
Which autoimmunities and treatment
match is incorrect
A. myasthenia gravis - neostigmine
B. good pasture’s syndrome corticosteroids
C. multiple sclerosis - baclofen
D. sjogren’s syndrome - dantrolene
E. SLE - oral methyl prednisolone
69.In this type of autoimmunity
absorption o f vitamin B ]2 is decreased
A.
B.
C.
D.
E.
autoimmune pernicious anemia
autoimmune hemolytic anemia
thrombocytopnea
neutropenia
none
70. Which one o f the following is NOT
included in the pathogenesis o f SLE?
A.
B.
C.
D.
progressive necrotizing vasculitis
hypertension may develop
behavioral changes
inhibition o f exocrine gland
secretion
E. hemolytic anemia
71. All the following therapies suppress
only lymphocytes that are activated,
EXCEPT
A. corticosteroids
B. feeding auto antigens
C. administration o f conjugates o f
interleukin-2
D. vaccination with auto reactive T
cells
E. A & B
72.All the following are primary
immunodeficiencies, EXCEPT
A.
B.
C.
D.
X-linked agammmaglobulinemia
Digeorge syndrome
Leukemias
Chronic granulomatous
deficiency
E. Chediak-higashi syndrome
( For Questions 73 and 74)
I. X-linked agamaglobulinemia
I], common variable immunodeficiency
III. selective IgA deficiency
IV. Digeorge syndrome
V. N ezelof syndrome
VI. SCIDs
VII. CGD
VIII. LAD
IX. Chediak-higashi syndrome
X. defects in complement
73. Which ones are associated with T-cell
deficiency?
A.
B.
C.
D.
E.
I, I I , III, V
I, IV, V, VI
I, III, V, IX
I, VI, IX
Ill, VI, IX
74. Which ones are associated with a
defect with phagocytic cells?
A.
B.
C.
D.
E.
V, VII, X
VII only
VII, VIII,X
VIII only
VII &VIII
75.This immuno deficiency occurs
primarily in men
A. selective IgA deficiency
B. commone-variable
immunodeficiency
C. X-linked agammaglobulinemia
D. B & C
E. none
76.filgrastim is a drug used in the
treatment o f secondary immunodeficiency
due to
A.
B.
C.
D.
E.
leukemias
myelomas
cytotoxic drugs
lymphomas
none
77.Optimal anti-HIV therapy is
combination therapy with antiretroviral
drugs
A.
B.
C.
D.
two
Three
four
it depends on the stage o f the
disease
E. none
78.A11 the following are non-nucleoside
reverse transcriptase inhibitors (NNRTIs),
EXCEPT
A.
B.
C.
D.
E.
nevirapine
didanosine
delavirdine
efavirenz
none
D. Herpes simplex virus( HSV)
E. all
80.The HIV, viral envelope glycoprotein
120(gpl20) has a strong affinity to
A.
B.
C.
D.
E.
CD8
CD4
APCs
Macrophases
none
81. Which of the following statements is
incorrect?
A. because o f molecular differences,
grafts are likely to be
antigenically different from the
recipient and therefore may
stimulate an immune response
B. class 1 glycoproteins are known
as HLA-DR, -DP and -D Q
antigens
C. human leukocyte antigen is each
person’s set o f MHC
glycoproteins
D. the likelihood of two siblings to
be HLA identical is
approximately 25%
82. Which o f the following are common
solid-organ transplants?
A.
B.
C.
D.
kidney
heart-lung
pancreas
All
83. In which organ transplant is HLA
matching not important?
79.Opportunistic infections are the major
consequences of AIDS, particularly by
A. P. carinii
B. Candida albicans
C. Mycobacterium-avium
intracellulare
A.
B.
C.
D.
kidney
Cornea
pancreas
all
84. In which type o f transplant is rejectic
decreased if HLA-KR and HLA-B are
matched?
A. cardiac graft
B. liver graft
C. pancreas graft
D. none
89. All are correct about bone marrow
transplantation EXCEPT
85.AH are correct about graft rejection
EXCEPT
A. HLA matching is not always a
factor in rejection
B. Parents and children are almost
always haploidentical
C. The only reason for tissue
rejection is HLA-incompatibility
D. HLA matching is not important
in liver transplantation
86.A T-cell macrophage-mediated attack
on the graft based on HLA and other
tissue antigen mismatch is
A.
B.
C.
D.
chronic rejection
hyperacute rejection
acute rejection
all
kidneys and atherosclerosis in the
heart
C. is resistant to therapy
D. All
-
A. it is attempted in patients with
immunodeficiency disease,
aplastic anemias, some leukemias
and certain genetic diseases
B. graft T-cell recognition o f the
host is important in GVH disease
C. in bone marrow transplantation,
the host-versus-graft response is
very important
D. HLA matching is important in
bone marrow transplantation
90.The clinical symptoms o f GVH
disease are
A.
B.
C.
D.
desguamation o f the skin
intestinal bleeding
necrosis o f the liver
agranulocytosis
91 .All are immunosuppression o f the
graft recipient EXCEPT
87.Hyperactue rejection is
A. T-cell-macrophage-mediated
attack on the graft
B. An ABO-mismatched graft
C. The release o f inflammatory
cytokines by macrophages
D. A rejection that occurs in 10-14
days
88.Chronic
rejection
A. occurs several months to years
after transplantation
B. causes fibrosis and occlusion of
small arteries and arterioles in the
A.
B.
C.
D.
corticosteroids
tacrolimus
azathioprine
methotrexate
92.For the prophylaxis and treatment o f
graft rejection, corticosteroids are used in
combination with
A.
B.
C.
D.
ALG/ATG
Tacrolimus
Muromonab CD3
Rampamycin
93.Which o f the following drugs is
primarily used for bone marrow
transplantation in combination with
antilymphocyte globulins/antithymocyte
globulins (ALG/ATG)?
A.
B.
C.
D.
98. All are correct about muromonab-CD3
(OKT3) EXCEPT
azathioprine
methotrexate
cyclosporine
tacrolimus
A. it may also be used in vitro to
purge host(recipient) bone
marrow o f T cells to reduce the
risk o f GVH disease
B. OKT3 is contraindicated in
patients with fluid overload
C. The side effects o f OKT3 include
high fever, chills blood pressure
changes and vomiting
D. The main action o f OKT3 is the
opsonization o f T cells for
enhanced phagocytosis
94.Cyclosporine inhibit
A. TH-cell response to IL-2 and
prevents TH-cell activation
B. T-cell antigens by a variety of
antibody specificities
C. Specific CD3 antigen by a
monoclonal antibody
D. TH-cell secretion o f IL-2 and
lFN-y and prevents T-cell
activation
99. All are true about active vaccination,
EXCEPT
95.
Which o f the following drugs should
NOT be used together?
A.
B.
C.
D.
rampamycin and cyclosporine
corticosteroids and cyclosporine
cyclosporine and tacrolimus
azathioprine and corticosteroids
96. Which o f the following is an antisera
derived from animals and is used in bone
marrow and organ transplantation?
A.
B.
C.
D.
cyclosporine
ALG and ATG
Tacrolimus
None
97. Which o f the following is used to h alf
and reverse acute rejection?
A. muromonab-CD3
B. ALG
C. Tacrolimus
A. the immunity produced by active
vaccine is long lasting
B. the response o f active vaccination
generates antibody, activated T
cells and specific memory
C. active vaccination is the
intramuscular or intravenous
injection o f antibody preparations
to enhance a patient’s immune
competence
D. protection through memory
varies with the vaccine
100. Which o f the following is incorrect
about standard human serum immune
globulin for intramuscular vaccination?
A. they are individual sera prepared
from plasma lots o f subjects
actively immunized against or
recovering from specific disease
B. it is a polyclonal antiserum
prepared from pooled plasma o f
donors
C. it is unsuitable for intravenous
injection
D. the side effects are confined to
minor inflammation and pain at
the site o f in jection
101. Tetanus immune globulin (TIG) is
A.
B.
C.
D.
IVIGs
Animal antisera
Special IGIM
IGIM
102. All are correct about IVIGs
EXCEPT
A. the side effects can be diminished
by reducing the rate of
intravenous infusion
B. premeditation with
corticosteroids is recommended;
C. intravenous epinephrine is usedi
anaphylaxis occurs
1
D. chills, nausea and abdominal p a h
occurs in all patients
103.
Which o f the following is an
example o f passive vaccination for the
prophylaxis o f infectious diseases?
A. hepatitis immune globulin
B. IGIM for
hypogammaglobulinemia
C. Muromonab CD-3 for acute renkl
graft rejection
D. 1VIG for idiopathic
thrombocytopenic purpura
104. Which o f the following vaccine is
used for the prophylaxis and therapy fOi
snakebite?
A.
B.
C.
D.
botulism antiserum
black widow antivenin
polyvalent antivenin
none
105. All are equine (horse) antisera
EXCEPT
A.
B.
C.
D.
Rho(D) immune globulin
Botulism antiserum
Polyvalent antivenin
Black widow antivenin
106. For which o f the following illness is
intravenous passive vaccines used?
A.
B.
C.
D.
measles
rubella
chronic lymphocytic leukemia
varicella
107. For which o f the following illnesses
both intramuscular and intravenous
passive vaccine is used?
A.
B.
C.
D.
hypogammaglobulinemia
measles
cytomegalovirus infection
idiopathic thrombocytopenic
pupurea
-
108. The contents of active vaccines is
A.
B.
C.
D.
low doses of antibiotics
one or more antigens
whole pathogenic organisms
all of the above
109.
AH are routes o f administration o f
active vaccines EXCEPT
A.
B.
C.
D.
Intravenous
intranasal
oral
intradermal
110. A vaccine whose seroconversion
does not indicate established immunity is
A. botulism antiserum
B. bacillus calmette-Guerin
C. rubella
D. oral polio(opvj trivalent)
111. The vaccines that can be given
immediately after birth is
A.
B.
C.
D.
bacillus calmette-Guerin
varicella
HBV
Measles, mumps, rubella(MMR)
produce a strong immune
response
D. live attenuated vaccines multiply
after vaccination but are
attenuated to reduce their
pathogenecity
115. Tetanus toxoid is an example of
A.
B.
C.
D.
live, attenuated vaccine
subunit vaccine
killed inactivated vaccines
experimental vaccines
112. All vaccines require booster
vaccinations EXCEPT
A. rabies
B. diptitheria, tetanus,
perussis(DTP)
C. tetanus and diphtheria
toxoids(Td)
D. Rubella
113. All are true about active vaccine
EXCEPT
A. it is used for prophylaxis
B. the side effects are inflammation
at the site o f injection, malaise,
mild fever, chills, headache,
myalgia and arthralgia
C. all vaccines require a series of
vaccinations
D. the success o f the series of
vaccinations is indicated by
seroconversion o f the patient
114. All are correct about live,
attenuated vaccines EXCEPT
A. it is safe to give live, attenuated
viral vaccines to pregnant women
B. some vaccines elicit life long
immunity in two doses
C. because the antigen concentration
increases when the organism
multiplies, a small dose can
116. All are true about killed, inactivated
vaccines EXCEPT
A. the inactivation o f isolated
antigens eliminates pathogenicity
but preserves some antigenicity
B. vaccines in which the antigenic
fragment is a polysaccharide are
usually best at eliciting immune
response and memory
C. in killed, inactivated vaccines,
reversion to pathogenicity is not a
problem
D. the doses o f cells or antigens
must be higher than in live,
attenuated vaccines
117. HBV vaccine and the lyme disease
vaccine are example of
A.
B.
C.
D.
experimental vaccines
killed inactivated vaccines
live, attenuated vaccines
subunit vaccines
118. Experimental vaccines are
A. peptides produced by chemical
B. anti-idiotype antibodies used for
active vaccination
C. recombinant DNA viruses
D. All
119. Which o f the following vaccines has
a risk o f vaccine-induced paralysis?
A.
B.
C.
D.
measles, mumps, rubella(MMR)
rubella
varicella
oral polio(opvj trivalent)
120. Which o f the following vaccine is
given to adolescent girls not previously
vaccinated?
A.
B.
C.
D.
Rubella
varicella
MMR
Influenza
121. Which vaccine is a live, attenuated
bacterial vaccine?
A.
B.
C.
D.
varicella
rubella
BCG tuberculosis
Oral polio
B. hepatitis B
C. influenza
D. all
125. All are correct regarding inactivated
polio EXCEPT
A. there is a risk o f vaccine-induced
paralysis
B. the number o f vaccination is 4
C. the target population are
immunodeficient children and
families and as booster in health
and day car workers
D. one vaccine is given at school
entry
126. Which killed inactivated bacterial
subunit is given to children above 7 years
and as a booster every 10 years or on
exposure through a wound if more than
10 years or vaccine history is unavailable?
A.
B.
C.
D.
diphtheria, tetanus, pertussis
meningococcus
tetanus and diphtheria toxoid
none
122. A vaccine that is given to animalcare workers is
A.
B.
C.
D.
127. All are correct regarding diphtheria,
tetanus, pertussis(DTP) EXCEPT
influenza
rubella
rabies
none
123.
Which vaccine is given annually for
maximum protection?
A.
B.
C.
D.
Influenza
hepatitis B
inactivated polio
rabies
124. A vaccine that is a recombinant
subunit is
A. rabies
~
A. it is given for infants and children
only
B. there are 4 vaccination with
boosters
C. it is given on the 2nd, 3rd, 4lh , 15th
- 18th months and one at school
entry
D. since it is a polysaccharide
vaccine, conjugate vaccines
should be used
128. A vaccine that is given for infants,
children and HIV infected adults is
A. haemophilus b
B. pneumococcus
C. meningococcus
D. rubella
129. A vaccine that is given to college
freshmen living in dormitories is
A.
B.
C.
D.
pneumococcus
haemophilus
meningococcus
all
130. A killed inactivated bacterial
subunit that is given for at risk adults such
as immunocompromised patients and
geriatric patients is
A.
B.
C.
D.
varicella
hepatitis B
menigococcus
pneumococcus
131. Active and passive vaccines are
administered simultaneously in
A. infants with HBV who are born
to mothers who have the hepatitis
B surface antigen
B. as a2 post exposure prophylaxis
for rabies
C. a tetanus prone wound that
produces anaerobic conditions
D. All
132. AH are correct about vaccine
EXCEPT
A. combined active and passive
vaccines are sometimes used
B. if the last dose was received
more than 10 years ago. Td but
not TIG is given
C. if the patient’s history o f active
vaccination is uncertain both
TIG and Td are administered
D. for tetanus prone wound , no
treatment is necessary if the
patient has received a full series
o f active vaccination
333. Which o f the following statements
is incorrect?
A. for a clean, minor wound, no
treatment is necessary if the
patient received a full series and
the last Td dose was received
within 5 years
B. for a tetanus prone wound( and
clean, minor wound), if the last
dose was received more than 10
years ago, Td but not TIG is
given to boost memory immunity
and antibody production
C. combined prophylaxis o f tetanus
is sometimes used depending on
the type o f wound and the
patient’s history o f active
vaccination
D. if the patient’s history o f active
vaccination is uncertain or
includes fewer than three doses,
both TIG and Id are administered
134. All are correct about monoclonal
antibodies EXCEPT
A. monoclonal antibodies are used for in
vitro diagnostic tests
B. it is used for screening cancer-related
antigens
C. it is useful to treat certain leukemias
and lymphomas
D. it is used for testing HIV infection
E. it is used for HIV treatment
135. Monoclonal antibodies against
neoplastic cells are used to treat all
EXCEPT
A. certain leukemias and
lymphomas
B. breast cancer
C. bone cancer
D. colon cancer
136. Which o f the following shows
improvement in certain autoimmune
disorders?
A. Fab antidigoxin antibody
B. Muromonab-CD3
C. Monoclonal antibodies against T
cells
D. Monoclonal antibodies against
neoplastic cells
137. Monoclonal antibodies are
conjugated to
A.
B.
C.
D.
enzymes
drugs
prodrugs
All
138. Diphtheria toxin is an example o f
A. immunotoxins
B. monoclonal antibodies
conjugated to radioisotopes
C. monoclonal antibodies
conjugated to enzymes
D. none
139. Which o f the following is used to
treat hairy cell leukemia, kapaosi’s
sarcoma in patients with AIDS and genital
warts?
A.
B.
C.
D.
IFN -y
IF N -a
Muramyl dipeptide
Levamisole
140. Which o f the following is incorrec t
about interferons?
A. IFN- y provides greater
immunosuppression in the intait
immune system
B. The combined use o f IF N -a ar('
IFN - y yields better results
C. IFN- y is used to treat hair cell
leukemia and genital warts
D. Influenza-like symptoms are the
most common side effects
141. All are correct regarding
immunostimulation EXCEPT
A. in adoptive immunotherapy, a
patient’s blood lymphocyte or
tumor-infiltrating lymphocytes
are removed
B. the effect o f sulfur-containing
compounds such as levamisole
and diethyldithiocarbamate is
greater on humoral immunity
than on cell mediated immunity
C. certain cell-mediated immune
functions are increased by
hormones o f the thymus which
induce T-cell maturation and
other functions
D. inosine pranobex induces T-cell
differentiation and auguments
cell-mediated immune functions
with minimal toxicity
142. Which o f the following is a
component o f mycobacterial cell walls
and stimulates macrophage activation?
A.
B.
C.
D.
muramyl dipeptide
levamisole
interferon a
inosine pranobex
mmunology
Answers
Immunology
1. Answer: B. Antigens.
Explanation:
Immunogens are chemical compounds th t cause specific immune response. While antigens are
compounds that bind to products o f an im nune response. Haptens are low molecular weight
compounds that act, as immunogens after chemically complexing to a larger molecule or cell
surface and tolerogens are chemical comj ounds that elicit specific non-responsiveness.
2. Answer: D. A and B.
Explanation:
Haptens may be present in the environment (e.g. pentadecyl catechol o f poison ivy) and several
types o f drugs (e.g. penicillin). Haptens n a k e a complex with a larger molecule or cell surface
and after they stimulate the immune systi m in this complex, these compounds, act as antigens in
the uncomplexed or complexed state.
Where as pollens are an immunogen-antilgen that can be contacted environmentally.
3. Answer: D. the route o f administrati >n o f a compound may lead to immunogen-antigen
effect.
Explanation:
Immunogen-antigens are compounds ass ociated with or secreted by parasitic bacteria, protozoa,
fungi and viruses, and o f molecular weij; ht greater than 10000 daltons may act as immunogens
and antigens. Molecular complexity is a: , important as molecular weight in determining the status
of a compound as an immunogen. For a molecule to be very good immunogenic, it must contain
protein or peptide. Therefore proteins, g ycoproteins, lipoproteins and nucleoproteins are the most
potent immunogen antigens. Drugs o f sufficient molecular weight (e.g. insulin) can act as
immunogen-antigens. The cells o f anotl er individual and the cells o f one’s own body can act as
immunogen antigens. Immunogen antig :ns can also be contacted from the environment (e.g.
pollens). But the route o f administration (e.g. oral administration) may be the cause o f specific
non responsiveness thus being a tolerog ;n.
4. Answer: D. A and C
Explanation:
B-lymphocytes and T-lymphocytes are the primary cells o f specific immune responses. AH B & T
lymphocytes are antigen specific becau >e they have specific antigen receptors as part o f their
plasma membranes.
Neutrophils simply assist in eliminating antigens from body.
Explanation:
Natural killer (NK) cells are large, granular lymphocytes without specific T- or B- cell antigen
receptor. Their cytotoxicity is similar to that o f cytotoxic T lymphocyte (CTL) cells. NK cells
recognize and destroy tumors.
6. Answer: E. None
Explanation:
B-cells have thousands o f identical antibodies in their membrane that allow them to bind
chemically to a small group o f chemically related antigens. This group defines the antigen
specificity o f each B-cell. Different B-cells have different antigen specificities, but each B-cell
has only one specificity. B-cells that recognize specific antigens divide to form new B-cells
(memory B-cells) and plasma cells (antibody forming cells) which secrete free, soluble (humoral)
antibody molecules into extracellular fluids.
7. Answer: D. 1, IV, V
Explanation:
Virgin B-cells have never responded to an antigen since their release into the circulation from
bone marrow and their membrane. Antibodies are o f immunoglobulin M and D (IgM, IgD)
classes. Memory cells are derived by cell division from another B-cells that has responded to an
antigen. Their membrane antibodies are o f immunoglobulin classes A, E, or G (IgA, IgE. IgG).
8. Answer: B. thymus-gland
Explanation:
T-cells originate in pluripotential stem cells in the bone marrow and differentiate into immune
cells in the thymus gland.
9. Answer: B. Tr
Explanation:
Tr cells have recently been described; most o f these cells are CD4+, although there is CD8+ subset
as well. All o f these cells suppress immune responses through the secretion o f IL-10 and TGF-|3,
in addition cells designated CD4+CD25+ are able to inhibit through direct contact. Tc (cytotoxic
T-lymphocyte) is able to kill cells that are infected by viruses and T h cells are the ‘helper’ cells.
10.Answer: C. CD3
Explanation:
Most T-cells can be classified by the presence o f membrane glycoprotein known as CD4, the
helper, or TH cell, or the presence o f CD8, the cytotoxic T lymphocyte (CTL) or Tc cell. Antigen
receptors o f T cells have two membrane proteins (a and p or y and 8) that define the antigen
specificity o f each T cell and several other integral membrane proteins known as CD3 complex
(T cells are CD3+).
i 1.Answer: B. MHC
Explanation:
The antigen receptors o f T cells do not recognize antigens alone. Rather, they normally recognize
peptide epitopes (fragments o f antigen) that are chemically combined with MHC proteins (Major
Histocompatibility Complex). MHC proteins are divided into two classes o f class 1 proteins
(which are present on all nucleated cells) and class II proteins (which are present on the surfaces
o f special APCs).
12. Answer: B. TH2 cells
Explanation:
T h cells (the helper) can be divided into two functional groups, TH1 and TH2. These cells have
different functions in the immune response. These cells regulate immune responses through the
production o f lymphokines, which are small proteins that act on other cells in an autocrine,
paracrine or endocrine manner. TH1 cells activate other cells, including some TH cells, Tc cells,
and macrophages. In addition they decrease antibody (Ab) production by inhibiting the formation
o fT H2 cells. TH2 cells activate B cells to divide and produce Ab. They can also inhibit the
production TH1 cells. Lymphokines are part o f a larger net work o f regulatory cytokines and CD8
are suppressor T cells. While virgin T cells are T cells that are released from thymus into
circulation.
13. Answer: D. All of the above
Explanation:
APCs are essential for most immune responses and are found in the sites at which these responses
originate and the best understood APCs are macrophags and dendritic cells o f lymph nodes,
spleen. Most immune responses with in these organs begin when these cells present epitopes
bound to their surface MHC class II molecules to Th cells and secrete cytokines as accessory
signal.
14. Answer: A. CTL cells
Explanation:
Any cell in the body can act as an APC for immune responses involving CTL cells. Nucleated
cells can present fragments of antigens bound to their surface MHC class 1 molecules to Tc (CD8)
lymphocytes.
15.Answer: E. all
Explanation:
Neutrophils, macrophages, eosinophils, basophils, platelets and mast cells assist in eliminating
antigens from the body. Their functions may be phagocytic, pro inflammatory, cytotoxic, and
regulatory or a combination o f these
16.Answer: E. A & B
Explanation:
In most humoral immune responses, antigen is recognized by antigen specific B cells and TH
cells.
17.Answer: C. IgM
Explanation:
The first time a specific antigen is encountered only virgin B cells and virgin TH cells are present
to respond to the antigen. Initially, these cells produce plasma cells that secrete IgM antibody.
Later in the immune response, plasma cells producing other classes o f antibody develop. In a
primary immune response, IgM is produced first and is followed by IgG. Memory B and TH2
cells are also produced. Memory B-cells can also be activated to produce the other classes o f
antibody in subsequent immune responses.
18.Answer: B. IgG
Explanation:
The second or subsequent encounter with the same antigen or a closely related antigen produces
responses by memory B cells and memory TH2 cells. These responses are more rapid because
memory cells require less antigen for stimulation and are o f greater magnitude because there are
more antigen specific B & T cells to respond. Most antibody produced is IgG, with smaller
amounts o f IgA and IgE.
19.
Answer: E. All
Explanation:
The first function o f an antibody is to act as an antigen receptor for B cells so that the B-cells can
recognize and respond to antigens. The second function is to aid in the elimination o f antigen.
Elimination occurs through non specific functions, such as phagocytosis or complement
activation. The mechanism o f elimination depends on the class o f antibody involved. And the
third function o f an antibody is neutralization o f toxins which occurs when the antibody binds to
the toxin and prevents it from reaching the target.
20.Answer: C. the C-terminal constant region is responsible for antigen binding
Explanation:
The standard immunoglobulin has four polypeptide chains: two identical light polypeptides
chains and two identical heavy polypeptide chains. The structure is represented as H2L2. Each
chain can be divided into a C-terminal constant region and an N-terminal variable region of
amino acids. The N-terminal variable region formed from the H & L variable domains is
responsible for antigen binding by the immunoglobulin. The C-terminal constant regions o f the H
chain determine the class o f the immunoglobulin.
21 .Answer: A. I only
Explanation:
IgA is secreted across mucosal surfaces into gastrointestinal, respiratory, lachrymal, mammary
and genitourinary secretions, where it protects mucosa from colonization.
IgE mediates allergic reactions while IgG opsonizes antigens for phagocytosis and activates the
complement system and IgM is the most potent activator o f the complement system. But IgD has
no known function as a secreted immunoglobulin.
22. Answer: D. II, V , I , III
Explanation:
IgG accounts for approximately 70% o f adult serum immunoglobulin while IgM accounts for
20% o f adult serum immunoglobulin and IgA accounts for approximately 10% o f serum
immunoglobulin. But IgD and IgE account for less than 1% o f serum immunoglobulin.
23.Answer: A. IL-5
Explanation:
IL-5(secreted by TH2 cells) is responsible for memory cell formation and eosinophil production.
IL-6(secreted from TH2 cell and other types) is responsible for plasma cell maturation while IL7(secreted from bone marrow stroma) is responsible for lymphocyte maturation; IL-8(secreted
from Th 1 cells, macrophages, endothelial cells) is responsible for neutrophil activation and 1L9(secreted by TH1 cells) is responsible for proliferation and differentiation o f bone marrow cells
and thrombocytes as is IL-11(secreted from bone marrow stroma).
24.
Answer: B. 1L-12
Explanation:
IL-1 (secreted form macrophages, APCs) is responsible for T and B-cell activation, pyrogenic
and pro-inflammatory actions. IL-12(secreted from macrophages, B-cells) is responsible for
promotion o f cell-mediated immunity, activation o f TC and NK cells and suppression o f humoral
immunity; IL-13 (secreted from TH cells) is responsible for activation o f B-cells, inhibition o f
production o f inflammatory cytokines by monocytes. IL-14(secreted from TH cells) is important
for the generation o f B memory cells and IL-10(secreted from macrophages, TH2 cells, CD8+ Tcells, B-cells) is responsible for increased humoral (antibody), decreased cell mediated immunity
and mast cell growth.
25.Answer: E. All
Explanation:
Each immunoglobulin specificity can bind to several different, but closely related antigens. The
ability illustrates the phenomenon o f cross-reactivity o f a single antibody for multiple antigens.
Cross reactivity may also occur through the sharing o f some, but not all. antigens by two strains
o f bacteria, viruses or other microorganisms.
26.Answer: D. they are class specific
Explanation:
Immunoglobulins can be enzymatically cleaved into fragments [e.g. Fab and F (ab')2(antigenbinding fragments), Fc (crystallizable fragment), Fv (variable region fragment)]. Fab and F (ab’) 2
fragments are clinically useful because they retain antigen specificity, but not class-specific (e.g.
inflammatory) functions, and are readily excreted renally. Conversely, this characteristics limits
their effectiveness in certain situations.
27.Answer: E. None
Explanation:
Compliment is a group o f approximately 20 serum proteins that, when activated, form a
proteolytic cascade similar to clotting and fibrinolytic sequence. With in this complex o f proteins,
there are some that inhibit complement activation. Complement is responsible for increasing the
inflammatory response, phagocytosis o f antigen, lysis o f cells and clearance o f immune
complexes. But opsonization is the preparation o f extra cellular antigen for phagocytosis through
binding o f antibody. But certain complement proteins also provide opsonization.
28.
Answer: A. classic activation pathway
Explanation:
In classic activation pathway, immune complexes o f IgM or IgG antibodies bind subunits of
complement component 1 (C l) and trigger an initial series o f proteolytic cleavages. In an
alternative activation pathway, the cell walls o f certain microorganisms
(e.g. gram negative bacteria) are able to bind C3b and other complement proteins that initiate a
different sequence o f proteolytic cleavages and in the mannose-binding pathway, mannosebinding protein (MBP) is produced by the liver during the acute-phase response.
29.Answer: E. A & C
Explanation:
Circulating basophiles and connective tissue mast cells are mainly proinflammatory cells that
rapidly initiate acute inflammation. Triggers o f secretion include mechanical and thermal trauma
and immunologic triggers, compliment and IgE.
30.Answer: E. none
Explanation:
Mast cells and basophile, when triggered, immediately secrete the contents o f their storage
granules, including histamine, proteases and chemotactic proteins for neutrophils and eosinophils.
In additions, activation o f phospholipase A2 releases arachidonic acid from membrane
phospholipids and results in the synthesis o f various leukotrienes, prostaglandins and
throrriTJoxanes. The primary effect of these mediators is vascular dilation, increased vascular
permeability, contraction o f respiratory and gastrointestinal smooth muscles, neutrophil and
eosinophil chemotaxis.
31 .Answer: E. All
Explanation:
Antibody dependent cell-mediated cytotoxicity is mediated by cells with cytotoxic potential as
well as receptors for IgG. These cells NK cells, macrophages and some Tc cells bind to and lyse
target cells coated with IgG.
32.Answer: E. AH
Explanation:
Cell mediated immune responses are those in which antibody is not involved in the elimination o f
antigen. Non-viral intracellular parasite, viruses, tumors and graft rejection trigger cell mediated
immunity.
33.Answer: C. T-cell macrophage
Explanation:
Non-viral intracellular parasites o f macrophages such as myobacteria, listeria and certain
protozoa are primarily eliminated by T-cell macrophage immunity. CD4+ TH1 cells recognize
infected macrophages and secrete lymphokines, particularly interferon-y (IFN-y).
34.
Answer: D. All except B
•
Explanation:
Viruses must be eliminated from both extracellular sites and infected cells. Antibodies opsonize
virus particles in blood and tissue fluids for phagocytosis, but antibodies are generally ineffective
against infected cells and CTL cells recognize infected cells and directly kill them in an antigen
specific manner secreting lymphokines, such as tumor necrosis factor-P(IFN-P) while NK cells
are believed to kill infected( and tumor) cells in a non-antigen specific manner.
35.Answer: C. Macrophages
Explanation:
INF-y is secreted by CTL, NK and TH 1 cells and IFN-a and IFN-p is secreted by macrophages
and other cells thus providing antiviral immunity by binding to receptors on other end.
36.Answer: E. All
Explanation:
NK cells are primarily responsible for killing tumor cells. They may act by recognizing changes
in cell surface proteins or by antibody dependent cell mediated cytotoxicity. CTL cells recognize
tumor cells in an antigen specific manner and kill them by secreting lymphokines (TNF-P) and
macrophages also kill tumor cells in a non-specific manner through the release o f TNF-a.
37.Answer: B. IgE
Explanation:
A type I hypersensitivity reaction is caused by inappropriate production and hyper secretion of
IgE to specific allergens, plus auxiliary factors such as increased mucosal permeability to
allergens (e.g. S 0 2, N 0 2, diesel fumes). Type II hypersensitivity reaction is mediated by IgM or
IgG.
38.Answer: C. 75%
Explanation:
The tendency to hypersecrete IgE is inheritable; a child’s probability o f being hypersecetor is
50% with one hyper secretor parent and 75% with two hyper secretor parents.
39.Answer: B. local mast cells are armed
Explanation:
In normosecretors ( 1 - 1 0 pg/dl), arming local mast cells occurs. And in hyper secretors
( typically 100 pg- 1 mg/dl) , IgE spill over occurs, arming basophils and non-local mast cells and
causing increased occupancy o f mast cell and basophile IgE receptors by IgE.
40.Answer: D. intravenous allergens
Explanation:
Respiratory allergens include pollens o f various plants(ragweed, grasses, trees); gastrointestinal
allergens include dietary products, shellfish, soybeans and peanuts; skin and mouth allergens
include topically applied drugs( e.g. procaine) and intravenous allergens include insect venoms
and drugs that act as cell or plasma protein bound haptens( e.g. penicillin,
cephalosproins,vaccines). These drugs may cause type II or III hypersensitivity reactions in
people who do not hypersecrete IgE in response to these drugs.
41 .Answer: A. histamine
Explanation:
Vasodilation and increased capillary permeability are caused by histamine; the leukotrienes C4,
D4 and E4; PGD2 secreted by mast cells. Gastrointestinal and respiratory smooth muscle
constriction is caused primarily by the leukotrienes C4, D4 and E4; PGD2; and platelet activating
factor secreted by mast cells and other leukocytes. And eosinophil and neutrophil infiltration is
caused by chemotactic factors secreted by mast cells.
42.Answer: E. all
Explanation:
In sensitized individuals; intravenous injection o f an allergen (e.g. bee venom) or absorption
across the mucus membranes (e.g. peanuts) can cause systemic edemic and hypovolemic shock,
with cardiac arrhythmia, asphyxiation as a result o f bronchoconstriction and mucous hyper
secretion and urticaria. Death usually occurs because o f asphyxiation.
43.A nsw er:B . 1-2 min
Explanation:
Immediate hypersensitivity reaction has two phases. The early reaction, resulting from mediator
secretion by mast cells, begins with in 1-2 min after allergen contact and peaks with in 1-2 hours.
The late phase reaction begins 3-12 hours after contact with the allergen and lasts for several
hours.
44.Answer: D. A & B
Explanation:
In scratch tests, a variets o f allergens are injected intradermally to screen for the presence of
wheal and flare (i.e. edema and erythema) response in the skin. Radioallergenosorbent (RAST)
and radio immuno-sorbent (R1ST) assays used radio labeled reagents to detect serum IgE
concentrations. But the results o f these assays do not always agree with each other or with clinical
manifestations o f type I hypersensitivity.
45.Answer: B. passive immunization
Explanation:
In type I hypersensitivity reaction, prophylaxis includes hyposensitization (injecting weekly,
increasing does o f allergen intramuscularly to elicit an allergen specific IgG response and
decrease the allergen specific IgE) and the therapy includes competitive H] antagonists of
histamine, epinephrine, cromolyn sodium and topical steroids. But passive immunization is used
in the prophylaxis and therapy o f type 11 hypersensitive reactions
(e.g. anti RhD administered during pregnancy and with in 72 hours postpartion for each RH+
pregnancy in RH‘ mothers).
46.Answer: B. epinephrine
Explanation:
Competitive Hj-antagoinsts are useful in local forms they do not completely reverse inflammation
and have a little effect on anaphylaxis. Epinephrine reverses anaphylaxis through its a-agonist
(e.g. oti agonist phenyl propanolamine decreases nasal congestion) and p-agonist (e.g. (32 agonist,
albuterol promotes brochodilation); cromolyn sodium (cormoglycate) is locally administered
inhibitor o f mast cell degranulation and topical steroids inhibit inflammation and immune
responses.
47.Answer: D. A & B
Explanation:
Non-IgE mediated type I hypersensitivity reactions (anaphylactoid reactions) are contributed by
the factors like respiratory p2-receptors unresponsiveness which leads to diminished
bronchodilator effect o f the sympathetic nervous system and hyper reactivity o f mast cells
through H2 receptor unresponsiveness, this decrease the negative feed back o f histamine on the
activation o f mast cells.
48.Answer: B. cytotoxicity
Explanation:
In type II hypersensitivity reaction, antibody mediated cytotoxicity occurs through the production
o f IgM or IgG. These antibodies are able to bind to specific allergens located on cell surfaces.
Anaphylaxis is IgE mediated type I hypersensitivity reaction while immune complexes’
persistence in the circulation or at local tissues causes type III hyper sensitivity reaction. Type II
reactions may exhibit anaphylactic signs and symptoms if enough complement is activated; how
ever they usually do not progress to this stage.
49.Answer: B. antisera
Explanation:
Antisera is a common allergen in type III hyper sensitivity reactions (others include bacterial or
protozoan antigens, drugs, fungal or bacterial spores and self antigens is most non-organ specific
autoimmune disorder). The common antigens in type U hypersensitivity reactions include foreign
blood surface antigens that produce transfusion mismatches or Rh disease; drug allergens( or
metabolites) that act as haptens; self allergens which are the allergens in certain autoimmune
diseases and hyperactue rejection o f transplanted tissue.
50.Answer: B. drug allergens
Explanation:
Drug allergens( or metabolites) acting as haptens are the leading cause o f hemolytic anemia they
may directly adsorb to cell surfaces and be specifically bound by antibodies( e.g. penicillin ,
cephalosporin, quinidine). Alternately they may form serum-phase immune complexes, which
adsorb nonspecifically to blood cells surfaces. This makes the cell susceptible to lysis due to the
“innocent bystander” effect (e.g. rifampicin, sulfonamides, and chlorpromazine).
51 .Answer: A. a-methyl dopa
Explanation:
Autoimmune hemolytic anemia is sometimes associated with administration o f a-methyldopa,
which induces autoantibodies against the red blood cells but the drugs like penicillin,
sulfonamides, and thiouracil are one o f the common allergens in type III hypersensitivity
reactions.
52. Answer: D. A & B
Explanation:
In type II hypersensitivity, complement proteins produce cytotoxicity and inflammation, which
stimulate macrophages and granulocytes to secrete cytokines and enzymes, which in turn enhance
inflammation. And in type III anti-inflammatory reactions, complement proteins cause
inflammation and stimulate mast cell and basophile secretion.
53.Answer: B. 7-10 days
Explanation:
In the first sensitization to a drug allergen, the blood cell lysis and inflammation begin 7-10 days
after initiation o f drug therapy. The second exposure to the drug causes symptoms within 3 days.
But in type III hypersensitivity reactions, patients with no prior exposure to the allergen, the
symptoms appear in 1-2 weeks (possibly longer) after the exposure. In patients with preexisting
antibodies symptoms appear with in several hours to one day after exposure. This is in case o f
systemic reaction, incase o f local reactions, for patients with preexisting antibodies,
hypersensitivity pneumonitis symptoms appear 6-8 hours after exposure to the antigen.
54.Answer: D. A & C
Explanation:
Clinical symptoms o f type II hypersensitivity reactions depend on the type o f antigen/allergen
involved. Hemolytic anemia and thromboxytopnea are the major clinical signs o f type II
hypersensitivity reactions. But the clinical symptoms o f type III hypersensitivity reactions include
the first symptoms lymphadenopathy, splenomegaly, fever and rash. And a more serious
symptoms like vasculitis and glomerulonephritis.
55.Answer: D. 1-2 hours after transfusion
Explanation:
Transfusion mismatch hemolysis begins 1-2 hours after transfusion. Peak effects occur after
approximately 12 hours.
56.Answer: C. neutrophils
Explanation:
In the pathogenesis o f type III hypersensitivity, immune complexes activate complement, cause
inflammation and induce positive chemotaxis in neutrophils. Persistence o f immune complexes
may be caused by a high concentration o f antigen or antibody. Chronic formation of immune
complexes and other factors, which cause insoluble immune complexes to from and precipitate
intravascularly or on basement membranes.
57.Answer: B. pneumonitis
Explanation:
The most common types o f local type III hypersensitivity reactions are pneumonitis to inhaled
fungi and bacteria to which the patient is occupationally exposed (e.g. mold hay in farmer’s lung)
and reactions to spores borne in aerosol micro droplets from dirty ultrasonic humidifiers( e.g.
humidifier lung). The etiology o f these diseases is not completely understood, but both IgE and
IgG are involved. IgE causes the first inflammation and trapping o f antigen, and IgG is
responsible for the long term effects. Symptoms include nasal congestion, bronchoconstriction,
joint pain and inflammation of rheumatoid arthritis. Lymphadenopathy is the first symptom
exhibited but granulomas and contact sensitivity is symptoms exhibited by type IV reactions.
58.Answer: E. B & C
Explanation:
Type IV reactions include prolonged inappropriate and appropriate immune responses mediated
by antigen-specific TH1 cells in concert with activated macrophages. The TH1 cells infiltrate
tissue in which the antigens are presented and recruit and activate macrophages. The release of
enzymes and cytokines by these cells results in inflammation and disruption o f tissue structure in
the absence o f antibodies.
59. Answer: B. contact dermatitis
Explanation:
Contact dermatitis is an inappropriate skin reaction to haptens (e.g. pentadecyl cathecoles o f
poison ivy) which binds to epidermal cell surfaces and elicits TH1 response. Tuberculin reactions
observed in the dermis and are an appropriate reaction to mycobacterial antigens. This reaction
indicates the state o f active TH1 immunity (due to an active infection) or T cell memory to the
organism. Granulomas are local aggregations o f T cells, macrophages and giant epitheoloid cells
(derived from fusion o f activated macrophages). They occur at sties o f chronic infection and
serve to restrict the spread o f infection. And erythema is caused by tuberculin tests.
60.Answer: C. E. coli
Explanation:
From the common allergens, infectious allergens include M. tuberculosis, M. leprae, lysteria
monocytogens, trypanosomes and viruses. Haptens allergens include pentadecayl cathechols from
poison ivy, poison oak, chromates, nickel ions( leached from watch backs and other jewelry),
acrylates, hair dyes that contain P. phenylene diamine, paraminobenzoic acid, and certain
antibiotic ointments( topical neomycin). And antigens that induce tuberculin reactions include
purified protein derivatives (PPD), tuberculin (mantoux reactions), Candida, malps and other
antigens from microorganisms.
61 .Answer: A. granulomas
Explanation:
Granulomas form at various times after the onset o f a chronic immunoresponse but generally
require a minimum o f 2 weeks while contact dermatitis may not occur with the first transient
exposure, however in sensitized individual, skin inflammation will appear 12-24 hours after
contact and reaches peak between 24 and 48 hours after exposure. And tuberculin reactions
follow the same time course as contact sensitivity; this reaction is often called cutaneous
hypersensitivity.
62. Answer: D. a high concentration o f antibody
Explanation:
The etiology o f autoimmune responses (response directed specifically and inappropriately against
one or more self-antigens) is not generally known and probably involves several deregulations in
the control networks that normally prevent development o f autoimmune disease. This
deregulations may include aberrant regulation o f T h and Tc cells, cross reactivity with antigens
from microorganisms loss o f self-tolerance or failure to develop tolerance, and aberrant
presentation o f self-antigen on specific HLA molecules. And the predisposition is associated with
specific MHC types (e.g. rheumatoid arthritis with the MHC class II molecules HLA-DR4).
63.Answer: E. C & D
Explanation:
These reactions are more common in women. Myasthenia gravis, with a female to male ratio o f
2:1, SLE with a ratio o f 10:1 but in contrast, Sjogren’s disease and good pasture’s syndromes is
more common in men than in women.
64.Answer: E. Obesity
Explanation:
Environmental factors are thought to contribute to pathogenesis. However, specific associations
have been found in only a few cases; these include streptococcus group A pharyngitis and
rheumatic fever, exposure to organic solvents and good pasture’s syndrome, ultraviolet irradiation
and SLE. It is likely that environmental factors act in concert with genetic predisposition to
induce disease.
65.Answer: B. sjogren’s syndrome
Explanation:
Organ-specific autoimmunites include rheumatic fever, antithyroid autoimmunities, myasthenia
gravis, autoimmune pernicious anemia, good pasture’ssyndrome, autoimmune hemolytic anemia,
thrombocytopenia, neutropenia, lymphopenia, insulin dependent diabetes mellitus (IDDM) and
multiple sclerosis. And non organ-specific autoimmunities include sjogren’s syndrome and SLE.
66.Answer: C. graves’ disease
Explanation:
An antithyroid autoimmunities, aspects o f several subtypes may occur in the same patient. In
primary autoimmune myxedema, antibodies against TSH receptor on thyroid follicle cells act as
antagonists to the stimulation o f growth o f the follicle cells normally provoked by TSH; in
hashimoto’s thyroiditis, antibodies against thyroid peroxidase on follicle cells cause cytotoxicity
and inflammation through the activation o f complement. But in grave’s disease antibodies act as
agonists o f TSH, binding to TSH receptor and stimulating hyper secretion o f thyroid hormone
[(thyroid stimulating immunoglobulin (TSIs)].
67. Answer: B. myasthenia gravis
Explanation:
In myasthenia gravis, antibodies against the nicotine acetylcholine receptor on skeletal muscle
plasma membrane at neuromuscular junctions act as competitive antagonists o f acetylcholine
binding.
In goodpasture’s syndrome, antibodies against glomerular capillary basement membrane (GBM)
activate compliment and neutrophil mediated damage; in multiple sclerosis (MS), T-cells and
macrophages which are thought to be cytocidal for oligodendrocyts, infiltrate the central nervous
system (CNS) and attack the basic protein o f myelin as an autoantigen; in IDDM, progressive and
ultimately complete destruction o f pancreatic p-cells occurs in diabetes. But rheumatic fever is
not technically an auto immune response because antibodies are produced against group A
streptococci and cross react with cardiac muscle fibers that are damaged by complement.
68.Answer: D. sjogren’s syndrome - dantrolene
Explanation:
Anticholinestrase therapy( e.g. neostigmine) is indicated for myasthenia gravis; in good pasture’s
syndrome immunosuppressive therapy(corticosteroids) ; in multiple sclerosis, spasticity is treated
with baclofen, the peripheral skeletal muscle relaxant dantrolene is effective is some patients and
adrenocortioctropic hormone(ACTH) is the favored immunosuppressive agent. But sjogren's
syndrome, mild cases are treated with artificial tears and frequent drinking of water and for most
serious cases (e.g. vasculitis) treatment is similar to that o f SLE which is systemic corticosteroids
like methyl prednisolone.
69.Answer: A. autoimmune pernicious anemia
Explanation:
In autoimmune pernicious anemia, antibodies against intrinsic factor are secreted into the
stomach lumen, where they inhibit the association of intrinsic factor with vitamin B 12thus the
absorption o f B 12 is decreased, therapy includes intramuscular injection o f cyanocobalamin or
oral administration o f concentrated intrinsic factor preparations. But in case o f autoimmune
hemolytic anemia (red blood cell), thromobocytopenia (platelet), neutropenia (neutrophil) and
lymphopenia (lymphocyte), antibodies against membrane antigens o f one or more o f the indicated
cell types may activate complement and posonize the cells for rapid splenic phagocytosis. These
disorders are often acute and self limiting but when they become chronic, treatment begins with
corticosteroids.
70.
Answer: D. inhibition of exocrine gland secretion
Explanation:
SLE’s pathogenesis is that of type III hypersensitivity patients have hyperactivity o f B cells of
unknown origin. This hypcractivity causes hypergammaglobulinemia, with circulating immune
complexes o f DNA and other nuclear antigens that precipitate onto vascular basement membranes
and active complement. Mild arthritis, fever rash and fatigue occur, hypertension may develop
secondary to kidney disease, hemolytic anemia and thromobocytopnea are common; behavioral
changes occur in approximately 25 % of patients and progressive necrotizing vasculitis with CNS
involvement and glomerulonephritis are the most serious consequences occurring in
approximately 50% of patients. In sjogren’s syndrome pathogenesis, primary symptoms include
inhibition o f exocrine gland secretion.
71 .Answer: A. corticosteroids
Explanation:
Current therapies involve approaches that suppress all immune responses for example
corticosteroids; however current clinical trials seek to suppress only lymphocytes that are
activated e.g. feeding autoantigens(to induce immunologic suppression), vaccination with
autoactive T cells( to induce immunologic suppression), administration o f anti-TH monoclonal
antibodies(particularly anti-CD4, to eliminate auto reactive T cells) and administration o f
conjugates of interleukin-2(lL-2) and toxins from plants or bacteria to eliminate auto reactive T
cells with out generalized T-cell suppression.
72.Answer: C. Leukemias
Explanation:
Primary immunodeficiencies include X-linked agammaglubulinemia, common variable
immunodeficiency, selective IgA deficiency, Digeorge syndrome, Nexelof syndrome, severe
combined immunodeficiency disorders(SClDs), chronic granulomatous disease(CGD), leukocyte
adhesion deficiency(LAD), Chediak-higashi syndrome and defects in complement while
secondary immunodeficiencies include, cytotoxic drugs, leukemias, lymphomas, myelomals,
protein calorie malnutrition, aging, acute infections and AIDS.
73.Answer: B. I, IV, V, VI
Explanation:
Digeoge syndrome results from development failure o f the thymus and parathyroid glands,
accompanied by cardiovascular and the other developmental anomalies, patients have a decrease
in total T-cell numbers (but normal immunoglobulin level), nezelof syndrome is probably
inherited and cause lymphopenia and thymus abnormalities, but normal serum immunoglobulin
levels. Gram negative sepsis may occur in addition to the opportunistic infections associated with
T-cell deficiency and SCIDs are heterogeneous group of inherited disorders with deficiencies in
T-cells, B-cells(variable) and serum immunoglobulin X-linked agammaglobulinemia is an
inherited deficiency in antibody production(humoral immunity) in which T-cell function is
relatively normal but B-cells do not fully mature. Common variable immunodeficiency is an
acquired deficiency o f B-cell maturation to plasma cells while Chediak-higashi syndrome is a
deficiency in fusion of lysosomes with phagocyte vesicles and selective IgA deficiency has low
secretary IgA (slgA).
74.Answer: E. VII&VIIJ
Explanation:
Chronic granulomatous disease (CGD) is a defect in the ability o f phagocytes to kill bacteria and
leukocyte adhesion deficiency (LAD) is associated with a defect in phagocytic cells. But defects
in complement may be due to defects in the activation pathways, membrane attack complex or
regulatory proteins.
75.Answer: C. X-linked agammaglobulinemia
Explanation:
X-linked agammaglobulinemia is liked to the X-chromosome so it occurs primarily in men.
Treatment is passive immunization with intravenous human immune globulin. But commonvariable immuno deficiency and selective IgA deficiency may occur in either sex.
76.Answer: C. cytotoxic drugs
Explanation:
Cytotoxic drugs prevent the division o f responding lymphocytes, suppress the production o f
blood cells in bone marrow and may directly kill cells. Patients who receive chemotherapy and
exhibit a significant loss o f neutrophils may be treated with filgrastim, or recombinant G-CSF
(neupogen), to restore the WBCs count to normal levels. But leukemias, lymphomas and
myelomas are associated with decreased immune responsiveness.
77.Answer: B. Three
Explanation:
Optimal anti-HIV therapy is combination therapy with three antiretroviral drugs.
78.Answer: B. didanosine
Explanation:
At present, there are three classes o f antiretroviral drugs approved by the FDA; these are
nucleoside reverse transcriptase inhibitors (NRTIs) (i.e. zidovadie, lamivodine, stavudine,
zalcitabine, didanosine and abacavir), NNRTIs (e.g. nevirapine, delavirdine, efavirenz) and
protease inhibitors (e.g. saquinavir, indinavir, ritonavir, nelfinavir).
79.Answer: E. all
Explanation:
Opportunistic infections are the major consequences o f AIDS, particularly by P. carinii. Candida
albicans, Mycobacterium-avium intraccllulare, Herpes simplex virus (HSV), cytomegalovirus
(CMV) and others. TB occurs as a reactivation o f latent infection in carriers.
80.
Answer: B. CD4
Explanation:
The viral envelope g p l2 0 has a strong affinity for CD4, allowing the virus to directly infect TH
cells. In addition, these proteins use a chemokine receptor CCR5 to gain entry to macrophages
and dendritic cells. APCs are also affected by the infection. There is a loss o f follicular dendritic
cells and interdigitating cells in the lymphoid tissue; this loss leads to decreased APCs to the
CD4+ T cells. Macrophages may produce new viruses with out being killed and may spread the
virus to uninfected T cells and other cell types. CD8+ T cells are not significantly affected and the
ratio o f circulating CD4+ to CD8 cells is inverted after infection.
81 .Answer: B. class 1 glycoproteins are known as HLA-DR, -DP and DQ antigens
Explanation:
There are individual differences in the molecular structures o f cells and tissues except in identical
twins because o f the genetic variation inherent in humans. Because o f these molecular
differences, transplanted tissues or organs i.e. grafts are likely to be antigenically different from
the recipient and there fore may stimulate an immune response. Human leukocyte antigen (HLA)
or histocompatibility type is each person’s set o f MHC glycoproteins. Class-] glycoproteins are
known as HLA-A, -B, and -C antigens. Class II glycoproteins are known as HLA-DR, -DP and DQ antigens. Each person receives from each parent one set o f genes encoding these protein
antigens. Only identical twins have the same histocompatibility type. The probability o f two
siblings with the same parents to be HLA-identical or matched is 25%.
82.Answer: D. All
Explanation:
The common solid-organ transplants are kidney, heart, liver, heart-lung and pancreas. The organs
can be obtained from cadavers or living donors. In a cadaver graft, the probability o f an exact
HLA match is approximately 1 in 10 million.
83.Answer: B. Cornea
Explanation:
In cornea transplant, is HLA matching not important.
84.
Answer: A. cardiac graft
Explanation:
The rejection reaction is decreased in renal and cardiac grafts if HLA-DR and HLA-B are
matched. But rejection does occur in HLA-matched situations.
85.Answer: C. The only reason for tissue rejection is HLA-incompatibility
Explanation:
The probability o f two siblings with the same parents to be one-half HLA-matched or
haploidentical is 50%. But parents and children are almost always haploidentical. Some
transplanted tissues are rejected because o f HLA incompatibility where as in other cases, the
reason is unknown. HLA-matching is not always a factor in rejection.
86.Answer: C. acute rejection
Explanation:
Acute rejection is a T-cell-macrophage- mediated attack on the graft based on HLA and other
tissue antigen mismatches. They cause cellular necrosis and inflammation perivascularly after the
T-cell and macrophages infiltrate the graft in 10-14 days. I f untreated, the entire graft starts to
necrose.
87. Answer: B. An ABO-mismatched graft
Explanation:
Hyperacute rejection is mediated by preexisting antibody in the recipient, usually against ABO
mismatches. Rejection occurs within 2 days after transplantation. Complement is activated,
clotting occurs and the vasculature o f the transplanted organ is occluded. ABO-mismatched graft
is rarely attempted and the rejection is untreated.
88.Answer: D. All
Explanation:
Chronic rejection occurs several months to several years after transplantation. It causes fibrosis
and occlusion o f small arteries and arterioles in the kidneys and atherosclerosis in the heart. It
may be controlled by immunologic injury, through antibody or cells, and includes the release o f
inflammatory cytokines by macrophages. This form o f rejection is resistant to therapy.
89.Answer: C. in bone marrow transplantation, the host-versus-graft response is very important
Explanation:
Bone marrow transplantation is sometimes attempted in patients with immunodeficiency diseases,
aplastic anemia, some leukemias and certain genetic diseases. A high proportion o f donor
lymphocytes that respond to the host HLA and other antigens are contained in the graft. This
response causes GVH disease. Graft T-cell recognition o f the host is important in GVH disease as
shown by the decreased incidence o f GVH disease after procedures that purge mature T cells
from the donor marrow.
Although HLA matching is important in bone marrow transplantation, the failure rate even for
matched grafts is high because o f GVH disease. The host-versus-graft response is less important
because the host is immunosuppressed due to primary immunodeficiency or by drugs or radiation.
90.Answer: D. agranulocytosis
Explanation:
Clinical symptoms of GVH disease is seen on the skin which causes rash, and desquamation,
gastrointestinal tract such as pain, vomiting and intestinal bleeding and liver necrosis indicated by
increased serum bilirubin levels. Death commonly occurs.
91.Answer: B. tacrolimus
Explanation:
Corticosteroids, azthioprene and methotrexate are used for immunosupression o f the graft
recipient. But tacrolimus is used to specifically suppress the T-cell.
92.Answer: A. ALG/ATG
Explanation:
Corticosteroids such as prednisolone and methyl prednisolone are administered just before
transplantation. They are tapered rapidly because o f their side effects. Corticosteroids are used in
combination with azathioprine, cyclosporine or antilymphocyte elobulins/antithymocyte
globulins (ALG/ATG).
93.Answer: B. methotrexate
Explanation:
Methorexate is used primarily for bone marrow transplantation in combination with ALG/ATG. It
is administered either a few days before or at the time o f transplantation. Azathioprine is used for
immunosuppression o f the graft recipient. It is given before transplantation followed by a
maintenance dose afterwards. Cyclosporine and tacrolimus are specific suppressants o f T cells.
94.
Answer: D. TH-cell secretion o f IL-2 and IFN-y and prevents T-cell activation
Explanation:
Cyclosporine binds to an intracellular protein known as cylcophilin and blocks the transcription
o f cytokine agents in a T cell that has recognized antigens. It inhibits TH-celi secretion o f IL-2
and IFN-y and prevents complete T-cell activation. Because it is more effective if it is present
when rejection begins, it is administered prophylactically. It is commonly combined with other
agents. Nephrotoxicity is the major side effect.
95. Answer: C. cyclosporine and tacrolimus
Explanation:
Since cyclosporine and tacrolimus function through the same pathway i.e. by inhibition o f TH-cell
secretion o f IL-2 and IFN-y and complete prevention of T-cell activation. Rampamycin functions
by inhibiting TH cell response o f IL-2 to prevent T h- ccII activation. Since it functions through a
different pathway, it is more effective in combination with cyclosporine and tacrolimus.
Corticosteroids are used in combination with cyclosporine, azathioprine or antilymphocyte
globulins/antithymocyte globulins (ALG/ATG).
96. Answer: B. ALG and ATG
Explanation:
ALG and ATG are antisera derived from animals. They contain a variety o f antibody specificities
against T-cell antigens. They are used prophylactically and therapeutically in bone marrow and
organ transplantation.
97.Answer: A. muromonab-CD3
Explanation:
Muromonab-CD3 is a mouse monoclonal antibody specific for the CD3 antigen, which is present
on all peripheral T cells. It is used therapeutically to half and reverses acute rejection.
98. Answer: A. it may also be used in vitro to purge host(recipient) bone marrow o f T cells to
reduce the risk o f GVH disease
Explanation:
Muromonab-CD3’s main actions are the opsonization o f T cells for enhanced phagocytosis. It can
be administered daily for 10-14 days. Only one course is typically used because it causes an
immune response against the foreign mouse antibody. Because o f nonspecific T-cell activation
which causes the release o f cytokines, acute side effects are common. The side effects include
high fever, chills, blood pressure changes, vomiting, diarrhea and respiratory distress. Patients
with fluid overload should not use OKT3 because it may cause fatal pulmonary edema. OKT3
may also be used in vitro to purge donor bone marrow o f T cells to reduce the risk o f GVH
disease.
99. Answer: C. active vaccination is the intramuscular or intravenous injection o f antibody
preparations to enhance a patient’s immune competence
Explanation:
Active vaccination is the intramuscular, subcutaneous or oral introduction o f one or more
antigens designed to stimulate the immune system to produce a specific immune response. This
response generates antibody, activated T cells and specific memory. Protection through memory
varies with the vaccine but immunity is long-lasting. Passive vaccination is the intramuscular or
intravenous injection o f antibody preparations used to enhance a patient’s immune competence.
The protection o f passive vaccination depends on the serum half-life o f the injected antibody and
is limited to several weeks to several months for each administration o f human sera.
100. Answer: A. they-are individual sera prepared from plasma lots o f subjects actively
immunized against or recovering from specific disease
Explanation:
Standard human serum immune globulin for intramuscular vaccination (IGIM) is a polyclonal
antiserum prepared from pooled plasma o f donors. It contains 165 mg/ml human
immunoglobulin, predominantly the four subclasses o f IgG i.e. IgG 1-4. The side effects are rare,
minimal and usually confined to minor inflammation and pain at the site of injection. Since
antibody aggregates form and may activate complement and platelets, it is unsuitable for
intravenous injection.
101.
Answer: C. Special IGIM
Explanation:
Special IGIM are individual sera prepared from plasma lots o f subjects actively immunized
against or recovering from specific diseases. Each serum is enriched for antibody o f the desired
specificity e.g. tetanus immune globulin (TIG) contains more antibodies against tetanus toxin
than would be found in IGIM.
102.
Answer: D. chills, nausea and abdominal pain occurs in all patients
Explanation:
IVIGs are prepared from polled human serum and modified to minimize antibody aggregation.
Approximately 10% o f patients experience chills, nausea and abdominal pain. By reducing the
rate o f intravenous infusion, the side effects can be diminished. Premeditation with
corticosteroids is recommended and intravenous epinephrine is used if prophylaxis occurs.
103.
Answer: A. hepatitis immune globulin
Explanation:
Passive vaccination is used for the prophylaxis o f infectious disease e.g. tetanus immune globulin
is used for the prophylaxis o f Clostridium tetani infection, hepatitis B immune globulin for
individuals exposed to hepatitis virus, prophylaxis or therapy which prevents or attenuates the
effects o f infection in special populations e.g. varicella zoster immune globulin for
immunocompromised patients. IGIM is used in pregnant women exposed to rubella. Treatment o f
antibody deficiency are used for persons who are deficient in antibody production, either because
o f primary immunodeficiency or as a result o f chronic lymphocyte leukemia receive IVIG or
IGIM every 2-4 weeks to maintain humoral immunity. It is also used for other situations such as
for idiopathic thrombocytopenia purpura, intramuscular Ro (D) immune globulin as a prophylaxis
for Rh disease and muromonab-CD3 for acute renal graft rejection. IGIM is used for
hypogammaglobulinemia that is for antibody deficiency therapy.
104.
Answer: C. polyvalent antivenin
Explanation:
Polyvalent antivenin is used for the prophylaxis and therapy for snakebite. Botulism antiserum is
used for prophylaxis and therapy o f botulism. For the prophylaxis and therapy o f black widow
bite, black widow antivenin is used.
105.
Answer: A. Rho(D) immune globulin
Explanation:
Animal antisera i.e. equine(horse) antisera are used in certain situations such as in the preparation
o f botulism antiserum for botulism, polyvalent antivenin for snakebite, black widow antivenin for
black widow bites and mouse monoclonal antibody for acute renal rejection. Rho (D) immune
globulin is used for the prophylaxis o f Rh disease.
106.
Answer: C. chronic lymphocytic leukemia
Explanation:
Intramuscular passive vaccines are used for the prophylaxis o f hepatitis A and hepatitis B viruses,
measles, rabies, rubella, varicella, tetanus, hypogammaglobulinemia, Rh disease, botulism,
snakebite and black widow bite. As a therapy, intravenous passive vaccines are used for
hypogammaglobulinemia, idiopathic thrombocytopenic purpura, chronic lymphoctyic leukemia,
cytomegalovirus infection. To reverse acute rejection, intravenous passive vaccine i.e.
muromonab-CD3 is used.
*
Explanation:
> ----------------- ~ « , , r , „ „ 1 n h i i 1 i n e m
i a
Explanation:
In the therapy for antibody deficiency caused by hypogammaglobulinemia, both intramuscular
(1GJM) and intravenous (IVIM) passive vaccines can be used.
In all the other illnesses, either intravenous or intramuscular passive vaccines can be used.
108.
Answer: D. all o f the above
Explanation:
Active vaccines contain low doses o f antibiotics, one or more antigens or whole pathogenic
organisms. It may also contain preservatives and other compounds that do not affect the immune
response.
109.
Answer: A. Intravenous
Explanation:
Active vaccines are administered subcutaneously, or intramuscularly, intradermally. Some are
introduced adsorbed to aluminum hydroxide or aluminum phosphate adjuvants. The antigenicity
o f the vaccine is increased by an adjuvant. A few vaccines are administered orally or intranasally.
110.
Answer: B. bacillus calmette-Guerin
Explanation:
Seroconversion indicates that a person who previously did no have specific serum antibodies (i.e.
seronegative) now has these antibodies( i.e. seropostivie). The success o f the series o f vaccination
for most active vaccines is indicated by seroconversion o f the patient. For certain vaccines,
seroconversion does not indicate established immunity e.g. bacillus calemtte-Guerin vaccine for
tuberculosis.
111.
Answer: A. BCG
Explanation:
The vaccine that can be given immediately after birth is BCG vaccine. Most o f the vaccines are
given after the infant is 6 weeks old because responses are normally inadequate in newborns and
because maternal antibodies remain in the new born circulation.
112.
Answer: D. Rubella
Explanation:
Most vaccines require a series o f vaccinations where as other are effective with a single
vaccination. For those that require a series, the protection does not diminish if the interval
between vaccinations is greater than the recommended. Booster vaccinations are often necessary
for vaccines in which the duration o f memory varies with each vaccine. Rabies, DTP and Td
require booster vaccinations after 4 or 5, 4 and 3 vaccines respectively.
113.
Answer: C. all vaccines require a series o f vaccinations
Explanation:
Active vaccination is used for prophyl axis. It contains one or more antigens or whole pathogenic
organisms, preservatives low doses of antibiotics and other compounds that do not affect the
immune response. It can be administe ied intramuscularly, intradermally, subcutaneously,
adsorbed to aluminum hydroxide or a.l uminum phosphate adjuvants, orally or intranasally. For
most active vaccines, the success o f th e series o f vaccination is indicated by seroconversion o f the
patient. A schedule o f active vaccinati 3n is recommended for infants and children. But some
vaccines are intended for use primaril; in noninfant populations. Most vaccines require a series o f
vaccination where as others are effecti ve with a single vaccination. The side effects include
inflammation at the site o f vaccinatidr malaise, mild fever, chills, headache, myalgia and
arthralgia. Febrile illness, somnolence seizures or anaphylactic hypersensitivity to vaccine
antigens or accessory components sue i as antibiotic, chicken protein is the more sever side
effects. Sever reactions contraindicate continuation o f a series. A person with sever febrile illness
should not be actively vaccinated unti the illness resolves.
114.
Answer: A. it is safe to give live, attenuated viral vaccines to pregnant women
Explanation:
Live, attenuated vaccines consists o f jjwhole organisms usually viruses. Since these organisms
multiply after vaccination, they are att enuated to reduce their pathogenecity. A small dose can
produce strong immune response becj£use the antigen concentration increases when the organism
multiplies. Some vaccines such as me isles, mumps, and rubella (MMR) vaccine elicit life long
immunity in two doses. Because o f th : ir relative genetic instability, viruses can revert to
virulence and cause the disease again't which the patient is vaccinated e.g. oral polio
vaccine(OPV). Live attenuated viral y accines are not recommended for pregnant women or those
intending to become pregnant within months o f vaccination. Immunocompromised individuals
should not be given live, attenuated Vi ral or bacterial vaccines.
115.
Answer: C. killed inactivated vaccines
Explanation:
Killed, inactivated vaccines may contk:in whole killed cells for e.g. phenol-killed bordetella
petussis or any antigenic fraction isolated from the organism. They are usually given adsorbed to
adjuvant. Tetanus toxiod(Td) is an ex;ample o f killed, inactivated vaccine which is isolated
antigen which may require inactivatiion before they are used in a vaccine. The inactivation
eliminates pathogenicity but preserves; some antigenicity.
116. Answer: B. vaccines in whidl the antigenic fragment is a polysaccharide are usually best
at eliciting immune response and mernory
Explanation:
In killed, inactivated vaccines, isolate|d antigens may require inactivation before they are used in a
vaccine. This inactivation eliminates; pathogenicity but preserves some antigenicity. Since no live
organisms are present, reversion to pjiJathogenicity is not a problem. The doses o f cells or antigens
must be higher than in live, attenuated vaccines. Flypersensitivity reactions to vaccine
components are more common. Vac<j; nes in which the antigenic fragment is a polysaccharide are
usually poor at eliciting immune resp<j>nses and memory, probably because they do not evoke T-
cell activation. In this type o f vaccines, the polysaccharides are conjugated to another antigenic
compound. These vaccines are known as conjugate vaccines.
117.
Answer: D. subunit vaccines
Explanation:
HBV vaccine and the vaccine that is not currently available lyme disease vaccine are examples of
subunit vaccines.
Subunit vaccines are proteins and glycoprotein of an organism that are produced by recombinant
DNA technology in bacteria, yeast or mammalian cells. These are used as the antigens for
vaccination.
118.
Answer: D. All
Explanation:
Experimental vaccines include other subunit vaccines i.e. peptides produced by chemical, cellfree synthesis, recombinant DNA viruses containing genes for the antigens o f multiple organisms
and anti-idiotype antibodies used for active vaccination.
119.
Answer: D. oral polio(opvj trivalent)
Explanation:
Oral polio(opvj trivalent) is a live attenuated viral vaccine. The target populations were infants,
children, health and day-care workers. It was given four times with a schedule o f 2,4,15-18
months and one at school entry. Because of 1 in 2.6 million risk o f vaccine-induced paralysis; it
is no longer recommended and is substituted by killed vaccine.
120.
Answer: A. Rubella
Explanation:
Rubella is the vaccine hat is given to adolescent girls not previously vaccinated. It is given to
protect future fetus from congenital rubella injury. It is given once after puberty. MMR(measles,
mumps rubella) is given to infants and children. It is given twice on the 15 month and at school
entry. This vaccine affords life long immunity. Varicella virus is given to children and to
individuals at risk. It is given once but if the patient is 13 year or older it is given twice. In
children below 13 years or older it is given twice. In children below 13 years o f age it is given
between the 12 and 18 months or 2-3 years. For individuals above 13 years it is given 2-4 weeks
apart. Influenza(tri or polyvalent) is given.to geriatric patients, health care workers and for those
who are at risk for complications o f flu. It is given annually for maximal protection . the vaccine
must be updated annually because variant strains may appear each year.
121.
Answer: C. BCG tuberculosis
Explanation:
Oral polio(opv trivalent, measles, mumps rubella(MMR) rubella and varicella are live attenuated
viral vaccine. BCG tuberculosis is a live attenuated bacterial vaccine. It is given to persons
exposed to sputum-positive tuberculosis patients. The schedule o f BCG tuberculosis vaccine
depends on the success o f the initial vaccination. Its effectiveness is unpredictable. It induces cell
mediated immunity.
122.
Answer: C. rabies
Explanation:
Rabies is given to animal-care-workers 4 or 5 times with booster vaccination. It should be taken 7
days apart. The boosters are taken as required to maintain immunoglobulin. Only tow doses are
given to exposed, already immune individuals. Influenza vaccine is given to geriatric patients,
health care workers and to those who are at risk for complications o f flu. Rubella vaccine is given
to adolescent girls not previously vaccinated.
123.
Answer: A. Influenza
Explanation:
A vaccine that is given annually is influenza vaccine. It is given to geriatric patients, health care
workers and those at risk for complications o f flu. The vaccine must be updated annually because
variant strains may appear each year. 3 vaccines o f hepatitis B are given inactivated polio 4
vaccines and rabies 4 or 5 vaccines.
124.
Answer: B. hepatitis B
Explanation:
Hepatitis B is a recombinant subunit. It is given to each individual. Three vaccines are given, the
first between 1-2 months, the second 2-3 months and the last one after 6 months.
125.
Answer: A. there is a risk of vaccine-induced paralysis
Explanation:
Inactivated polio vaccine is given to immunodeficient children and families. It is given as booster
vaccination in health and day care workers. Four vaccinations are given scheduled at 2,4,15-18
months and one at a school entry. Inactivated polio has no paralysis risk.
126.
Answer: C. tetanus and diphtheria toxoid
Explanation:
Tetanus and diphtheria toxiod(Td) is given for children 7 years or older , and for adults with no
vaccination. It is three vaccination with boosters. The second dose is given in 4-8 weeks and the
third dose 6 months later. Td booster is given every 10 years or on exposure through a wound if
more than 10 years or vaccine history is unavailable.
127.
Answer: D. since it is a polysaccharide vaccine, conjugate vaccines should be used.
Explanation:
Diphtheria, tetanus pertussis(DTP) is given for infants and children. There are four vaccinations
with boosters. It is given on the 2nd, 4th, 15th - 18th month and one at school entry. Tetanus
toxiod(Td) boosters are given every 10 years or on exposure through a wound.
128.
Answer: A. haemophilus b
Explanation:
Hemophilus b is given to infants, children and HIV infected adults. The number o f vaccine and
schedule depends on the formulation. Conjugated vaccines enhance the potency polysaccharide
capsule is poor antigen. Pneumococcus is given to adults or children 2 years or older and are at
risk o f e.g. immunocompromised patients and geriatric patients.
129.
Answer: C. meningococcus
Explanation:
Menigococcus(quadrivalent A,C,Y, and W-135) is given to college freshmen living in
dormitories, high-risk adults or children 2 years or older including individuals with terminal
complement component deficiencies or anatomic or functional asplenia. It is given once
subcutaneously. It is given as necessary to individuals at risk, in 3-5 year intervals.
Polysaccharide vaccine gives poor response in children younger than 2 years. It dose not protect
against serotype B, which accounts for 46% o f cases.
130.
Answer: D. pneumococcus
Explanation:
Pneumococcus is a polyvalent vaccine. The target population are adults at risk or children 2 years
or older for e.g. immunocompromised patients, geriatric patients. It is given once or once per
year. It can be given once per year in geriatric patients, it is given as necessary in at risk patient
who were not given during active infection. In children younger than 2 years o f age, the
polysaccharide antigen has poor response.
131.
Answer: D. All
Explanation:
Active and passive vaccines are administered simultaneously to maximize post exposure
prophylaxis. The immune globulin offers immediate protection where as the active vaccine
stimulates an immune response. In order to prevent antigen and antibody from reacting and
inactivating one another these vaccines are given at separate sites. Infants with HBV who are
bom to mothers who have the hepatitis B surface antigen, this combined prophylaxis is given to
protect them from becoming chronic carriers. Combined active and passive vaccines are used as a
post exposure prophylaxis o f rabies. Because o f the lethal nature o f the unchecked infection. The
exceptions are patients with a previous active vaccination with sufficient existing serum antibody
concentration.
132.
Answer: B. if the last dose was received more than 10 years ago, Td but not TIG is given
Explanation:
Active and passive tetanus vaccine is sometimes used depending on the type of wound and the
patient’s history o f active vaccination. A tetanus-prone wound is one that produces anaerobic
conditions for e.g. deep puncture or one in which exposure to clostridium or its spores is probable
e.g. contaminated with animal feces. Both TIG and Td vaccines are administered if the patients
vaccination history is uncertain or includes fewer than three doses. The patient must return to
complete the toxoid series for tetanus prone wound no treatment is necessary if the last Td dose
was received with in the last 5 years and if the last dose was received more than 10 years ago, Td
and not TIG is given to boost memory immunity and antibody production.
133. Answer: A. for a clean, minor wound, no treatment is necessary if the patient received a
full series and the last Td dose was received within 5 years
Explanation:
For a clean minor wound, if the patient’s history o f active vaccination is uncertain or includes
fewer than three doses only Td is administered. No treatment is necessary if the last Td dose was
received within 10 years and full series o f active vaccination was received by the patient. If the
last dose was received more than 10 years ago, Td but not TIG is given to boost memory
immunity and antibody production.
134.
Answer: E. it is useful for HIV treatment
Explanation:
Monoclonal antibodies are used for in vitro diagnostic tests such as blood group and tissue typing
for HLA, screening o f cancer-related antigens e.g. carcinoembryonic antigen, urine testing for
drugs and metabolites and testing for HIV infection. Monoclonal antibodies are conjugated to
enzymes, radioisotopes or florescent dyes for these and many other diagnostic applications.
135.
Answer: C. bone cancer
Explanation:
Monoclonal antibodies against neoplastic cells show some success and are used to treat certain
leukemias and lymphomas, breast cancer and colon cancers.
136.
Answer: C. Monoclonal antibodies against T cells
Explanation:
The clinical trials o f monoclonal antibodies against T cells have shown improvement in certain
autoimmune disorders. Fab antidigoxin antibody which is obtained from sheep is approved for the
reversal o f toxicity associated with toxic digoxin serum levels. Muromonab-CD3 is used to treat
acute graft rejection. Monoclonal antibodies against neoplastic cells are useful in treating certain
leukemias and lymphomas as well as breast and colon cancers.
137.
Answer: D. All
Explanation:
Monoclonal antibodies are conjugated to enzymes, drugs, prodrugs, radioisotopes or plant and
bacterial toxin. It is conjugated in order to provide specific delivery o f the conjugated agent to
one or more focused in vivo sites o f action.
138.
Answer: A. immunotoxins
Explanation:
Immuotoxins are usually produced by the conjugation o f a monoclonal antibody to a biological
polypeptide toxin that is modified to reduce nonspecific toxicity e.g. diphtheria toxin.
Immunotoxins are primarily as antineoplastic agents but they are being tested for graft rejection
and autoimmunity.
139.
Answer: B. IFN- a
Explanation:
Since IFN-a inhibits cell growth, it is used to treat hairy cell leukemia, kaposPs sarcoma in
patients with AIDS and genital warts. Immune cellular functions are stimulated by interferons at
low dose e.g. T cclls, NK cells, macrophages but higher doses have immunosuppressive effects.
140.
Answer: C. IFN- y is used to treat hair cell leukemia and genital warts
Explanation:
IFN- a and IFN- y are the only approved interferons. IFN- a is used to treat hairy cell leukemia,
kaposi’s sarcoma in patients with AIDS and genital warts. The low doses o f IFN- a are immune
cellular function stimulants where as higher doses are immunosuppressants. Greater immune
stimulation is provided by IFN- y in the intact immune system. Its effect depends on dose and
timing. IFN- y is used as a macrophage-activating factor in chronic granulomatous disease. The
most common side effects o f interferons are influenza like symptoms. Better results are obtained
when IFN- a and
IFN- y are used in combination.
141. Answer: B. the effect o f sulfur-containing compounds such as levamisole and
diethyldithiocarbamate is greater on humoral immunity than on cell mediated immunity
Explanation:
Sulfur-containing compounds such as levamisole( a phenylimidothiazole anthelmintic) and
diethyldithiocarbamate( imuthiol) have immunostimulatory activity. Their effect is greater on cell
mediated immunity than on humoral immunity. Adoptive immunotherapy is a technique in which
a patient’s peripheral blood lymphocytes or tumor-infiltrating lymphocytes are removed.
Hormones o f thymus which induce T-cell maturation and other functions are used to increase
certain cell-mediated immune functions. Inosine pranobex induces T-cell differentiation and it
augments cell mediated immune functions.
142.
Answer: A. muramyl dipeptide
Explanation:
Muramyl dipeptide is a component o f mycobacterial cell walls and it stimulates macrophage
activation. They may be used as an adjuvant given with antigen or given alone as an
immunostimulant.
Infectious Diseases
“A man can succeed at almost anything for which he has unlimited enthusiasm.”
Charles Schwab
1. Which o f the following statements is
(are) TRUE?
l.Anti-infective agents treat infection b>
suppressing or destroying the causatm
microorganisms
ILAnti-infective agents derived frorr
natural substances are called antibiotics.
111.Anti-infective agents produced fron
synthetic substances are called anti
microbials
A.
B.
C.
D.
E.
i f l only is correct
if HI only is correct
if I & II are correct
if II&III are correct
ifl , II, and 111 are correct
2. Which o f the following statements is
NOT TRUE about gram staining?
A. Gram staining can be done on a)ll
specimens except blood cultures
B. By determining if the causath
agent is gram-positive or gramnegative, the test allows a bett
choice o f drug therapy
C. Gram-positive
microorganisms
stain blue or purple
D. Fungi cannot be identified fey
gram stain
E. Gram-negative
microorganisijis
stain red or rose pink
3. All o f the following are termed
microorganisms EXCEPT:
A.
B.
C.
D.
E.
Bacteria
Fungi
Protozoa
Viruses
Lice
4. Which o f the following should be
performed before anti-infective therapy i
initiated?
A. Microbiological cultures
B. Gram staining
C. Susceptibility tests o f the infective
microorganism
D. All o f the above
E. A and C are enough
5. Which of the following statements best
describes the minimum inhibitory
concentration in the micro dilution method
o f susceptibility testing?
A. It is the lowest drug concentration
that prevents microbial growth after
18-24 hours o f incubation.
B. It is the minimum number of
bacteria that can survive after 24
hours o f incubation in anti-microbial
drug susceptibility testing.
C. It is the lowest concentration o f a
drug that reduces bacterial density
by 99.9%
D. It is the concentration o f a drug that
kills the lowest number o f bacteria.
E. None
6. Which o f the following statements are
true about break point concentrations of
antibiotics?
A. They are used to characterize
antibiotic activity.
B. They are determined by considering
pharmacokinetics, serum and tissue
concentrations following normal
doses o f antibiotics.
C. The interpretive categories are based
on break point concentrations are
susceptible, moderately susceptible,
and resistant.
D. All o f the above
E. A and B only
7. As compared to the microdilution
method the diffusion method o f
susceptibility testing is:
A. Less expensive
B. More expensive
C. Less reliable
D. More reliable
E. A and C
8. Which o f the following may suggest the
effectiveness o f a particular drug in treating
a given syndrome (mostly infections)?
A.
B.
C.
D.
E.
Structure o f a drug
Physical properties o f a drug
Susceptibility testing
Clinical experience
C and D
9. An anti-infective agent should be chosen
for a particular infection based on:
A.
B.
C.
D.
E.
Its pharmacological properties
Spectrum o f activity
Various patient related factors
All o f the above
A and C only
10. A bactericidal agent is:
A. A drug that inhibits the growth or
reproduction o f a bacterium.
B. A drug that rapidly destroys the
bacteria
C. A drug that stimulates the growth o f
bacteria
D. A drug that acts as food for bacteria
E. None
11 .Which o f the following patient related
factors affect the outcome o f anti-infective
therapy?
A. Impaired
immunological
mechanisms
B. Preexisting kidney or liver damage
C. Pregnancy if the patient is female
D. All o f the above
E. A and C only
12. Which of the following statements is
NOT TRUE about drug therapy during
pregnancy?
I.Plasma drug concentrations tend to
decrease in pregnant women
II.Most drugs, including antibiotics,
appear in the breast milk o f nursing
mothers and may cause adverse effects
in infants
III .The m other's need for the antibiotic
should be weighed against the drug’s
potential harm
A.
B.
C.
D.
E.
I only
Ill only
I & II
II&III
1,11, and III
13. Which o f the following class o f
antibiotics may lead to toxic bilirubin
accumulation in a newborn’s brain?
A.
B.
C.
D.
E.
Tetracyclines
Sulfonamides
Aminoglycosides
Erythromycins
None
14.Sulfonamides may cause hemolytic
anemia in patients with hereditary
deficiency o f the enzyme:
A.
B.
C.
D.
E.
Salivary amylase
Glucose-6-phosphate dehydroganse
Ri bose-6-phosph ate
Topoisomerase
None
15.Patients who rapidly metabolize drugs
(i.e. rapid acetylators) may develop
hepatitis when receiving the antitubercular
drug:
A.
B.
C.
D.
Isoniazid
Streptomycin
Rifamipicin
Ethambutol
E. None
16. Which o f the following should be done
when a serious life-threatening infection
occurs?
A. A broad-spectrum antibiotic should
be given until the specific organism
has been identified
B. Any antibiotic should be given in
doses higher than those used in the
treatment o f less severe infections
C. The antibiotic therapy should not be
given until the infective organism is
known
D. Combination o f any antibiotics
should be used
E. None
17. The disadvantages o f combination
therapy o f anti-infective agents are:
A. It may increase the toxic drug
effects
B. It may result in drug antagonism
C. It is always ineffective
D. A and B
E. None
18. The indications for multiple-drug
therapy include:
A. Need
for increased
antibiotic
effectiveness
B. To prevent the proliferation o f drugresistant organisms
C. Treatment o f an infection caused by
multiple pathogens
D. Treatment o f any infection
E. A, B and C only
19. Which o f the following statements
is/are FALSE about the duration o f antiinfective therapy?
I.In
acute
uncomplicated
infection
treatment should generally continue until
the patient has been afebrile and
asymptomatic for atleast 72"Rours
II.In chronic infection treatment may
require duration o f 4-6 weeks.
III.Treatment o f acute infection should
continue until the patient feels better.
A.
B.
C.
D.
E.
1 only
111 only
I & 11
II&III
I,II, and III
20.The role o f radiographic findings in
monitoring therapeutic effectiveness is:
A. They help in identification o f the
infecting organism.
B. They help indicate the locus of
infection.
C. They act as therapeutic agents by
directly
killing
the
infecting
organism.
D. They help in the management of
symptoms o f acute infection.
E. None
21 .Which o f the following statements is
NOT TRUE about erythrocyte
sedimentation rate?
A. Large elevations in erythrocyte
sedimentation rate are associated
with acute or chronic infection
B. Elevated erythrocyte sedimentation
rate does not occur due to
noninfectious cases
C. Elevated sedimentation rates are
common with infections such as
endocarditis
D. A normal erythrocyte sedimentation
rate may occur in some infections
E. Erythrocyte sedimentation rates are
elevated
with
intraabdominal
infections
22. Which of the following are useful in
indicating a locus o f infection?
A. Radiographic findings
B.
C.
D.
E.
F.
Pain and inflammation
ESR measurements
White blood cell count
A and B
C and D
23.A patient was admitted to a hospital for
a severe infection. The physician in charge
ordered proper laboratory tests for
identification o f the infecting
microorganism.
The laboratory result was obtained and the
physician ordered an antibiotic based on the
laboratory result, but the patient’s condition
didn’t improve. Which o f the following may
be causes o f the lack effectiveness o f the
antibiotic?
A. Misdiagnosis o f the infecting
microorganism
B. Improper drug regimen
C. Inappropriate choice o f an antibiotic
agent
D. All o f the above
E. A and B
24. Which o f the following can be causes of
fever?
A. Infections
B. Drug reactions
C. Neoplasms
D. All o f the above
E. B and C only
F. A and C only
25. Which o f the following non-infcctious
conditions respond to antimicrobial agents?
A.
B.
C.
D.
E.
Metabolic disorders
Phlebitis
Arthritis
Neutropenic cancer
None
26. Which o f the following statements is
NOT TRUE about perioperative antibiotic
prophylaxis?
A. It is a short course o f antibiotic
administered before there is clinical
evidence o f infection
B. Initiation o f prophylaxis is done
often at induction o f anesthesia
C. The most commonly used route o f
administration o f the drugs is the
oral route
D. The
antibiotic
should
be
administered in order to ensure that
appropriate antibiotic levels are
available
at
the
site
of
contamination before the incision
E. The most commonly used route o f
administration o f the drugs is IV or
1M
27. First generation cephalosporins are
drugs o f choice for most procedures and
patients in perioperative antibiotic
prophylaxis because:
A. They have appropriate spectrum
B. They have less frequency o f side
effects
C. They have favorable half-life
D. They have low cost
E. All o f the above
28. Which o f the following statements are
TRUE about Aminoglycosides?
I.They are primarily used in the
treatment o f infections caused by gramnegative enterobacteria and in suspected
sepsis
II.They act as antibacterial by inhibiting
protein synthesis.
III.The toxic potential o f these drugs
limits their use.
A.
B.
C.
D.
E.
i f l only is correct
i f III only is correct
if I & 11 are correct
if I1&I11 are correct
if I,II, and III are correct
29.An amino glycoside antibiotic most
commonly used in treatment o f tuberculosis
in combination with other antitubercular
drugs is:
A.
B.
C.
D.
E.
Gentamicin
Kanamycin
Streptomycin
Tobramcyin
None
30.The amino glycoside antibiotic with the
broadest-spectrum activity against most
aerobic gram-negative bacilli as well as
many anaerobic gram-negative bacterial
strains that resist gentamicin and
tobramycin is:
A.
B.
C.
D.
E.
Kanamycin
Neomycin
Amikacin
Netilmicin
None
A.
B.
C.
D.
E.
Aminoglycosides
Tetracycline
Amikacin
Penicillin
None
34. Aminoglycosides can cause vestibular
or auditory damage. Which o f the following
Aminoglycosides are primarily associated
with vestibular damage?
A.
B.
C.
D.
E.
Streptomycin
Amikacin
Netilmicin
Gentamicin
A and D
35. All o f the following Aminoglycosides
are associated with auditory damage
EXCEPT:
A.
B.
C.
D.
E.
Amikacin
Netilmicin
Kanamycin
Neomycin
None
31.The amino glycoside antibiotic with the
least ototoxic adverse effect is:
A.
B.
C.
D.
E.
Streptomycin
Gentamicin
Netilmicin
Kanamycin
None
36. An aminoglycoside that results in both
vestibular and auditory damage is:
A.
B.
C.
D.
E.
Tobramycin
Gentamicin
Amikacin
Streptomycin
None
32. Which o f the following organisms are
neomycin resistant?
A.
B.
C.
D.
E.
E.coli
Klebsiella pneumoniae
P.aeruginosa
Streptococci
C and D
33.Streptomycin is used in the treatment of
acute brucellosis in combination with:
37. Aminoglycosides accumulate in the
proximal tubule; mild renal dysfunction
develops in up to 25 % o f patients receiving
these drugs. Which o f the following is the
most nephrotoxic?
A.
B.
C.
D.
E.
Neomycin
Kanamycin
Amikacin
Gentamicin
Streptomycin
38. The risk factors for the development o f
nephrotoxicity in patients taking
Aminoglycosides are:
A. Preexisting renal disease
B. Impaired renal flow unrelated to
renal disease
C. Concurrent
administration
of
another nephrotoxic drug
D. Previous
or
prolonged
aminoglycoside therapy
E. All o f the above
39. A carbapenem which should be
administered with cilastatin is:
A.
B.
C.
D.
E.
Ertapenem
Meropenem
Imipenem
Cefuroxime
None
40. Which one o f the following statements
is FALSE about carbapenems?
A. They have broader spectrum of
activity than do most p-lactams
B. They inhibit bacterial cell wall
synthesis
C. They are destroyed easily by most
p-lactam ases
D. They are
active against gram
positive cocci
■
E. They are
active against gramnegative rods and anaerobes
41. Cephalosporins are known as p-lactam
antibiotics because their chemical structure
consists o f a p-lactam ring adjoined to a:
A.
B.
C.
D.
E.
Thiazolidine ring
Imidazole ring
Benzene ring
Tetrazole ring
None
42.All o f the following are first generation
cephalosporins EXCEPT:
A.
B.
C.
D.
E.
Cefadroxil
Cefazolin
Cephalexin
Cefmetazole
Cephapirin
43. Which o f the following is a fourth
generation cephalosporin?
A.
B.
C.
D.
E.
Cefdinir
Cefazolin
Cefonicid
Cefepime
None
44. First generation cephalosporins are
active against all o f the following grampositive cocci EXCEPT:
A.
B.
C.
D.
E.
Staphylococcus
Streptococcus
Pneumococci
Enterococci
None
4 5 .Both first generation and Second
generation cephalosporins are active against
all of the following organisms EXCEPT:
A.
B.
C.
D.
E.
coli
Klebsiella Pneumoniae
Proteus mirabilis
Haemophilis influenzae
None
46. Which o f the following statements is not
TRUE?
A. Generally
each
generation
of
cephalosporin has shifted toward
increased gram-negative activity but
lost activity toward gram-positive
organisms
B. Fourth-generation
cephalosporins
have improved activity toward
gram-positive organisms over third
generation cephalosporins
C. Cephalosporins inhibit bacterial cell
wall
synthesis, reducing wall
stability, thus causing membrane
lysis.
D. Cephalosporins
are
generally
classified in four groups based
mainly on structural similarity.
E. None
50. Probenecid may impair the excretion o f
all o f the following cephalosporins
EXCEPT:
A.
B.
C.
D.
E.
Cephapirin
Cephradine
Ceftazidime
Ceftriaxone
None
51. Alcohol consumption may result in a
disulfiram-type reaction in patients taking:
47. A second generation cephalosporin
commonly administered for communityacquired pneumoniae is:
A.
B.
C.
D.
E.
Cefprozil
Cefoxitin
Cefuroxime
Cefonicid
None
48. Third generation cephalosporins are
valuable in the treatment o f meningitis
caused by meningococci, pneumococci and
H. influenzae because:
A. They penetrate the cerebrospinal
fluid
B. They are resistant to destruction by
p-lactamases produced by these
organisms.
C. They have the broadest spectrum o f
activity as compared to other
generation o f cephalosporins.
D. They are administered only orally.
E. None
49. All o f the following cephalosporins are
eliminated renally EXCEPT:
A.
B.
C.
D.
E.
Cephalexin
Cefproxil
Cefoperazone
Cefixime
None
A.
B.
C.
D.
E.
Cefmetazole
Cefotetan
Cefoperazone
All o f the above
B and C only
52. The ring found in the chemical structure
of macrolide antibiotics is known as:
A.
B.
C.
D.
E.
lactone
Tetrazole
Thiazolidine
(3-lactam
None
53. Which o f the following erythromycin
salts are given parenterally?
A.
B.
C.
D.
E.
Erythromycin
Erythromycin
Erythromycin
Erythromycin
C and D
estolate
ethylsuccinate
lactobionate
gluceptate
54.The erythromycin salt commonly
associated with cholestatic hepatitis is:
A.
B.
C.
D.
E.
erythromycin
erythromycin
erythromycin
erythromycin
None
gluceptate
estolate
ethylsuccinate
lactobionate
55. Which of the following macrolide
antibiotics increase the plasma
concentration o f terfenadine and
astemizole?
A.
B.
C.
D.
E.
Erythromycin
Azithromycin
Dirithromycin
Clarithromycin
A and D
56. Coadministration o f one o f the follwing
is contrainidacted with an ongoing
pimozide therapy.
A.
B.
C.
D.
E.
Erythromycin
Clarithromycin
Dirithromcyin
Azithromycin
None
57. The advantages o f the semi-synthetic
macrolide antibiotics as compared to
erythromycin are:
A.
B.
C.
D.
E.
they are cheap
:
they are well tolerated
they are administered once daily
All o f the above
B and C only
58. A semi-synthetic macrolide antibiotic
used in combination with omeprazole or
lansoprazole for helicobacter pylori
eradication is:
A.
B.
C.
D.
E.
Azithromycin
Dirithromcyin
Clarithromycin
Erythromycin
None
59. Which o f the following statements are
not TRUE?
A. Macrolide antibiotics act by binding
to the 50S ribosomal subunit,
inhibiting bacterial protein synthesis
B. Gastrointestinal distress may occur
with all forms o f erythromycin.
C. Azithromycin is more effective than
erythromycin against gram-positive
cocci.
D. Clarithromycin is less active than
erythromycin against staphylococci
and streptococci.
E. C and D
60.A macrolide antibiotic known to
concentrate itself within cells and its tissue
levels are higher than serum levels is:
A.
B.
C.
D.
E.
Troleandomycin
Clarithromycin
Azithromycin
Erythromycin
None
61 .Which o f the following natural
penicllins are repository drug forms
administered intramuscularly?
A.
B.
C.
D.
E.
Penicillin G
Penicillin G procaine
Penicillin V
Penicillin G benzathine
B and D
62.How many times is Penicillin G more
active than penicillin V against gramnegative organisms and some anaerobic
organisms.
A.
B.
C.
D.
E.
5-10 times
30-40 times
40-50 times
50-60 times
None
63.Resistance is emerging to penicillin G
by S.pneumoniae. The alternative drug for
such organisms is:
A.
B.
C.
D.
E.
Vancomycin
Penicillin V
Penicillin G procaine
Penicillin G benzathine
None
64. Which o f the following statements is
NOT TRUE about hypersensitivity
reactions associated with penicillin
therapy?
A. They occur in up to 10% o f patients
receiving penicillin
B. They do not occur in patients with a
negative history o f penicillin allergy
C. A
life-threatening
anaphylaxis
occurs
with
parenteral
administration o f penicillins
D. A positive history places the patient
at a heightened risk for a subsequent
reaction
E. Manifestaions range from mild rash
to anaphylaxis
65 .A severe adverse effect that most
commonly occurs in patients taking highdose penicillin is:
A.
B.
C.
D.
E.
Vomiting
Depression
Seizures
Diarrhea
None
66. Antibiotic antagonism occurs when
penicillin is given within 1 hour o f the
administration of:
A.
B.
C.
D.
E.
Erythromycins
Tetracyclines
Chloramphenicol
All o f the above
A and C only
67. Penicillinase resistant isoxazolyl
penicillin(s) is/are
A.
B.
C.
D.
E.
Cloxacillin
Dicloxacillin
Oxacillin
Methicillin
A,B,C
68. A penicillinase resistant penicillin
excreted by the liver and thus may be useful
in treating staphylococcal infections in
patients with renal impairment is:
A.
B.
C.
D.
E.
Methicillin
Nafcillin
Cloxacillin
Dicloxacillin
None
69. Which o f the following penicillinase
resistant penicillins are most valuable in
long-term therapy o f serious staphylococcal
infections such as endocarditis and
osteomyelitis.
A.
B.
C.
D.
E.
Oxacillin
Cloxacillin •
Dicloxacillin
All o f the above
B and C only
70. Which o f the following statements is
FALSE about aminopenicillins?
A. They are also known as broadspectrum penicillins.
B. They have a spectrum o f activity
broader than that o f natural
penicllins.
C. Their spectrum o f activity is
narrower than that of penicillinase
resistant penicillins.
D. They are easily destroyed by
staphylococcal penicillinases.
E. None
71. All o f the following drugs are
aminopenicillins EXCEPT:
A.
B.
C.
D.
E.
Bacampicillin
Cyclacillin
Ampicillin
Amoxicillin
Penicillin
72. For infections resulting from penicillinresistant organisms, ampicillin may be
given in combination with:
A.
B.
C.
D.
E.
Ampicillin
Penicillin G potassium
Sulbactam
Bacampicillin
None
73.Amoxicillin is more effective against
S.aureus, Klebsiella and bactcroides fragilis
when given in combination with clavulanic
acid because:
A. Clavulanic acid inactivates
penicillinases
B. Clavulanic acid enhances the
absorption o f an orally administered
amoxicillin
C. Clavulanic acid inhibits the renal
elimination o f amoxicillin
D. Clavulanic has a bactericidal effect.
E. None
B. Carbenicillin is active against
ampicillin-resistant proteus strains
and other gram-negative organisms.
C. Carbenicillin is two to four times
more active than Ticaricillin against
P.aeruginosa.
D. Piperacillin is 10 times as active as
carbenicillin against Pseudomonas
organisms.
E. None
76. All of the following organisms are
sensitive to a combination o f Tazobactam
with piperacillin EXCEPT:
A.
B.
C.
D.
E.
Haemophilis
Enterobacteriaceae
Bacteroides
Pseudomonas
None
77. The extended spectrum penicillins
which may cause hypokalemia are:
A.
B.
C.
D.
E.
Mezlocillin
Ticaricillin
Carbenicillin
All o f the above
B and C
78.The mechanism o f antibacterial action
o f sulfonamides is:
74. Which o f the following extendedspectrum penicillins are Ureidopencillins?
A.
B.
C.
D.
E.
Carbenicillin
Ticaricillin
Mezlocillin
Piperacillin
C and D
75.All o f the following statements are true
EXCEPT
A. Amoxicillin is more effective than
ampicillin against shigellosis.
A. They suppress bacterial growth by
triggering a mechanism that blocks
folic acid synthesis.
B. They inhibit bacterial cell wall
synthesis.
C. They damage the bacteria] DNA.
D. They inhibit an enzyme involved in
the detoxification o f bacteria]
metabolites.
E. None
79. Sulphonamides may cause blood
dyscrasias in patients with hereditary
deficiency of the enzyme:
A. Pyruvate dehydrogenase
B. Glucose-6-phosphate
dehydrogenase
C. Aminotransferase
D. Serum glutamic-pyruvic
transaminase
E. None
80. All o f the following antibacterial agents
have bactericidal property EXCEPT
A.
B.
C.
D.
E.
Aminoglycosides
Cephalosporins
Penicillins
Sulfonamides
None
81 .A sulfonamide used in combination with
erythromycin ethylsuccinate to treat acute
otitis media (caused by H. influenzae) and in
combination with phenazopyridine for
relief o f symptoms o f pain and burning in
urinary tract infections is:
A.
B.
C.
D.
E.
Sulfamethoxazole
Sulfisoxazole
Sulfamethizole
Sulfacytine
None
82. All o f the following organisms are
susceptible to tetracyclines EXCEPT:
A.
B.
C.
D.
E.
Mycoplasma
Chlamydial organisms
Rickettsial organisms
Pseudomonas
Spirochetes
83. A tetracycline highly effective in the
prophylaxis o f “traveler’s diarrhea” is:
A.
B.
C.
XT.
Demeclocycline
Methacycline
Doxycycline
Chlortetracycline
84. Doxycycline is the safest tetracycline
for the treatment o f extrarenal infections in
patients with renal impairment because:
A.
B.
C.
D.
it is excreted by the renal route
it is excreted mainly in the feces
it is concentrated in the kidney
it is metabolized by gastrointestinal
enzymes
E. None
85.The tetracycline commonly used as an
adjunctive agent to treat the syndrome o f
inappropriate antidiuretic hormone
secretion is:
A.
B.
C.
D.
E.
Chlortetracycline
Methacycline
Minocycline
Demeclocycline
None
86.Phototoxic reactions (reactions which
develop upon exposure to sunlight) are
common in patients taking:
A.
B.
C.
D.
E.
Demeclocycline
Minocycline
Doxycycline
Methacycline
A and C
87. Member o f the tetracycline group
which can cause vestibular toxicity is:
A.
B.
C.
D.
E.
Demeclocycline
Chlortetracycline
Minocycline
Methacycline
None
88. Which o f the following statements is
NOT TRUE about tetracyclines?
A. Tetracyclines are useful alternatives
to penicillin in the treatment o f
anthrax, syphilis, gonorrhea, and
H.influenzae infections
B. The gastrointestinal distress
associated with tetracyclines can be
minimized by administering them
with food
C. Tetracyclines may induce
permanent tooth discoloration
D. Members o f the tetracycline group
do not have cross-sensitivity among
themselves.
E. None
89. Iron preparations, antacids, magnesium
containing laxatives reduce the absorption
o f tetracyclines. The only exception is:
A.
B.
C.
D.
E.
Minocycline
Methacycline
Chlortetracycline
Doxycycline
None
90. The mechanism o f action o f
fluoroquinolone antibacterials is:
A. They inhibit bacterial cell wall
synthesis.
B. They inhibit the enzyme DNA
gyrase
C. They inhibit bacteria] cell wall
synthesis by binding to the 30S
ribosomal subunit.
D. They inhibit bacterial cell wall
synthesis by binding to the 50S
ribosomal subunit.
E. None
91. Which o f the following
fluoroquinolones has the greatest activity
against Chlamydia?
A. Ciprofloxacin
B. Trovafloxacin
C. Norfloxacin
D. Ofloxacin
E. None
92. All o f the following are first generation
quinolones EXCEPT:
A.
B.
C.
D.
E.
Sparfloxacin
Cinoxacin
Enoxacin
Norfloxacin
Nalidixic acid
93. A fluoroquinolone that has been
associated with serious liver injury leading
to liver transplantation or death is:
A.
B.
C.
D.
E.
Gatifloxacin
Grepafloxacin
Trovafloxacin
Levofloxacin
None
94.The blood level o f one antiasthmatic
drug is increased when it is administered
with ciprofloxacin. The drug is most likely:
A.
B.
C.
D.
E.
Bitolterol
Terbutaline
Epinephrine
Theophylline
None
95. Which o f the following
fluoroquinolones should be avoided in
patients with known prolongation o f QTC
interval?
A.
B.
C.
D.
E.
Gatifloxacin
Moxifloxacin
G repatof! oxacin
Enoxacin
A and B
96. Which o f the following statements is/are
TRUE about urinary tract antiseptics?
I .They get concentrated in the renal
tubules and bladder, exerting local
antibacterial effects.
Il.M ost o f them do not achieve blood
levels high enough to treat systemic
infections.
Ill .All urinary tract antiseptics have the
same mechanism o f action.
A.
B.
C.
D.
E.
i f l only is correct
if III only is correct
if I & II are correct
if II&III are correct
if I,II, and III are correct
97.The mechanism as to how methenamine
acts as a urinary antiseptic is that it
hydrolyses in acidic urine into:
A. Ammonia and formaldehyde
B. Carbonic acid and bicarbonate.
C. Ammonium
hydroxide
and
Sulphuric acid.
D. Nalidixic acid and ammonium
chloride
E. None
98. Fosfomycin tromethamine acts as
antibacterial by inactivation o f the enzyme:
A. Enolylpyruvyl transferase
B. Glucose-6-phosphate dehydrogenase
C. Topoisomerase II
D. DNA gyrase
E. None
99.Nalidixic acid and oxolinic acid are
active against all o f the following
organisms EXCEPT:
A.
B.
C.
D.
E.
Proteus mirabilis
Escherichia Coli
Pseudomonas
Klebsiella
Enterobacter organisms
100. A urinary antiseptic indicated for
the treatment o f uncomplicated urinary tract
infection (acute cystitis) in women caused
by susceptible strains o f E.coli and
E.faecalis is:
A.
B.
C.
D.
E.
Cinoxacin
Enoxacin
Fosfomycin
Nalidixic acid
None
101. Which o f the following agents are
likely to antagonize the effects o f
methenamine?
A.
B.
C.
D.
E.
Aspirin
Acetozolamide
Sodium bicarbonate
All o f the above
B and C only
102. Which o f the following anti-gout
drugs increase the blood level and decrease
the urine level o f nitrofurantoin?
A. Probenecid
B .Sulfinpyrazone
C.Colchicine
D.Allopurinol
E.A
and B
103.
All o f the following statements are
true about aztreonam EXCEPT:
A. It is a monocyclic fi-lactam
compound
B. It resembles the Aminoglycosides in
its efficacy against many gramnegative organisms, and its ototoxic
and nephrotoxic adverse effects.
C. It is active against many gentamicin
resistant organisms.
D. It lacks cross-allergenicity with
penicillin.
E. It preserves the body’s normal
gram-positive and anaerobic flora
104.
Chloramphenicol is chemically:
A. a nitrobenzene derivative
B. a phenyl alkyl derivative
C. a naphthalene derivative
D.an imidazole derivative
E. None
105.
Which o f the following drugs are
active against Rickettsial infections?
A.
B.
C.
D.
E.
Chloramphenicol
Tetracycline
Amoxicillin
Cefaclor
A and B
106. Which o f the following statements
is FALSE about Chloramphenicol?
A. It is primarily a bacteriostatic drug
B. Because o f its toxic side effects, it is
used only to suppress infections that
cannot be treated effectively with
other antibiotics
C. The bone marrow suppression
associated with Chloramphenicol is
not dose-related
D. Severe Hypersensitivity reactions
due to Chloramphenicol include
angioedcma or anaphylaxis
E. Chloramphenicol therapy may lead
to gray baby syndrome in neonates
107. The gray baby syndrome which
occurs in neonates taking Chloramphenicol
is due to:
A. Inadequate liver detoxification o f
chloramphenicol
B. Interaction o f chloramphenicol with
plasma proteins
C. Necrotic effects of chloramphenicol
on renal tissues
D Inadequate absorption of
chloramphenicol from the
gastrointestinal tract
108. The anti-epileptic drug whose
metabolism is inhibited by chloramphenicol
is:
A.
B.
C.
D.
E.
Zonisamide
Carbamazepine
Lamotrigine
Phenytoin
None
109. Which o f the following analgesic
drugs elevates the levels of
chloramphenicol?
A. Aspirin
B. Acetaminophen
C. Naproxen
D..Ibuprofen
E.
None
110. Clindamycin is used only against
infections for which it has proven to be
most effective drug. It is most commonly
used in the treatment o f abdominal and
female genitourinary tract infections caused
by:
A.
B.
C.
D.
E.
Bacillus fragilis
Escherichia Coli
Staphylococcus aureus
Salmonella typhi
None
111. Dapsone is a member o f which class
o f antibiotics
A.
B.
C.
D.
E.
Sulfone
Penicillin
Aminoglycoside
Cephalosporin
None
112. All o f the following drugs have
bacteriostatic action EXCEPT:
A.
B.
C.
D.
E.
Dapsone
Clindamycin
Chloramphenicol
Cefonicid
tetracyclines
3.
Dapsone is active against
I.P.carinii
II.Plasmodium
III.Mycobacterium leprae
A.
B.
C.
D.
E.
if l only is correct
if III only is correct
if I & II are correct
if II&III are correct
if I,II, and III are correct
114. Maloprim is a combination product
containing dapsone and:
A.
B.
C.
D.
E.
115.
Pyrimethamine
Trimethoprim
Procaine penicillin
Erythromycin
None
Linezolid is chemically a synthetic:
A. Oxazolidine
B. Imidazole
C. Tetrazole
D. P-lactam
E. None
116. Linezolid has bactericidal action
against:
A.
B.
C.
D.
E.
Enterococci
Streptococci
Staphylococci
A and C
All the above
117. In which of the following cases is
enhanced effect o f the antibiotic linezolid
expected?
A. Patients taking adrenergic agents
B. Patients taking serotonergic agents
C. Patients consuming more than 100
mg o f tyramine a day
D. All o f the above
E. B and C only
118.
to:
A.
B.
C.
D.
E.
Spectinomycin is related structurally
Penicillins
Cephalosporins
Aminoglycosides
Sulfonamides
None
119.
route o f administration o f
Spectinomycin is
A.
B.
C.
D.
E.
IM
IV
Oral
Subcutaneous
Sublingual
120. Trimethoprim is chemically a
substituted:
A.
B.
C.
D.
E.
Purine
Pyrimidine
Sugar
Amino acid
None
121. Trimethoprim acts as antibacterial
by inhibiting the enzyme:
A. Lactate dehydrogenase
B. Dihydrofolate reductase
C. Glucose-6-phosphate
dehydrogenase
D. Topoisomerase 11
E. None
122. When a combination o f
Trimethoprim and sulfamethoxazole is
used; many organisms resistant to one
component are susceptible to the
combination. This effect is known as;
A.
B.
C.
D.
E.
124.
A.
B.
C.
D.
E.
Nelfinavir
Phenytoin
Rifamipicin
Cyclosporine
None
Flucytosine is chemically a:
Fluorinated
Fluorinated
Fluorinated
Fluorinated
None
cryptococcus and Candida
III.Use o f Flucytosine alone is
recommended
A.
B.
C.
D.
E.
synergism
antagonism
agonism
synchronism
None
123. All o f the following drugs result in
an increase in the clearance o f caspofungin
EXCEPT:
A.
B.
C.
D.
E.
II.lt is prim arily active against
pyrimidine
purine
amino acid
sugar
125. The mechanism o f action of
Flucytosine is:
A. It inhibits DNA synthesis
B. It inhibits bacterial cell wall
synthesis
C. It is converted to fluorouracil, which
results
in
defective
protein
synthesis.
D. It inhibits an enzyme involved in
fatty acid synthesis.
E. None
126. Which o f the following statements
is TRUE about Flucytosine?
I. It is usually given in combination
with amphotericin B
if l only is correct
if 111 only is correct
i f l & II are correct
if 1I&I11 are correct
if 1,11, and III are correct
127.
Which o f the following drugs have
demonstrated synergy with Flucytosine
against cryptococcus and Candida?
A.
B.
C.
D.
E.
128.
A.
B.
C.
D.
E.
Griseofulvin
Amphotericin B
Fluconazole
Nyastatin
B and C
Griseofulvin is produced from:
Penicillium griseofulvum dierckx
Cryptococcus species
Apsergillus species
Candida albicans
None
129. Griseofulvin is active against which
o f the following fungal species
A.
B.
C.
D.
E.
Microsporum
Epidermophyton
Trichophyton
Aspergillus
A, B and C
130. Which o f the following statements
is TRUE about the therapeutic uses of
griseofulvin?
A. It is effective against tinea
infections o f the skin, hair, and nails
caused by microsporum,
epidermophyton and trichophyton.
B. Generally it is given only for
infections that do not respond to
topical antifungal agents.
C. It may used in the treatment of
Raynaud’s diseases
D. It may be used in the treatment o f
gout.
E. All o f the above
131. The mechanism o f action of
griseofulvin is similar to:
A.
B.
C.
D.
E.
Amphotericin B
Caspofungin
Flucytosine
Colchicine
None
132. Which o f the following adverse
effects associated with griseofulvin is
classified as rare?
A.
B.
C.
D.
E.
Headache
Leukopenia
Hepatotoxicity
Confusion
None
133. The dosage o f griseofulvin is
dependent on:
A. The particle size o f the product
B. The color of the product
C. The bioequivalence of the product
with other standard product.
D. The solubility o f the product in
water
E. None
134. Which of the following drugs result
in tachycardia and flushing when given
with griseofulvin?
A.
B.
C.
D.
Barbiturates
Alcohols
Cimetidine
Warfarin
135. Which o f the following statements
best describes the mechanism o f action o f
imidazole antifungals?
A. They inhibit the synthesis of
proteins involved in membrane
transport
B. They inhibit sterol synthesis in
fungal cell membranes and increase
cell wall permeability.
C. They result in the synthesis o f
defective fungal DNA.
D. They bind to 30 S ribosomal subunit
o f fungal cells and inhibits protein
synthesis.
E. None
136.
Which o f the following are
susceptible to imidazole antifungal agents?
A.
B.
C.
D.
E.
Dermatophytes
Actinomycetes
Phycomycetes
Yeasts
All o f the above
137. Ketoconazole is less effective than
other antifungal agents for the treatment o f
severe and acute systemic infections
because:
A.
B.
C.
D.
E.
it is not distributed well on our body
it is only given topically
it is slow-acting
it requires a long duration o f therapy
C and D
138. Which o f the following statements
are NOT TRUE about miconazole?
A. It is available for topical application
only.
B. It is available in parenteral form
only.
C. Topical miconazole is highly
effective in vulvovaginal
candidiasis.
D. Parenteral miconazole therapy is
associated with CNS toxicity.
E. A and B
139. Which o f the following statements
are true about parenteral miconazole:
LAs a first line therapy
II.When other antifungal drugs are
ineffective
III.
When other antifungal drugs cannot
be tolerated.
A.
B.
C.
D.
E.
if I only is correct
if III only is correct
if I & II are correct
if II&III are correct
if 1,11, and III are correct
140. An imidazole antifungal drug used
in the treatment o f CNS infections
involving Cryptococcus and Candida is:
A.
B.
C.
D.
E.
Miconazole
Ketoconazole
Itraconazole
Voriconazole
Fluconazole
141. Which o f the following infections
is/are susceptible to itraconazole?
A.
B.
C.
D.
E.
Blastomycosis
Coccidioidomycosis
Cryptococcosis
Histoplasmosis
All o f the above
142. Itraconazole is preferred to
amphotericin B against systemic and
invasive pulmonary aspergillosis because:
A. Amphotcricin B is less effective
B. Amphotericin B is associated with
hematological toxicity
C. Amphotericin is not available in the
market
D. Itraconazole has broader spectrum
E. None
143.
Which o f the following adverse
effects are common to all imidazole
antifungal agents?
A.
B.
C.
D.
E.
Nausea
Vomiting
Hepatotoxicity
CNS toxicity
A and B
144.
Antacids, H2-blockers, or proton
pump inhibitors should not be
co-administered with ketoconazole and
itraconazole because:
A. They decrease the absorption of
ketoconazole and itraconazole
B. They decrease the level o f gastric
acidity, which is necessary for
ketoconazole and itraconazole to
act.
C. They increase the enzymatic
degradation o f ketoconazole and
itraconazole.
D. They increase the urinary
elimination o f ketoconazole and
itraconazole
E. None
145. Ketoconazole may antagonize the
antibiotic effects of:
A.
B.
C.
D.
E.
Nyastatin
Flucytosine
Caspofungin
Amphotericin B
None
146.
The blood level o f which o f the
following drugs is elevated by fluconazole?
B.
C.
D.
E.
Cyclosporine
Warfarin
Sulfonylureas
All o f the above
147. Which o f the following enzyme
systems are inhibited by Voriconazole?
A.
B.
C.
D.
E.
148.
A.
B.
C.
D.
E.
149.
A.
B.
C.
D.
E.
Cytochrome P4502C19
Cytochrome C Y P2C19
Cytochrome CYP3A4
All o f the above
A and B
Nyastatin is related chemically to:
Voriconazole
Itraconazole
Amphotericin B
Ketoconazole
None
Nyastatin is primarily active against:
Aspergillus
Candida
Fusarium
Cryptococcus
None
151.
as:
A.
B.
C.
D.
E.
3% cream
Lotion
Oral suspension
All o f the above
A and C only
152. Which o f the following adverse
effects are likely to occur with lotion and
cream dosage forms o f amphotericin B?
A.
B.
C.
D.
E.
Pruritis
Local irritation
Nausea
Vomiting
A and B
153.
Which o f the following statements
is FALSE about butenafine?
A. It interferes with sterol biosynthesis
B. It may be fungicidal in certain
concentrations against susceptible
organisms such as dermatophytes.
C. It alters fungal membrane
permeability
D. It is ineffective against Candida
species
E. It is effective against Trichophyton
rubrum
150. Which o f the following statements
is FALSE about terbinafine?
A. It is a synthetic allylamine
B. It possesses some activity against
yeasts
C. It is useful in patients who may not
tolerate the adverse effect profile of
imidazole antifungals.
D. It has been shown to be ineffective
against tinea capitis and tinea
corporis
E. Oral terbinafine iws useful in
treating toe nail and finger nail
infections
154.
In the treatment o f dermatophytes,
butenafine is used as:
A.
B.
C.
D.
E.
10 % lotion
10 % cream
10 % solution
1 % cream
None
155.
An azole antifungal available as a
cream for vaginal use is:
A. Miconazole
B. Fluconazole
C. Ketoconazole
D. Butoconazole
E. None
156.
Butoconazole is effective against
which of the following bacteria
I. S.aureus
II. S.pyrogenes
III. E. Faecalis
A.
B.
C.
D.
E.
if l only is correct
if III only is correct
if I & II are correct
if II&III are correct
if 1,11, and III are correct
157.
Which o f the following drugs has
different mechanism o f action from the
other?
A.
B.
C.
D.
E.
Terbinafine
Naftifme
Ciclopirox
Butoconazole
Nystatin
158. Clioquinol is a topical antifungal
agent that is most commonly used ointment
form in combination with:
A.
B.
C.
D.
E.
Hydrocortisone
Griseofulvin
Voriconazole
Ketoconazole
None
bacteria. Which o f the following bacteria
are susceptible to clotrimazole
A.
B.
C.
D.
E.
161. Clotrimazole may be available in
all o f the following dosage forms EXCEPT:
A.
B.
C.
D.
E.
A.
B.
C.
D.
E.
Sterols in membrane
Phospholipids in membrane
Amino acids
Calcium ions
None
160. At higher concentrations,
clotrimazole inhibits some strains o f
Lozenges
Parenteral solutions
Creams
Lotion
None
162. Which o f the following statements
are NOT TRUE about clotrimazole?
A. Below normal liver enzyme levels
has occurred in patients taking
clotrimazole lozenges.
B. Abnormal liver function tests have
occurred in patients taking topical
clotrimazole formulations.
C. Vaginal clotrimazole tablets are
associated with mild burning, skin
rash, and itching.
D. Cross-sensitization occurs with
imidazole antifungals.
E. A and B
F. C and D
163.
159.
Clotrimazole alters fungal cell
membrane permeability by binding with
S.aureus
S.pyogenes
Proteus vulgaris
Salmonella
All o f the above
Gentian violet is:
A. A dye
B. An antibiotic derived from fungal
cultures.
C. A synthetic antifungal antibiotic
D. It an antibiotic derived from
164. Which o f the following formulations
of ketoconazole is used in the treatment of
fungal keratitis?
A.
B.
C.
D.
E.
Ophthalmic suspension
2% shampoo
2% topical cream
Oral tablets
None
165.
Ketoconazole when comibined with
one o f the follwoing is useful in treating
dermatitis, diaper rash, impetigo, and
psoriasis.
A.
B.
C.
D.
E.
Gentian violet
Clioquinol
Steroids
Butenafine
None
166. Topical dosage form(s) o f
Miconazole is/are
A.
B.
C.
D.
E.
Aerosol powder
Cream
Tincture
Vaginal suppositories
All o f the above
167. Miconazole is advantageous over
other agents such as Nyastatin and
tolnaftate in that its activity covers:
A.
B.
C.
D.
E.
T. mentagrophytes
T. rubrum
Candia species
All o f the above
A and C only
168. Use o f condoms and diaphragms
concurrently with vaginal suppositories (e.g
vaginal tablets o f miconazole) is
contraindicated because:
A. Condoms antagonize the antifungal
activity o f any drug
B. Vaginal
suppositories
are
manufactured from a vegetable oil
base that may interact with latex
products
"
C. Vaginal suppositories worsen the
hypersensitivity reactions caused by
latex products
D. Drugs given in the form o f vaginal
suppositories have anti-infertility
effects.
E. None
169.
Which o f the following statements
is FALSE about naftifine?
A. It is a synthetic allylamine
B. It acts by interfering with fungal
protein synthesis
C. It is active against aspergillus flavus
and aspergillus fumigatus in vitro
D. It possesses some local anti­
inflammatory activity
E. None
170.
All o f the following antifungal
agents may be fungistatic or fungicidal
depending on concentration EXCEPT:
A.
B.
C.
D.
E.
Amphotericin B
Griseofulvin
Terbinafine
Nyastatin
None
171.
The antibacterial mechanism of
action o f sulconazole is:
A. It has a direct physicochemical
effect on the destruction of
unsaturated fatty acids present in
fungal cell membranes.
B. It damages bacterial DNA.
C. It inhibits bacterial protein synthesis
D. It inhibits an enzyme involved in
protein synthesis.
E. None
172. All o f the following antifungal
agents are active against M furfur
EXCEPT:
A.
B.
C.
D.
E.
Miconazole
Ketoconazole
Nyastatin
Sulconazole
Oxiconazole
173. Which of the following antifungal
agents have antibacterial activity?
A. Sulconazole
B. Tetraconazole
C. Econazole
D. Miconazole
E. A and B
174.
Malaria results from infection by
any o f four species o f the protozoal genus:
A.
B.
C.
D.
E.
Plasmodium
Amoeba
Isoporidium
Microsporidia
None
175. Which o f the following antimalarial
agents bind to and alter the properties o f
microbial and mammalian DNA?
A.
B.
C.
D.
E.
Chloroquine
Hydroxychloroquine
Primaquine
Mefloquine
A and B
176.
All o f the following have blood
schizonticidal activity (kill the schizont
forms o f plasmodium) EXCEPT:
A.
B.
C.
D.
E.
Chloroquine
Fansidar
Mefloquine
Primaquine
None
177. A schizonticidal antimalarial drug
active against erythrocytic forms of
susceptible plasmodium and toxoplamsa
Gondii is:
A.
B.
C.
D.
E.
Chloroquine
Hydroxychloroquine
Fansidar
Mefloquine
None
178. Which o f the following anti-malarial
drugs is active against liver forms of
P. Vivax and P. Ovale?
A.
B.
C.
D.
E.
Primaquine
Mefloquine
Chloroquine
Fansidar
None
179.
An antimalarial drug now used
almost exclusively in combination with a
sulfonamide or sulfone is:
A.
B.
C.
D.
E.
Quinine
Pyrimethamine
Mefloquine
Chloroquine
None
180.
A Parenteral form of quinine used
in severe cases o f chloroquine-resistant
malaria is:
A.
B.
C.
D.
E.
Quinine dihydrochloride
Quinine sulfate
Quinine carbonate
Quinine
None
181.
Fansidar is used in the prophylaxis
o f an infection in AIDS patients unable to
tolerate co-trimoxazole. The infective agent
is:
A.
B.
C.
D.
E.
Plasmodium falciparum
Pneumocystis carinii
Toxoplamsa Gondii
Plasmodium vivax
None
182. Which o f the following antimalarial
drugs are contraindicated in patients with
hereditary deficiency o f the enzyme
glucose-6-phosphate dehydrogenase?
A.
B.
C.
D.
E.
Chloroquine
Quinine
Mefloquine
Primaquine
B and D
183. Which o f the following antibacterial
agents are contraindicated in patients taking
primaquine?
A.
B.
C.
D.
E.
Penicillins
Aminoglycosides
Sulfonamides
Cephlosporins
None
184. Fansidar is a combination
containing sulfadoxine and:
A. pyrimethamine.
B. chloroquine
C. primaquine
D. Mefloquine
E. None
185. Concomitant use o f Mefloquine
with one o f the following may increase the
risk o f convulsions.
A.
B.
C.
D.
E.
Primaquine
Fansidar
Pyrimethamine
Chloroquine
None
D. Paromomycin
E. Emetine
187. Paromomycin is not effective in
extra-intestinal amoebiasis because:
A. It is absorbed very quickly
B. It is poorly absorbed
C. It is always given in solid dosage
forms
D. It is an amino-glycoside antibiotic
E. None
188. Which o f the following drugs have a
mechanism o f action related to DNA?
A. Metronidazole
B. Paromomycin
C. Emetine
D. Quinacrine
E. A and D
189. Which o f the following amebicidal
drugs is effective in giardiasis,
trichomoniasis and against bacterial
anaerobes?
A.
B.
C.
D.
E.
Diloxanide
Quinacrine
Emetine
Metronidazole
None
190.
Quinacrine is useful in the
treatment of:
A.
B.
C.
D.
E.
Giardiasis
Tapeworm infection
Malaria
A and B only
B and C only
186. Which one o f the following drugs is
an alkaloid?
A. Diloxanide
B. Quinacrine
C. Metronidazole
191.
Which o f the fol lowing is known for
its cardiovascular toxicity?
A. Paromomycin
B.
C.
D.
E.
Diloxanide
Emetine
Quinacrine
None
1
192. Concomitant use o f alcohol v^ith
one o f the following drugs results in a
typical disulfiram like reaction :
A.
B.
C.
D.
E.
Iodoquinol
Metronidazole
Quinacrine
Diloxanide
None
193. Which o f the following drugs may
produce optic neuritis or peripheral
neuropathy with high doses?
A.
B.
C.
D.
E.
Emetine
Quinacrine
Iodoquinol
Metronidazole
None
194. Pentamidine can be administered by
which route?
A.
B.
C.
D.
E.
Intra-muscular route
Intravenous route
Inhalation
A, B&C
A& B only
195.
Pentamidine is indicated for the
prevention and treatment of:
A.
B.
C.
D.
E.
196.
Infections due to P. carinii
Trypanosomiasis
Visceral leishmaniasis
Babesiosis
None
Pentamidine is chemically:
A. An aromatic diamide
B. A hydroxyquinoline
C. A dichloroacetamide
D. An aminoquinoline
E. None
197. After initial administration of
intravenous pentamidine the blood sugar
level:
A.
B.
C.
D.
E.
Increases
Decreases
Does not change
All o f the above
None
198. Atovaquone acts as antiprotozoal by
blocking mitochondrial electron transport
o f complex III o f the respiratory chain of
protozoa, resulting in inhibition of:
A.
B.
C.
D.
E.
Pyrimidine synthesis
Purine synthesis
Amino acid synthesis
Protein synthesis
None
199. Which o f the following statements
are NOT TRUE about Atovaquone?
A. It is highly protein bound (99%)
B. It is a second line drug in the
treatment o f P.carinii pneumonia in
patients intlerant of co-trimoxazole
or other sulfonamides.
C. Its oral absorption is decreased
when administered with food.
D. It results in elevated liver function
tests.
E. None
200. Eflomithine HC1 is an antiprotozoal
drug given through the:
A.
B.
C.
D.
E.
Intravenous route
Intravenous rote
Inhalational route
Oral route
None
201. The mechanism o f antiprotozoal
action ofEflom ithine is:
A. It inhibits the enzyme glucose-6phosphate dehydrogenase.
B. It inhibits the enzyme ornithine
decarboxylase
C. It inhibits protozoal protein
synthesis
D. It inhibits protozoal cell wall
synthesis.
E. None
202. Organisms susceptible to
atovaquone is/are:
A.
B.
C.
D.
E.
T.Gondii
P.Carinii
Microsporidia
P.falciparum
All o f the above
203. The most frequent serious side
effect of Eflomithine is:
A.
B.
C.
D.
E.
Nausea
Vomiting
Myelosuppression
Hearing impairment
None
204. Which o f the following
antitubercular agents have the lowest
incidence o f resistance?
A.
B.
C.
D.
E.
Isoniazid
Rifamipicin
Pyrazinamide
Ethambutol
A and B
205. Most patients with tuberculosis are
started on:
A. Isoniazid, rifamipicin, Pyrazinamide
B. Ethambutol, streptomycin, Isoniazid
C. Pyrazinamide, streptomycin,
Isoniazid
D. Ethambutol, ethionamide,
capreomycin
E. None
206. In the treatment o f tuberculosis
combination therapy is recommended:
A. In order to overcome resistance
B. Tn order to minimize the incidence
o f adverse effects.
C. In order to decrease the overall cost
o f a drug therapy.
D. B and C
E. None
207. Ethambutol is used in combination
with which of the following in the
treatment of mycobacterium avium
complex.
A.
B.
C.
D.
E.
Clarithromycin
Azithromycin
Isoniazid
Pyrazinamide
A and B
208.
Which o f the following statements
is NOT TRUE about Isoniazid?
A. It is a hydrazide o f isonicotinic acid.
B. It is bacteriostatic for resting bacilli
C. It is bactericidal for dividing
organisms.
D. Its mechanism o f action is that it
inhibits the enzyme DNA gyrase.
E. None
209.
Isoniazid is active against which of
the following organisms:
A. tuberculosis
B. bovis
C. kansasii
D. A& B only
E. A, B&C
210.
Pyridoxine 15-50 mg/day should be
administered to patients taking Isoniazid in
order to:
A. Decrease the gastrointestinal
absorption o f Isoniazid
B. Minimize the peripheral neuropathy
associated with Isoniazid use
C. Increase the gastrointestinal
absorption o f Isoniazid
D. Decrease the hepatic metabolism o f
Isoniazid.
E. None
211. Use o f Isoniazid concurrently with
Carbamazepine increases the risk of:
A.
B.
C.
D.
E.
Blood dyscriasis
Hepatitis
Convulsions
Peripheral neuropathy
None
212.
Which o f the following antitubercular agents may cause additive
nervous system effects when given with
Isoniazid?
A.
B.
C.
D.
E.
Cycloserine
Ethionamide
Pyrazinamide
Rifampin
A and B
213. The antitubercular effect o f
Rifampin is due to:
A. Inhibition o f mycobacterial cell wall
synthesis.
B. Impairment o f bacteria] RNA
synthesis by binding to DNAdependent RNA polymerase.
C. Disruption o f mycobacterial cell wall
synthesis by inhibiting mycolic acid
synthesis.
D. Inhibition o f mycobacterial protein
synthesis.
E. None
214. Which o f the following organisms
are susceptible to Rifampicin?
A.
B.
C.
D.
E.
S.aureus
H.influenzae
Legionella pneumophilia
Most mycobacterial strains
All o f the above
215. Rifampin, colors urine, sweat, tears.
saliva, and feces:
A.
B.
C.
D.
E.
Orange-red
Yellow
Red
Pink
None
216. Which of the following statements
is FALSE about Rifampin?
A. It may be used in combination with
dapsone in the treatment o f leprosy.
B. Probenecid decreases the blood level
o f Rifampin.
C. It may induce influenzae like
syndrome.
D. It should not be administered alone
because this may lead to the
emergence o f highly drug-resistant
organisms.
E. None
217.
of:
A.
B.
C.
D.
E.
Pyrazinamide is a pyrazine analogui
Nicotinamide
Isonicotinic acid
Ascorbic acid
Lactic acid
None
218.
Pyrazinamide is a highly specific
agent and has activity only against:
A.
B.
C.
D.
E.
avium
bovis
Kansasii
tuberculosis
None
219.
Which of the following statements
is NOT TRUE about retreatment
antitubercular agents?
A. They are more effective than primary
agents.
B. They are more toxic than primary
agents.
C. They are always used in combination
with primary agents.
D. They are less effective than primary
agents.
E. None
220.
All o f the following antitubercular
drugs are retreatment agents EXCEPT:
A.
B.
C.
D.
E.
Kanamycin
Capreomycin
Ethionamide
Cycloserine
Ethambutol
221.
The mechanism o f action o f amino
salicylic acid is similar with that of:
A.
B.
C.
D.
E.
Penicllins
Aminoglycosides
Cephalosporins
Trimethoprim
None
222.
Concomitant use o f Capreomycin
and streptomycin is contraindicated
because:
A. Capreomycin is ototoxic
B. Streptomycin is nephrotoxic
C. Both are ototoxic
D. Both are nephrotoxic
E. Both are ototoxic and nephrotoxic
223.
A retreatment anti-tubercular agent
implicated in peripheral neuropathy is:
A.
B.
C.
D.
E.
Capreomycin
Ethionamide
Cycloserine
Kanamycin
None
224.
Which o f the following gives the
correct composition o f the antitubercular
product rifater?
A. Rifampin 120mg, Isoniazid 500 mg,
Pyrazinamide 50mg.
B. Ethambutol 300mg, Rifampin
200mg. amikacin 600mg
C. Rifampin 120 mg, Isoniazid 50 mg,
Pyrazinamide 300mg
D. Cycloserine 250mg, Isoniazid
1OOmg, Rifampin.
E. None
-
225. The quinolone antibacterials used in
tuberculosis therapy are:
A.
B.
C.
D.
E.
Enoxacin
Cinoxacin
Ciprofloxacin
Levofloxacin
C and D
226.
Which o f the following statements
is FALSE about rifabutin?
A. It has been reported to inhibit
reverse transcriptase and block the
in vitro infectivity and replication o f
HIV.
B. Its use has resulted in mild elevation
o f liver enzymes and
thrombocytopenia.
It is more effective than Rifampin in
the treatment o f tuberculosis. ;
D. It may increase the hepatic
metabolism o f drugs, but to a lesser
extent than Rifampin.
E. None
c.
227. Which o f the following statements
is NOT TRUE:
A. Viruses lack independent metabolic
activity
Viruses can replicate only within
B.
living host cells.
C. Antiviral agents tend to injure host
cells.
D. Antiviral agents tend to injure viral
cells
E. Antiviral agents act by inhibiting
viral cell wall synthesis.
228. All o f the following anti-DNA viral
agents are prodrugs that require viral and
host cellular enzymes to phosphorylate
them to the active triphosphate form before
exerting their antiviral activitv EXCEPT:
A.
B.
C.
D.
E.
Acyclovir
Ganciclovir
Valacyclovir
Foscamet
None
229. Which o f the following is an RNA
virus:
A.
B.
C.
D.
E.
Herpes simplex virus
HIV-1
Varicella- Zoster virus
Cytomegalovirus
None
230. Antiviral agents which act against
DNA viruses inhibit viral DNA synthesis
by inhibiting the enzyme:
A. Viral DNA polymerase
B.
C.
D.
E.
231.
A.
B.
C.
D.
E.
Viral thymidine kinase
Viral topoisomerase 11
Viral deoxykinase
None
Acyclovir is active against:
Herpes simplex-1 ( HSV-1)
Herpes simplex-1 (HSV-2)
Varicella-zoster virus
Cytomegalovirus
A,B&C
232. Amantadine inhibits replication o f
influenzae A virus by:
A. Inhibiting the enzyme DNA
polymerase.
B. Interfering with viral attachment and
uncoating.
C. Inhibiting the enzyme thymidine
kinase.
D. Inhibiting the enzyme deoxyadenosine kinase.
E. None
Which o f the following anti-viral
233.
drugs is used in the treatment o f
Parkinsonism?
A.
B.
C.
D.
E.
234.
A.
B.
C.
D.
E.
Acyclovir
Famciclovir
Ganciclovir
Amantadine
None
Cidofovir is a synthetic:
Acyclic Purine nucleoside
Pyrimidine nucleoside
Amino acid
Amine
None
235. All o f the following may occur as
side effects o f amantadine EXCEPT:
A.
B.
C.
D.
E.
Dry mouth
Blurred vision
Bradycardia
CNS depression
Insomnia
236. Famciclovir is prodrug o f the
antiviral drug:
A.
B.
C.
D.
E.
Acyclovir
Ganciclovir
Penciclovir
Zanamivir
None
237. Famciclovir is rapidly
phosphorylated in virus infected cells to
Penciclovir monophosphate by:
A.
B.
C.
D.
E.
Viral deoxyguanosine kinase
Viral thymidine kinase
Viral DNA polymerase
Viral topoisomerase II
None
238. Which of following statements best
describes the chemical nature o f Foscamet?
A.
B.
C.
D.
E.
It is a pyrophosphate analogue.
It is disubstituted benzene.
It is a phenyl alkyl amine.
It is a modified amino acid
None
239. Which one o f the following
statements is FALSE about Foscamet?
A. It is the drug o f choice in cases of
acyclovir or ganciclovir resistance.
B. It is not active against H IV -1
C. It is a noncompetitive reversible
inhibitor o f HIV reverse
transcriptase.
D. It competitively binds to DNA
polymerase to form an inactive
complex.
E. None
'
240. Foscamet is highly nephrotoxic if it
is given by:
A.
B.
C.
D.
E.
IV route
IM route
Inhalational route
Oral route
None
241.
All o f the following are electrolyte
abnormalities associated with Foscamet
EXCEPT:
A.
B.
C.
D.
E.
Hypomagnesemia
Hypophosphatemia
Hypokalemia
Hypercalcemia
Hypocalcemia
242. Foscarnet is not recommended for
patients with creatinine clearance o f less
than:
A.
B.
C.
D.
E.
243.
by:
A.
B.
C.
D.
E.
80 mL/min
75 mL/min
150 mL/min
50 mL/min
None
Foscamet is exclusively excreted
Glomerular filtration
Tubular secretion
Feces
All o f the above
A and B
244. Which o f the following drugs
should not be given concurrently with
Foscamet?
A.
B.
C.
D.
Streptomycin
Amikacin
Ceftibuten
Cefuroxime
E. A and B
249. The hydrolysed product o f
Oseltamivir invivo is:
245. Which o f the following statements
is NOT TRUE about ganciclovir?
A. It is converted to triphosphate form
and then gets incorporated into viral
DNA which results in inhibition of
DNA polymerase.
B. It is available in oral and IV
formulations.
C. It is incapable o f penetrating the
CNS.
D. Its oral formulation is only approved
for prevention and maintenance
treatment o f Cytomegalovirus
infections.
E. None
246. Ganciclovir is associated with all o f
the following adverse effects EXCEPT:
A.
B.
C.
D.
E.
Neutropenia
Thrombocytopenia
Anemia
Ototoxicity
Teratogenic
247. Which o f the following antibiotics
may induce generalized seizures when
given concurrently with ganciclovir?
A.
B.
C.
D.
E.
Imipenem -cilastatin
Ertapenem
Meropenem
Cefuroxime
None
248. Oseltamivir is related
pharmacologically to:
A.
B.
C.
D.
E.
Cidofovir
Famciclovir
Ganciclovir
Zanamivir
None
A.
B.
C.
D.
E.
Oseltamivir Phosphate
Oseltamivir Carboxylate
Oseltamivir Sulfate
Oseltamivir Carbonate
None
250. An enzyme of the influen
inhibited by Oseltamivir is:
A.
B.
C.
D.
E.
Neuraminidase
DNA polymerase
Reverse transcriptase
Thymidine kinase
None
251.
Which o f the following agents is
the best for the prophylaxis o f influenzae
infections?
A.
B.
C.
D.
E.
Amantadine
Influenzae virus vaccine
Rimantadine
Oseltamivir
None
252. Valacyclovir is prodrug o f the
antiviral agent:
A.
B.
C.
D.
E.
Valganciclovir
Cidofovir
Acyclovir
Zanamivir
None
253. The mechanism o f action o f
ribavarin is:
A. It inhibits RNA and DNA synthesis
by depleting intracellular nucleotide
reserves.
B. It inhibits the enzyme DNA
polymerase.
c. It inhibits the early viral replication
cycle, possibly by inhibiting the
uncoating o f the virus.
D. It inhibits the enzyme reverse
transcriptase.
E. None
D. It does not have carcinogenic
potential.
None
E.
258.
Which o f the following anti-viral
drugs are active against both influenzae A
and influenzae B virus infections?
254.
The antiviral drug ribavarin is
administered by which route.
A.
B.
C.
D.
E.
Intramuscular route
Intravenous route
Inhalational route
Oral route
None
A.
B.
C.
D.
E.
Zanamivir
Oseltamivir
Amantadine
Rimantadine
A and B
259.
Which o f the following are classes
of antiretroviral drugs
255.
Ribavarin is not recommended in
patients using ventilators because:
A. It corrodes the internal wall of
ventilators.
B. It may precipitate on respirator
valves and tubing causing lethal
malfunction.
C. It may result in hypersensitivity
reactions.
D. It may result in bacterial pneumonia.
E. None
256. Valganciclovir is a prodrug o f the
antiviral agent;
A.
B.
C.
D.
E.
Acyclovir
Ganciclovir
Famciclovir
Valacyclovir
None
A. Nucleoside reverse transcriptase
inhibitors
B. Nucleotide reverse transcriptase
inhibitors
C. Nonnucleoside reverse transcriptase
inhibitors
D. Fusion inhibitors
E. All o f the above
260. AH o f the following drugs are
Nucleoside reverse transcriptase inhibitors
EXCEPT:
A.
B.
C.
D.
E.
Abacavir
Zidovudine
Stavudine
Tenofovir
Didanosine
261. The fusion inhibitor used in the
treatment o f HIV-1 and HIV-2 infections is:
257. The advantage o f Valganciclovir
over ganciclovir is:
A. That it has broader spectrum o f
activity.
B. It has markedly increased
bioavailability when given with
A. Enfuvirtide
B. Zalcitabine
C. Lamivudine
D. Indinavir
E. None
Infectious Diseases
A.
B.
C.
D.
Dry mouth
Blurred vision
Bradycardia
CNS depression
240.
Foscamet is highly nephrotoxic if it
262. Which of the following is/are
Nonnucleoside reverse transcriptase
inhibitors
A.
B.
C.
D.
E.
Delaviridine
Efavirenz
Nevirapine
A, B&C
Stavudine
263. Which one o f the following
statements is FALSE about reverse
transcriptase inhibitors?
A. They are competitive inhibitors of
the enzyme reverse transcriptase.
B. They are inactive until
phosphorylated by human cellular
kinases into the active triphosphate
metabolite.
C. All agents in the nucleoside class
have a black box warning
concerning the potential for the
development o f lactic acidosis and
severe hepatomegaly.
D. They canbe used alone in the
treatment o f HIV infection.
E. None
264. A reverse transcriptase inhibitor
with good penetration into the
cerebrospinal fluid is:
A.
B.
C.
D.
E.
Zidovudine
Didanosine
Stavudine
Lamivudine
Abacavir
265. Abacavir has a black box warning
about
~
A. A hypertensive crisis
B. A life threatening hypersensitivity
reaction
C. Lactic acidosis
D. Liver damage
E. None
266. The anti-retroviral drug Didanosine
results in hyperuricemia because:
A. It stimulates the degradation o f body
proteins.
B. It stimulates the enzyme xanthine
oxidase.
C. It is metabolized to uric acid.
D. It inhibits the elimination of uric
acid.
E. None
267. Didanosine is available in a
specially buffered formulation in order to:
A. Prevent degradation at acidic pH.
B. Increase gastrointestinal absorption.
C. To control rate o f drug release.
D. To decrease the urinary elimination
o f Didanosine.
E. None
268. Which o f the following anti­
retroviral drugs is used in the treatment o f
chronic hepatitis B?
A.
B.
C.
D.
E.
Abacavir
Didanosine
Stavudine
Lamivudine
None
269. The major toxicity associated with
Stavudine is:
A.
B.
C.
D.
E.
Headache
Sleep disorders
Abdominal pain
Peripheral neuropathy
None
270. Which o f the following anti­
retroviral drugs have not been reported to
interact with any drug?
A.
B.
C.
D.
E.
Lamivudine
Stavudine
Abacavir
Didanosine
B and C
C. Co-trimoxazole
D. Fansidar
E. None
275.
of
271. The nucleoside reverse transcriptase
inhibitor Tenofovir is available in prodrug
form as:
A.
B.
C.
D.
E.
Tenofovir disoproxil fumarate
Tenofovir sulfate
Tenofovir gluconate
Tenofovir estolate
None
272. Tenofovir may increase the serum
concentrations o f one o f the following if
they are given together:
A.
B.
C.
D.
E.
Lamivudine
Abacavir
Didanosine
Stavudine
None
273. Zalcitabine is indicated for
combination therapy with one o f the
following for the treatment o f adult patients
with advanced HIV infection.
A.
B.
C.
D.
E.
Zidovudine
Stavudine
Lamivudine
Abacavir
None
274. An HIV patient was taking a
medication for P.carinii infection. The same
patient was taking the nucleoside reverse
transcriptase inhibitor Zalcitabine. The
patient suffered from severe pancreatitis,
this suggests that the drug used in the
treatment o f the P.carinii infection is:
A. Pentamidine
B. Atovaquone
A.
B.
C.
D.
E.
Zidovudine is a synthetic analogue
Guanosine
Thymidine
Adenosine
Cytosine
None
276. Zalcitabine should not be used in
combination with which o f the following
drugs
A.
B.
C.
D.
E.
Didanosine
Lamivudine
Stavudine
Zidovudine
A,B&C
277. Combivir is a combination product
containing Zidovudine and:
A.
B.
C.
D.
E.
Lamivudine
Stavudine
Zalcitabine
Didanosine
None
278. Which one o f the following
statements is NOT TRUE about Combivir?
A. It has improved compliance in
patients by decreasing the number
o f tablets typically ingested daily
when administered as individual
agents.
B. It has fewer incidences o f adverse
effects and drug interactions than
the individual agents.
C. It is administered as Lamivudine
150mg/zidovuidne 300 mg per
tablet twice daily.
D. It is the first FDA
combination
product
treatment o f HIV.
E. None
approved
for
the
279. The first triple nucleoside
combination product approved by the FDA
contains Zidovudine. Lamivudine and:
A.
B.
C.
D.
E.
Didanosine
Abacavir
Stavudine
Lamivudine
None
280. All o f the following result in
increased blood levels o f Zidovudine,
leading to toxicity EXCEPT:
A.
B.
C.
D.
E.
Valproic acid
Methadone
Probenecid
Acetaminophen
Co-trimoxazole
281. Delavirdine inhibits its own
metabolism by reducing the activity of:
A.
B.
C.
D.
E.
CYP3A4
CYP2A6
CYP2C8
CYP2C9
A and D
282. Inhibition o f the metabolism of
which the following drugs by Delavirdine
may result in cardiac arrhythmias?
A.
B.
C.
D.
E.
Terfenadine
Astemizole
Alprazolam
Midazolam
A and B
283. The advantage o f Efavirenz over
other Nonnucleoside reverse transcriptase
inhibitors is:
A.
B.
C.
D.
Its broader spectrum o f activity.
Its better tolerability.
Its once daily dosing.
Its effect on the hepatic metabolism
o f drugs.
E. None
284. Which o f the following hepatic
enzymes is induced by Efavirenz?
A.
B.
C.
D.
E.
CYP3A4/5
CYP2E1
CYP3A4
CYPC19
None
285.
All o f the following anti-retroviral
drugs are protease inhibitors EXCEPT:
A.
B.
C.
D.
E.
Lopinavir
Nelfinavir
Ritonavir
Nevirapine
Amprenavir
286. All o f the following protease
inhibitors are indicated for use in the
pediatric population EXCEPT:
A.
B.
C.
D.
E.
Lopinavir
Nelfinavir
Amprenavir
Ritonavir
None
287. The protease inhibitor with the
longest half-life is:
A.
B.
C.
D.
E.
Nelfinavir
Ritonavir
Amprenavir
Indinavir
None
288. Fortovase is a soft gel cap
formulation o f a protease inhibitor that has
improved bioavailability and efficacy. The
protease inhibitor is:
A.
B.
C.
D.
E.
Lopinavir
Saquinavir
Indinavir
Ritonavir
Amprenavir
289. Nelfinavir has few adverse effects.
The most commonly reported adverse
effect is:
A.
B.
C.
D.
E.
Constipation
Diarrhea
Hyperglycemia
Hypersensitivity reactions
None
D. Carbamazepine
E. A and B
293. The first FDA approved
combination o f protease inhibitors is:
A.
B.
C.
D.
E.
Lopinavir/Amprenavir
Lopinavir/Ritonavir
Ritonavir/Nelfinavir
Saquinavir/Indinavir
None
294.
In the Lopinavir/Ritonavir
combination product the ratio o f Ritonavir
to Lopinavir is:
A.
B.
C.
D.
E.
1:4
4:1
1:5
2:3
None
290. The vitamin included in Amprenavir
capsules is:
A.
B.
C.
D.
E.
Vitamin
Vitamin
Vitamin
Vitamin
None
A
B
C
E
291. Amprenavir is contraindicated in
certain patient populations due to the
potential toxicity from high amounts o f the
excepient:
A.
B.
C.
D.
E.
Starch
Acacia
Propylene glycol
Sucrose
None
292. Which o f the following drugs
increase the blood levels o f saquinavir?
A. Ketoconazole
B. Clarithromycin
C. Phenytoin
295. The protease inhibitor with the
shortest half-life is:
A.
B.
C.
D.
E.
Lopinavir
Saquinavir
Amprenavir
Nelfinavir
None
296.
Which o f the following anti­
retroviral drugs does not have any effect on
the metabolism o f drugs by CYP450?
A.
B.
C.
D.
E.
Delaviridine
Nevirapine
Amprenavir
Enfuvirtide
None
297. The mechanism o f anthelmintic
action o f mebendazole includes:
A. Inhibition o f the formation o f
microtubules.
B.
C.
D.
E.
Blockage o f glucose uptake.
Inhibition o f protein synthesis.
All o f the above
A and B only
298.
Which one o f the following
represents a wrong pair o f a scientific name
o f a parasite and its common name?
A.
B.
C.
D.
E.
Ancylostoma duodenale-hookworm
Ascaris lumbricoides-roundworm
Necator americanus-hookworm
Trichinella spiralis-threadworm
Trichuris thrichiura-whipworm
299. Which o f the following anti­
epileptic may reduce the blood levels and
subsequent efficacy o f mebendazole?
A.
B.
C.
D.
E.
Carbamazepine
Phenytoin
Zonisamide
Lamotrigine
A and B
300. Which o f the following
anthelmintics are structurally related to
each other?
A.
B.
C.
D.
E.
301.
A.
B.
C.
D.
E.
Mebendazole
Diethylcarbamazine
Albendazole
Pyrantel
A and C
headache and general malaise if they are
treated with diethylcarbamazine.
A.
B.
C.
D.
E.
Mansonella pertans
Dipetalonema streptocera
Wuchereria bancrofti
L oaloa
None
303. Pyrantel is used in the treatment of
all o f the following infections EXCEPT:
A.
B.
C.
D.
E.
Round worm infection
Pinworm infection
Hook worm infection
Tape worm infection
Hair worm infection
304. An anthelmintic drug which
antagonizes the action of Pyrantel is:
A.
B.
C.
D.
E.
Albendazole
Mebendazole
Piperazine
Diethylcarbamazine
None
305. An anthelmintic drug with anti­
inflammatory, antipyretic, and analgesic
effects is:
A. Albendazole
B. Thiabendazole
C. Mebendazole
D. Niclosamide
E. None
Albendazole is active against:
Taenia saginata
Taenia solium
Echinococcus granulosis
Ascaris lumbricoides
B and C
302. Patients treated for one o f the
following infections often present with
306. Which o f the following fungi are
susceptible to the anthelmintic drug
thiabendazole?
A.
B.
C.
D.
E.
Trichophyton
Candida albicans
Aspergillus
Microsporum
A and D
307. The most common adverse effects
o f thiabendazole are:
A.
B.
C.
D.
E.
Nausea and vomiting
Anorexia
Seizures
Vertigo
A and B
A. Dihydrofolate reductase
B. Glucose-6-phosphate
dehydrogenase
C. Fumarate reductase
D. Glycogen synthetase
E. None
311. Which o f the following
anthelmintics is also active against giardia?
308. Which of the following statements
describes the mechanism o f action
Piperazine?
A. It causes flaccid paralysis o f the
helminth by blocking the response
o f the ascaris muscle to
acetylcholine.
B. It inhibits the formation o f
microtubules.
C. It inhibits glucose transport of the
helminth.
D. Its mechanism o f action is unknown.
E. None
309.
A.
B.
C.
D.
E.
Piperazine is active against:
Ascaris lumbricoides
Enterobius Vermicularis
Hymenolepis Nana
Necator americanus
A and B
310. Thiamebendazole was shown to
inhibit the helminth-specific enzyme,
A.
B.
C.
D.
E.
Thiamebendazole
Mebendazole
Pyrantel
Quinacrine
None
312. Niclosamide is not active against
cycticercosis because:
A. It is not active against T.solium
B. It affects only cestodes o f the
intestine.
C. It has short half life.
D. It is not active against cestodes
E. None
313.
Which of the following
anthelmintics should be taken in empty
stomach?
A.
B.
C.
D.
E.
Piperazine
Albendazole
Oxamniquine
Pyrantel
None
A n sw ers
Infectious Diseases
1. Answer: E. I,II and III are correct
Explanation:
Anti-infective agents treat infection by suppressing or destroying the causative
microorganisms.Anti-infective agents derived from natural substances are called antibiotics.Antiinfective agents produced from synthetic substances are called anti-microbials.
2. Answer: D. Fungi cannot be identified by gram stain
Explanation:
'
Gram staining is a technique, which helps determine
1. Gross morphology o f the bacteria and
2. Differentiation into two groups -(a) gram-positive and (b) gram negative
Gram staining is performed on all specimens except blood cultures. It helps identify if the
causative agent is gram-positive or gram-negative, and allows for a better choice o f drug therapy.
Gram-positive microorganisms stain blue or purple and gram-negative microorganisms stain red
or rose pink.
Fungi can also be identified by gram stain
3. Answer: E. Lice
-
Explanation
The microorganism is any organism o f microscopic size. Bacteria, mycobacterium, fungi,
protozoa and viruses. Lice can be seen with naked eye.
4. Answer: D. All o f the above
Explanation:
Gram stain, microbiological culturing, and susceptibly tests should be performed before antiinfective therapy is initiated. Microbiological cultures are useful to identify the specific causative
agent; specimens o f body fluids or infected tissue are collected for analysis. Most bacteria can be
cultured artificially on culture media containing. Different strains o f the same pathogenic species
may have widely varying susceptibility to a particular agent. Susceptibility tests determine
microbial susceptibility to a given drug and, can be used to predict whether the drug will combat
the infection effectively.
5. Answer: A. It is the lowest drug concentration that prevents microbial growth after 18-24
hours o f incubation.
Explanation:
The minimum inhibitory concentration s the lowest concentration of a drug that prevents
microbial growth after 18-24 hours o f incu bation.
The lowest concentration o f a drug that red'uces bacterial density by 99.9% is called the minimum
bactericidal concentration.
6. Answer: D. All o f the above
Explanation:
Break point concentrations o f antibiotits are used to characterize antibiotic activity. The
interpretive categories are susceptible, moderately susceptible (intermediate), and resistant.
These concentrations are determined by considering pharmacokinetics, serum and tissue
concentrations following normal doses and the population distribution o f M1CS o f a group of
bacteria for a given drug.
7. Answer: E. A and C
Explanation:
Disk diffusion technique is less expensive but less reliable than the microdilution method but it
provides qualitative susceptibility information.
8. Answer: E. C and D
Explanation:
In order to treat infectious disease effectively, an anti-infective agent must be active against the
causative pathogen.
Susceptibility testing or clinical experience in treating a given syndrome may suggest the
effectiveness o f a particular drug.
9. Answer: D. All o f the above
Explanation:
An anti-infective agent should be chosen on the basis o f its pharmacological
properties.Pharmacological properties include the ability o f the drug to reach the infection site
and to attain a desired level in the target tissue.
10. Answer: B. A drug that rapidly destroys the bacteria
i
Explanation:
Bactericidal agent is a drug that inhibits tjie growth or reproduction o f a bacterium.
A drug that only inhibits the growth and reproduction o f a bacterium is known as a bacteriostatic
agent
11. Answer: D. All o f the above
Explanation:
Impaired immune mechanisms may require a drug that rapidly destroys pathogens (i.e.
bactericidal agent) rather than one that merely suppresses a pathogen’s growth or reproduction
(i.e.. bacteriostatic agent).
Preexisting kidney or liver disease increases the risk o f nephrotoxicity or hepatoxicity during the
administration o f some antibacterial agents.
Drug therapy during Pregnancy and lactation can cause unwanted effects.
12.Answer: E. 1,H&1I1
Explanation:
Drug therapy during pregnancy and lactation can cause unwanted effects. Therefore, the
mother’s need for the antibiotic must be weighed against the drug’s potential harm.
Pregnancy can increase the risk o f adverse effects for both mother and fetus. Most drugs,
including antibiotics, appear in the breast milk o f nursing mothers and may cause adverse effects
in infants. Also, plasma drug concentrations tend to decrease in pregnant women, reducing a
drug’s effectiveness.
13.Answer: B. Sulfonamides
Explanation:
Sulfonamides lead to toxic bilirubin accumulation in a newborn’s brain.
Bilirubin is a by-product o f erythrocyte degradation.
Sulfonamides may cause hemolytic anemia in susceptible individuals. The excessive degradation
o f erythrocytes results in the formation o f excess bilirubin in the pregnant mother and this affects
the infant. (The permeability o f the blood brain barrier to bilirubin is very high and accumulates
in the brain)
-
14.Answer: B. Glucose-6-phosphate dehydroganse
Explanation:
Sulfonamides may cause hemolytic anemia in patients with hereditary deficiency o f the enzyme
glucose-6-phosphate dehydrogenase.
Glucose-6-phosphate is an enzyme linked to metabolic pathways, which produce substances
necessary in maintaining the integrity b f the membrane o f red blood cells. Sulfonamides interfere
with these processes and it gets worse.
In patients taking sulfonamides having hereditary deficiency o f this enzyme are exposed to
hemolytic anemia (an anemia that results from lysis o f red blood cells).
15.Answer: A. Isoniazid
Explanation:
Patients who rapidly metabolize dru^s (rapid acetylators) may develop hepatitis receiving the
antitubercular drug Isoniazid. The hepatitis may occur due to increased metabolic activity in liver.
(The main organ where most drugs are metabolized).
16.Answer: A. A broad-spectrum antibiotit should be given until the specific organism has been
identified
Explanation:
In serious life threatening disease, antiLinfective therapy must begin before the infecting
organism is identified.A broad-spectrum antibiotic usually is the most appropriate choice until
specific organism has been determined. In all cases, culture specimens should be obtained before
therapy begins.
17.Answer: D. A and B
Explanation:
A combination o f drugs should be given only when clinical experience has shown such therapy to
be more effective than single-agent therapy in a particular setting. A multiple-drug regimen can
increase the risk o f toxic drug effects and, in a few cases, may result in drug antagonism and
subsequent therapeutic ineffectiveness.
18.Answer: E. A,B and C only
Explanation:
A multiple-agent regimen can increase the risk o f toxic drug effects and, in a few cases, may
result in drug antagonism and subsequent! therapeutic ineffectiveness. Indications for multipleagent regimen include:
j
- Treatment o f an infection caused by multiple pathogenic organisms
Need for increased antibiotic effectiveness. The synergistic (intensified) effect of
two or more agents may ajlow a dosage reduction or a faster or enhanced effect
fof the drug
Prevention o f drug-resistant organisms
19.Answer: C. I&II
Explanation:
.
In chronic infections such as endocarditis, osteomyelitis the treatment may require a longer
duration (4-6 weeks) with follow-up culture analyses to assess therapeutic effectiveness. In acute
uncomplicated infection treatment generally should continue until the patient has been afebrile
and asymptomatic for at least 72 hours.
20. Answer: B. They help indicate the locus o f infection
Explanation:
Small effusions, abscesses, or cavities that appear on radiographs indicate the focus o f infection.
21 .Answer: B. Elevated erythrocyte sedimentation rate does not occur due to noninfectious
cases
Explanation:
Large elevations in erythrocyte sedimentation rate are associated with acute or chronic infection,
particularly endocarditis, chronic osteomyelitis, and intra-abdominal infections. A normal ESR
does not exclude infection. Erythrocyte sedimentation rate is elevated in noninfectious causes
such as collagen vascular diseases.
22.Answer: E. A and B
Explanation:
Small effusions, abscesses, or cavities that appear on radiographs indicate the focus o f
infection.Pain and inflammation may occur when infection is superficial or within a joint or bone,
also indicating a possible focus of infedtion.
23 .Answer: D. All o f the above
!
Explanation:
Causes o f therapeutic infectiveness include:Misidentification o f the isolated organism may lead
to misdiagnosis.Improper drug regimen. The drug dosage, administration route, dosing frequency,
or duration . Survival o f microbes due to microbial resistance to a specific antibiotic, and
inappropriate choice of antibiotic agent.
24. Answer: D. All o f the above
Explanation:
Fever frequently signifies infection, but it sometimes stems from non-infectious conditions such
as drug reactions, phlebitis, neoplasmsj, metabolic disorders, arthritis.
25.Answer: D. Neutropenic cancer
I
Explanation:
Conditions such as metabolic disorders, phlebitis, arthritis and drug reactions result in fever, but
they do not respond to anti-microbial therapy .But Neutropenic cancer patients suffering from
fever are widely treated with antimicrobial agents.
26. Answer: C. The most commonly used route o f administration o f the drugs is the oral route.
Explanation:
In perioperative antibiotic prophylaxis intravenous or intramuscular routes are preferred to
guarantee good serum and tissue levels at the time o f incision.All other choices are true.
27. Answer: E. All o f the above
Explanation:
In general, first-generation cephalosporins are drugs o f choice for most procedures and patients.
These agents have an appropriate spectrum] a low frequency o f side effects, and a favorable half­
life, and low cost.
I
28.Answer: E. I,II,&I1I are correct
Explanation:
They are primarily used in the treatment of infections caused by gram-negative enterobacteria and
in suspected sepsis.The toxic potential o f these drugs limits their use.Aminoglycosides are
bactericidal; they inhibit bacterial protein synthesis by binding to and impeding the function o f
the 30 S ribosomal subunit. (Some Aminoglycosides also bind to the 50 S ribosomal subunit).
29.Answer: C. Streptomycin
i
Explanation:
Streptomycin is used in the treatment o f mycobacterium tuberculosis in combination with other
antitubercular drugs.
30. Answer: C. Amikacin
;
i
Explanation:
Amikacin is the broadest spectrum antibiotic with activity against most aerobic gram-negative
bacilli as well as anaerobic gram-negative bacilli strains that resist gentamicin and tobramycin. It
is also active against M.tuberculosis and mycobacterium tuberculosis.
31 .Answer: C. Netilmicin
j
Explanation:
Netilmicin appears to be less ototoxic than other Aminoglycosides. Ototoxicity involves
progressive damage to and destruction o f the sensory cells in the cochlea and vestibular organ of
the ear.
32. Answer: E. C and D
Explanation:
Pseudomonas aeruginosa and most streptococci are now resistant to neomycin.
33.Answer: B. Tetracycline
Explanation:
Streptomycin is used to treat plague, acute tularemia, acute brucellosis (given in combination
with tetracycline), bacterial endocarditis caused by streptococcus viridans (given in combination
with penicillin), and tuberculosis (given in combination with other antitubercular agents).
34.Answer: E. A and D
Explanation:
Gentamicin and streptomycin primarily cause vestibular damage (manifested by tinnitus, vertigo,
and ataxia)
35.Answer: B. Netilmicin
Explanation: Amikacin, kanamycin, an i neomycin cause mainly auditory damage (hearing loss)
36.Answer: A. Tobramycin
,
Explanation:
Tobramycin can cause both vestibular and auditory damage.
37.Answer: A. Neomycin
i
Explanation:
j
Nephrotoxicity consists o f damage to; the kidney tubules and can be reversed if the use o f the
drugs is stopped. Neomycin is the mbst nephrotoxic aminoglycoside; streptomycin is the least
nephrotoxic. Gentamicin and tobramycin are nephrotoxic to approximately the same degree.
38. Answer: E. All o f the above
|
i
Explanation:
Aminoglycoside associated nephrotoxicity is more likely to occur in patients with pre-existing
renal disease or in conditions in which urine volume is reduced,concomitant use o f other
nephrotoxic drugs or previous or prolonged aminoglycoside therapy.
39.Answer: C. Imipenem
Explanation:
Imipenem is given intravenously. In the kidneys it is partly broken down by a dipeptidase in the
proximal tubule and is,therefore, givdn in combination with cilastatin, a specific inhibitor o f this
enzyme.( cilastatin is not required with Meropenem or Ertapenem since these are not sensitive to
renal dipeptidases).
40.Answer: C. They are destroyed easily by most |3-lactamases.
Explanation:
Carbapenems are resistant to destruction by most (3-lactamases.
They are derived from streptomyces jspecies.These drugs have the broadest spectrum o f activity
as compared to other (3-lactam antibiotics.
41 .Answer: A. Thiazolidine ring
Explanation:
Cephalosporins are known as p-lactam antibiotics because their chemical structure consists o f a
p-lactam ring adjoined to a thiazolidine ring.
42.Answer: D. Cefmetazole
Explanation:
Cefmetazole is a second generation cephalosporin.
43.Answer: D. Cefepime
i
Explanation:
Cefepime is a fourth generation cephalosporin.
44.Answer: D. Enterococci
Explanation:
First generation antibiotics are active against most gram-positive cocci (except enterococci)
45.Answer: D. Haemophilis influenzae
Explanation:
First and second generation cephalosporins are active against E.coli, K. Pneumoniae, and Proteus
Mirabilis and second generation cephalosporins have extended gram-negative coverage,
including p-lactamase producing strains o f Haemophilis influenzae.
46.
Answer: D. Cephalosporins are generally jclassified in four groups based mainly on structural
similarity.
Explanation:
Cephalosporins are classified into four major groups based on their spectrum o f activity (not
based on structural similarity). Each generation o f cephalosporin has shifted toward increased
gram-negative activity but lost activity toward gram-positive organism. Fourth-generation
cephalosporins have improved activity toward gram-positive organisms over third generation
cephalosporins.
47.Answer: C. Cefuroxime
Explanation:
Cefuroxime is commonly administered for community-acquired pneumoniae.
48.Answer: A. They penetrate the cerebrospinal fluid
Explanation:
Third generation cephalosporins are , valuable in the treatment o f meningitis caused by
meningococci, pneumococci and H. influenzae because they penetrate the cerebrospinal fluid.
49.Answer: C. Cefoperazone
Explanation:
All cephalosporins (except cefoperazone) are eliminated renally, so doses should be adjusted for
patients with renal impairment.Cefoperazone is eliminated by liver.
50.Answer: C. Ceftazidime
Explanation:
Probenecid may impair the excretion o f cephalosporins (except ceftazidime), causing increased
cephalosporin levels and possible toxicity.
51 .Answer: D. All o f the above
Explanation:
Alcohol consumption may result in a disulfiram-type reaction in patients taking cefmetazole,
cefotetan, and cefoperazone.
52.Answer: A. Lactone
Explanation:
The chemical structure o f macrolide antibiotics is characterized by a lactone ring to which sugars
are attached.
53.Answer: E. C and D
Explanation:
Erythromycin base and the estolate, i ethylsuccinate and stearate salts are given orally;
erythromycin lactobionate and gluceptate are given parenterally.
54.Answer: B. Erythromycin estolate
;
Explanation:
Cholestatic hepatitis may arise in patients treated for 1 week or longer with erythromycin estolate;
symptoms usually disappear within a few days after drug therapy ends.
55.Answer: E. A and D
|
Explanation:
I
Clarithromycin and erythromycin increase terfenadine and astemizole concentrations. Cardiac
arrhythmia may result. Azithromycin and dirithromcyin do not appear to interfere with
terfenadine metabolism; however, if used Concomitantly,patients should be closely monitored.
56.Answer: B. Clarithromycin
!
Explanation:
Sudden deaths have been reported when Clarithromycin was added to ongoing pimozide
therapy .Therefore, co-administration is coiitraindicated.
57.Answer: E. B and C only
Explanation:
Semi-synthetic macrolides Azithromycin,clarithromycin and dirithromycin are well tolerated as
compared to erythromycin and they are given once daily.They are expensive.
58.Answer: C. Clarithromycin
Explanation:
Clarithromycin is used in combination with omeprazole or lansoprazole for H.Pylori eradication.
59.Answer: E. C and D
Explanation:
Azithromycin is less active than erythromycin against gram-positive cocci.
Clarithromycin is more effective than erythromycin against staphylococci and streptococci.
60.Answer: C. Azithromycin
Explanation:
Azithromycin persists in high concentrations in the tissues (which could be significant in some
infections) but its peak plasma concentration can be quite low (which needs to be taken into
account in infections such as pneumococcal: pneumonia which can be complicated by septicemia).
61 .Answer: E. B and D
Explanation:
'
Penicillin G procaine and penicillin benzathine are repository drug forms.
Administered intramuscularly, these insoluble salts allow slow drug absorption from the
injection, and thus, have a longer duration o f action (12-24 hours).
62.Answer: A. 5-10 times
Explanation:
Penicillin G is 5-10 times more active than penicillin V against gram-negative organisms and
some anaerobic organisms
63.Answer: A. Vancomycin
Explanation:
j
The alternative drug for penicillin G resistant S.pneumoniae is vancomycin.
64. Answer: B. They do not occur in patients with a negative history o f penicillin allergy.
Explanation:
The hypersensitivity reactions may occur even in patients with a negative history.All other
choices are correct.
65.Answer: C. Seizures
Explanation:
With high dose therapy of penicillins seizures may occur, particularly in patients with renal
impairment.
!
66.
Answer: D. All o f the above
-
Explanation:
Antibiotic antagonism occurs when erythromycins, tetracyclines or chloramphenicol is given
within 1 hour of the administration o f penicillin. The clinical significance of such antagonism is
not clear.
j
67. Answer: E. A,B,&C
Explanation:
I
The isoxazolyl penicillins are cloxacillin, Dicloxacillin and Oxacillin.
i
68.Answer: B. Nafcillin
[
Explanation:
Nafcillin is excreted by the liver and!thus may be useful in treating staphylococcal infections in
patients with renal impairment.
|
69.
Answer: D. All o f the above
Explanation:
Oxacillin, cloxacillin, and dicloxacillin are most valuable in long-term therapy o f serious
staphylococcal infections (e.g. endocarcjiitis, osteomyelitis) and in the treatment o f minor
staphylococcal infections o f the skin and soft tissues.
70.Answer: C. Their spectrum o f activity iis narrower than that o f penicillinase resistant
penicillins.
Explanation:
Aminopenicillins have a spectrum o f activity that is similar to but broader than that o f the natural
and penicillinase resistant penicillins.; They are easily destroyed by staphylococcal
penicillinases,and thus they are ineffective; against most staphylococcal organisms.
71 .Answer: E. Penicillin
Explanation:
The aminopenicillin group includes the semi-synthetic agents ampicillin and amoxicillin and their
derivatives, Bacampicillin and cyclacillin.
72.Answer: C. Sulbactam
Explanation:
For infections resulting from penicillin-resistant organisms, ampicillin may be given in
combination with sulbactam.
73.Answer: A. Clavulanic acid inactivates penicillinases
Explanation:
Amoxicillin is more effective against S. aureus, Klebsiella and bacteroides fragilis when given in
combination with clavulanic acid because clavulanic acid inactivates penicillinases.
74.Answer: E. C and D
Explanation:
Extended-spectrum penicillins include the carboxypenicillins (e.g. carbenicillin, carbenicillin
indanyl, ticaricillin) and the ureidopenicilHns (e.g. mezlocillin, piperacillin)
75. Answer: C. Carbenicillin is two to four times more active than Ticaricillin against
P.aeruginosa.
Explanation:
Ticaricillin is 2 to 4 times as active as carbenicillin against Pseudomonas aeruginosa.
76.Answer: D. Pseudomonas
Explanation:
Tazobactam is a [3-lactamase inhibitor that expands the spectrum o f activity to include some
organisms not sensitive to piperacillin alone ( if resistance is due to p-lactamase production) ,
including strains o f staphylococci, Haemophilis ,bacteriodes, and enterobacteriacae. Generally,
Tazobactam does not enhance activity against pseudomonas.
77.Answer: E. B and C
Explanation:
Carbenicillin and ticaricillin may cause hypokalemia.The high sodium content o f carbenicillin
and ticaricillin may pose a danger to patients with heart failure.
78. Answer: A. They suppress bacterial!growth by triggering a mechanism that blocks folic acid
synthesis.
Explanation:
Sulfonamides suppress bacterial growth by triggering a mechanism that blocks folic acid
synthesis, thereby forcing bacteria to synthesize their own folic acid.
79.Answer: B. Glucose-6-phosphate dehydrogenase
Explanation:
In patients with hereditary deficiency Of the enzyme glucose-6-phosphate dehydrogenase, there
is problem in maintaining the integrity o f the red blood cells.The rate o f rupture o f erythrocytes
increases and results in hemolytic anemia.
80.Answer: D. Sulfonamides
Explanation:
Sulfonamides are bacteriostatic; they suppress bacterial growth by triggering a mechanism that
blocks folic acid synthesis.
81 .Answer: B. Sulfisoxazole
j
Explanation:
Sulfisoxazole is sometimes used in combination with erythromycin ethylsuccinate to treat acute
otitis media caused by H. influenzae organisms.
82.Answer: D. Pseudomonas
Explanation:
Pseudomonas and proteus organisms are resistant to tetracyclines.
83.Answer: C. Doxycycline
j
Explanation:
Doxycycline is highly effective in the prophylaxis o f “traveler’s diarrhea”
commonly caused by E.coli.
84.Answer: B. It is excreted mainly in the feces
j
i
Explanation:
Doxycycline is excreted mainly in the feces, thus it is the safest tetracycline
for the treatment o f extrarenal infections in patients with renal impairment.
85.Answer: D. Demeclocycline
Explanation:
Demeclocycline antagonizes the action o f antidiuretic hormone (ADH) in the renal tubules;
therefore, it is used as an adjunctive to treat the syndrome o f inappropriate antidiuretic hormone
secretion.
86. Answer: E. A and C
Explanation:
Phototoxic reactions are common with Demeclocycline and Doxycycline.
87.Answer: C. Minocycline
Explanation:
Minocycline can cause vestibular toxicity! The vestibular toxicity includes
nausea, and vomiting.
Dizziness, vertigo,
88.Answer: D.Members o f the tetracycline group do not have cross-sensitivity among
themselves.
Explanation:
I f a patient is hypersensitive to any one o f the tetracyclines, he/she is likely to be sensitive to any
other tetracycline.Cross sensitivity within the tetracycline group is common.
89.Answer: D. Doxycycline
Explanation:
Dairy products and other foods, and antacids and laxatives containing aluminum, calcium, or
magnesium can cause reduced tetracycline absorption. Absorption o f Doxycycline is not inhibited
by these factors.
Explanation:
Fluoroquinolone antibacterials inhibit thfe enzyme DNA gyrase topoisomerase 11, an enzyme that
produces a negative supercoil in DNA, permitting transcription or replication.
91 .Answer: D. Ofloxacin
!
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Explanation:
Ofloxacin has the greatest activity against Chlamydia.
92.Answer: A. Sparfloxacin
Explanation:
Sparfloxacin is a third generation quinolone.
93.Answer: C. Trovafloxacin
Explanation:
Trovafloxacin has been associated with serious liver injury leading to liver transplantation and /or
death. Liver injury has been reported with both short term and long-term drug exposure.
94.Answer: D.Theophylline
Explanation:
Ciprofloxacin has been shown to increase itheophylline levels.
95.Answer: E. A and B
Explanation:
Gatifloxacin, moxifloxacin should be avoided in patients with known prolongation o f the QTC
interval o f cardiac action potential, with uncorrected hypocalcaemia, or who are receiving class
IA or class III antiarrhythmic drugs.
96.Answer: C.I &II are correct
Explanation:
They get concentrated in the renal tubules and bladder, exerting local antibacterial effects.Most of
them do not achieve blood levels high (enough to treat systemic infections.All urinary tract
antiseptics do not have the same mechanistn o f action.
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97.Answer: A. Ammonia and formaldehyde
Explanation:
Methenamine is hydrolyzed to ammonia and formaldehyde in acidic urine; formaldehyde is
antibacterial against gram-positive and gram-hegative organisms.
98.Answer: A. Enolylpyruvyl transferase
Explanation:
j
The bactericidal action fosfomycin tromethamine occurs due to inactivation o f the enzyme
enolylpyruvyl transferase thereby blocking the condensation o f uridine diphosphate-Nacetylglucosamine with penolpyruvate, one Of the first steps in bacterial cell wall synthesis.
99.Answer: C. Pseudomonas
Explanation:
Nalidixic acid and oxolinic are active against most gram-negative organisms that cause urinary
tract infections, including P.mirabilis, E.colij, Klebsiella, and enterobacter organisms. These drugs
are not effective against Pseudomonas organisms.
100.
Answer: C. Fosfomycin
Explanation:
I
Fosfomycin is indicated for the treatment o f uncomplicated urinary tract infection (acute cystitis)
in women caused by susceptible strains o f S.coli and E.faecalls.
101.
Answer: E. B and C only
Explanation:
Acetozolamide is inhibitor o f the enzyme Carbonic anhydrase. Carbonic anhydrase is the enzyme
responsible for catalyzing the reaction between carbon dioxide and water to give carbonic acid. If
this enzyme is inhibited the urine will have an alkaline pH which is unfavorable for methenamine
to act.
Sodium bicarbonate makes the pH o f urine alkaline thus rendering it unsuitable for methenamine
to act.
Aspirin is an acidic drug, and thus it makes the pH o f urine acidic and this does not have affect on
the antibacterial effect of methenamine. (Acidic media is required for methenamine to act).
102.
Answer: E. And B
Explanation:
Nitrofurantoin blood levels are increased and urine levels decreased by sulfinpyrazone and
probenecid, leading to increased toxicity and reduced therapeutic effectiveness.
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I
103. Answer: B. It resembles the Aminoglycosides in its efficacy against many gram-negative
organisms, and its ototoxic and nephrotoxic adverse effects.
Explanation:
Aztreonam resembles the aminoglycoside;s in its efficacy against many gram-negative organisms
but it does not cause nephrotoxicity or oto toxicity .All other statements are true.
104.
Answer: A. a nitrobenzene derivative
Explanation:
Chloramphenicol is a nitrobenzene derivative.
105.
Answer: E. A and B
Explanation:
Chloramphenicol and tetracyclines are active against ricketsia.Cefaclor and amoxicillin are not
active against Rickettsial organisms.
106.
Answer: C. The bone marrow suppression associated with Chloramphenicol is not doserelated.
Explanation:
The bone marrow suppression associated with chloramphenicol is dose-related. It is more likely
to occur at higher doses. All other statements are true.
107.
Answer: A. Inadequate liver detoxification o f Chloramphenicol
Explanation:
The gray baby syndrome which commonly occurs in neonates taking chloramphenicol is due to
inadequate liver detoxification o f chloratnphenicol.Several enzymes that is important for drug
metabolism, for example hepatic microsomal oxidase, glucuronyltransferase and plasma
transferases have low activity in neonates, especially if they have been born prematurely. These
enzymes take 8 weeks or longer to reach the adult level o f activity. The relative lack o f
conjugating activity in the newborn cah have serious consequences such as the gray baby
syndrome caused by chloramphenicol.
108.
Answer: D. Phenytoin
Explanation:
Chloramphenicol inhibits the metabolism o f phenytoin, tolbutamide and chlorpropamide and
dicumarol, leading to prolonged action and intensified effect o f these drugs.
109.
Answer: B. Acetaminophen
Explanation:
Acetaminophen elevates the blood levels o f chloramphenicol and may cause toxicity. This may
be due to the structural similarity between chloramphenicol and acetaminophen.
Explanation:
Because o f its marked toxicity, clindamy ;in is used only against infections for which it has
proven to be the most effective drug. Typ cally, such infections include abdominal and female
genitourinary tract infections caused by B.fr agilis.
111.
Answer: A. Sulfone
Explanation:
Dapsone is a member o f the sulfone class o f antibiotics.
112.
Answer: D. Cefonicid
Explanation:
Cefonicid is a second generation cephalosporin and it has bactericidal action. All others have
bacteriostatic action.
113.
Answer: E. I,II,&III are correct
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:
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Explanation:
Dapsone has been shown to be active against all the three: P.carinii,Plasmodium, and
Mycobacterium leprae.
114.
Answer: A. Pyrimethamine
Explanation:
Maloprim is a combination product o f dapsone and Pyrimethamine. It is used in the prophylaxis
and treatment o f malaria.
115.
Answer: A. Oxazolidine
Explanation:
Linezolid is chemically a synthetic Oxazolidine.
116.
Answer: B. Streptococci
Explanation:
Linezolid is bacteriostatic against Enterococci and Staphylococci, and bactericidal against
Streptococci.
117.
Answer: D. All o f the above
Explanation:
Patients receiving concomitant therapy jwith adrenergic or serotogenic agents or consuming more
than 100 mg o f tyramine a day may experience an enhancement o f linezolid’s effect.
118.
Answer: C. Aminoglycosides
Explanation:
Spectinomycin is an aminocyclitol related structurally to the aminoglycosides.
119.
Answer: A. 1M
Explanation:
Spectinomycin is given only as a single dose IM injection.
120.
Answer: B. Pyrimidine
Explanation:
Trimethoprim is chemically a substituted Pyrimidine.
121.
Answer: B. Dihydrofolate reductase
Explanation:
Trimethoprim inhibits the enzyme Dihydrofolate reductase, thus blocking bacterial synthesis o f
folic acid.
122.
Answer: A. synergism
!
Explanation:
The trimethoprim-sulfamethoxazole combination is synergistic; many organisms resistant to one
component are susceptible to the combination.
123.
Answer: D. Cyclosporine
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Explanation:
Cyclosporine does not increase the plasma concentration o f caspofungin.
When cyclosporine is combined with caspofungin, clinically significant rises in ALT were
observed. Serum transaminases should be monitored, and this combination should be avoided in
patients with pre-existing liver diseases.
When used in combination, carbamazepine, nelfinavir, nevirapine, phenytoin, and rifampin
increase the clearance o f caspofungin. Higher doses o f caspofungin should be considered when
this combination is administered.
124.
Answer: A. Fluorinated pyrimidine
Explanation:
Flucytosine is chemically a fluorinated py imidine.
125.
Answer: C. It is converted to fluorouracil, which results in defective protein synthesis.
Explanation:
Flucytosine penetrates fungal cells and is converted to fluorouracil , a metabolic antagonist,
Incorporated into the RNA o f the fungal c ill, Flucytosine causes defective protein synthesis.
126.
Answer: C. I&II are correct
Explanation:
Flucytosine is primarily active against cryptococcus and Candida. It is most commonly used in
conjunction with amphotericin B. Flucytosine alone is not recommended.
127.
Answer: E. B and C
Explanation:
Flucytosine has demonstrated synergy with amphotericin B and fluconazole against cryptococcus
and Candida species.
128.
Answer: A. Penicillium griseofulvum dierckx
Explanation:
Griseofulvin is produced from penicillium griseofulvum dierckx.
129.
Answen.E. A,B&C
Explanation:
Griseofulvin is active against various strains o f microsporum, Epidermophyton, and trichophyton.
It has not been shown to be active against aspergillus.
130.
Answer: E. All o f the above
Explanation:
Griseofulvin is effective in tinea infectioris o f the skin, hair, and nails (including athlete’s foot,
jock itch, and ringworm) caused by microsporum, epidermophyton, and trichophyton.lt is used in
infections that do not respond to topical antifungal agents.lt may be used in raynaud’s disease. It
can also be used in the treatment o f gout, i
131.
Answer: D. Colchicine
'
Explanation:
Griseofulvin inhibits fungal cell activity by interfering with mitotic spindle structure. Its
mechanism o f action is similar to Colchicine and that is why it is also used in the treatment of
gout.
132.
Answer: C. Hepatotoxicity
Explanation:
The most common adverse effects associated with griseofulvin are: headache, fatigue,
syncope,impaired performance and lethargy.
Occasional adverse effects: leukopenia, neutropenia, and agranulocytopenia
Rare adverse effects: serum sickness, angioedema, urticaria, and hepatotoxicity.
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133.
Answer: A. The particle size o f the product
j
Explanation:
The dosage o f griseofulvin is dependentlon the particle size o f the product.
For example 350 ultramicrosize is to equivalent 700 mg o f micro size in therapeutic
effectiveness.
!
134.
Answer: B. Alcohols
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Explanation:
Alcohol consumption in patients taking griseofulvin may cause tachycardia and flushing.
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135. Answer: B. They inhibit sterol Synthesis in fungal cell membranes and increase cell wall
permeability
Explanation:
Imidazoles inhibit sterol synthesis in fungal cell membranes and increase cell wall permeability;
this, in turn, makes the cell more vulnerable to osmotic pressure.
136.
Answer: E. All o f the above
Explanation:
Imidazole antifungals are active against many fungi, including yeasts, dermatophytes,
actinomycetes, and some phycomycetes.
I
137.
Answer: E. C and D
Explanation:
Ketoconazole is slow-acting and requires a long duration o f therapy (up to 6 months for some
chronic infections).
138.
Answer: E. A and B
Explanation:
Miconazole is available both in oral and parenteral forms.
139.
Answer: D.II & III are correct
Explanation:
Parenteral miconazole serves as a second-line agent in severe systemic fungal infections only
when other antifungal drugs are ineffective or cannot be tolerated.
The reason for this could be the adverse effefcts associated with the drug.
140.
Answer: E. Fluconazole
i
Explanation:
Fluconazole is used in the treatment o f CNS'infections involving cryptococcus and Candida.
141.
Answer: E. All o f the above
Explanation:
Deep mycotic infections susceptible to itraconazole include blastomycosis, coccidioidomycosis,
cryptococcosis, and histoplasmosis.
142.
Answer: B. Amphotericin B is associated with hematological toxicity
Explanation:
Itraconazole is preferred to amphotericin B against systemic and invasive pulmonary aspergillosis
because it is devoid o f hematological toxicity.
143.
Answer: E. A and B
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Explanation:
Nausea and vomiting are common to all imidazole antifungal agents.
144.
Answer: B. They decrease the level d>f gastric acidity, which is necessary for
ketoconazole and itraconazole to act.
Explanation:
Both ketoconazole and itraconazole need the presence o f stomach acid for adequate absorption.
Use with antacids, H2-blockers, or proton pump inhibitor is contraindicated.
145.
Answer: D. Amphotericin B
Explanation:
Ketoconazole may antagonize the antibiotic effects o f amphotericin B.
146.
Answer: E. All of the above
Explanation:
Fluconazole has been shown to elevate the serum levels o f phenytoin, cyclosporine, warfarin, and
sulfonylreas.
147.
Answer: D. All o f the above
.
Explanation:
Voriconazole inhibits cytochrome P4502C19. CYP2C9, and CYP3A4.
148.
Answer: C. Amphotericin B
Explanation:
Nyastatin is related chemically to amphotericin B. Both o f them are polyene antibiotics.
149.
Answer: B. Candida
Explanation:
Nyastatin is active primarily against Candida species.
150.
Answer: D. It has been shown to be ineffective against tinea capitis and tinea corporis
Explanation:
Terbinafine is very effective against tinea capitis and tinea corporis infections. All other
statements are true.
151.
Answer: D.
All o f the above
Explanation:
Amphotericin B is available as a 3% cream or lotion or an oral suspension that is not absorbed.
152.
Answer: E. A & B
Explanation:
Dry skin and local irritation with er> threma, pruritis, or burning, along with mild skin
discoloration, has occurred with the lotion and cream.
153.
Answer: D.
It is ineffective against Candida species
Explanation:
Butenafine is active against Trichophytor rubrum, Trichophyton mentagrophytes, microsporum
canis, Sporothrix schenckii, and yeasts inc luding Candidaparapsilosis and Candida albicans.
154.
Answer: D.
1 % cream
Explanation:
1 % cream o f butenafine is used in the treatment o f infection due to dermatophytes.
155.
Answer: D.
Butoconazole
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Explanation:
Butoconazole is an azole antifungal available for vaginal use to treat vulvovaginal candidiasis.
156.
Answer: E. I,II, & III
Explanation:
Butoconazole contains antibacterial activity against some gram-positive organisms such as
S. aureus, S. pyrogenes and E. Faecalfs. But E.coli is a gram-negative bacterium and
butoconazole is not active against gram-positive bacteria.
157.
Answer: C.
Ciclopirox
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Explanation:
Ciclopirox is a synthetic antifungal agent! that is chemically unrelated to any other antifungal
agent. It causes intracellular depletion o f amino acids and ions necessary for normal cellular
function.
Naftifine, terbinafine, and butoconazole interfere with fungal cell wall synthesis and permeability.
158.
Answer: A.
Hydrocortisone
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Explanation:
Clioquinol is a topical antifungal in a 3% ointment that can be used alone or in combination with
hydrocortisone.
i
159.
Answer: B. Phospholipids in membrane
Explanation:
Clotrimazole alters fungal cell membrane permeability by binding with phospholipids.
160.
Answer: E. All o f the above
Explanation:
Clotrimazole is active against yea:its dermatophytes (T.rubrum, T.mentagrophytes, and
E.floccosum, M.canis), and some grant -positive bacteria. At higher concentrations, clotrimazole
inhibits M.fufur, Aspergillus fumigatus, C. albicans, and some strains o f S. aureus, S.pyogenes,
Proteus vulgaris, and Salmonella.
161.
Answer: B. Parenteral solution^
Explanation:
|
Clotrimazole is available in the following formulations
Lozenges: Clotrimazole 10 mg
Topical:
Cream:
Lotion:
- Solution: Clotrimazole 1%
It is not used in parenteral formulations.
162.
Clotrimazole
Clotrimazole
1%
1%
Answer: E. A and B
Explanation:
Abnormal liver function tests (elevated AST) have occurred in patients taking clotrimazole
lozenges. (The interference with liver function tests seems to occur with oral formulations only).
Vaginal tablets are associated with mild burning, skin rash, itching, vulval irritation, lower
abdominal cramps vaginal soreness during intercourse, and an increase in urinary frequency.
Cross-sensitization occurs with imidazole antifungals.
163.
Answer: A.dye
Explanation:
Gentian violet is a dye and is useful as an antifunagal agent against Candida,
Epidermophyton,Cryptococcus,Trichophyton,and some Staphylococcus species.
164.
Answer: A. Ophthalmic suspension
Explanation:
Extemporaneously prepared ophthalmic suspension is used in the treatment o f fungal keratitis
165.
Answer: C. Steroids
Explanation:
j
When combined with a steroid, ketoconazole is useful in treating the following: diaper rash,
eczema, impetigo, lichenoid dermatitis, and psoriasis.
Explanation:
,
Miconazole is available topically as a 2 % kerosol, 2 % aerosol powder. 2 % cream, 2 % powder,
and 2 % vaginal cream, 100 mg and 200 m^ vaginal suppositories.
167.
Answer: D. All o f the above
Explanation:
j
Miconazole is advantageous over other ageAts such as Nyastatin and tolnaftate in that its activity
covers dermatophytes {Tinea mentagrophites, Tinea rubrum, and E.Floccosum) as well as
Candida.
I
168.
Answer: B. Vaginal suppositories art manufactured from a vegetable oil base that may
interact with latex products
:
Explanation:
j
Vaginal suppositories are manufactured from a vegetable oil base that may interact with latex
products. Avoid using diaphragms or condorris concurrently with suppositories.
169.
Answer: B. It acts by interfering withi fungal protein synthesis
Explanation:
j
Naftifine interferes with sterol biosynthesis by accumulating squalene in the fungal cell.
170.
Answer: B. Griseofulvin
Explanation:
Nyastatin, Terbinafine, and Nyastatin mdy be fungistatic or fungicidal
concentration of the drug. Griseofulvin has fungistatic action only.
depending on
171. Answer: A. It has a direct physicochemical effect on the destruction o f unsaturated fatty
acids present in fungal cell membranes
Explanation:
i
The antibacterial effects exerted by sulconazole are thought to be due to a direct physicochemical
effect on the destruction o f unsaturated fatty acids present in fungal cell membranes
i
172. Answer: C. Nyastatin
j
Explanation:
Nyastatin is prim arily used as a topical agent inivaginal and oral Candida infections. It has not
been shown to be active against M.furfur
173.
Answer: E. A and B
Explanation:
Sulconazole is active against selected gram-positive aerobes (S.aureus, S. epidermidis and
Staphylococcal saprophyticus, E.faecdlis and Bacillus subtilis) and anaerobes (Clostridium and
Propionibacterium)
\
Tetraconazole is active against gram-positive and gram-negative bacteria.
Miconazole and Econazole have not beLn shown to have antibacterial activity.
174.
Answer: A. Plasmodium
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Explanation:
Malaria results from infection by any o f four species o f the protozoal genus plasmodium.
175.
Answer: E. A and B
Explanation:
Chloroquine and Hydroxychloroquine^ bind to and alter the properties o f microbial and
mammalian DNA.
The mechanism o f action o f primaquine and Mefloquine is not known.
176.
Answer: D. Primaquine
Explanation:
Schizonts are cells that reproduce by schizogony, producing a varied number o f daughter
trophozoites and merozoites.
177.
Answer: C. Fansidar
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Explanation:
;
Fansidar is a blood schizonticidal agent that is active against the erythrocytic forms o f susceptible
plasmodia. It is active against T.Gondii, i
178.
Answer: A. Primaquine
Explanation:
Primaquine is active against liver forms of P. Vivax and P.Ovale.
179.
Answer: B. Pyrimethamine
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Explanation:
*
Pyrimethamine is effective in the prevention and treatment o f chloroquine-resistant strains o f
P.falciparum. It is now almost exclusively iused with a sulfonamide or sulfone.
180.
Answer: A. Quinine dihydrochlorid
Explanation:
Quinine dihydrochloride is a parenteral form used in severe cases o f chloroquine-resistant
malaria. Quinine sulfate is an oral form use d in the prophylaxis.
181.
Answer: B. Pneumocystis carinii
Explanation:
Co-trimoxazole (a combination product containing Sulfamethoxazole and trimethoprim) is used
in the prophylaxis o f pneumonia caused by Pneumocystis carinii, which occurs most commonly
in AIDS patients. Fansidar is used in the prophylaxis o f Pneumocystis carinii infection in AIDS
patients unable to tolerate co-trimoxazole.
182.
Answer: E. B and D
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Explanation:
Quinine and Primaquine may result in hemolytic anemia in patients with hereditary deficiency of
the enzyme glucose-6-phosphate dehydrogenase.
183.
Answer: C. Sulfonamides
Explanation:
Primaquine is contraindicated in patients with rheumatoid arthritis and in those receiving
potentially hemolytic drugs or bone marrow depressants.
Sulfonamides may result in hemolytic anemia in patients with hereditary deficiency o f the
enzyme glucose-6-phosphate dehydrogenase.
184.
Answer: A. pyrimethamine
Explanation:
Fansidar is a combination containing sulfadoxine and pyrimethamine.
185.
Answer: D. Chloroquine
Explanation:
Concomitant use o f Mefloquine and quinine or chloroquine may increase the risk o f convulsions.
186.
Answer: . E. Emetine
Explanation:
Emetine is an alkaloid, Quinacrine is an acridine derivative, Diloxanide is a dichloroacetamide
derivative, Metronidazole is an imidaz ole derivative,and Paramomycine is an aminoglycoside.all
these agents are useful as amebicides and trichomonacides.
187.
Answer: B. It is poorly absorbed
Explanation:
Paromomycin is not effective in extral-intestinal amoebiasis because it is poorly absorbed when
given by the oral route.
188.
Answer: E. A and D
Explanation:
Metronidazole acts as amebicidal drug by disrupting the helical structure o f DNA. Quinacrine
inhibits DNA metabolism. Emetine and paromomycin inhibit protein synthesis.
189.
Answer: D. Metronidazole
Explanation:
Metronidazole is the drug o f choice in the treatment o f urogenital trichomoniasis, amebic
dysentery, giardiasis and against bacterial anaerobes.lt is also a drug o f choice in the treatment o f
C.difficile colitis infections.
190.
Answer: D. A and B only
Explanation:
Quinacrine is useful in the treatment o f giardiasis and tapeworm infection.
191.
Answer: C. Emetine
Explanation:
!
Emetine may induce potentially lethal systemic toxicity. The most serious symptoms and findings
o f cardiovascular toxicity are tachycardia and other symptoms, precordial pain, and congestive
heart failure.
192.
Answer: B. Metronidazole
Explanation:
Metronidazole has a disulfiram-like iffect, so that nausea and vomiting occur if alcohol is
consumed while the drug is still in the body.
193.
Answer: C. Iodoquinol
Explanation:
Iodoquinol can produce severe neurotoxicity, particularly if they are given at greater than
recommended dose and for long periods o f t me.
Iodoquinol has not been implicated in the production o f neurotoxic effects when used at the
standard dosage o f 650 mg 3 times daily for 21 days.
194.
Answer: D. A ,B&C
Explanation:
Pentamidine can be administered intramuscularly, intravenously, or by inhalation. It is not given
by oral route because it is not well absorbed from the gastrointestinal tract.
195.
Answer: A. Infections due to P. carinii
Explanation:
Pentamidine is indicated for the prevention and treatment o f infections due to P.carinii. Its
unlabeled uses include treatment o f Trypanosomiasis, visceral leishmaniasis and Babesiosis.
196.
Answer: A. An aromatic diamide
i
Explanation:
Pentamidine is chemically an aromatic dianliide.
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197.
Answer: B. Decreases
Explanation:
Hypoglycemia may occur with initial admihistration o f drug via the IV, IM, or inhalational route.
After the patient has been on the drug for a period o f time, hyperglycemia will result. The effect
o f the drug may actually induce a reversible insulin-dependent diabetes mellitus.
198.
Answer: A. Pyrimidine synthesis
Explanation:
Atovaquone blocks mitochondrial electron synthesis at complex III o f the respiratory chain o f
protozoa, resulting in inhibition o f Pyrimidine synthesis.
199.
Answer: C. Its oral absorption is decreased when administered with food
Explanation:
The oral absorption o f atovaquone increases when it is administered with food. (Especially a high
fat meal)
j
Atovaquone is used as a second-line treatment o f mild to moderate P.carinii pneumonia in
patients intolerant o f Co-trimoxazole or other sulfonamides, or nonresponsive to co-trimoxazole.
200.
Answer: A. Intravenous route
Explanation:
Eflomithine HC1 is an antiprotozoal driig given intravenously.
201.
Answer: B. It inhibits the enzyine ornithine decarboxylase
Explanation:
Eflomithine is an irreversible inhibitor b f the enzyme ornithine decarboxylase.
202.
Answer: E.A11 o f the above
Explanation:
Atovaquone is active against P.carinii T.Gondii, and Cryptosporidium parvum, P.falciparum,
Isoporidium, and Microsporidia.
\
203.
Answer: C. Myelosuppression
Explanation:
I
Myelosuppression is the most frequent serious side effect ofEflom ithine.
Nausea and vomiting are not reported.Ckses o f Hearing impairment have been reported.
204.
Answer: E. A and B
Explanation:
Antitubercular agents such as Isonia zid,rifamipicin and streptomycin have relatively low
incidence o f adverse effects as comparec to Pyrazinamide or Ethambutol.
205.
Answer: A. Isoniazid, rifamipicih, Pyrazinamide
Explanation:
Most patients are started on isoniazic), rifamipicin, and Pyrazinamide. A fourth drug (e.g
Ethambutol, streptomycin,) is added wijth suspected resistance (i.e. if patients were previously
treated or if resistance is expected). Patients failing this therapy must be treated with five drugs
(isoniazid, rifamipicin, Pyrazinamide, Ethambutol. and streptomycin). If one or more o f these
agents can not be used ethionamide, para-aminosalicyclic acid, cycloserine, or capreomycin can
be used.
206.
Answer: A. In order to overcome; resistance
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Explanation:
Combination therapy is used in the treatmjent o f tuberculosis in order to overcome resistance.
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207.
Answer: E. A and B
!
Explanation:
Ethambutol is used in combination with Clarithromycin or Azithromycin and rifabutin in the
treatment of mycobacterium avium complex.
208.
Answer: D. Its mechanism of action is that it inhibits the enzyme DNA gyrase
Explanation:
j
The mechanism o f action o f Isoniazid is probably disruption o f bacterial cell wall synthesis by
inhibiting mycolic acid synthesis.
[
209.
Answer: E.A,B&C
Explanation:
Isoniazid has activity only against organisms in the genus mycobacterium.
More specifically, it has demonstrated activity against M.tuberculosis, M.bovis and selected
strains o f M.kansasii.
210.
Answer: B. Minimize the peripheral neuropathy associated with Isoniazid use
Explanation:
Pyridoxine 15-50 mg/day should be administered to patients taking Isoniazid to minimize the
peripheral neuropathy associated with its uSe.
211.
Answer: B. Hepatitis
!
i
!
Explanation:
j
Concurrent Carbamazepine therapy may increase the risk o f hepatitis.
212.
Answer: E. A and B
Explanation:
Cycloserine and ethionamide may cause additive nervous system effects when used along with
isoniazid.
213.
Answer: B. Impairment o f bacterial RNA synthesis by binding to DNA-dependent RNA
polymerase
i
i
Explanation:
Rifampicin impairs bacterial RNA synthesis by binding to DNA-dependent RNA polymerase.
214.
Answer: E. All o f the above
Explanation:
Rifampin has activity against most mycobacterial strains. In addition, Rifampin has activity
against many other organisms, including N.meningitidis, S.aureus, and H. influenzae, Legionella
pneumophilia, and C. trachomatis.
215.
Answer: A. Orange-red
Explanation:
Rifampin colors urine, sweat, tears, saliva and feces orange red.
216.
Answer: B. Probenecid decreases the blood level of Rifampin
Explanation:
Probenecid may increase the blood levels o f Rifampicin.
217.
Answer: A. Nicotinamide
Explanation:
Pyrazinamide is a pyrazine analogue of nicotinamide.
218.
Answer: D. M.tuberculosis
Explanation:
Pyrazinamide is a highly specific agent and has activity only against M.tuberculosis.
219.
Answer: A. They are more effecti ye than primary agents
Explanation:
Retreatment agents are less effective, more toxic, and are used in combination with primary
agents.
220.
Answer: E. Ethambutol
Explanation:
Retreatment agents include aminosalicylic acid, capreomycin, cycloserine, ethionamide,and
Kanamycin. Ethambutol is a primary anti-tubercular agent.
221.
Answer: D. Trimethoprim
Explanation:
Amino salicylic acid inhibits the enzymes responsible for folic acid synthesis.Trimethoprim has
almost similar mechanism o f action.
Explanation:
Capreomycin and streptomycin are ototo xic and nephrotoxic, they should not be administered
together.
223.
Answer: B. Ethionamide
Explanation:
Ethionamide may induce nausea, vomiting and orthostatic hypotension, metallic taste, epigastric
distress, and peripheral neuropathy.
224.
Answer: C. Rifampin 120 mg, Isoniazid 50 mg, Pyrazinamide 300mg
Explanation:
Rifater is a combination o f Rifampin 120 i)ng, Isoniazid 50 mg, and Pyrazinamide 300mg
225.
Answer: E. C and D
Explanation:
Ciprofloxacin and Levofloxacin are used ih the treatment o f tuberculosis.
226.
Answer: C. It is more effective than Rifampin in the treatment o f tuberculosis
Explanation:
Rifabutin is an antimycobacterial agent that is similar to Rifampin, with activity against both
tubercular and non-tubercular mycobacter al, and offers no clear advantage over Rifampin.
227.
Answer: E. Antiviral agents act b> inhibiting viral cell wall synthesis
Explanation:
Antiviral agents act by inhibiting viral rep ication.
228.
Answer: D. Foscarnet
Explanation:
Foscarnet does not need to be activated to act against viruses.
229.
Answer: B. HIV-1
Explanation:
HIV is an RNA virus. Others are DNA viiiises.
Explanation:
Antiviral agents which act against DNjj\ viruses are virustatic and arrest DNA synthesis by
inhibiting the enzyme viral DNA polymerase.
i
231.
Answer: E.A,B&C
|
Explanation:
Acyclovir is active against HSV-1, HSV-2, and Varicella Zoster virus.
232.
Answer: B. Interfering with viral attachment and uncoating
Explanation:
Amantadine inhibits replication o f the influenzae A virus by interfering with viral attachment and
uncoating.
233.
Answer: D. Amantadine
Explanation:
Amantadine is an-anti-viral drug used in the treatment o f Parkinsonism.
234.
Answer: A. Acyclic Purine nucleoside
Explanation:
Cidofovir is a synthetic acyclic purine nucleoside.
235.
Answer: C. Bradycardia
Explanation:
The most pronounced adverse effects o f amanatadine are ataxia,nightmares,and insomnia.The
anticholinergic side effects of amantadine include dry mouth, blurred vision, and tachycardia.
236.
Answer: C. Penciclovir
Explanation:
Famciclovir is a prodrug o f the antiviral agent Penciclovir.lt has activit against HSV-1,HSV2,and VZV.The drug is indicated for managemnt o f acute herpes zoster(shingles) and oral genital
herpes.
237.
Answer: B. Viral thymidine kinase
Explanation:
Famciclovir is rapidly phosphorylated in virus infected cells by viral thymidine kinase to
Penciclovir monophosphate. Penciclovir is a competitive inhibitor o f viral DNA polymerase and
prevents viral replication by inhibition o f hp;rpes virus DNA synthesis.
238.
Answer: A. It is a pyrophosphate analogue
Explanation:
Foscarnet is a synthetic pyrophosphate analogue.
239.
Answer: B. It is not active against HIV-1
Explanation:
Foscarnet is active against HIV-1.
240.
Answer: A. IV route
Explanation:
IV Foscamet is highly nephrotoxic, causing acute tubular necrosis.
241.
Answer: D. Hypercalcemia
Explanation:
Foscamet
The electrolyte
abnormalities
associ ated with
hypomagnesemia, Hypokalemia and Hypo phosphatemia.
242.
include
hypocalcaemia,
A nsw er:. 50 mL/min
Explanation:
Foscarnet is not recommended for patients \ vith creatinine clearance of less than 50 mL/min.
243.
Answer: E. A and B
Explanation:
Foscamet is exclusively eliminated by glom :rular filtration and tubular secretion.
244.
Answer: E. A and B
Explanation:
Foscarnet should not be given concurr ently with drugs having nephrotoxic adverse effects,
Aminoglycosides (e.g. streptomycin and amikacin) should not be given with Foscamet.
245.
Answer: C. It is incapable o f penbtrating the CNS.
Explanation:
Ganciclovir is capable o f penetrating the CNS.
246.
Answer: D. Ototoxicity
Explanation:
Ganciclovir has not been associated with ototoxicity.Ganciclovir has blackbox warnings
concerning increased potential for dose-limited neutropenia,anemia,and thrombocytopenia.lt is
also potentially teratogenic and carcinogenic.
247.
Answer: A. Imipenem-cilastatin |
Explanation:
Imipenem is always given in combination with cilastatin (in order to protect the degradation of
imipenem by renal dipeptidases), when this combination is given concurrently with ganciclovir it
may induce generalized seizures.
248.
Answer: D. Zanamivir
Explanation:
Oseltamivir is pharmacologically related to Zanamivir but structurally different.
249.
Answer: B. Oseltamivir Carboxylate
Explanation:
Oseltamivir is a prodrug that must be hydrolyzed to Oseltamivir carboxylate to exert antiviral
activity.
:
250.
Answer: A. Neuraminidase
j
Explanation:
Oseltamivir is a potent selective inhibitor o f the influenzae virus enzyme, neuraminidase.lt is
approved for symptomatic treatment o f infjluenza-A& B infections.
251.
Answer: B. Influenzae virus vaccine
Explanation:
Although amantadine, Rimantadine and Oseltamivir are approved for the prophylaxis o f
influenzae virus infections, the influenzae virus vaccine is still the gold standard for prophylaxis
o f influenzae virus infection.
252.
Answer: C. Acyclovir
Explanation:
Valacyclovir is the L-valine ester o f acyclovir.
253.
Answer: A. It inhibits RNA and D liA synthesis by depleting intracellular nucleotide
reserves.
Explanation:
Ribavarin inhibits RNA and DNA synthesis by depleting intracellular nucleotide reserves.
254.
Answer: C. Inhalational route
Explanation:
Ribavarin is administered in aerosol form by the inhalation in the treatment o f respiratory
syncytical virus (RSV).
255.
Answer: B. It may precipitate on respirator valves and tubing causing lethal malfunction.
Explanation:
Ribavarin is not recommended in patiehts using ventilators because it may precipitate on
respirator valves and tubing, causing lethal malfunction. However, use o f prefilter may permit
ribavarin therapy in such patients.
256.
Answer: B. Ganciclovir
Explanation:
Valganciclovir is L-valine ester (prodrug) o f the antiviral agent ganciclovir.
257.
Answer: B. It has markedly increased bioavailability when given with food.
Explanation:
Valganciclovir has the same spectrum of activity as ganciclovir. Valganciclovir is a potential
carcinogen and teratogen.
The advantage o f Valganciclovir over ganciclovir is it has markedly increased bioavailability
when given with food.
258.
Answer: E. A and B
Explanation:
Zanamivir and Oseltamivir are active against influenzae A and influenzae B, but amantadine and
Rimantadine are active against influenzae A virus infection.
259.
Answer: E. All o f the above
Explanation:
Currently 4 classes o f antiretroviral drugs are approved, these include Nucleoside reverse
transcriptase inhibitors, nucleotide reverse transcriptase inhibitors, Nonnucleoside reverse
transcriptase inhibitors, and fusion inhibitors and protease inhibitors.
260.
Answer: D. Tenofovir
Explanation:
i
Tenofovir is a Nucleotide reverse transcriptase inhibitor.
261.
Answer: A. Enfuvirtide
Explanation:
Enfuvirtide is the fusion inhibitor used in the treatment of HIV-1 and HIV-2 infection.
Zalcitabine and Lamivudine are nucleoside reverse transcriptase inhibitors.Indinavir is a protease
inhibitor.
262.
Answer: D. A,B&C
Explanation:
Stavudine is a nucleoside reverse transcriptase inhibitor.
263.
Answer: D. They can used alone in the treatment o f HIV infection.
Explanation:
Monotherapy with any single antiretroviral agent is no longer considered acceptable in the
treatment o f HIV infection.
264.
Answer: E. Abacavir
Explanation:
Abacavir has good penetration into the cerebral spinal fluid, unlike other agents in this class.
265.
Answer: B. A life threatening hypersensitivity reaction
Explanation:
Abacavir has a black box warning about a life-threatening hypersensitivity reaction that can lead
to death. It occurs in approximately 5% o f patients taking this drug, typically within the first 6
weeks o f therapy. This reaction involves respiratory symptoms fever, rash, and GI complaints.
Explanation:
Didanosine results in hyperuricemia beca use it is catabolized to uric acid.Didnosine carries a
balck box warning for its potential to cause lethal pancratitis.
267.
Answer: A. Prevent degradation at acidic pH.
Explanation:
Didanosine is available in a specially buffered formulation in order to prevent degradation at
acidic pH.
268.
Answer: D. Lamivudine
Explanation:
j
Lamivudine is used in the treatment oi[ chronic hepatitis B in patients with active liver
inflammation.
269.
Answer: D. Peripheral neuropathy
Explanation:
The major toxicity associated with Stavudine is a dose-related peripheral neuropathy occurring in
up to 21% o f patients. Other adverse effects include headache, rash, sleep disorders and
abdominal pain.
270.
Answer: E. B and C
Explanation:
No drug interactions have been reported with abacavir and Didanosine.
271.
Answer: A. Tenofovir disoproxil fumarate
Explanation:
Tenofovir is available as Tenofovir disoproxil fumarate. Tenofovir disoproxil fumarate is rapidly
hydrolyzed by plasma esterases to Tenofovir, with subsequent conversion to the active Tenofovir
diphosphate.
272.
Answer: C. Didanosine
Explanation:
Tenofovir may increase Didanosine serum cc ncentrations.
273.
Answer: A. Zidovudine
Explanation:
Zalcitabine is indicated for combination therapy with Zidovudine for the treatment o f adult
patients with advanced HIV infection.
274.
Answer: A. Pentamidine
Explanation:
Zalcitabine has been associated with high incidence o f pancreatitis (inflammation o f the
pancreas). Pentamidine has also a potential to result in pancreatitis when given in therapeutic
doses.
Zalcitabine treatment should be interrupted, when a drug with a potential to cause pancreatitis.
(E.g. pentamidine)
275.
Answer: B. Thymidine
Explanation:
Zidovudine is a synthetic thymidine analogue.
276.
Answer: E.A,B&C
Explanation:
Zalcitabine should not be used in combination with Didanosine, Lamivudine, or Stavudine, in
order to minimize the incidence o f drug antagonism. Zidovudine (Azidothymidine) is always
used in combination with Zalcitabine.
277.
Answer: A. Lamivudine
Explanation:
Combivir is a combination product containing Zidovudine and Lamivudine.
278. Answer: B. It has fewer incidences o f adverse effects and drug interactions than the
individual agents.
Explanation:
Even though it is a combination product the adverse effects and drug interaction are the same as
the single agents.
279.
Answer: B. Abacavir
Explanation:
The first triple nucleoside combination product approved by the FDA is
Zidovudine/Lamivudine/Abacavir.
i
Infectious Diseases
Explanation:
n __ *
* -r-
Explanation:
|
Acetaminophen, ribavirin, rifabutin, and Rifampin may decrease blood levels o f Zidovudine.
281.
Answer: E. A and D
Explanation:
j
Cytochrome P450 enzymes are heme proteins, comprising a large family o f different enzymes
(each referred to as CYP followed by a defining set o f numbers and letter). These enzymes differ
from one another in amino acid sequencfe, in regulation by inhibitors and inducing agents.
Delavirdine is a Nonnucleoside reverse trariscriptase inhibitor which inhibits its own metabolism
by reducing the activity o f CYP3A4 and CYIP2C9.
282.
Answer: E. A and B
|
i
Explanation:
j
Delavirdine inhibits the metabolism o f terfehadine, astemizole, and Cisapride, and this increases
the risk o f cardiac arrthymias.
Alprazolam and Midazolam are benzodiazepines (a class o f sedative hypnotics) and an increase
in their plasma level results in excessive sedation.
283.
Answer: C.
Itsonce daily dosing.
!
Explanation:
]
The advantage o f Efavirenz over other Nomiucleoside reverse transcriptase inhibitors is its once
daily dosing.
j
284.
Answer: C.
CYP3A4
j
Explanation:
j
Efavirenz induces CYP3A4 enzyme and sljould not be used concomitantly with astemizole,
Cisapride, Midazolam, Triazolam, or ergot derivatives.
I
285.
Answer: D.
p ^
Nevirapine
j
j
Explanation:
j
Nevirapine is Nonnucleoside reverse transcriptase not a protease inhibitor.
Indinavir, Lopinavir, nelfinavir, Ritonavir and jsaquinavir are protease inhibitors.
286.
Answer: D.
Ritonavir
Amprenavir,
Explanation:
Saquinavir, Ritonavir, and Indinavir are not approved for use in the pediatric population.
287.
Answer: C. Amprenavir
Explanation:
Amprenavir is the protease inhibitor with the longest half-life. It has a half-life o f 7.1-10.6 hrs.
288.
Answer: B. Saquinavir
Explanation:
Saquinavir hard caps should be administered with fatty foods to improve bioavailability because
the oral bioavailability alone is only 4 %.
Fortovase is a soft gel cap formulaticfn o f a saquinavir that has improved bioavailability and
efficacy.
I
289.
Answer: B. Diarrhea
Explanation:
The most commonly reported adverse effect of nelfinavir is diarrhea.
290.
Answer: D. Vitamin E
Explanation:
Vitamin E is given in Amprenavir capsules, because it increases the absorption o f Amprenavir. 36
international units (IU) o f vitamin E arb included in 50mg o f Amprenavir.
291.
Answer: C. Propylene glycol
Explanation:
|
The oral liquid formulation o f Amprenavir contains a large amount o f propylene glycol.
Therefore, it must not be used in infants and children under 4 years old, pregnant women, patients
with severe kidney or liver problems, nor in patients who take disulfiram or metronidazole.
292.
Answer: E. A and B
Explanation:
Rifabutin, Phenobarbital, Phenytoin, dexamethasone, and Carbamazepine also lower saquinavir
plasma concentrations. Ketoconazole and Clarithromycin have increased saquinavir levels by
130%-180%.
293.
Answer: B. Lopinavir/Ritonavir
Explanation:
Lopinavir/Ritonavir is the first FDA approv i:d combination o f protease inhibitors.
294.
Answer: B. 4:1
Explanation:
The Lopinavir/Ritonavir combination is formulated as a 4:1 ratio o f Lopinavir to Ritonavir,
Ritonavir markedly reduces the metabcjl ism o f Lopinavir, resulting in increased plasma
concentrations.
295.
Answer: A. Lopinavir
Explanation:
Lopinavir has the shortest half-life.
296.
Answer: D. Enfuvirtide
Explanation:
Enfuvirtide is an antiretroviral drug that indibits the entry o f HIV-1 and CD4+ cells by interfering
with the fusion o f viral and cellular mem branes. It does not have drug interactions with the
CYP450 enzyme system.
297.
Answer: E. A and B only
Explanation:
Mebendazole interferes with reproduction and survival o f helminthes by inhibiting the formation
o f microtubules and irreversibly blocking glucose uptake, there by depleting glycogen stores in
the helminthes.
298.
Answer: D. Trichinella spiralis-threadworm
Explanation:
Trichinella spiralis is commonly known as pork worm.The scientific name o f threadworm is
strongyloides stercoralis.
299.
Answer: E. A and B
Explanation:
Carbamazepine and hydantoins may ieduce the blood levels and subsequent efficacy of
mebendazole.
300.
Answer: E. A and C
Explanation:
Both Albendazole and mebendazole ard synthetic imidazole derivatives.
Pyrantel is a Pyrimidine, and diethylcarbamazine is a synthetic organic compound which is not
structurally related to the above mentioned anthelmintics.
301.
Answer: E. B and C
i!
Explanation:
Albendazole is active against Taenia solium and Echinococus granulosis.
|
I
i
302.
Answer: C. Wuchereria bancrofti
Explanation:
Patients treated for W.bancrofti infection often present with headache and general malaise.
303.
Answer: D. Tape worm infection
i
Explanation:
;
Pyrantel is not used in the treatment o f tape worm infection.
304.
Answer: C. Piperazine
Explanation:
I
Piperazine is an anthelmintic drug which antagonizes the action o f Pyrantel.
305.
Answer: B. Thiabendazole
Explanation:
j
Thiabendazole besides its anthelmintic property, it exhibits anti-inflammatory, antipyretic, and
analgesic effects.
306.
Answer: E. A and D
j
'
Explanation:
Thiabendazole is active against trichophyton, and Microsporum species.
307.
Answer: E.A&B
Explanation:
The most common adverse effects o f thiabendazole are anorexia, nausea, vomiting, and dizziness.
Seizures, vertigo, paresthesias, and psychic disturbances may also occur less frequently.
308. Answer: A. It causes flaccid parah sis o f the helminth by blocking the response o f the
ascaris muscle to acetylcholine.
Explanation:
Piperazine causes flaccid paralysis of the helminth by blocking the response o f ascaris muscle to
acetylcholine.
309.
Answer: E. A and B
Explanation:
Piperazine is active against Ascaris lumbrit aides and Enterobius Vermicularis.
310.
Answer: C. Fumarate reductase
Explanation:
Thiamebendazole was shown to inhibit the helminth-specific enzyme, fumarate reductase.
311.
Answer: D. Quinacrine
Explanation:
Quinacrine is used for the treatment o f gi irdiasis and cestodiasis. It is active against T.saginata,
T.solium, H.nana, diphyllobothrium latum and the protozoa Giardia lamblia.
312.
Answer: B. It affects only cestodcs o f the intestine.
Explanation:
Niclosamide is used against T.saginata (beef tapeworm), D.latum (fish tapeworm), and H.nana
(dwarf tapeworm). It is not active agair st cysticercosis (a disease caused by the presence o f
tapeworm larvae of the species Taenia s k iu m in any o f the body tissues) because it affects the
cestodes o f the intestine only.
313.
Answer: A.
Piperazine
Explanation:
Piperazine should be taken in empty stom ich in order to be effective.
1. Catecholamines are
from the amino acid
A.
B.
C.
D.
E.
synthesized
Glycine
Alanine
Tyrosine
Methionine
Proline
A.
B.
C.
D.
E.
Alkyl substitution at the a-carbon
(adjacent to amino group) in
adrenergic agonists shows all the
below effects EXCEPT
^
2. Number of hydroxyl groups in
Dopamine
A.
B.
C.
D.
E.
1
2
3
4
5
3. Common chemical chain present in
adrenergic agonists is
A.
B.
C.
D.
E.
Methylamine
Ethylamine
Acetic acid
Chlorobenzene
Pentylamine
4. All the following statements are
TRUE regarding direct acting
adrenergic agonists EXCEPT
A. Catecholamines are activated by
the enzymes COMT (Catechol
ortho methyl transferase)
and
MAO (Monoamino oxidase)
B. Smaller substituents on N-, like
hydrogen, a-methyl group produce
a-receptor activity.
C. Larger substituents on N-; like
isopropyl group produces p­
receptor activity.
D. For a- and p-receptor activity,
hydroxyl group on meta position
is necessary.
E. Catecholamines are inactivated by
the enzymes COMT (Catechol
ortho methyl transferase) and
MAO (Monoamino oxidase)
5. One of the following is indirect
acting adrenergic agonist
Epinephrine / Adrenaline
NaphazoJine
Terbutaline
Dobutamine
Amphetamine
A.
B.
C.
D.
E.
Retards destruction of compound
Increases lipophilicity
Produces prolonged action
Increases water solubility
None
7. a-adrenergic antagonist that is a
quinazoline derivative
A.
B.
C.
D.
E.
8.
A.
B.
C.
D.
E.
Phentolamine
Tolazoline
Phenoxybenzamine
Prazosin
Amphetamine
Isopropylamine is the common side
chain in all the drugs mentioned
below EXCEPT in
Propranolol
Acebutolol
Pindolol
Atenolol
Tyramine
9. The common linking group between
aromatic ring and nitrogen in
Propranolol, Pindolol, Atenolol
and Timolol is
A.
B.
C.
D.
E.
Ethoxy
2-hydroxy-prpoxyOxy butyl
Methyl
Methoxy
10.Choline is chemically
A.
B.
C.
D.
E.
1° amino
2° amino
3° amino
4° amino
None
alcohol
alcohol
alcohol
alcohol
1
l.The link, functional group, between
acetic acid and choline
in
Acetylcholine is
A.
B.
C.
D.
E.
Ester
Ether
Amine
Lactone
Lactam
12. Which of the following is
chemically unstable and hence not
useful systemically
A.
B.
C.
D.
E.
Propantheline
Dicyclomine
Atropine
Glycopyrrolate
Tropicamide
16.Quaternary nitrogen is present in
A.
B.
C.
D.
E.
Tropicamide
Ipratropium
Pirenzepine
Dicyclomine
Cyclopentolate
17.
A.
B.
C.
D.
E.
Methacholine
Bethanechol
Acetylcholine
Carbachol
None
13. Which of the following statement is
FALSE
A. Acetylcholine is extremely short
acting as it undergoes rapid
hydrolysis by acetylcholinesterase
enzyme
B. Replacement of acetyl group by
carbamoyl group in Acetylcholine
produces Carbachol, which is less
susceptible to hydrolysis and
hence more stable
C. Substitution of methyl group on pcarbon of Carbachol produces
Bethanechol
D. Substitution of methyl group on pcarbon of Acetylcholine produces
Methacholine
E. Acetylcholine is more stable than
Carbachol, Methacholine and
Bethanechol
14. Which of the following is direct
acting cholinergic agonist
A.
B.
C.
D.
E.
Carbachol
Physostigmine
Neostigmine
Echothiophate
Isoflurophate
15.All the below agents are synthetic
anti-cholinergic agents EXCEPT
A.
B.
C.
D.
E.
Cholinomimetic drug is
Dicycloverine
Tyramine
Neostigmine
Tropicamide
Ipratropium
18.d-tubocurarine is an example of
A.
B.
C.
D.
E.
Neuromuscular blocking agent
Sympathomimetic agent
Sympatholytic agent
Cholinomimetic agent
Para sympatholytic agent
19.
WRONG
choline
Which o f the following statement is
regarding
succinyl
A. Succinyl
choline
is
non­
competitive depolarizing agent
B. Aliphatic molecule
C. Short duration of action
D. Contains ester functional group
E. Shows neuromuscular blocking
effect by blocking the receptor
because of its bulky nature like
Tubocurarine
.Natural
competitive
non­
depolarizing agent that comes
under Neuromuscular blocker
A.
B.
C.
D.
E.
Atracurium
Doxacurium
Tubocurarine
Vecuronium
Pancuronium
21. Which of the following is NOT a
steroidal derivative
A.
B.
C.
D.
E.
D. Contains one chlorine and two
fluorine groups
E. Available with the name Amidate
Pancuronium
Mivacurium
Pipecuronium
Vecuronium
None
27.Ester type of Local anesthetic drug
A.
B.
C.
D.
E.
22. What is the chemical ring structure
commonly present in Atracurium,
Doxacurium,
Tubocurarine,
Metocurine and Mivacurium
A.
B.
C.
D.
E.
28.
Pyrrole
Piperidine
Quinoline
Isoquinoline
Imidazole
Ketamine
Fenatanyl citrate
Midazolam
Thiopental
Etomidate
24.
General
contain ether group
A.
B.
C.
D.
E.
Enflurane
Desflurane
Sevoflurane
Isoflurane
Halothane
anesthetic
25.General anesthetic that is also called
as laughing gas
A.
B.
C.
D.
E.
Desflurane
Nitrous oxide
Fentanyl
Propofol
Midazolam
Which of the following statement is
FALSE with Etomidate
A. Non volatile general anesthetic
B. Water soluble and available as
aqueous propylene glycol solution
C. Contains imidazole ring in the
structure
Which o f the following statement is
FALSE regarding Local anesthetic
A. Ester type of drugs are longer
acting comparing to amide type of
drugs
B. Site of action of local anesthetic is
the inner surface of the cell
membrane
C. Upon ionization, the cationic form
is the active form
D. Drugs
pKa influences
the
chemical state of the drug
E. None
23.Cyclohexanone ring is present in
A.
B.
C.
D.
E.
Lidocaine
Dibucaine
Mepivacaine
Benzocaine
Prilocaine
that
29.Xylidine ring is not present in
doesn’t
A. Lignocaine / Lidocaine B. Bupivacaine
C. Procaine
D. Etidocaine
E. Mepivacaine
30.Which of the following drug
structure contains Quinoline ring
A.
B.
C.
D.
E.
Benzocaine
Lidocaine
Etidocaine
Butamben
Dibucaine
31.Benzisoxazole derivative having
Anti-psychotic drug action is
A.
B.
C.
D.
E.
Chlorprothixene
Loxapine
Pimozide
Clozapine
Risperidone
32.Haloperidol
is a derivative of
A.
B.
C.
D.
E.
Thioxanthine
Butyrophenone
Phenothiazine
Dibenzoxazepine
Dihydroindolone
D. Quetiapine
E. Butamben
37. Which of the following is NOT a
dibenzazepine derivative
33. Which of the following is WRONG
statement
A. Chlorprothiazine is thioxanthene
derivative
B. Fluphenazine and Fluoperazine
are phenothiazine derivatives
C. Clozapine is dibenzodiazepine
derivative
D. Pimozide is a dihydroindolone
derivative
E. Risperidone is benzisoxazole
derivative
34. All statements are true regarding
phenothiazines as Anti-psychotic
agents EXCEPT
A.
B.
C.
D.
E.
Fluphenazine and long
chain
alcohols form highly hydrophilic
compounds
Substitution of nitrogen containing
side chain on ring nitrogen is must
for anti-psychotic activity.
Ring and side chain nitrogens are
to be separated by three carbon
chain
Side chains may be
either
aliphatic, piperidine or piperazine
derivatives
None
A.
B.
C.
D.
E.
Amitriptyline
Imipramine
Desipramine
Clomipramine
Trimipramine
38.A tetra cyclic Anti-depressant agent
A.
B.
C.
D.
E.
Doxepin
Amitriptyline
Nortriptyline
Protriptyline
Maprotiline
39.Dibenzoxazepine derivative
A.
B.
C.
D.
E.
Doxepin
Amoxapine
Imipramine
Phenelzine
Tranylcypromine
40.Which
of the following is NOT a
serotonin reuptake inhibitor
A.
B.
C.
D.
E.
Fluoxetine
Paroxetine
Trazodone
Sertraline
Fluvoxamine
41.Lithium carbonate is used as
35.Thioxanthenes
differ
phenothiazines in
A.
B.
from
Having extra nitrogen
Lacking thering nitrogen and
having link to the side chain by
double bond
C. Not having anti-psychotic action
D. Having analgesic action
E. None
A.
B.
C.
D.
E.
42.
A.
Which o f the following is NOT B.
an
C.
Anti-psychotic agent
D.
E.
A. Loxapine
B. Sertindole
36.
C.
Remoxipiride
Anthelmintic
Anti-manic
Anti-diarrhoeal
Anti-spasmodic
Local anesthetic
Which o f the following is NOT a
benzodiazepine derivative
Diazepam
Alprazolam
Lorazepam
Chlrodiazepoxide
Thiopental
43.Which of the following statements
is
WRONG
regarding
Benzodiazepines
A. Compound with 3-OH group are
metabolized by Phase-I reactions
B. Agents lacking 3-OH group will
undergo phase I metabolism
C. Metabolite of diazepam is having
more potency and longer duration
of action than diazepam
D. Benzodiazepines
contains
an
additional phenyl substituent to
show anxiolytic activity
E. None
44.
A.
B.
C.
D.
E.
Which of the following drugs is an
azaspirone derivative
Buspirone
Zolpidem
Glutethimide
Paraldehyde
Pentobarbital
45.Buspirone structure doesn’t contain
A.
B.
C.
D.
E.
Piperazine
Pyrimidine
Benzene
Butyl group
Cyclopentane
46.Two
side chains in position 5- of
barbituric acid is essential for
A.
B.
C.
D.
E.
Sedative-hypnotic activity
Analgesic activity
Anti-pyretic activity
Anti-spasmodic activity
None
47. In barbiturates, substitution of
oxygen at 2 nd position with sulfur
produces
the below
effects
EXCEPT
A. Lipophilicity
B. Rapid distribution into lipid tissue
C. Ultra-short acting agents that
induce anesthesia
D. Thiopental is an example
E. Looses its lipophilicity
48.Long acting barbiturates have below
substituents in position-5
A.
B.
C.
D.
E.
Phenyl and chloride
Phenyl and ethyl
Chloride and ethyl
Phenyl and chloride
None
49.Hypnotic drug that is barbiturate
derivative
A.
B.
C.
D.
E.
Glutethimide
Methypiylon
Phenobarbitol
Paraldehyde
Chloral hydrate
50. Anti-epileptic drug that
under hydantoin derivative
A.
B.
C.
D.
E.
comes
Phenytoin
Ethosuximide
Primidone
Trimethadione
Clorazepate
51. Valproic acid used as Anti-epileptic
agent is a derivative of
A.
B.
C.
D.
E.
Iminostilbine
Dialkyl acetate
Oxazolidine dione
Succinimide
Hydantoin
52.Phenyl triazine derivative used as
Anti-epileptic agent
A.
B.
C.
D.
E.
Gabapentin
Carbamazepine
Dimethadione
Lamotrigine
Felbamate
53.1midazolidinedione ring is present
in
A.
B.
C.
D.
E.
Ethosuximide
Trimethadione
Phenytoin
Clonazepam
Primidone
54.An example for Anti-parkinsonism
agent
A.
B.
C.
D.
E.
55.
A.
B.
C.
D.
E.
Cocaine
Tubocurarine
Levodopa
Amitriptyline
Carbamazepine
A.
B.
C.
D.
E.
Selegiline
Tolcapone
Carbidopa
Fluoxetine
Fluvoxamine
Piperidine
Pyrimidine
Pyrazine
Pyradiazine
Pteridine
Naphthalene
Phenanthrene
Isoquinoline
Phenothiazine
Barbituric acid
-
58.Morphinan derivative having opioid
action is
A.
B.
C.
D.
E.
in
cardiac
Selective inhibitor of COMT is
57.The
basic ring present in Morphine,
Codeine and Heroin is
A.
B.
C.
D.
E.
Digitoxin
Digoxin
Gitoxin
Ouabain
None
61.Glycosidic linkage
glycosides is
56.Meperidine, an opioid analgesic
contains the ring structure of
A.
B.
C.
D.
E.
A.
B.
C.
D.
E.
Morphine
Pentazocine
Levorphanol
Buprenorphine
Naloxane
Ether
Ester
Amide
Disulfide
Peptide
62.As
the number of hydroxyl groups
increases in the cardiac glycoside
structure the following results will
be observed EXCEPT
A. Increases polarity
B. Decreases protein binding
C. Decreases
renal
tubular
reabsorption
D. Decreases liver bio-transformation
E. Increases duration of action
63.The positive ionotropic agent that
contains bipyridine moiety
A.
B.
C.
D.
E.
Amrinone
Digoxin
Digitoxin
Gitoxin
None
64.An Anti-anginal drug that is an
organic ester of nitrous acid
A. Nitroglycerin
B. Isosorbide
C. Amylnitrite
D. Propranolol
59.
Which of the following is an opioid E. Nifedipine
antagonist
65.Dipiperdino-dipyrimidine derivative
used as peripheral vasodilator
A. Morphine
B. Codeine
A. Verapamil
C. Methadone
B. Nifedipine
D. Tramadol
C. Amlodipine
E. Naltrexone
D. Dipyridamole
60. Cardiac glycoside obtained from
E. Milrinone
Strophanthus gratus
66
.Xyly] derivative that comes under
both Local anesthetic and: Anti­
arrhythmic agent
A.
B.
C.
D.
E.
A.
B.
C.
D.
E.
68
72. Which of the following statement is
WRONG
regarding
thiazide
diuretics
Lidocaine
Quinidine
Acebutolol
Diltiazem
Phenytoin
67.Anti-arrhythmic
drug that
diiodobenzyloxyethylamine
derivative
is
Lidocaine
Quinidine
Verpamil
Dipyridamole
Amiodarone
.Which
of the following Anti­
hypertensive agent is similar in
structure to the thiazide diuretics
A.
B.
C.
D.
E.
69.
A.
B.
C.
D.
E.
Diazoxide
Clonidine
Diltiazem
Captopril
Losartan
Which of the following is NOT a
cardiovascular agent
Propranolol
Nadolol
Esmolol
Acebutolol
Halothane
70.Carbohydrate derivative used as
osmotic diuretic
A.
B.
C.
D.
E.
71.
Glucose
Starch
Mannitol
Sucrose
None
D. Pyrrole
E. Thiazole
A. Benzthiadiazide is the basic ring
in almost all the thiazide diuretics
B. Substitution
of
sulfonamide
moiety on position-7 is not
compulsory
C. Saturation of 3,4-double bond
produces increases potency
D. Lipophilic substituents at position3 increases potency and provides
prolong activity
E. Replacement of sulfonyl group in
postion- 1 with carbamoyl group
prolongs the activity
73.Anthranilic acid derivative used as
Loop diuretic
A.
B.
C.
D.
E.
Ethacrynic acid
Triamterene
Spironolactone
Chlorothiazide
Furosemide
74.Potassium
sparing
diuretic,
Triamterene is having the basic
ring moiety
A.
B.
C.
D.
E.
Pyridine
Piperidine
Pteridine
Pyrimidine
Pyradiazine
75.Steroidal moiety containing diuretic
A.
B.
C.
D.
E.
Spironolactone
Amiloride
Bumetanide
Acetazolamide
Quinethazone
Carbonic anhydrase inhibitors used
76.All the below statements regarding
as diuretics contain the basic
Cholestyramine are true EXCEPT
structural ring
A. Non-absorbable
antiA. Benzene
hyperlipidemic agent
B. Thiadiazole
B. Bile acid sequestrant
C. Pyridine
C. Basic anion-exchange resin
D. Consists co-polymer of styrene
and divinyl benzene
E. Consists co-polymer of diethyl
pentamine and epichlorohydrin
77. Which of the following is NOT an
absorbable
Anti-hyperlipidemic
agent
A.
B.
C.
D.
E.
Clofibrate
Probucol
Lovastatin
Colestipol
Gemfibrozil
78.Anti-coagulant used both in vivo
and in vitro
A.
B.
C.
D.
E.
Heparin
Lepirudin
Warfarin
Dicumarol
Phenindione
A.
B.
C.
D.
E.
Streptokinase
Urokinase
Alteplase
Anistreplase
Reteplase
A.
B.
C.
D.
E.
Iron dextran
Ferrous sulfate
Ferrous gluconate
Ferrous fumarate
None
83.Vitamin that contains cyanide ion
and cobalt atom and used as Antianemic agent
A.
B.
C.
D.
E.
Vitamin BI
Vitamin B2
Vitamin B 6
Vitamin B l2
Vitamin C
84.Amino acid present in the structure
of Folic acid
A. Aspartic acid
B. Glutamic acid
C. Tyrosine
D. Glycine
E. Leucine
79.
Which of the following is NOT a
85.Hematopoietic
growth
factors
low molecular heparin fragment
include
A. Enoxaparin
A. Erythropietin
B. Dalteparin
B. Filgrastin
C. Tinzaparin
C. Oprelvekin
D. Ardeparin
D. All the above
E. Lepirudin
E. None
80. Salicylic acid derivative having
86.
Which of the following is NOT a
Anti-platelet activity
Hi-receptor antagonist
A. Paracetamol
A. Chlorpheniramine
B. Ticlopidine
B. Meclizine
C. Aspirin
C. Nizatidine
D. Dipyridamole
D. Cyproheptadine
E. Piroxicam
E. Pyrilamine
81. Serine protease obtained from
87. Which of the following has
human kidney cells and having
piperazine ring in its structure
thrombolytic activity
82. Anti-anemic agent that is NOT used
for oral administration
A.
B.
C.
D.
E.
88
Dimenhydrinate
Cetirizine
Promethazine
Cyproheptadine
Astemizole
.Anti-histamine drug Acrivastine
and cetirizine shows less sedation
A.
B.
C.
D.
E.
comparing to other anti-histamines
due to their
94. Which of the following statement is
FALSE regarding prostaglandins
Limited ability to cross BBB
High molecular molecular weight
Complex structure
Piperidine ring structure
None
A. COX-1 is a constitutive enzyme
B. COX-11 is a pathologic enzyme
C. Thromboxanes
differ
from
prostaglandins mainly by the
substitution of tetrahydropyran
ring structure for pentane ring
found in prostaglandins
D. Prostaglandin is a derivative of
prostanoic acid
E. Prostaglandins are synthesized
from glutamic acid
89.Proton pump inhibitors are specific
inhibitors of
A.
B.
C.
D.
E.
Na+ K+ ATPase pump
H+ Na+ ATPase pump
H+ K+ ATPase pump
C ai+ channel pump
None
90.5-Hydroxy
called as
A.
B.
C.
D.
E.
Tryptamine
95. Thromboxane that is clinically
relevant as platelet aggregating
agent
is
also
Epinephrine
Acetyl choline
Dopamine
Serotonin
Nor-epinephrine
91. Which of the following serotonin
agonist is NOT an indole
derivative
A.
B.
C.
D.
E.
Sumatriptan
Zolmetriptan
Almotriptan
Rizatriptan
Cisapride
92. An indole derivative that acts as 5HT 3 antagonist
A.
B.
C.
D.
E.
Ondasetron
Sumatripton
Rizatripton
Zolmetriptan
Almotriptan
93.Prostaglandins are synthesized from
A.
B.
C.
D.
E.
Maleic acid
Fumaric acid
Arachidonic acid
Mandelic acid
Phthalic acid
A.
B.
C.
D.
E.
TXA]
TXA2
TXB,
TXB 2
None
96.Leukotrienes
differ
prostaglandins in that
from
A. They contain no ring structure and
are covalently linked to 2 or 3
amino acids
B. They are 20-carbon derivatives of
fatty acids
C. They are not autocoids
D. They have different nomenclature
E. They won’t have physiological
actions
97.Lipoxygenase inhibitor
A.
B.
C.
D.
E.
Zafirlukast
Montelukast
Zilueton
Misoprostol
Carboprost
98.
A.
B.
C.
D.
E.
Acetyl ester of salicylic acid is
Aspirin
Piroxicam
Paracetamol
Diclofenac
Nimesulide
99. Winter green oil is the synonym of
A.
B.
C.
D.
E.
Diflunisai
Sodium thiosalicylate
Methyl salicylate
Choline salicylate
Sulphasalazine
100. NSAID (Non Steroidal Anti­
inflammatory Drug) used as
uricosuric agent
A.
B.
C.
D.
E.
Acetaminophen
Sulfinpyrazone
Etodolac
Valdecoxib
Piroxicam
101. Gout is the disease condition,
which involves deposition of
A.
B.
C.
D.
E.
Prostaglandins
Leucotrienes
Histamines
Bradykinis
Sodium urate crystals
102. Propionic acid derivative used as
NSAID is
A. Etodolac
B. Sulindac
C. Diclofenac
D. Naproxen
E. Paracetamol
103. Anthranilic acid derivative used as
NSAID is
A.
B.
C.
D.
E.
Nabumetone
Ibuprofen
Mefenamic acid
Aspirin
Diclofenac
104. Which of the following is a
selective COX-11 inhibitor
A.
B.
C.
D.
E.
Celecoxib
Ketorolac
Naproxen
Ketoprofen
Aspirin
105. Which of the following is NOT an
Autocoid
A.
B.
C.
D.
E.
Histamine
Prostaglandin
Leukotriene
Serotonin
Cyclooxygenase
ANSWERS
Medicinal Chemistry
1.
Answer: C. Tyrosine
Explanation:
Naturally occuring catecholamines include epinephrine (adrenaline) and norepinephrine
(noradrenaline). They are biosynthesized from tyrosine, an amino acid.
MH,
»°
H~ C00H
Tyrosine
I Tyrosine hjdioxytsse
HH,
i
HO
D O P A (D ih ^ ia iy p k n ^ lih iu n e )
| Aromatic L'amino aciddecasboxyiase
HO
i
HO
D o p a m in e
|Dop*jwi* Plijriroxyiise
HO
Norep inep h rin e f N ora d re n a lin e
| Phe-rijfe tlianoiarau* N '
OM
MO-
^
^ — CH
C H j— NH— C H j
2. Answer: B. 2.
Explanation:
Dopamine is a neurotransmitter biosynthesized from tyrosine by the action of tyrosine
hydroxylase and aromatic L-amino acid decarboxylase. It is a catechol derivative and hence it
contains two hydroxyl groups in its structure.
3. Answer: B. Ethylamine.
Explanation:
Adrenergic agonists either direct acting or indirect acting contains ethylamine as a common
chain and is essential to their activity.
I t
..'V
CHj
HO
HO
Norepinephrine
(Ethylamine chain)
Epinephrine
(Ethylamine chain)
Naphazoline
(Ethylamine chain)
Terbutaline
(Ethylamine chain)
Dobutamine
(Ethylamine chain)
4. Answer: A.
Explanation:
Direct acting adrenergic agonists interact directly with adrenergic receptors to produce a
response. E.g., Epinephrine (adrenaline), norepinephrine (noradrenaline), naphazoline,
terbutaline, dobutamine etc.
1
2
.
.
3.
4.
5.
6
Chemical Factor
Ethylamine chain
Smaller substituents on N-.
E.g., hydrogen, a-methyl group
Larger substituents on N-.
E.g., isopropyl group
Hydroxyl / sulfonamide on meta position
Catechol ortho methyl tranferase (COMT)
.
Monoaminooxidase (MAO).
5.
Effect
Essential for activity
a-receptor activity
E.g., norepinephrine
p-receptor activity
E.g., isoproterenol
Essential for a- and p-receptor activity
Inactivation (Methylation o f the meta hydroxyl
group)
Inactivation (Oxidative Deamination)
Answer: E. Amphetamine.
Explanation:
Indirect acting adrenergic agonists even though chemically related to the catecholamines they
do not interact directly with the adrenergic receptors. They act by stimulating the release of
endogenous catecholamine neurotransmitters. Hence they are also called as sympathomimetic
agents. E.g., amphetamine, ephedrine and tyramine.
Epinephrine/Adrenaline, Naphazoline, Terbutaline and Dobutamine are direct acting
adrenergic agonists.
CHL
CH,
CH*
1
CH---- NH>
HO
Amphetamine
OH
I
CH —
Hydroxy amphetamine
CH,
1
CH—
Methamphetamine
^ //
N H -C H 3
HO
Tyramine
Ephedrine
6
.
Answer: D.
Explanation:
1
.
2
.
Chemical Factor
Alkyl substitution on a-carbon
(adjacent to amino group)
More Hydroxyl groups
3.
Substitution of bulky groups on N7.
Effect
Increased lipophilicity > Increased absorption
> Decreased destruction > Prolonged Activity
Increased hydrophilicity > Decreased
absorption > Increased destruction >
Decreased Activity
Increased direct [3-receptor activity
Answer: D. Prazosin.
Explanation:
a -adrenergic antagonists include:
Ergot alkaloids: Ergotamine
Dibenzamines: Phenoxybenzamine
Benzolines: Tolazoline
Quinazolines: Prazosin
Nonselective a -receptor blockers (adrenergic antagonists) include phenoxybenzamine and
phentolamine.
Selective cti-receptor blockers include prazosin, terazosin, doxazosin and indoramin.
Selective a 2-receptor blockers include yohimbine, tolazoline and rauwolscine.
NHj
Prazosin
(Quinazoline, piperazine, furan rings; ketone
link)
I'wp-x
Phenoxybenzamine
(Dibenzamine; ether link)
Phentolamine
(Imidazoline ring)
8
. Answer: E. Tyramine
Explanation:
Nonselective p-receptor blockers (p-adrenergic antagonists) commonly contain isopropyl
chain in their structure. E.g., Propranolol, pindolol, timolol, sotalol, penbutolol, carteolol etc.
Selective Pj-receptor blockers include acebutolol, atenolol,, betaxolol, celiprolol, esmolol and
metoprolol.
Selective p2-receptor blocker includes butoxamine.
Tyramine is an indirect acting adrenergic agonist that doesn’t contain isopropyl chain in its
structure.
(Naphthalene ring, ether link,
isopropylamine side chain)
Pindolol
(Indole ring, ether link,
isopropylamine side chain)
(Ether link, isopropylamine side chain)
(Ehter link, isopropylaminb side chain)
ch 2— c h 2- imh2
//
HO
Tyramine
(Ethylamine side chain)
9. Answer: B. 2-hydroxy-propoxyExplanation:
In all the drugs propranolol, pindolol, atenolol, timolol the common linking chain between
ring structure and nitrogen is 2 -hydroxy-propoxy- chain.
ch3
Atenolol
( 2 -hydroxy-propoxy- link)
Propranolol
(2 -hydroxy-propoxy- link)
QH
H
.N
H
.NY
C«3
ch
CH3
A
H3 G OH 3
3
Timolol
(2 -hydroxy-propoxy- link)
(2 -hydroxy-propoxy- link)
10. Answer: D. 4° amino alcohol.
h3c + ch3
Acetylcholine chloride
(Acetic acid + choline = Acetylcholine + water)
(Choline = Quaternary amino alcohol
[trimethyl amino ethanol])
11. Answer: A. Ester
Explanation:
Acetylcholine, the most potent neurotransmitter acting at cholinergic receptor as agonist, is an
endogenous neurotransmitter. It is an ester of acetic acid and choline (quaternary amino
alcohol).
h3c ch3
C f
CH3
Acetylcholine (Ester link)
12. Answer: C. Acetylcholine.
Explanation:
Acetylcholine, methacholinb, bethanechol, carbachol; all are cholinergic agents (direct acting
cholinergic agonists), but vary in their stability and duration of action.
Acetylcholine is chemically very unstable and readily undergoes hydrolysis both in vivo and
in vitro resulting in extremely short duration of action and hence didn’t got attention as
therapeutic agent. Acetylcholinesterase is the enzyme that causes hydrolysis of acetylcholine
in vivo.
Substitution of methyl group on p-carbon of acetylcholine produces methacholine.
Replacement of acetyl group by carbamoyl group in acetylcholine produces carbachol, which
is less susceptible to hydrolysis and hence more stable.
Substitution of methyl group on p-carbon of carbochol produces bethanechol.
Methacholine, Carbachol and Bethanechol, which are less susceptible to acetylcholinesterase,
are said to be stable and produces longer duration o f action.
9
N
h 3c
CHjH sC .C h,
Cl
"c h 3
Acetylcholine chloride
Methacholine chloride
0
o
h3c
+/ch 3
Ct
Cl
h2n
ch 3
Carbachol chloride
H2 N
jQ
ch3
Bethanechol choride
13. Answer. E.
Explanation:
Acetylcholine is chemically very unstable and undergoes hydrolysis readily hence not used
systemically whereas Methacholine, Bethanechol and Carbachol are stable than acetylcholine
and somehow more resistant to hydrolysis hence got therapeutic value and utility.
14. Answer: A. Carbachol.
Explanation:
Direct acting cholinergic agonists: They act directly on the cholinergic receptors and show the
cholinergic actions. E.g., Acetylcholine, methacholine, bethanechol and carbachol.
Indirect acting cholinergic agonists: They act by increasing the levels o f acetylcholine in vivo
by inhibiting the acetylcholinesterase enzyme that causes degradation (hydrolysis) of
acetylcholine. These are again of two types:
Reversible inhibitors (short acting) E.g., Cambamates (carbamic acid esters): physostigmine
(eserine), neostigmine
Irreversible inhibitors (long acting) E.g., Organophosphorous agents (organophosphorate
esters): echothiophate, isoflurophate, parathion, malathion.
Physostigmine
Neostigmine
15. Answer: C. Atropine.
Explanation:
Anti-cholinergic agents or cholinergic antagonists are those that block the actions of
acetylcholine at muscarinic or nicotinic receptors.
Atropine is a natural alkaloid obtained from plant source, Atropa.belladona. A pah of the
structure of atropine is similar to acetylcholine allowing it to bind to postganglionic
parasympathetic receptors. Atropine has no intrinsic activity and it simply acts by its bulky
structure, preventing acetylcholine from binding to the receptor and thereby inhibiting the
cholinergic actions.
Propantheline, dicyclomine, glycopyrrolate, tropicamide, pirenzapine, ipratropium and
benzatropine are synthetic anti-cholinergic agents.
T
n -c h
3
L
OH
OH
Atropine
Homatropine
Propantheline
Dicyclomine
16. Answer: B. Ipratropium.
Explanation:
Propantheline, dicyclomine, glycopyrrolatc, tropicamide, pirenzapine, ipratropium and
benzatropine are synthetic anti-cholinergic agents.
Quaternary nitrogen is present in propantheline, glycopyrrolate and ipratropium; hence
positive charge, thereby reducing passage across the blood brain barrier.
Tertiary nitrogen is present in dicyclomine, pirenzapine, tropicamide and benzatropine, hence
no significant charge, which provide higher volume of distribution.
j N rC H j
OH
CH3
Tropicamide
(Tertiary amine)
Br
ck3
Ipratropium
(Quaternary amine)
OH
17. Answer: C. Neostigmine
Explanation:
Neostigmine is the indirect acting cholinergic agonist that acts by reversibly inhibiting the
acetylcholinesterase enzyme thereby increasing the concentration o f acetylcholine hence also
called as cholinomimetic agent.
Tyramine is an indirect acting adrenergic agonist.
Tropicamide, dicycloverine (dicyclomine) and ipratropium are synthetic anti-cholinergic
agents.
18. Answer: A. Neuromuscular blocking agent.
Explanation:
d-tubocurarine is a neuromuscular blocking agent. It is a competitive non-depolarizing agent
obtained naturally as curare alkaloid. It is rigid and bulky molecule.
d-Tubocurarine
(Isoquinoline ring, quaternary amine)
19. Answer: E.
Explanation:
Neuromuscular blocking agents are of two types. Competitive non-depolarizing agents and
noncompetitive depolarizing agents.
Former type include curare derivatives as examples, they act by competitively blocking
nicotinic receptor because of their bulky structure and inhibits the action of acetylcholine
thereby resulting in neuromuscular blocking effect and produces skeletal muscle relaxant
effect.
Noncompetitive depolarizing agents include succinyl choline and gallamine. These agents are
aliphatic molecules. Succinyl choline has a short duration of action because of rapid
hydrolyzing nature in the liver and plasma by pseudo cholinesterase (butylcholinesterase) as it
contains simple ester functional group.
20. Answer: C. Tubocurarine.
Explanation:
d-tubocurarine is a natural competitive non-depolarizing neuromuscular blocking agent
whereas Atracurium, Doxacurium, Vecuronium and Pancuronium are synthetic competitive
non-depolarizing neuromuscular blockers.
21. Answer: B. Mivacurium.
Explanation:
A wide number o f compounds structurally related to naturally available d-tubocurarine used,
as neuromuscular blockers are available synthetically.
E.g., Isoquinoline derivaties: metocurine, atracurium, doxacurium and mivacurium.
Steroidal derivatives: pancuronium, vecuronium and pipecuronium.
o
Pancuronium bromide
(Quaternary amine, steroidal moiety)
22. Answer: D. Isoquinoline.
23. Answer: A. Ketamine
Explanation:
Cyclohexanone ring is present in Ketamine.
General anesthetics include:
Volatile or inhalation anesthetics: These agents exist as gases or vapors and are lipophilic in
nature. E.g., Nitrous oxide (inorganic agent; flammable; laughing gas), Halothane
(halogenated hydrocarbon) and Ethers (methoxyflurane, isoflurane, desflurane, sevoflurane).
Nonvolatile or intravenous anesthetics (occasionally intramuscular). These agents are
available as aqueous solutions, aqueous propylene glycol solutions or emulsions. E.g., ultra­
short acting barbiturates (thiopental, methohexital, thiamylal), cyclohexylamines (ketamine),
benzodiazepines (diazepam, midazolam), butyrophenones (droperidol), opioid analgesics
(morphine, fentanyl), imidazole derivative (etomidate; an aqueous propylene glycol solution),
dialkylphenol (propofol; as an emulsion)
ch3
I
H 3C H 2C
Ketamine
(Cyclohexanone ring)
Etomidate
(Imidazole ring, ester link)
24.
Midazolam
(Benzodiazepine ring)
C H C H i C H 2C H 3
Thiopental
(Dihydropyrimidine
dione)
Fentanyl
(Piperidine ring)
Answer: E. Halothane
Explanation:
Halothane doesn’t contain ether link whereas enflurane, desflurane, sevoflurane and
isoflurane contains ether link in their structure. All these drugs comes under inhalation type of
volatile genera] anesthetics.
F
F
F
Cl
F
F
Enflurane
(Ether link)
F
F
F
Desflurane
(Ether link)
F
CF3
Sevoflurane
(Ether lnik)
H
Br F
I
I
H — C — C— F
I
F
I
Cl
I
I
ci
F
I
F
Halothane
(Halogenated hydrocarbon)
Isoflurane
(Ether link)
25. Answer: B. Nitrous oxide
Explanation:
Nitrous oxide (N 2 0 ) is a colorless gas also called as laughing gas. It is a nonflammable gas
but it can support combustion. It can produce narcosis effect.
26. Answer: D.
Explanation:
Etomidate is a non volatile general anesthetic that is water soluble and available as aqueous
propylene glycol solution. It is available commercially with the name Amidate.
Structurally etomidate contains imidazole ring, ester link, but it won’t contain any chlorine or
fluorine groups.
N
Etomidate
(Imidazole ring, ester link)
27. Answer: D. Benzocaine.
Explanation:
Local anesthetics are similar in structure to natural alkaloid cocaine. These agents consist of a
lipophilic aromatic group linked to hydrophilic moiety through an ester or amide bonding.
Ester type of agents includes cocaine, benzocaine, procaine, chloroprocaine, butamben and
tetracaine. These agents because o f simple ester group undergo rapid hydrolysis by plasma
esterases resulting in short duration of action.
Amide type of agents includes lidocaine(lignocaine/xylocaine), dibucaine, prilocaine,
mepivcaine, bupivacaine and etidocaine. These are less susceptible to hydrolysis and hence
show longer duration of action.
H2 N
Benzocaine
(Ester link)
Procaine
(Ester link)
H
Tetracaine
(Ester link)
CHj
V ^ n^
WH3
UH3
Lignocaine or Lidocaine
(Amide link)
Prilocainc
(Amide link)
CH!
Mepivacaine
(Amide link)
28. Answer: A.
Explanation:
Ester type o f local anesthetics are short acting than amide type as they undergo hydrolysis
rapidly by plasma esterases whereas amide type drugs are less susceptible to degradation by
esterases. The drugs pKa influences its chemical state and the site of action of local anesthetic
drug is at the inner surface of the cel] membrane. Based on the form (charged or uncharged)
of drug the mechanism of action of local anesthetic depends. At ordinary tissue pH, the drug
is in uncharged form (secondary or tertiary amine) providing lipophilic nature and hence gets
diffused through the tissue and cell membrane and enters the nerve cell, where it gets ionized
(converts to charged form) into quaternary ammonium compound. This form of the drug
(charged; cationic) is the active form that block the sodium channel thereby preventing the
generation of action potential (impulse) at the membrane receptor complex. Because of its
positive charge the drug gets trapped within the cell and hence results in prolonged action
generally.
29. Answer: C. Procaine.
Explanation:
Xylidine is 2,6-dimethyl aniline. This ring structure is present in lignocaine
(lidocaine/xylocaine), bupivacaine, etidocaine and mepivacaine whereas it is absent in
procaine. All these drugs are local anesthetics.
30. Answer: E. Dibucaine.
Explanation:
Dibucaine is a quinoline derivative local anesthetic agent. Benzocaine and butamben are ester
type local anesthetics whereas lidocaine and etidocaine are xylidine derivatives and amide
type local anesthetics.
Dibucaine
(Quinoline ring, amide link)
31. Answer: E. Risperidone.
Explanation:
Anti-psychotic agents include:
Phenothiazines:
chlorpromazine,
triflupromazine,
fluoperazine etc.
Thioxanthenes: chlorprothixene, thiothixene
Dibenzodiazepines: clozapine
Butyropbenones: haloperidol
Benzisoxazoles: risperidone
Dihydroindolones: molindone
Dibenzoxazepines: loxapine
Diphenyibutyl piperidines: pimozide
prochlorperazine,
fluphenazine,
Pimozide
(Diphenyibutyl piperidine,
Benimidazolidinone)
(Pyrimidinone, Piperidine, Benzisoxazole)
Ci
Chlorprothixene
(Thioxanthene)
Clozapine
(Dibenzodiazepine, piperazine)
32. Answer: B. Butyrophenone.
Explanation:
Haloperidol is an anti-psychotic agent that comes under butyrophenone derivatives.
C!
Haloperidol
(Butyrophenone, Piperidine)
33. Answer: D.
Explanation:
Pimozide is a diphenyibutyl piperidine derivative that comes under anti-psychotic agents.
34. Answer: A.
Explanation:
Phenothiazines as anti-psychotic agents must have a nitrogen containing side chain as
substitution on the ring nitrogen. There must be a three -carbon chain between the ring and
side chain nitrogens (if two-carbon chain is present, then those phenothiazines show antihistaminic or sedative activity rather than anti-psychotic activity). The side chains may be
either aliphatic, piperidine or piperazine (imparts more potentcy) derivatives. Fluphenazine
and long chain alcohols form stable, highly lipophilic esters e.g., enantate or decanoate
provides prolonged activity.
35. Answer: B.
Explanation:
Thioxanthene derivatives used as anti-psychotic agents include chlorprothixene and
thiothixene. These agents differ from phenothiazines in that they won’t contain the ring
nitrogen and gets linked to the side chain by a double bond.
CHS
CHj
Chlorprothixene
(Thioxanthene)
Chlorpromazine
(Phenothiazine)
36. Answer: A. Butamben.
Explanation:
Butamben is an ester type of local anesthetic whereas loxapine, sertindole, remoxipride and
quetiapine are anti-psychotic agents.
37. Answer: A. Amitriptyline.
Explanation:
Anti-depressants include:
MAO inhibitors (Mono amino oxidase inhibitors): phenelzine, isocarboxazid (hydralazine
derivative), tranylcypromine (phenylcyclopropylamine derivative).
Tricyclic anti-depressants: Dibenzazepines (imipramine, desipramine, clomipramine,
trimipramine), dibenzocycloheptadienes (amitriptyline, nortriptyline, protriptyline),
dibenzoxepine (doxepin) and dibenzoxazepine derivative (amoxapine).
Tetracyclic agent: maprotiline.
Atypical anti-depressants: Bupropion (aminopropiophenone), complex heterocyclics
(trazodone, nefazodone).
Serotonin reuptake inhibitors: fluoxetine, fluvoxamine, paroxetine, sertraline and venlafaxine.
Cl
Imipramine
(Dibenzazepine)
Desipramine
(Dibenzazepine)
Clomipramine
(Dibenzazepine)
Trimipramine
(Dibenzazepine)
Amitriptyline
(Dibenzocycloheptadiene)
38. Answer: E. Maprotiline.
XHj
Maprotiline
(Ethanoanthracene; tetracyclic)
. CH-i
Doxepin
(dibenzoxepine)
(Dibenzocycloheptadiene)
(Dibenzocycloheptadiene)
39. Answer: B. Amoxapine.
Explanation:
Amoxapine is a dibenzoxazepine derivative.
Doxepin is a dibenzoxapine derivative, Imipramine is dibenzazepine derivative, Phenelzine is
hydrazine derivative and Tranylcypromine is a phenylcyclopropylamine derivative.
40. Answer: C. Trazodone.
j
Explanation:
Trazodone is a complex heterocyclic atypical anti-depressant whereas fluoxetine, paroxetine,
sertraline and fluvoxamine are serotonin reuptake inhibitors.
41. Answer: B. Anti-manic agent
Explanation:
Lithium is an element used as carbonate salt in the treatment of manic depression or bipolar
disease. Valproic acid and carbamazepine are also used as anti-manic agents.
42. Answer: E. Thiopental.
Explanation:
Cl
(Dihydropyrimidine dione)
(Benzodiazepine)
Alprazolam
(Benzodiazepine)
OH
Cl t
Lorazepam
(Benzodiazepine)
Chlordiazepoxide
(Benzodiazepine)
43. Answer: A.
Explanation:
Benzodiazepines can be used as anxiolytics and sedative-hypnotics. E.g., alprazolam,
diazepam, lorazepam, halazepam, oxazepam, flurazepam, chlordiazepoxide etc.
Agents with 3-OH group are easily metabolized by phase-11 reactions (conjugation reactions)
particularly glucuronidation and hence short acting. Benzodiazepines that lack 3-OH group
will preferably undergo phase-I metabolism E.g., 3-hydroxylation. These are long acting.
Diazepam produces a metabolite desmethyldiazepam which is still potent and has very long
half life. Thus, these agents can have cumulative action. As a structural feature these agents
contain phenyl substitution.
44. Answer: A. Buspirone.
Explanation:
'
Anxiolytics and sedatives-hypnotics include:
Benzodiazepines: diazepam, alprazolam, lorazepam, oxazepam etc.
Azaspirodecanediones or azaspirones: buspirone, gepirone, tiaspirone, ipsapirone (Buspirone
lacks CNS depressant activity unlike benzodiazepines)
Imidazopyridine: zolpidem
Barbiturates: Phenobarbital
Aldehydes: paraldehyde, chloralhydrate
Piperidinediones: glutethimide, methyprylon
Buspirone
(Azaspirodecanedione, butyl chain, piperazine, pyrimidine)
'H3C
Y
.CHa
.0
ch3
H3C
Glutethimide
(Piperidinedione)
Oi
Zolpidem
(Imidazopyridine)
Paraldehyde
(Cyclic trimer of acetaldehyde)
(Barbituric acid derivative,
pentyl chain, ethyl chain)
45. Answer: C. Benzene.
Explanation:
Buspirone
is an
azaspirone derivative.
Structurally
it contains biispirone
(cyclopentane+piperidinedione), butyl chain, piperazine and pyrimidine moieties. It won’t
contain benzene ring.
46. Answer: A. Sedative-hypnotic activity.
Explanation:
Barbiturates are 5,5-disubstituted derivatives of barbituric acid (saturated triketopyrimidine).
At position 5, two side chains are essential for sedative-hypnotic activity. Phenyl and an ethyl
group in position 5 produce long acting agents. Lipophilicity and metabolism rate gets
enhanced due to the presence of branched side chains, unsaturated side chains or side chains
longer than ethyl group, which results in shorter onset of action, shorter duration of action and
increased potency.
Since barbiturates and almost all their metabolites are weak acids, urinary pH h is great
impact on their excretion.
47. Answer: E.
Explanation:
In barbiturates, substitution of oxygen at 2nd position with sulfur produces highly lipophilic
molecule that distributes rapidly into the lipid tissues and are categorized as ultra-short acting
barbiturates. These are not useful as sedative-hypnotics but they can effectively; induce
anesthesia. E.g., thiopental.
48. Answer: B. Phenyl and ethyl
Explanation:
j
Alkyl chains are substituted at 5-position in short and intermediate acting barbiturates.:
E.g., Pentobarbital (Short acting), Butabarbital (Intermediate acting)
Aryl and alkyl chains are substituted at 5-position in long acting barbiturates.
E.g., Phenobarbital.
Phenobarbital
(Barbituric acid derivative)
(ethyl chain, phenyl moiety)
ch3
Amobarbital
(Barbituric acid derivative)
(ethyl chain, methylbutyl chain)
49. Answer: C. Phenobarbital.
Explanation:
Phenobarbital is a barbituric acid derivative used as hypnotic agent.
Glutethimide and Methyprylon are piperidinedione derivatives; Paraldehyde and Chloral
hydrate are aldehyde derivatives.
50. Answer: A. Phenytoin
Explanation:
Anti-epileptics or anti-convulsants include:
Long-acting barbiturates: Phenobarbital, mephobarbital, metharbital, primidone
Hydantoins: phenytoin, ethotoin
Succinimides: ethosuximide, phensuximide
Oxazolidinediones: trimethadione, dimethadione
Dialkylacetates: valproic acid
Iminostilbines: carbamazepine
Benzodiazepines: diazepam, clonazepam, clorazepate
Phenyltriazine derivative: lamotrigine
GABA-analogues: gabapentin
Dicarbamate: felbamate
Primidone acts as prodrug for phenobarbial. Upon metabolism primidone produces
Phenobarbital and phenyethylmalonamide (PEMA). These metabolites tend to accumulate
during chronic medication.
(Hydantoin derivative:
imidazoilidinedione)
Ethosuximide
(Succinimide derivative:
pyrrolidinedione)
(Pyrimidinedione derivative)
o
h 3c
h 3c
c o 2h
Cl
Trimethadione
(Oxazolidinedione, trimethyl
groups)
Clorazepate
(Benzodiazepine derivative)
51. Answer: B. Di alkyl acetate
Explanation:
Valproic acid is an anti-epileptic (anti-convulsant) agent and chemically it is a dialkyacetate
derivative. Its IUPAC name is 2-propyl pentanoic acid.
Iminostilbine derivative include carbamazepine; Oxazolidinedione derivatives include
trimethadione, dimethadione; Succinimide derivative include ethosuximide and Hydantoin
derivative include phenytoin.
Valproic acid
Carbamazepine
(Iminostilbine
derivative,
Dibenzazepine)
52. Answer: D. Lamotrigine.
Explanation:
Lamotrigine is phenyltriazine derivative used as anti-epileptic agent.
Gabapentin is a cyclohexane derivative, Carbamazepine is an iminostilbine derivative
(dibenzazepine), Dimethadione is an oxazolidinedione derivative and Felbamatei is a
dicarbamate derivative.
1
H-JM
H2N
N
nh2
Lamotrigine
(Phenyltriazine derivative)
COOH
Gabapentin
(Cyclohexane
ring)
O
II
Felbamate
(Dicarbamate derivative)
53. Answer: C. Phenytoin.
Explanation:
Phenytoin is hydantoin derivative used as anti-epileptic agent. Chemically hydantoin is
Imidazolidinedione.
Pyrrolidinedione ring (succinimide) is present in ethosuximide, Oxazolidinedione ring is
present in trimethadione, Benzodiazepine ring is present in clonazepam and Pyrimidinedione
ring is present in primidone.
Ring strucutre
Drug strucuture
^O
NH
Imidazolidinedione
(Hydantoin)
O
CH,
Pyrrolidinedione
(Succinimide)
ch3
Ethosuximide
O
O —
NH
O
Oxazolidinedione
Trimethadione
g 2m '
1,4-Benzodiazepine
,NH
Pyrimidinedione
54. Answer: C. Levodopa.
JI
J
Clonazepam
N
Explanation:
Levodopa is an anti-parkinsonism agent whereas Cocaine is a local anesthetic agent,
Tubocurarine is a neuromuscular blocking agent (skeletal muscle relaxant), Amitriptyline is
an anti-depressant agent and Carbamazepine is an anti-epileptic agent.
Levodopa
Dopamine
Anti-parkinsonism drugs include:
Anti-cholinergic anti-parkinsonism agents: Atropine, benzatropine, trihexyphenidyl,
procyclidine, orphenadrine and biperiden.
i
Dopaminergic anti-parkinsonism agents: Levodopa, ergot alkaloids (ergolines: bromotriptine,
pergolide and nonergolines: pramipexole, ropinirole)
55. Answer: B. Tolcapone.
Explanation:
Levodopa is a prodrug that gets converted in vivo to dopamine by the action of enzyme dopadecarboxylase that is available both centrally and peripherally. Action o f that dopainine is
required in brain. But if levodopa gets converted to dopamine in peripheral tissues, it is
unable to cross BBB (blood brain barrier) hence peripheral conversion o f levodopa into
dopamine is to be minimized by using agents that can inhibit peripheral dopa-decarb<j>xylase
enzyme.
!
Carbidopa, selegiline and tolcapone are the agents that improve the therapeutic efficacy and
safety of levodopa.
;
An analogue o f Levodopa namely carbidopa is able to inhibit the enzyme, dopadecarboxylase peripherally (as carbidopa is unable to cross BBB), hence more Levodopa is
available to brain for better therapeutic action. Hence their combination (Levodopa +
carbidopa) gained good attention.
Selegiline is a MAO-B (selective monoamine oxidase-B) inhibitor, which inhibits the
intracerebral degradation of dopamine.
;
Tolcapone is a selective inhibitor of COMT (catechol ortho methyl transferase).
j
(COMT converts levodopa to 3-ortho methyl dopa, an inactive metabolite)
Fluoxetine and Fluvoxamine are serotonin reuptake inhibitors used as anti-depressants.
56. Answer: A. Piperidine.
:
Explanation:
Pethidine (meperidine) is a synthetic opioid analgesic. Chemically it contains phenyl Nmethyl Piperidine ring in its strucuture.
j
CH3
Mepiridine/Pethidine (N-methyl piperidine)
Explanation:
. . .
Phenanthrene is the basic ring present in almost all natural and semi-synthetic opioid
analgesics. Opiate alkaloids are derived from the natural source, opium.
Both natural and synthetic opioids can be classified as:
Natural: Morphine, codeine
Semi-synthetic: Hydromorphone, oxycodone, pholcodeine, heroin (diacetylmorphine
/diamorphine)
Synthetic: Pethidine (Mepiridme), fentanyl, methadone, tramadol etc.
Tramadol is a new opioid analgesic agent that is chemically unrelated to the natural, semi­
synthetic and synthetic opiate derivatives.
N
CH3
N
CHg
h 3c
...
N
/C H j
ch
3
CHs
HO
OH
Hydromorphone
Morphine
M
Methadone
CH3
H 3C _ Ki„ C H 3
N
o c h
Codeine
(Methylated morphine)
N3 C0 ;
0
Oxycodone
°
3
Tramadol
58. Answer: C. Levorphanol.
Explanation:
Phenanthrenes:
Morphine,
hydromorphine,
codeine,
hydrocodone, nalbuphine,
buprenorphine, nalorphine, naltrexone and naloxone.
Phenylheptylamines: Methadone, propoxyphene
Phenylpiperidines: Meperidine, fentanyl, sufentanil, diphenoxylate and loperamide
Morphone derivatives: Naloxone, naltrexone
Morphinan derivatives: Dexromethorphan, levorphanol (levallorphan), Cyclorphan,
oxilarphan and butorphanol
Benzomorphan derivatives: Pentazocine, cyclazocine
Thebaine (oripavine) derivatives: Buprenorphine, diprenorphine
59. Answer: E. Naltrexone
Explanation:
Substitution of bulky groups in the place o f methyl group on nitrogen atom produces opioid
antagonists.
Mixed agonist-antagonists (phenanthrene derivatives): Nalbuphine, buprenorphine,
pentazocine
Pure antagonists (phenanthrene derivatives): Naltrexone, naloxone
Morphinan derived antagonists: Butorphanol, levallorphan
60. Answer: D. Ouabain
Explanation:
Cardiac glycosides also called as cardiotonics are used to increase myocardial contractility
and efficiency without the consumption o f extra energy hence the name cardiotonics. These
are steroidal glycosides obtained from natural sources (plants). E.g., Digitoxin (Digtalis
purpurea), Digoxin (Digitalis lanata), Gitoxin (Digitalis purpurea and Digitalis lahata) and
Ouabain (Strophanthus gratus).
61. Answer: A. Ether
Explanation:
Cardiac glycosides consist of a carbohydrate residue (e.g., digitoxose, rhamnose!), known
generally as a glycone, linked to a non-sugar residue steroidal moiety, known generally as an
aglycone or genin, by a so called glycosidic link to the anomeric carbon of the glycone. Since
the glycosidic link is formed to the anomeric carbon both a- and b-isomers of a glycoside are
known. The structures of glycosidic links vary, the most common being an ether group
(oxygen glycosidic links) but amino (nitrogen glycosidic links), sulphide (sulphur glycosidic
links) and carbon to carbon links (carbon glycosidic links) are also known to exist. Each type
of glycosidic link will exhibit the characteristics of the structure forming the jlink. For
example, oxygen glycosidic links are effectively acetals and so undergo hydrolysis iiji aqueous
solution.
Glycone portion helps in the bio-distribution of glycoside.
Cardiac glycosides also contain an unsaturated lactone (cyclic ester) substituent on the
aglycone (genin) moiety. Digoxin has an additional hydroxyl group at position 12. Ouabain
has a rhamnose glycone portion and additional hydroxyl groups at positions 1,5, 1 1 and 19.
sugar residues [P ip to x o so j^ <ciycou-e portion)
Digitoxin
62. Answer: E.
Explanation:
Increased number o f hydroxyl groups produces increased polarity resulting in increased
tubular excretion (decreased tubular reabsorption), decreased protein binding, decreased
biotransformation and thereby resulting in decreased duration of action. The same thing
happens in cardiac glycosides.
Digoxin has longer duration o f action and can undergo accumulation hence frequency is an
important issue. Whereas ouabain which is having more hydroxy] groups shows extremely
short duration of action and hence to be given intravenously for its effective action.
63. Answer: A. Amrinone.
Explanation:
Alternatives to cardiac glycosides obtained synthetically are Positive ionotropic agents. These
agents contain bipyridine moiety in their structures.
E.g., Amrinone, inamrinone and milrinone.
Whereas cardiac glycosides contain steroidal ring (aglycone/genin), sugar moiety
(digitoxose/rhamnose) and lactone ring in their structures. E.g., Digitoxin, digoxin, gitoxin.
64.
Answer: C. Amyl nitrite
Explanation:
Organic nitrates are polyol esters of nitric acid, whereas organic nitrites are esters of nitrous
acid. Nitrate esters (C 0 N 0 2) and nitrite esters (-C-O-NO) are characterized by a sequence of
carbon-oxygen-nitrogen, whereas nitro compounds possess carbon-nitrogen bonds (C N 02).
Amyl nitrite is a highly volatile liquid that must be administered by inhalation and is of
limited therapeutic utility. Organic nitrates of low molecular mass (such as nitroglycerin also
called as glyceryl trinitrate) are moderately volatile, oily liquids (very unstable drug and
undergoes extensive first pass metabolism), whereas the high-molecular-mass nitrate esters
(e.g., erythrity] tetranitrate, isosorbide dinitrate, and isosorbide mononitrate) are solids. In the
pure form (without an inert carrier such as lactose), nitroglycerin is explosive.
The organic nitrates and nitrites, collectively termed nitrovasodilators, must be metabolized
(reduced) to produce NO, the active principle of this class o f compounds (similar to EDRF
(Endothelium Derived Relaxing Factor)).
HC—O—N Q j
HC
H fi
O
NOj
O - NO?
Q
Nitroglycerine (glyceryl
trinitrate)
-----------CM*
Isosorbide dinitrate
"CHb
Isosorbide-5-mononitrate
CM
i
OCH2CM£5*jNHCH(CH3)j2
H jC
Propranolol
(Naphthalene ring)
ch
3
: >£>'■
Nifedipine (Pyridine and
nitrobenzene moieties)
Anti-anginal drugs are used in the treatment of angina pectoris. These agents also include:
Nitrites and nitrates:
p-blockers: Propranolol, atenolol.
Calcium channel blockers: Verapamil, nifedipine
\
65.
Answer: D. Dipyridamole
Explanation:
Dipyridamole is a dipiperidino-dipyrimidine derivative used as peripheral vasodilator.
H
OCHj'
HjCO
■OCHji
ch3
H3 C ''
o
CHj
Verapamil (methoxy anisole moieties, tertiary
amine group)
o
Nifedipine
(Pyridine and nitrobenzene moieties)
nh2
O
ON ! :
:
kilter Jmk
o .
^ch
r
3
-j
HO.
t
OH
Amlodipine (Pyridine and chloro benzene
moities; ether and ester links)
66
OH
"OH
N *-■-l)?pvfmij<i's'iw
sU!
I’tperulmc
Dipyridamole
(Dipiperidino-dipyrimidine moiety)
. Answer: A. Lidocaine
Explanation:
Drugs that comes under both local anesthetics and anti-arrhythmics include Procainamide
(amide derivative) and Lidocaine/lignocaine (xylidine derivative).
N
'CH 3
'c h 3
Lignocaine (Lidocaine, Xylocaine)
(Xylidine moiety, amide link,
tertiary amine)
o^,ch
C8
t
3
3
CH3
Acebutolol (Isopropyl amine)
Diltiazem (Anisole, Benzo thiazepane)
Phenytoin (lmidazolidine dione derivative)
67. Answer: E. Amiodarone.
Explanation:
Anti-arrhythmic drugs have diverse chemical structures. They include:
Cinchona alkaloids: Quinidine (an optical isomer o f quinine)
p-blockers: Propranolol, esmolol, acebutolol, nadolol
Amide derivatives: Procainamide, disopyramide, flecainide
Xylidine derivatives: Lidocaine (lignocaine, xylocaine), mexiletine
Quaternary ammonium salts: Bretylium
Diiodobenzyloxyethylamines: Amiodarone
Calcium channel blockers: Diltiazem
Hydantoins: Phenytoin.
68
. Answer: A. Diazoxide:
Explanation:
Thiazide (chlorthiazide), diuretic and diazoxide, anti-hypertensive agent, both are having the
common structural ring benzothiadiazine. Even though both are having structural similarity
and shows diuretic activity, only chlorthiazide is a potent diuretic whereas diazoxide is K+
channel opener and shows anti-hypertensive action. The prerequisite for thiazide diuretics is
presence of electron-withdrawing group like halogen in its structure, ortho to sulfonamide
group on the benzene nucleus. Since diazoxide doesn’t have this feature it lacks diuretic
property. On overall, benzothiadiazines without sulfonamide moiety exhibit anti-hypertensive
activity but lack diuretic activity.
69. Answer: E. Halothane.
Explanation:
Halothane is a general anesthetic.
Propranolol, nadolol, esmolol and acebutolol are cardiovascular drugs that comes under anti­
hypertensives, anti-arrhythmics and anti-anginals.
70. Answer: C. Mannitol.
Explanation:
Osmotic diuretics are highly polar, water-soluble, freely filtered at glomerulus and poorly
reabsorbed from the renal tubule thereby increasing the osmolarity of the filtrate in the lumen
hence causing limited tubular reabsorption of water and thus results in diuresis. Osmotic
diuretics include mannitol, urea, glycerin and isosorbide.
Glucose is a monosaccharide.
Sucrose is a disaccharide.
i
Starch is a polysaccharide.
71. Answer: B. Thiadiazole.
Explanation:
Carbonic anhydrase inhibitors used as diuretics contain thiadiazole ring with sulfonamide
moiety. These agents act by noncompetitive inhibition of the enzyme carbonic anhydrase
thereby preventing the supply of tubular hydrogen ions required for exchange with sodium in
the proximal convoluted tubule of nephron resulting in sodium bicarbonate diuresis.
E.g., Acetazolamide.
N-Nj
O
Acetazolamide (Thiadiazole ring)
72. Answer: B r
Explanation:
Thiazide diuretics contain the common basic ring structure benzothiadiazine with variable
substituents. The structural features required for diuretic activity are:
• The benzene ring must have a sulfonamide moiety (preferably unsubstituted) at position-7
and a halogen (preferably chloride) or halogen like group (CF3) at position-6 .
E.g., Chlorothiazide.
• Saturation of 3, 4 double bond generally produces increased activity.
E.g., Hydrochlorthiazide
• Lipophilic substituents at position-3 prolong activity as with methyl groups at position- 2
produces increased activity. E.g., Cyclothiazide.
• Position-1 o f the heterocyclic ring may be carbonyl group or sulfonyl group.
E.g., Quinethazone
• Benzothiadiazines without sulfonamide moiety exhibit anti-hypertensive activity but lack
diuretic activity. E.g., Diazoxide.
• Some of the sulfamoylbenzamides have activity similar to benzothiadiazides.
E.g., Indapamide, Chlorthalidone
73. Answer: E. Furosemide.
Explanation:
Loop diuretics act by inhibiting the co-transport of sodium, potassium and chloride from the
filtrate at the ascending limb o f loop of Henle in nephron.
Loop diuretics include:
Anthranilic acid derivatives: Furosemide and Bumetanide
Aiyloxyacetic acid derivatives: Ethacrynic acid.
Triamterene, Amiloride and Spironolactone (aldosterone antagonist) are potassium sparing
diuretics. Triamterene is a pteridine derivative, Amiloride is pyrazine derivative and
spironolactoone is a steroidal analogue.
NH
A
00
2H
nh2
m2
Triamterene
(Pteridine ring)
Cl
Ethacrynic acid
(Aryloxyacetic acid)
0
(Pyrazine ring)
/X .
h3c \ f
CH
H j
>
Q
H*N
0
CO^H
« 2N
COatf;
.CH*
Spironolactone
(steroidal moiety)
Furosemide
(Anthranilic acid moiety,
furan ring)
Bumetanide
(Anthranilic acid moiety)
74. Answer: C. Pteridine.
Explanation:
Triamterene, Spironolactone and Amiloride are potassium sparing diuretics. Triamterene is a
pteridine derivative, Amiloride is pyrazine derivative and spironolactone is a steroidal
analogue.
75.
Answer: A. Spironolactone
Explanation:
Spironolactone is a steroidal analogue antagonist of aldosterone (mineralocorticoid) at
aldosterone receptors in the distal convoluted tubule and collecting duct. Eplerenone also
comes under this category. They interferes with aldosterone mediated sodium-potassium
exchange by inhibiting the Na+-K7 exchange pump thereby decreasing the potassium
excretion hence the name potassium sparing diuretics.
76. Answer: E.
Explanation:
Anti-hyperlipidemic agents acting locally in the intestine are classified as nonabsorbable
agents and those acting systemically as absorbable agents.
Nonabsorbable agents are hydrophilic in nature but water insoluble resins that bind to bile
acids in the intestine and inhibits their reabsorption hence also termed as bile acid
sequestrants. E.g., Cholestyramine. It is a basic anion exchange resin and it consists of
trimethylbenzyl ammonium groups in a large copolymer o f styrene and divinylbenzene.
Another example includes Colestipol, which is a copolymer of diethylpentamine and j
epichlorohydrin.
I
77. Answer: D. Colestipol.
Explanation:
Non-absorbable anti-hyperlipidemic agents:
Bile acid sequesterants: Cholestyramine, colestipol.
Ezetimibe, phytosterols: Selcetive inhibitors of dietary cholesterol absorption.
‘
Absorbable anti-hyperlipidemic agents:
Nicotinic acid
Aryloxyisobutyric acid derivatives: Clofibrate, fenofibrate (prodrug) and gemfibrozil. ;
HMG-CoA (3-hydroxy-3-methyIgIutaryl-coenzyme A) reductase inhibitors (Statins):
Atorvastatin, Lovastatin, simvastatin, pravastatin, fluvastatin and cerivastatin.
Bisphenol derivative (sulfur containing): Probucol.
O
O ^C H j
Clofibrate
h 3c
Fenofibrate
ch3
CHa
O
A .
OH
CH3
c h
Lovastatin
3
Simvastatin
78. Answer: A. Heparin:
Explanation:
Heparin is an anticoagulant, highly acidic mucopolysaccharide (sulfated D-glucosamine and
D-glucuronic acid) administered by parenteral route. Heparin has in vivo and in vitro effects
whereas oral anticogulants (mostly used are warfarin and phenindione) show only in vivo
effects.
Other anticoagulants include:
Heparins group: Heparin, Antithrombin III, Danaparoid and Sulodexide
Low molecular weight heparin: Bemiparin, dalteparin, enoxaparin, nadroparin, pamaparin,
reviparin, tinzaparin and ardeparin.
Direct thrombin inhibitors: Lepirudin, argatroban, desirudin, hirudin, melagatran,
ximelagatran and bivalirudin are used as anticoagulants.
Vitamin K antagonists: Warfarin and dicumarol (4-hydroxycoumarin lactone derivative),
acenocoumarol, clorindione, coumatetraly], diphenadione,. ethyl biscoumacetate and
phenindione (indanedione derivative).
Non-medical anticoagulants: EDTA (Ethylene diamino tetra acetate), citrates and oxalates.
Warfarin (Coumarin moiety)
Dicumarol (Coumarin moiety)
o
o
Phenindione (Indanedione
moiety)
79. Answer: E. Lepirudin.
Explanation:
Lepirudin is a rDNA derived polypeptide used as direct thrombin inhibitor.
Low molecular weight heparin (LMWH) fragments are produced by controlled
depolymerization of heparin. E.g., Bemiparin, dalteparin, enoxaparin, nadroparin, pamaparin,
reviparin, tinzaparin and ardeparin.
80. Answer: C. Aspirin.
Explanation:
Aspirin is the acetyl ester of salicylic acid, which is also having anti-platelet action.
Anti-platelet drugs include:
COX (Cyclooxygenase) inhibitor: Aspirin (salicylate derivative)
ADP (Adenosine diphosphate) inhibitors: Ticlopidine (thienopyridine) and Clopidogrel
Phosphodiesterase inhibitors: Cilostazol
Glycoprotein llb/Jlla inhibitors: Abciximab (monoclonal antibody), eptifibatide and tirofiban.
Adenosine reuptake inhibitors: dipyridamole (dipiperidino-dipyrimidine derivative; peripheral
vasodilator).
Decreasing platelet production: Anagrelide.
Paracetamol (acetaminophen, p-aminophenol derivative) comes under non-narcotic analgesic
& antipyretic whereas piroxicam (oxicam derivative) comes under NSAID’s (Non-steroidal
anti-inflammatory drugs).
C 0 2 Hj
CT
ch 3
Aspirin
(Salicylic acid moiety)
o
......... ;.......... 7
6
Ticlopidine
(Thienopyridine)
rt
Paracetamol
(p-aminophenol moiety)
Piroxicam
(Benzothiazine, Pyridine)
81. Answer: B. Urokinase
Explanation:
Thrombolytic agents include urokinase, alteplase, reteplase, tenecteplase, streptokinase and
anistreplase.
Urokinase, also called as urokinase-type Plasminogen Activator, is a serine protease obtained
from cultured human kidney cells.
Alteplase, reteplase and tenecteplase rDNA (recombinant DNA) derived tissue plasminogen
activators (t-PA), converts plasminogen to plasmin, a fibrinolytic enzyme.
Streptokinase is a potent plasminogen activator obtained from p-hemolytic streptococci.
Anistreplase is also a Thrombolytic agent that converts plasminogen to plasmin and is also
called as APSAC: Anisolyted plasminogen-streptokinase activator complex.
82. Answer: A. Iron dextran.
Explanation:
The important anti-anemic agents include:
:
j
Iron preparations: Oral (ferrous sulfate, ferrous fumarate, ferrous gluconate) and Parenteral
(iron dextran- a complex of ferric hydroxide and low molecular weight dextrans).
Vitamins: Cyanacobalamin (vitamin B12) and folic acid.
Hematopoietic growth factors: erythropoietin, colony stimulating factors and interleukin-11.
83. Answer: D. Vitamin B }2
Explanation:
Vitamin B [2 or cyanocobalamin is a water-soluble vitamin with a corrin ring (modified
porphyrin ring) containing a cobalt atom. Cyanide ion is also associated with cobalt atom.
84. Answer: B. Glutamic acid.
Explanation:
Folic acid and cyanocobalamin (vitamin B12) comes under anti-anemic agents therapeutically.
Folic acid consists of two ring structures (pteridine moiety linked to niteogen o f p-amino
benzoic acid) and one side chain Glutamic acid (linked through an amide bond).
Folic acid
(Pteridine moiety + para amino benzoic acid (PABA) + Glutamic acid)
85. Answer: D.
Explanation:
Hematopoietic growth factors include:
Erythropoietin (natural), similar agents like epoietin alfa and darbepoietin alfa are
glycoproteins derived from rDNA technology.
Colony stimulating factors (CSF): Filgrastin, prefilgrastin (granulocyte colony stimulating
factor; G-CSF), and sargramostim (granulocyte macrophage colony stimulating factor; GMCSF) are also glycoproteins derived from rDNA technology.
Interleukin-11 (oprelvekin) is a nonglycosylated growth factor derived from rDNA
technology.
86
. Answer: C. Nizatidine
Explanation:
Nizatidine is a H 2 receptor antagonist whereas chlorpheniramine, meclizine, ciproheptadine
and pyrilamine are Hi receptor antagonists.
Histamine is bioamine derived principally from dietary source, Histidine. Upon
decarboxylation by L-histidine decarboxylase, Histidine will be converted to histamine.
Anti-histamines are the drugs, which block the actions of histamine. They are classified as H]
receptor antagonists and H 2 receptor antagonists.
Hi receptor antagonists:
Ethylene diamines: Pyrilamine, Tripelennamine
Alkylamines: Chlorphenaramine, Bromphenaramine, Acrivastine
Ethanolamines: Diphenhydramine, Dimenhydrinate, Clemastine, Doxylamine
Piperazines: Meclizine, Cyclizine, Hydroxyzine, Cetirizine
Phenothiazines: Promethazine
Dibenzocycioheptenes: Cyproheptadine
Phthalazinone: Azelastine
Piperidiens: Terfenadine, Astemizole, Levocabastine, Fexofenadine, Loratidine
H2 receptor antagonists:
Ranitidine, Famotidine, Cimetidine, Nizatidine.
Cl
Diphenhydramine
(ethanolamine derivative)
(Alkylamine derivative)
o
:;.. "r
HsC CHS
-
. it J
X
C! '
Or
h bn
Terfenadine
(Piperidine derivative)
Azelastine
(Phthalazinone, Azepine)
h3c
N0
h 3c
NOj
2
N
,CH3
^
N
H
H
N
H
Ranitidine
(Furan moiety)
Nizatidine
(Thiazole moiety)
NH?
NH2
iCN:
.‘JN
r~~*H
:HN
:...r-
s
tj
0
h 3c
0
Famotidine
(Guanidine, Thiazole moieties)
-N A
H
N ' CH‘
Hi
Cimetidine
(Imidazole, Guanidine moieties)
87. Answer: B. Cetirizine
Explanation:
Cetirizine is an antihistaminic drug having H2 receptor blocking effect, hence classified as H 2
receptor antagonist. The structure of cetirizine contains piperazine ring. Other drugs that
contain piperazine ring structure include meclizine, cyclizine and hydroxyzine. And also
cetirizine comes under second generation anti-histamines, which is less sedating than the first
generation drugs, due to its limited ability to cross the blood brain barrier (BBB).
The ring structure present in diphenhydramine is phenyl (2 rings), in promethazine
phenothiazine ring is present, in cyproheptadine dibenzocycloheptene ring and in astemizole
piperidine ring are present.
X
N
r
Hydroxyzine
Cetirizine
(Piperazine derivative)
(Piperazine derivative)
(Piperazine derivative)
(ethanolamine derivative)
CH3
n
y CH3
H CH3
Prom ethazine
(Phenothiazine derivative)
(Dibenzocycloheptene)
H ,.......
i
V ' N •'
'....... .
Astemizole
(Benzimidazole, Piperidine)
88
. Answer: A. Limited ability to cross BBB.
Explanation:
Cetirizine and acrivastine comes under second generation anti-histamines. Because of their
limited ability to cross the blood brain barrier (BBB) they are less sedating than the first
generation drugs.
89.
Answer: C. H+K+ ATPase pump
Explanation:
Proton pump inhibitors are the alternative agents to H2 receptor antagonists. These drugs
inhibit gastric acid secretion by specifically inhibiting the enzyme (proton pump), H+ K+
ATPase, which is the key mediator of gastric acid secretion. Drugs that come under proton
pump inhibitors are omeprazole, lansoprazole, rabeprazole, pantoprazole and esomeprazole.
Omeprazole
(Benzimidazole, pyridine moieties)
90. Answer: D. Serotonin.
Explanation:
Serotonin (5-OH tryptamine), the neurotransmitter, is a bioamine obtained from the amino
acid Tryptophan by the action of enzymes tryptophan hydroxylase and L-amino acid
decarboxylase. Serotonin agonists and antagonists both are having specific therapeutic
applications.
Epinephrine is the naturally occuring catecholamine, neurotransmitter synthesized
biologically from the amino acid tyrosine by the action of various enzymes and is a directly
acting adrenergic agonist.
Acetylcholine, the most potent cholinergic agonist is an endogenous component,
neurotransmitter, which is an ester o f acetic acid and choline (quaternary amino alcohol).
Dopamine is also a neurotransmitter synthesized from tyrosine in the pathway of epinephrine
and nor-epinephrine synthesis.
91. Answer: E. Cisapride
Explanation:
Serotonin also called as 5-hydroxy tryptamine is a bioamine synthesized from the amino acid
tryptophan. Serotonin has various physiological functions based on the receptor on which it is
acting.
Serotonin agonists:
5-HT id receptor agonists: Indole derivatives: Sumatriptan, rizatriptan, almotriptan,
naratriptan, zolmetriptan and frovatriptan.
5-HT4 receptor agonists: Tegaserod (indole derivative) and cisapride (benzamide derivative,
piperidine, phenyl rings).
5-HT3 antagonists: Indole derivatives: Ondasetron, alosetron and dolasetron;
Benzimidozole derivative: Granisetron.
Partial agonists/antagonists: Ergot alkaloids: Ergonovine. dihydroergotamine, methysergide
and bromocriptine.
H
N
h 3c
\
ft
M -C
HjC
Sumatriptan
(Indole derivative)
O
Granisctron
(Benzimidazole derivative)
a
h 2n
Cisapride
(Benzamide, Piperidine derivative)
92. Answer: A. Ondasetron.
Explanation:
All the drugs ondasetron, sumatripton, rizatripton, zolmetriptan and almotriptan are indole
derivatives but ondasetron is 5-HT3 antagonist whereas other drugs are 5-HT,D receptor
agonists.
93. Answer: C. Arachidonic acid.
Explanation:
Prostaglandins are synthesized from arachidonic acid (obtained from membrane
phospholipids by the action of phospholipase) by the action of enzyme cyclooxygenase,
which exists as two isoenzymes, COX-I and COX-II.
Chemically prostaglandins are derivatives o f prostanoic acid, a 20-carbon fatty acid
containing a 5-carbon ring.
94. Answer: E.
Explanation:
Prostaglandins are synthesized from arachidonic acid by the action of enzymes COX-I or
COX-II. COX-I enzyme is considered as constitutive enzyme, which synthesizes
prostaglandins regularly and contributes to homeostasis. One example is protection of gastric
miicosa from gastric HC1 by forming a prostaglandin layer over it. Whereas COX-II enzyme
is considered as pathologic enzyme, which produces prostaglandins in pathologic states like
inflammation or injury.
The products o f cyclooxygenase are then converted into either prostaglandins by
prostaglandin synthase or thromboxanes by thromboxane synthase. Thromboxanes differ
from prostaglandins mainly by the presence of a tetrahydropyran ring structure instead of the
pentane ring presence in prostaglandins.
Chemically prostaglandins are derivatives of prostanoic acid, a 20-carbon fatty acid
containing a 5-carbon ring.
CO OH
</
\
Prostanoic acid
(Source o f Prostaglandin structure)
95. Answer: B. TXA 2
Explanation:
Clinically relevant thromboxane that causes platelet aggregation is TXA 2
96. Answer: A.
Explanation:
Leukotrienes are produced by the enzyme lipoxygenase. Like prostaglandins, they are aslo
20-carbon derivatives of fatty acids. Unlike prostaglandins, they wont contain any ring
structure and are covalently linked to 2 or 3 amino acids.
E.g., LTC4 and LTD 4 (differ by the presence of glutamine).
97. Answer: C. Zileuton
Explanation:
Leukotrienes are autocoids obtained by the action of lipoxygenase enzyme. Since leukotrienes
were found to be involved in anaphylaxis reactions, leukotriene antagonists got therapeutic
importance.
Lipoxygenase inhibitors: Zilueton (Benzothiophene derivative)
Leukotriene antagonists: Zafirlukast and Montelukast
PGE] analogues: Misoprostol and Alprostadil.
PGF2 analogues: Carboprost, Travoprost, Latanoprost, Bimatoprost and Unoprostone.
PGI analogue: Epoprostenol.
98. Answer: A. Aspirin:
Explanation:
Aspirin is a NSAID (Non Steroidal Anti-inflammatory Drug), which is an acetyl ester of
salicylic acid. Since, aspirin is a simple ester it undergoes hydrolysis readily and hence
unstable in aqueous environment.
Aspirin
(Acetyl ester o f salicylic acid)
Piroxicam
(Benzothiazine, Pyridine, amide link)
OH
COOH
‘C ll
Diclofenac
(Dichloro aniline derivative,
acetic acid derivative)
o
Paracetamol
(p-aminophenol moiety, acetaminophen
2n
'Nimesulide
(Methane sulfonamide derivative,
ether link)
99. Answer: C. Methyl salicylate.
Explanation:
Methyl salicylate is called as oil of wintergreen, which is used as topical agent. It is a stable
salicylic acid derivative. Other salicylate derivatives include Diflunisal, Salsalate, Sodium
thiosal icy late (injectable), choline salicylate oral liquid), mesalamine, olsalazine and
sulphasalazine.
Mostly salicylates are weak acids.
Methyl salicylate
Diflunisal
'OH
Olsalazine
100.
Answer: B. Sulfinpyrazone
Explanation:
Deposition of sodium urate crystals in joints results in inflammation and pain, the disease
condition callcd as Gout (metabolic arthritis). Uric acid is obtained from the metabolism of
purines. The excess uric acid produced gets deposited in the joints as sodium urate crystals.
Drugs used in the treatment of gout include:
sulfinpyrazone (Pyrazolone derivative, also used as NSAID), colchicines (alkaloid),
probenecid (benzoic acid derivative) and allopurinol (isopurine form).
Acetaminophen (p-aminophenol derivative), Etodolac (Acetic acid derivative), Valdecoxib
(Pyrazole derivative) and Piroxicam (Oxicam derivative) are NSAID’s but doesn’t show
uricosuric action.
Sulfinpyarazone
(Pyrazolone derivative)
101. Answer: E. Sodium urate crystals.
Explanation:
Gout or metabolic arthritis is the disease condition observed due to the excess deposition of
sodium urate crystals, in cartilage joints resulting in inflammation and injury, obtained from
the excess metabolism o f purines.
102. Answer: D. Naproxen.
Explanation
NSAID’s:
Acetaminophen (paracetamol) is a p-aminophenol derivative. Its prodrug forms include
phenacetin and acetanilide.
Acetic acid derivatives: Etodolac, diclofenac, ketorolac, indomethacin, nabumetone, sulindac
and tolmetin.
Propionic acid derivatives: Ibuprofen, ketoprofen, flurbiprofen, fenoprofen, carprofen,
naproxen and oxaprozin.
Fenamic acid or anthranilic acid derivatives: Mefenamic acid and meclofenamate
Oxicams: Piroxicam
Selective COX-II inhibitors: Pyrazole derivatives: Valdecoxib, celecoxib and rofecoxib
Naproxen
(Naphthalene, propionic acid
derivative)
\ss=>
Etodolac
(Acetic acid derivative)
HjC,
JU
o
Sulin dac
(Acetic acic; derivatve)
103. Answer: C. Mefenamic acid.
Explanation:
Mefenamic acid is an anthranilic ac id or fenamic acid derivative.
Nabumetone and Diclofenac are ac ;tic acid derivatives, Ibuprofen is propionic acid derivative
and Aspirin is salicylic acid derivat ive.
c o
2h
Mefenamic acic I
(Anthranilic acid deri
(Naphthalene, acetyl derivative)
Ibuprofen
(Propionic acid deri\ ative)
104. Answer: A. Celecoxib.
Explanation:
Celecoxib, rofecoxib and valdec jxib are selective COX-II inhibitors whereas ketorolac,
naproxen, ketoprofen and aspirin ane non-selective COX inhibitors.
105. Answer: E. Cyclooxygena se
Explanation:
Autocoids are also called as local hormones and autopharmacolgical agents. They have wide
range of physiological and pharma cological actions. They also have diversity in their
structures. Examples include Hista mines, prostaglandins, leukotrienes, bradykinins, kallidin,
cytokinins and serotonin. Some au|t<ocoids like serotonin and histamine can function as
neurotransmitters.
Cyclooxygenase is the enzyme that participates in the conversion o f arachidonic into
prostaglandins. It exists in isomeric forms namely COX-I (Cyclooxygenase-I) and COX-II
(Cyclooygenase-II)
■' /
RIO
Microbiology
“Never let yesterday's disappointments overshadow tomorrow's dreams.”
1. All o f the following are cellular
organisms EXCEPT:
A.
B.
C.
D.
Fungi
Bacteria
Viruses
Protozoa
2. Which one o f the following is NOT
TRUE about Archaea?
A. They have cell walls.
B. Their cells are biochemically same as
that o f eubacteria.
C. They inhabit in extremes o f
environments i.e., extreme hot, cold,
pH, or saline environments.
D. A and C
3. The domain Eukarya contains
organisms:
A.
B.
C.
D.
E.
Microscopic fungi, protozoa
Macroscopic fungi and algae
Plants
Animals
All o f the above
4. Fungi are classified into phyla based on:
A. The type o f reproductive structures
observed
B. The lack o f observable sexual
structures.
C. Shape and color
D. A and B
E. None
5. Dimorphic fungi exist in either
unicellular (yeast) or filamentous (mold)
phase depending on:
A.
B.
C.
D.
Humidity
pH
Temperature
Moisture
. Which o f the following are dimorphic
fungi?
6
A.
B.
C.
D.
E.
Histoplasma
Trichophyton
Blastomyces
Epidermophyton
A and C
7. Protozoa are unicellular, non­
photosynthetic eukaryotes characterized by:
A.
B.
C.
D.
E.
Type o f motility
Size o f cells
Shape
B and C
None o f the above
8 . Which one o f the following is NOT a
Protozoan?
A.
B.
C.
D.
E.
Giardia
Entamoeba
Balantidium
Plasmodium
Ascaris
9. Viruses are classified by:
A.
B.
C.
D.
E.
Capsid structure
Type o f nucleic acid
Envelope
Presence o f enzymes
All o f the above
1 0 .Infectious proteins, implicated in mad
cow disease and kuru are:
A.
B.
C.
D.
Sporozoa
Prions
Viruses
Flagellates
11 .Bacteria are grouped and named
primarily by:
A. Morphology
B. Biochemical and metabolic differences
C. Immunological and genetic relationships
D. All o f the above
1 2 .In cultural morphology o f bacteria each
colony originates from a colony-forming
unit, consisting of:
A.
B.
C.
D.
A single cell
Group o f adherent cells
Different types o f cells
A and B
13. Which one o f the following statement is
FALSE?
A. Because o f their small size and
relative
transparency, bacteria
must be stained to be visible with
the light microscope.
B. Staining cannot be used as a
classification system.
C. Microscopic morphology describes
bacteria on the basis o f the size,
shape, and arrangement o f the cells.
D. Cultural morphology is based on the
size, shape and texture o f colonies
that are grown in axenic or pure,
culture.
14. A differential staining procedure that
divides the bacterial cells into either grampositive (purple) or gram negative (pink) is:
A.
B.
C.
D.
A. To make the color more intense
B. To magnify the bacteria
C. To stain both the cell and the
background, allowing visualization
o f the unstained capsular material
D. In order to facilitate enhances the
permeation o f one of the dyes to the
cell.
17. All of the following bacteria are
spherical in shape EXCEPT:
A.
B.
C.
D.
18.Spherical shaped bacteria that exist in
clusters are known as:
A.
B.
C.
D.
A.
B.
C.
D.
20
A.
B.
C.
D.
Acid Fast stain
Gram stain
Simple stain
Spore stain
16. In capsule staining the purpose o f using
two dyes is:
Streptococci
Staphylococci
Sarcinae
Vibrios
19. Which one o f the following represents a
wrong pair?
Simple stain
Acid-fast stain
Gram stain
Spore stain
15.A staining procedure that stains cells
that have an outer layer o f a waxy-lipid but
not those that lack this layer material is:
Streptococci
Neisseria gonorrhea
Staphylococci
Treponema palladium
Actinomycetes-Branching
Vibrios-Comma shaped
Spirochete- Helical
Fusobacteria-Spherical
.Bacteria can be classified based upon:
A.
B.
C.
D.
Spores
Capsules
Flagella
All o f the above
21 .Bacteria that have flagella distributed
evenly over the entire cell are called:
A.
B.
C.
D.
Monotrichaete
Amphitrichaete
Peritrichaete
Lopotrichaete
22. Which one o f the following statements
is FALSE about Prokaryotic cells?
A. Their cytoplasm is immobile.
B. Multiply asexually by binary fission
rather than by mitosis or meiosis.
C. Bacterial genetic information is
arranged on a single super coiled
circular strand o f DNA, the
nucleoid.
D. They are more complex inside, but
less complex outside.
23. Which of the following organelles are
absent in prokaryotic cells
A.
B.
C.
D.
E.
True nucleus
Endoplasmic reticulum
Nuclear membrane
Plastids
All of the above
70
80
90
60
A.
B.
C.
D.
Microcapsule
Slime layer
Glycolyx
None o f the above
28.Transformation from smooth to rough
colonies on bacterial media is indicative of:
Loss o f Capsule
Loss o f cell wall
Multiplication
Enhanced virulence
-
S
S
S
S
25.The capsule o f Bacillus anthracis is
made up o f
A.
B.
C.
D.
27.If the polysaccharide o f a capsule is
nonadherent, it is called a:
A.
B.
C.
D.
24. In prokaryotic cells Protein synthesis is
mediated by ribosome o f :
A.
B.
C.
D.
A. Increases the virulence (degree of
organism pathogenicity) o f a
microorganism
B. Prevents phagocytosis o f the
organism by macrophages and
neutrophils.
C. Aids in adherence of the organism to
host cells.
D. It kills the host cells.
Polypeptide
Polysaccharide
Lipid
Lipopolysaccharide
26. Which one of the following is not a
function o f a Capsule?
29. The decrease in virulence of bacteria
after loss o f capsule is because:
A. The capsule is changed to a
substance that is harmful to the
bacterial cells.
B. The capsular material is
immunogenic, thereby inducing the
production o f antibodies.
C. The capsular material induces
antibody production, which enhance
phagocytosis.
D. B and C
E. None
SO.The main parts, that comprise flagella,
are:
A.
B.
C.
D.
E.
Basal body
Hook
Filament
All o f the above
A and B
31 .The number o f rings that make up the
basal body o f flagella in gram-positive
organisms is:
A. 2
B. 4
C. 6
D. 5
32.Most bacteria are designated as either
gram-negative or gram-positive, based on:
A.
B.
C.
D.
Components o f the cell wall.
Shapes
Color.
Composition o f capsule.
33.The function o f cell walls in bacteria is:
A. To provide the general shape o f the
cell.
B. To protect the cell from osmotic
shock.
C. To carry the genetic material
D. A and B
34.
Which one o f the following statements
is not true about movement in bacteria?
A. lagella are proteinaceous, helically
coiled organs o f locomotion that
extend outward from the cytoplasm
through the cell wall in to the
environment.
B. Flagella rotate either clockwise or
counterclockwise; allowing a series
o f runs and tumbles in response to
chemicals in the environment.
C. The direction o f movement is
controlled by a complex mechanism
involving chemoreceptors and an
intracellular cascade o f methylation
and phosphorylation
D. The intracellular reactions enable the
bacteria to move toward nutrient
chemo attraclants and away from
repellants.
E. None o f the above
35. Which o f the following are common to
the cell walls o f Gram-negative and Grampositive bacteria?
A. Peptide cross-links between
polysaccharides.
B. A wide variety o f complex lipids.
C. Rigid polysaccharide framework.
D. A and C
E. None
36. All o f the following are found within the
cell wall o f Gram-positive cells EXCEPT;
A.
B.
C.
D.
Proteins
Lipopolysaccharides
Teichoic acids
Polysaccharides
37. Which one o f the following is FALSE
about Teichoic acids o f bacterial cell
membranes?
A. Chemically they are glycerol or
ribitol phophodiesters.
B. Membrane-associated Teichoic acids
are covalently linked to glycolipids
of the cytoplasmic membrane.
C. Well-associated Teichoic acids are
covalently linked to the glycan
chain o f peptido glycan.
D. They are found in both Grampositive and Gram-negative
bacteria.
3 8 . In gram-negative bacteria part o f the
endotoxin responsible for nonspecific
inflammation including diarrhea, fever, and
septic shock is:
A.
B.
C.
D.
E.
Core polysaccharide
Phospholipid
Lipid A
Protein
None
45. Which one o f the following contains
genes for heavy metal and antibiotic
resistance?
A.
B.
C.
D.
Cytoplasmic membrane
Nuclear region
Plasmids
Ribosomes
39.In bacteria the periplasmic space is:
A. An area between the cell wall and
the cytoplasmic membrane.
B. A pore found in the cell wall
C. An organelle found in the nucleus.
D. The organelle, which contains the
genetic material.
Questions [40-44] Match the cellular units
with their description.
A. Periplasmic space
B. Ribosomes
C. Cytoplasmic membrane
D. Nuclear region
E. Plasmids
40. Contains a gel o f several types o f
molecules (e .g ., hydrolytic enzymes,
periplasmic-binding proteins ) that process
molecules before they enter the cytoplasm.
46. The proteins found in the Cytoplasmic
membrane are engaged in;
A. Transportation o f nutrients.
B. Secretion o f exotoxins.
C. Electron transport and energy
formation
D. All o f the above
Questions[ 4 7-51J Match the nutritional
types o f bacteria with the given nutrition
types
A.
B.
C.
D.
E.
Auxotrophs
Saprophytic
Parasitic
Chemoautotrophs
Photoheterotrophs
-
47.Mutated so that they cannot synthesize
the same essential nutrients (usually amino
acids) as their parent cell.
4 8 .Use
light as an energy source.
41. A phospholipid bilayer matrix o f a fatty
acid core and glycerol phosphate backbone
49.Organisms whose nutrients are obtained
from dead or decaying organic matter.
42.Cellular units that synthesize protein by
translation messenger RNA base sequences
in to amino acid protein sequences.
50.Organisms whose nutrients are obtained
from and at the expense o f a living
organism.
51 .Oxidize organic and inorganic
compounds to produce energy.
43.rCircular double-stranded pieces o f
DNA that are found outside of the bacterial
chromosomes.
44.
A condensed area containing the
bacterial DNA or genome that lacks a
nuclear membrane and consists o f a long,
double stranded, super coiled, circular
DNA molecule.
52. Which one o f the following bacteria can
grow at 55 °C or greater?
A.
B.
C.
D.
Psychophile
Mesophile
Thermophile
Autotrophs
53.Bacteria that have the ability to grow
with or without oxygen are known as:
A.
B.
C.
D.
Obligate Anaerobes
Facultative Aerobes
Facultative Anaerobes
Obligate Aerobes
54.Obligate Anaerobes do not tolerate
oxygen at all and die in its presence. One
reason could be;
A. Many strains lack catalase and
superoxide dimutase that protect
cells from the destructive oxidizing
capabilities o f hydrogen peroxide
and superoxide ions, which are
normally produced under Aerobic
conditions.
B. The oxygen molecule kills every
living cell
C. The oxygen molecule inhibits
respiration o f the bacterial cells.
D. B and C
A. The bacteria are replicating DNA
and enzymes needed for the new
environment induced.
B. The cells increase in number but not
in size.
C. The cells are most permeable.
D. The number o f cells increases in
geometric progression.
E. B and D
57.Most Bacteria cells are more susceptible
to cell wall inhibitors during
A. Death phase
B. Stationary phase
C. Log phase
D. Lag phase
58.In Death phase o f bacterial growth curve
the concentration of viable cells decreases
at a geometric rate because;
A. There is accumulation o f toxic
wastes and autocatalytic enzymes
B. The type o f reproduction is changed
from binary fission to sexual
reproduction
C. The growth rate is equal to death
rate.
D. B and C
55.Bacteria reproduce by:
A.
B.
C.
D.
Sexual reproduction
Mitosis
Binary fission
Meiosis
56. Which o f the following are WRONG
about the Lag phase o f bacteria] growth
curve?
5 9. An energy production process that
releases energy through direct transfer of
high-energy phosphate groups from an
intermediate metabolic compound to
adenosine diphosphate (ADP) is:
A.
B.
C.
D.
Oxidative phosphorylation
Substrate- level phosphorylation
Glucogenesis
Fermentation
60. All o f the following are pathways
involved in the production o f pyruvic acid
in microorganisms EXCEPT:
A.
B.
C.
D.
Em bden-M eyerhofpathway
Enter-Doudoroff pathway
Hexose monophosphate pathway
Lactic acid fermentation
A. It is transcribed in to RNA that can
be translated into protein
B. It contains control signals that
ultimately control the synthesis o f
protein.
C. It can be mutated to alter specific
characteristics that are encoded by
genes.
D. It does not directly catalyze
biological reactions.
E. All o f the above
61 .In glycolysis glucose is oxidized to
pyruvic acid with a yield of:
A.
B.
C.
D.
3 moles o f ATP
2 moles o f ADP
1 mole o f ATP
2 moles o f ATP
66
62. The products o f butyric acid
fermentation by Clostridium are:
A.
B.
C.
D.
Butanol
Isopropanol
Acetone
All o f the above.
63.All o f the following are electron
transport systems EXCEPT:
A. Cytochromes
B. Ribosomes
C. Flavoproteins
D. Ubiquinones
64. Which one o f the following statements
is FALSE?
A. Bacteria have only one chromosome.
B. In bacteria Duplication o f the genetic
material occurs by semi
conservative replication
C. In bcteria the nuclear material is
attached to cell membrane and as
the cell grows, it separates the
daughter chromosomes
D. Genes are RNA segments that are
processed in two steps to produce
various proteins.
.Bacterial replication involves:
A. Duplication o f the DNA, which enables
the formation o f two identical daughter
cells.
B. Processing o f the genetic information to
synthesize proteins.
C. Synthesis o f RNA from DNA.
D. B and C
67.Repression o f enzyme activity inhibits
the synthesis o f the enzyme at
A.
B.
C.
D.
At replication level
At transcription level
At translation level
None
6 8.
All o f the following are mechanisms by
which microorganisms can change their
genetic constitution by transfer o f genetic
material EXCEPT:
A.
B.
C.
D.
Transduction
Conjugation
Translation
Transformation
69. The gene transfer mechanism associated
with recombinant DNA technology is:
A.
B.
C.
D.
Transcription
Transformation
Conjugation
Translation
65.The functions o f DNA include;
70. Which one o f the following is FALSE
about cloning?
A. It involves splicing a gene into
plasmid DNA (vector)
B. The plasmids do hot contain a gene
essential for cellular survival.
C. The vectors code for a phenotypic
trait that can be used to detect the
presence o f foreign DNA.
D. The vectors contain at least one
replicon and can be replicated
within the host even when they
contain foreign DNA.
71 .The transfer o f genetic material by
bacteriophage (viruses that infect bacteria)
is known as:
A.
B.
C.
D.
74.0ne o f the following causes blindness
and sexually transmitted diseases.
Transduction
Transcription
Translation
Transformation
72.In lysogenic bacteriophages the viral
DNA that does not replicate is known;
A.
B.
C.
D.
Plasmid
Prophage
Transposons
Triplet codons
A. Lytic phages enter the cell, replicate,
and package their DNA and then
lyse the cell to release mature
infective virions
B. In temperate phages the prophage
suppresses the lytic state by
synthesizing a protein known as a
repressor, which protects the cell
from further infection by a virus.
C. Some phages can change the cell’s
phenotype, which allows the
organism to elaborate materials
(exotoxins or virulence factors) that
are detrimental to the human host.
D. None
-
73. Which one of the following statements
is FALSE about bacteriophages?
A.
B.
C.
D.
Rickettsia rickettsii
Mycoplasma pneumoniae
Chlamydia trachomatis
Clostridium tetani
75. All o f the following are true about
chlamydia EXCEPT:
A. They have the ability to generate
ATP
B. They are obligate intracellular
parasites.
C. They have a two-phase life cycle
D. The infectious form is a dense non­
replicating cell that is resistant to
drying in the environment.
Answers
Microbiology
1. Answer: C. Viruses
Explanation
Viruses are considered as non-cellular, but medically significant entities. Fungi, bacteria and
protozoa are cellular organisms as they have cellular organization.
2. Answer: B. Their cells are biochemically the same as that o f eubacteria
Explanation
Archaera includes prokaryotes with cells that are biochemically different from eubacteria and
inhabit extreme hot, cold, pH, or saline environments.
3. Answer: E. All o f the above
Explanation
Eukarya contains microscopic organisms like fungi, protozoa and algae? along with macroscopic
organisms like fungi and algae, plants, and animals.
4. Answer: D. A and B
Explanation
Fungi are classified into phyla based on the type o f reproductive structures observed or lack o f
observable sexual structures.
5. Answer: C. Temperature
Explanation Dimorphic fungi exist in either unicellular (yeast) or filamentous (mold) phase
depending on the temperature.
6
. Answer: E. A and C
Explanation
Histoplasma and Blastomyces are dimorphic fungi.
7. Answer: A. Type o f motility
Explanation
Protozoa are unicellular, non-photosynthetic eukaryotes characterized by type o f motility.
Motility organs for Mastigophora - Flagella, Sarcodina - Pseudopodia, Ciliophora - Cilia and
Sporozoa - Non motile.
8
. Answer: E. Ascaris
Explanation
All o f the above are Protozoas except Ascaris which is a helminth.
9. Answer: E. All o f the above
Explanation
Viruses are classified by:
1. Capsid structure
2. Type o f nucleic acid
3. Envelope
4. Presence o f enzymes
10.Answer: B. Prions
Explanation Prions are infectious proteins, implicated in mad cow disease and kuru. Sporozoa
and Flagellates are Protozoas.
11 .Answer: D. All o f the above
Explanation
Bacteria are grouped and named primarily by morphology, Biochemical and metabolic
differences, and immunological and genetic relationships.
12.Answer: D. A and B
Explanation
In cultural morphology o f bacteria each colony originates from a colony-forming unit, consisting
o f a single cell or a group o f adherent cells.
13.Answer: B. Staining cannot be used as a classification system.
Explanation
Because o f their small size and relative transparency, bacteria must be stained to be visible with
the light microscope. Staining is also used as a classification system. For example Gram’s
staining is used to classify bacteria into Gram positive and Gram negative.
14.Answer: C. Gram stain
Explanation
A differential staining procedure that divides the bacterial cells into either gram-positive (purple)
or gram negative (pink) is Gram stain.
In Simple stain a single dye is used that colors the cells.
In Spore stain heat is used to facilitate the entrance o f the dye to the spore.
15.Answer: A. Acid Fast stain
Explanation
A staining procedure that stains cells that have an outer layer o f a waxy-lipid (acid fast) but not
those that lack this layer material (non acid fast) is Acid Fast Stain.
16.
Answer: C. To stain both the cell and the background, allowing visualization o f the unstained
capsular material
Explanation
In Capsule staining two dyes are used to stain the cell and the background, allowing visualization
o f the unstained capsular material.
17.
A nsw er: D. Treponema palladium
Explanation
Streptococci, Neisseria gonorrhea and Staphylococci are spherical in shape but Treponema
pallidium is helical shaped like corkscrew.
18. Answer: B. Staphylococci
Explanation
Spherical shaped bacteria that exist in clusters are known as Staphylococci.
Streptococci exist in chains while sarcinae are found in packets o f four or eight.
Vibrios are not spherical instead they are comma shaped bacilli.
19. Answer: D. Fusobacteria-Spherical
Explanation : Fusobacteria do not have spherical shape instead they have tapered end and are
slightly curved.
20. Answer: D. All o f the above
Explanation
Bacteria can be classified based upon:
]. The presence or absence o f spores
2. The presence or absence of capsules
3. Arrangement o f flagella and type o f motility
21 .Answer: C. Peritrichaete
Explanation
Bacteria can be classified depending on Motility and the type o f flagella.
1. Monotrichous a single flagellum at either pole.
2. Amphitrichous: flagella at both poles.
3. Lophotrichous: a flagellum at either pole.
4. Peritrichous: flagella distributed evenly over the entire cell.
22.Answer: D. They are more complex inside, but less complex outside.
Explanation
Prokaryotic cells (bacteria) are more complex outside and less complex inside.
23.
Answer: E. All of the above
Explanation:
Reasoning Prokaryotic cells lack a true nucleus, a Nuclear membrane and intracytoplasmic
membranous organelles (e.g. Plastids, Endoplasmic reticulum
24.Answer: A.70 S
Explanation: 70 S ribosomal units mediate Protein synthesis in prokaryotic cells.
25.Answer: A. Polypeptide
Explanation
The composition o f capsule shell differs between genera and usually is polysaccharide in nature;
however, the capsule o f Bacillus anthracis is Polypeptide in nature
26.
Answer: D. It kills the host cells
Explanation
The Capsule has several functions;
1. Increases the virulence (degree o f organism pathogenicity) o f a microorganism
2. Prevents phagocytosis o f the organism by macrophages and neutrophils.
3. Aids in adherence o f the organism to host cells
But it does not directly involve in killing o f the host cells.
27.Answer: B. Slime layer
Explanation If the polysaccharide o f a capsule is nonadherent, it is called a Slime layer.
28.
Answer: A. Loss o f Capsule
Explanation:
Transformation from smooth to rough colonies on bacterial media is indicative o f loss o f Capsule.
Concurrently there is a loss o f virulence.
29.Answer: D. B and C
Explanation
The capsular material is immunogenic, thereby inducing the production o f antibodies, which act
as opsonins to enhance phagocytosis (opsonization).
30.
Answer: D. AH o f the above
Explanation
The three parts, which comprise flagella, are Basal body, Hook and Filament.
31 .Answer: A. 2
Explanation
The number o f rings that make up the basal body o f flagella differ in gram- positive
(two) and gram-negative (four) organisms.
32.Answer: A. Components o f the cell wall.
Explanation
Most bacteria are designated as either gram-negative or gram-positive, based on fundamental
differences in the components o f the cell wall.
33.Answer: D. A and B
Explanation
The function o f cell walls in bacteria is
a. To provide the general shape o f the cell.
b. To protect the cell from osmotic shock.
Bacterial genetic information is arranged on a single super coiled circular strand o f DNA, the
nucleoid. It is not kept in the cell membrane
34.Answer: E. None
Explanation
All o f the above are true.
35.Answer: D. A and C
Explanation
Peptidoglycan is the basic layer of the cell wall in gram- Gram-negative and Gram-positive
bacteria. Gram-positive cells are deficient in lipids; however, Gram-negative cells are rich in
complex lipids (e.g., lipopolysacchride). Both types o f cell walls have cross-links between
polysaccharides.
36.Answer: B. Lipopolysaccharides
Explanation
Lipopolysaccharides are not present in cell wall o f Gram-positive cells.
37.Answer: D. They are found in both gram-positive and gram-negative bacteria
Explanation
Teichoic acids are found only in Gram-positive bacteria.
38.Answer: C. Lipid A
Explanation
Lipid A is the toxic portion that can slough off intact cells or be released into circulation upon
lysis o f the cell, causing nonspecific inflammation including diarrhea, fever, and septic shock.
39.
Answer: A. An area between the cell wall and the cytoplasmic membrane.
Explanation
The periplasmic space is an area between the cell wall and the cytoplasmic membrane
40.Answer: -A
41.Answer: -C
42.Answer: -B
43.Answer: -E
44.Answer: -D
45.Answer: C. Plasmids
Explanation
Plasmids contain the information for heavy metal and antibiotic resistance.
46.
Answer: D. All o f the above
Explanation
The proteins found in the Cytoplasmic membrane are engaged in;
- Transportation o f nutrients.
- Secretion o f exotoxins.
- Electron transport and energy formation
47. Answer: - A
48. Answer: -E
49. Answer: -B
50. Answer: -C
51. Answer: -D
52.Answer: C. Thermophile
Explanation
1. Psychophile: an organism that grow well at 0 °C, has optimal growth at 15 °C or less and a
maximum growth temperature o f 2 0 °C
2 . Mesophile: an organism with optim il growth temperature between 20 °C and 45 °C
3. Thermopile; an organism that can grow at 55 °C
4. Autotrophs are organisms, which us e carbon dioxide as their sole or main carbon source.
53.Answer: B. Facultative Aerobes
Explanation
Obligate Anaerobes do not tolerate oxj/ gen at all and die in its presence,
Facultative Anaerobes do not require ixygen but grow better in its presence,
Obligate Aerobes are completely depe ndent on oxygen for growth. Oxygen serves as terminal
electron acceptor in Aerobic respiratic n.
Facultative Aerobes have the ability tc grow with or without molecular oxygen.
54.nswer: A. Many strains lack catalj.:se and superoxide dimutase that protect cells from the
destructive oxidizing capabilities o f hy drogen peroxide and superoxide ions, which are normally
produced under Aerobic conditions.
Explanation
Many Obligate Anaerobes strains lack catalase and superoxide dimutase that protect cells from
the destructive oxidizing capabilities c f hydrogen peroxide and superoxide ions, which are
normally produced under Aerobic con ditions.
55.Answer : C. Binary fission
Explanation
Bacteria reproduce asexually by Bina ry fission.
Mitosis and meiosis are cellular even s involved in sexual reproduction.
56.Answer: E. B and D
Explanation
In the Lag phase o f bacterial growth the bacteria are rcplicating DNA and enzymes needed for the
new environment induced.
The cells increase in size but not number. During this phase o f growth, the cells are most
permeable.
The number o f cells increases in geometric progression in the Log phase.
57.Answer: C. Log phase
Explanation: Most Bacteria cells are more susceptible to cell wall inhibitors during the Log
phase of their growth. This is because the cell wall is being synthesized rapidly during this phase.
58.Answer: A. There is accumulation o f toxic wastes and autocatalytic enzymes
Explanation
In the Death phase o f bacterial growth curve the concentration o f viable cells decreases at a
geometric rate because there is accumulation o f toxic wastes and auto catalytic enzymes.
The type o f reproduction is not changed from binary fission to sexual reproduction or to any type
o f reproduction.
59.Answer: B. Substrate- level phosphorylation
Explanation
Oxidative phosphorylation removes electrons from organic compounds and passes these electrons
through a series o f electron acceptors along an electron transport chain, with molecular oxygen.
Substrate- level phosphorylation releases energy through direct transfer o f high-energy phosphate
groups from an intermediate metabolic compound to adenosine diphosphate (ADP).
Fermentation refers to energy-producing oxidative sequences, in which organic compounds serve
as both electron donors and acceptors.
Glucogenesis refers to the build up o f glucose from varieties o f substrates.
60.Answer: D. Lactic acid fermentation
Explanation
Lactic acid fermentation is the simplest process in which pyruvate is converted to lactate.
61 .Answer: D. 2 moles o f ATP
Explanation
In glycolysis glucose is oxidized to pyruvic acid with a yield
62. Answer: D. All o f the above
Explanation
o f 2 moles o f ATP.
The products o f bacterial butyric acid fermentation are Butanol, Isopropanol and Acetone.
63.Answer: B. Ribosomes
Explanation
Ribosomes are not electron transport systems they are Cellular units that synthesize protein by
translating messenger RNA base sequences in to amino acid protein sequences.
64.Answer: D. Genes are RNA segments that are processed in two steps to produce various
proteins.
Explanation
Bacteria have only one chromosome - a single, continuous (closed), double stranded, circular
piece o f DNA.
Duplication o f the genetic material occurs by semi conservative replication, in which two strands
o f the helix separate and at this point new strands are synthesized, bidirectionally, with the
originals serving as templates.
In bacteria the nuclear material is attached to cell membrane and as the cell grows, it separates the
daughter chromosomes. Therefore, each daughter cell has one original and one new strand.
Genes are DNA segments that are processed in two steps to produce various proteins
65.Answer: D. DNA docs not catalyze biological reactions
Explanation
DNA does not catalyze biological reactions, Enzymes act as catalysts in biological reactions.
66
.Answer: A. Duplication o f DNA..
Explanation
Bacterial replication involves duplication o f the chromosomal DNA, which enables the formation
o f two identical daughter cells.
Processing o f the genetic information to synthesize proteins is known as translation.
67.Answer: B. At transcription level
Explanation
Repression o f enzyme activity inhibits the synthesis o f the enzyme at transcription level (transfer
o f information from DNA to RNA)
68
.Answer: C. Translation
Explanation
Translation is the processing of genetic information to synthesize proteins. Transduction,
Conjugation and Transformation are mechanisms by which microorganisms can change their
genetic constitution by transfer of genetic material.
69.Answer: B. Transformation
Explanation
The gene transfer mechanism associated with recombinant DNA technology is transformation.
70.Answer: B. The plasmids do not contain a gene essential for cellular survival
Explanation
Plasmids cannot maintain stability unless they are beneficial to the host, so the plasmid should
contain a gene essential for cellular survival -either an enzyme required in a metabolic pathway
or a gene that resists certain antibiotics.
71 .Answer: A. Transduction
Explanation
Transduction is the transfer o f genetic material by bacteriophage (viruses that infect bacteria).
Transcription is the process by which information is transferred from DNA to RNA to produce
necessary proteins.
Translation is the processing o f genetic information to synthesize proteins.
Transformation involves the recipient cell taking up cell free, fragmented, (i.e. naked) DNA and
recombining genetic elements.
72.Answer: B. Prophage
Explanation
In lysogenic bacteriophages the viral DNA that does not replicate is known Prophage.
Plasmids are circular double-stranded pieces o f DNA that are found outside the bacterial
chromosome and transposons are genetic elements carried by plasmids.
Triplet codons (three nucleotides) are nucleotide bases used in the transfer o f genetic information
to protein synthesis.
73.Answer: D. None
Explanation All o f the above are true.
74.
Answer: C. Chlamydia trachomatis
Explanation
Rickettsia causes Rocky Mountain spotted fever.
Mycoplasma pneumoniae is the causative agent o f pneumonia.
Chlamydia trachomatis is a bacterium, which causes blindness and sexually transmitted diseases.
75.Answer: A. they have the ability to generate ATP
Explanation
Lack the ability to generate ATP; hence, they must obtain it from the host cell.
7. Which o f the following direct acting
adrenergic agonists affect betaj and beta 2
but not: alpha receptors?
A.
B.
C.
D.
E.
Dobutamine
Norepinephrine
Epinephrine
Isopreterenol
Phenylephrine
A.
B.
C.
D.
E.
12
.Apraclonidine is used
A.
B.
C.
D.
E.
. Which o f the following is given
systemically to treat nasal decongestion?
8
A.
B.
C.
D.
E.
Phenylephrine
Oxymetazoline
Xylometazoline
B and C
All the above
9. Which o f the adrenergic agonists
(sympathomimetic agents) are used in the
treatment o f hypertension?
A.
B.
C.
D.
E.
Alphal selective
Alpha 2 selective
Beta 1 selective
Beta 2 selective
Beta selective (nonselective beta
agonists)
10. Which o f the following is a WRONG
match between an adrenergic agonist and
its therapeutic application?
A. Isoproterenol; bronchodilator and
cardiac stimulant
B. Dobutamine; systemic
bronchodilator
C. Epinephrine; treatment of
anaphylactic reactions
D. Terbutaline: in the treatment o f
asthma
E. A and D
.Which o f the following agents is used to
prolong the activity o f local anesthetic
agents and in the treatment of glaucoma?
11
Dobutamine
Phenylephrine
Epinephrine
Terbutaline
Salmeterol
13.
As antihypertensive agent
Bronchodilator
Cardiac stimulant
Glaucoma
To lower intraocular pressure during
surgery
Which o f the following is NOT correct?
A. Prazosin is alphal-selective
adrenergic antagonists
B. Propranolol is beta2-selective
adrenergic antagonist
C. Phenoxybezamine is irreversible,
nonselective alpha-adrenergic
antagonist
D. Metoprolol is betal selective
adrenergic antagonist
E. Beta selective antagonists lose their
selectivity at high doses
14. A drug used for topical treatment o f
glaucoma is
A.
B.
C.
D.
E.
Prazosin
Propranolol
Phenoxybenzamine
Tolazoline
Timolol
15.A drug that is used in the treatment
hypertension and symptomatic treatment o f
benign prostatic hyperplasia,
A.
B.
C.
D.
Prazosin
Propranolol
Phenoxybenzamine
Tolazoline
E. Timolol
16. Which o f the following statements about
labetalol are correct?
I. It is a selective alpahl blocking agent
II. It is a nonselective beta blocking agent
III. It is used in the treatment o f
hypertension
A. i f l only is correct
B. if III only is correct
C. i f l and II are correct
D. if II and III are correct
E. if l, II and III are correct
17. Which o f the following is NOT true
about the therapeutic application o f
propranolol?
A. It can be used to reduce the
frequency and intensity o f migraine
headache
B. It is effective in the treatment o f
both supraventricular and
- ventricular dysrhythmias
C. It can be used safely in patients with
asthma
D. It can be used as a prophylactic
agent in angina pectoris
E. It can be used in the management of
hypertension
19. Which one of the following statements
about acetylcholine is wrong?
A. It is the endogenous
neurotransmitter released at
neuromuscular junction and at the
synapses o f parasympathetic nerves
B. It is the most potent cholinergic
agonist
C. Chemically it is an ester o f acetic
acid and the quaternary amino
alcohol(choline)
D. It is long acting cholinergic agonist
E. It is not a satisfactory therapeutic
agent
20. Which of the following is a direct acting
cholinergic agonist?
A.
B.
C.
D.
E.
Methacholine
echothiophate
physostigmine
isoflurophate
neostigmine
21 .In peripheral nervous system muscarinic
receptors are located at
A.
B.
18. Which o f the following are therapeutic
applications of phenoxybenzamine and
phentolamine?
C.
D.
A. Relieving vasospasm in Raynaud’s
syndrome
B. Management o f hypertensive
emergencies resulting from
pheochromocytoma
C. Management o f hypertensive
emergencies resulting from over
dosage o f sympathomimetic drugs
D. Management o f hypertensive
emergencies resulting from over
dosage o f MAO inhibitors
E.
the ganglia o f parasympathetic
nervous system
Neuromuscular junctions o f
somatic nervous system
Parasympathetic postganglionic
neuroeffector sites
the ganglia o f sympathetic
nervous system
All but C
22. Which of the following is NOT true
about the therapeutic application of
cholinergic agonists?
A. The direct-acting agonist
bethanechol can be used to initiate
B.
C.
D.
E.
micturition in acute nonobstructive
urinary retention
Both direct-acting and indirectacting cholinergic agonists are used
to cause mydriasis to aid in eye
examination
The indirect acting agonists can be
used in the diagnosis and therapy of
myasthenia gravis
The indirect acting agonist
edrophonium is used in the
treatment o f hypercholinergic crisis
Physostigmine, indirect acting
agonist, may be used in
counteracting the toxic effects o f
anticholinergic drugs
23.All the following are correct about
cholinergic antagonist EXCEPT
A. atropine is the prototypical drug in
this group
B. they are bulky analogues o f
acetylcholine
C. the quaternary ammonium
antimuscarinic agents are designed
to produce more central effect
D. they are able to interact with the
postganglionic receptors but they do
not have intrinsic activity
E. none
24.The drug o f choice for alleviating
motion sickness is
A.
B.
C.
D.
E.
Atropine
Scopolamine
glycopyrrolate
trihexyphenidyl
A and B
25. Which o f the following are true matches
between a cholinergic antagonist drug and
its therapeutic indication?
A. Benztropine; controls Parkinson’s
disease and some nurolepticinduced extrapyramidal disorders
B. Scopolamine; to induce sedation
C. Homatropine; to produce mydriasis
and cycloplegia
D. ipratropium; to treat bronchospasm
associated with chronic obstructive
pulmonary disease
E. All o f the above
26.A11 the following are adverse effects of
cholinergic antagonists EXCEPT
A.
B.
C.
D.
E.
Increased intraocular pressure
Dry mouth
Urinary retention
Diarrhea
Mydriasis
27. Which o f the following is NOT true
about the competitive, nondepolarizing
neuromuscular blocking agents?
A. They are bulky and rigid molecules
B. pancuronium is a competitive
nondepolarizing agent, which is a
synthetic steroid derivative
C. atracurium is a competitive
nondepolarizing agent, which is an
isoquinoline
D. The principal active alkaloid in
curare is metocurine
E. None
28. Which o f the following is NOT true
about succinylcholine?
A. It is a noncompetitive depolarizing
agent
B. It has slender aliphatic structure
C. It has a long duration o f action
D. A and B
E. None
29. All o f the following are therapeutic
indications of neuromuscular blocking
agents EXCEPT
A. To cause total unconsciousness of
the body
B. Promote skeletal muscle relaxation
and facilitate endotracheal
intubation
C. Relax the skeletal muscles and
facilitate bone replacement and
manipulation during orthopedic
procedures
D. Limit trauma associated with
skeletal muscle contraction during
electroconvulsive shock therapy
E. None
30.One o f the following is NOT the adverse
effect of succinylcholine
A.
B.
C.
D.
E.
Respiratory paralysis
Muscle fasciculation with pain
Decreased intraocular pressure
Increased intragastric pressure
Bradycardia
B. Should permit rapid recovery
immediately after cessation of
administration
C. Should induce anesthesia rapidly
and smoothly
D. Devoid o f adverse effects
E. All o f the above
34. Which of the following is CORRECT
about the inhalation anesthetics?
I
They are inhaled as gases or vapors
IT They are hydrophilic
III They are all organic compounds
A.
B.
C.
D.
E.
i f l only is correct
if III only is correct
i f l and II are correct
if II and III are correct
if I, II and III are correct
3 5. Which o f the following nonvolatile
anesthetics is ultra-short acting?
31 .Which of the following are the adverse
effects o f tubocurarine?
A.
B.
C.
D.
E.
Respiratory paralysis
Hypotension
Histamine release
bronchospasm
All o f the above
32. General anesthetics induce which o f the
following actions?
A.
B.
C.
D.
Analgesia
Loss o f consciousness
Amnesia
Inhibition of sensory and autonomic
reflexes
E. All o f the above
A.
B.
C.
D.
E.
Ketamine
-Thiopental
Diazepam
Morphine
All the above
36. Which o f the following intravenous
anesthetics should not be mixed with other
therapeutic agents before administration?
A.
B.
C.
D.
E.
Thiopental
Etomidate
Propofol
Diazepam
Morphine
37.Inhalation anesthetics are excreted
primarily through
33. Which o f the following are ideal
properties o f a general anesthetic?
A. A wide margin o f safety
A. The kidneys
B. The liver
C. The lungs
D. The skin
E. A and B
38. Which o f the following agents allow
reduction in the concentration o f inhalation
anesthetics required to produce anesthesia?
A.
B.
C.
D.
E.
Muscarinic antagonists
Skeletal muscle relaxants
Muscarinic agonists
Analgesics
All but C
39. One o f the following nonvolatile
anesthetics is administered intramuscularly
A.
B.
C.
D.
E.
Thiobarbiturates
Benzodiazepines
Ketamine
A and B only
All the above
40. Which o f the following previously
popular volatile anesthetics is no longer in
use due to toxicity?
A. Chloroform
B. Cyclopropane
C. Diethylether
D. B and C
E. All the above
41 .The uncharged, lipophilic form o f a
local anesthetic is necessary
A. Because it is the active form o f the
drug
B. For rapid penetration o f biological
membranes
C. To enhance the duration o f action
D. For interaction with the receptors on
the surface o f cell membrane
E. All the above
B. loss o f consciousness
C. Temporary loss o f sensation at their
administration site
D. Complete analgesia o f well-defined
parts o f the body
E. None
43.Epinephrine is added to many local
anesthetic preparations in order to
A. Increase the duration o f action o f the
local anesthetic
B. Decrease the systemic side effects
o f the local anesthetic
C. Initiate the action o f the local
anesthetics
D. Help enhance the effectiveness o f
the local anesthesia by causing
analgesia
E. A and B
44.In order to provide anesthesia for
surgery o f the lower limbs and pelvis, the
local anesthetics should be
A. Injected close to the innervating
nerve
B. Injected into the epidural space or
the subarachnoid space o f the spinal
chord
C. Applied locally as a cream
D. Infiltrated around the tissue site
E. Injected intramuscularly
45.The antipsychotic agents that lack the
ring nitrogen o f phenothiazines and have a
side chain attached by a double bond are
A.
B.
C.
D.
E.
Butyrophenones
Clozapine
Pimozide
Thioxanthenes
Molindone
42.One o f the following is NOT the action
o f local anesthetics
A. Reversible blockage o f nerve
impulse conduction
46.Antipsychotic drugs block dopamine
receptors in which part o f the brain to elicit
antispychotic action?
A.
B.
C.
D.
E.
Cortical
Limbic
Basal ganglia
A and B only
All the above
47.Many antipsychotic drugs have strong
antiemetic effect. This is due to the
blockade o f
A.
B.
C.
D.
E.
Muscarinic receptors
Seretonin receptors
Dopamine receptors
Hj-histamonergic receptors
Alphaj-adrenergic receptors
48.
Which o f the following is NOT correct
about the pharmacological effect o f the
atypical antipsychotics such as clozapine?
A. They are very weak antagonists at
the serotonin receptors
B. They can ameliorate a wide range of
symptoms better than the classic
antipsychotic agents
C. Their extrapyramidal effect is less
than that o f the classic antipsychotic
agents
D. All o f the above
49. One o f the following is NOT an
extrapyramidal symptom that may occur as
a result o f the centrally mediated adverse
effect o f antipsychotic drugs?
A.
B.
C.
D.
E.
Akathisia
Acute dystonia
Akinesia
Tardive dyskinesia
Poikilothermy
50. All o f the following are adverse effects
o f antipsychotic drugs EXCEPT
A. Drowsiness
B. Hyperprolactinemia
C. Weight loss
E. Bone marrow depression
51 .AH o f the following are used in the
treatment o f manic depression and bipolar
disease EXCEPT
A.
B.
C.
D.
E.
Chlorpromazine
Lithium
Valproic acid
Carbamazepine
None
52.The drug/class o f antidepression and
antimaniac drugs, which act by blocking
the CNS neuronal reuptake o f biogenic
amines
A.
B.
C.
D.
E.
Tricyclic antidepressants
MAO inhibitors
Selective serotonin inhibitors
Bupropion
Trazadone
53. An antidepressant drug/class o f drugs,
w'hich is approved clinically but has unclear
mechanism o f action,
A.
B.
C.
D.
E.
Tricyclic antidepressants
MAO inhibitors
Selective serotonin inhibitors
Bupropion
Trazadone
54.The drug/class o f drugs that act mainly
by blocking the intraneuronal oxidative
deamination o f brain biogenic amines,
A.
B.
C.
D.
E.
T ricyclic anti depressants
MAO inhibitors
Selective serotonin inhibitors
Bupropion
Trazadone
55.The drug/group o f drugs that act by
selectively inhibiting the reuptake o f
serotonin into the nerve terminal,
A. Tricyclic antidepressants
B. MAO inhibitors
C. Selective serotonin reuptake
inhibitors
D. Bupropion
E. Trazadone
56. Which o f the following antidepressants
are agents o f choice for the treatment of
endogenous depression?
I MAO inhibitors
II Tricyclic antidepressants
III Atypical antidepressants
A.
B.
C.
D.
E.
only
III only
I and 1 1 only
11 and III only
1,11 and III
Clomipramine
Imipramine
Fluoxetine
Doxepin
Fluvoxamine
58. Which o f the following should be
avoided in a patient taking MAO
inhibitors?
A.
B.
C.
D.
E.
A.
B.
C.
D.
E.
Dry mouth
Bone marrow depression
Constipation
Urinary retention
All but B
60. Which o f the following is/are no longer
used for their anxiolytic and sedativehypnotic effect?
A.
B.
C.
D.
E.
Benzodiazepines
Imidazopyridines
barbiturates
Azaspirodecanediones
None
1
57.The tricyclic/atypical antidepressant
drug that is used to treat enuresis is
A.
B.
C.
D.
E.
antidepressants, and atypical
antidepressants?
Sympathomimetic agents
Wine
Cheese
Sausage
All the above
59. Which o f the following adverse effects
is shared by MAO inhibitors, tricyclic
61 .Which o f the following benzodiazepines
are expected to show short duration of
action?
I Temazepam
II Lorazepam
III Oxazepam
IV Diazepam
A.
B.
C.
D.
E.
I and II only
II and III only
I, II, and III only
I, II, and IV only
1,11, III, and IV
62 .IV solutions o f diazepam are prepared
using propylene glycol. This is because
A. Propylene glycol enhances the
action o f diazepam
B. Diazepam is insoluble in aqueous
solutions
C. Diazepam is unstable in aqueous
solutions
D. Propylene glycol prolongs the
biological half-life of diazepam
E. B and C
63. Which o f the following is NOT true
about the structure activity relationship of
barbiturates?
A. Chemically barbiturates are 5,5disubstituted derivatives of
barbituric acid
B. Two side chains in position 5 are
essential for sedative-hypnotic
activity
C. Decreasing the urinary pH,
increases the excretion o f
barbiturates
D. The presence o f phenyl and ethyl
groups in position 5 makes the
barbiturates to be long acting
E. None
64. Which o f the following are correct about
the barbiturates, which have branched side
chains, unsaturated side chains, or side
chains longer than an ethyl group?
A. These barbiturates have increased
metabolic rate
B. They have shorter onset o f action
C. They have short duration o f action
D. They are more potent
E. All o f the above
65. Which o f the following is NOT true
about the ultra-short acting barbiturates?
A. They are the most effective
sedative-hypnotics
B. The oxygen in C2 is replaced by
sulfur
C. Thiopental is the prototype drug in
this class
D. They are highly lipophilic drugs
E. They are effective in facilitating the
induction o f anesthesia
.Which of the following is CORRECT
about the pharmacological action o f
benzodiazepines?
66
A. They act by inhibiting the release
neurotransmitter GABA
B. They act by binding to and
activating GABA receptors
C. They act by increasing the
efficiency o f GABAergic synaptic
inhibition
D. They act by blocking GABA
receptors
E. A and B
67. Which o f the following are actions o f
benzodiazepines?
A.
B.
C.
D.
E.
Hypnosis
Anesthesia
Anticonvulsant
Muscle relaxation
All o f the above
6 8 .All the following are correct about the
pharmacological action of
azaspirones/buspirone EXCEPT
A. They do not interact with the
GABA-chloride ionophore receptor
complexes
B. Buspirone appear to exert its
anxiolytic effects by acting as
partial agonist at 5-HTIA receptors
C. Buspirone has minimum abuse
liability
D. Buspirone enhances the depressant
effect o f alcohols and other CNS
depressant drugs
E. A and C
69.One of the following is NOT correct
about the pharmacology o f barbiturates.
A. They bind to the GABA-chloride
ionophore complex at a site
different from that o f
benzodiazepines
B. They are more selective in their
action than the benzodiazepines
C. Unlike benzodiazepine, they
increase the duration o f the GABAgated channel openings
D. They induce hepatic microsomal
drug-metabolizing enzyme activity
E. They may act as respiratory
depressants
70. Which o f the following is NOT true
about chloral hydrate?
A. It is commonly used to induce sleep
in pediatric or geriatric patients
B. It induces the hepatic microsomal
drug metabolizing enzyme activity
C. It is relatively cheap drug
D. Its metabolites do not show any
activity
E. It may be used as a preanesthetic for
minor surgical and dental
procedures
71 .The drug, which is not effective against
panic disorders but is used for generalized
anxiety states is:
A.
B.
C.
D.
E.
Buspirone
Zolpidem
Long-acting barbiturates
Chloral hydrate
Benzodiazepines
72. One o f the following Drug/drugs may be
used as antiepileptics
A.
B.
C.
D.
E.
Buspirone
Zolpidem
Long-acting barbiturates
Chloral hydrate
Benzodiazepines
73.A drug, which may be used to induce
sleep but cannot be used clinically for its
anxiolytic activity is:
A. Buspirone
B. Zolpidem
C. Long-acting barbiturates
D. Chloral hydrate
E. Benzodiazepines
74.All the following adverse effects are
associated with the use o f benzodiazepines
EXCEPT
A. CNS depression, drowsiness,
sedation
B. Leukopenia
C. Nausea, vomiting, diarrhea
D. Paradoxical excitement, insomnia,
rage reactions
E. Liability to abuse and dependence
75.Intravenous diazepam, phenytoin, and
Phenobarbital are used in the management
of
A.
B.
C.
D.
E.
Tonic-clonic seizures
Absence (petit mal) seizures
Status epilepticus
Psychomotor seizures
All the above
76. Which o f the following is NOT effective
against absence (petit mal) seizures?
A.
B.
C.
D.
E.
Phenobarbital
Clonazepam
Phenytoin
Valproic acid
Ethosuximide
77. Which o f the following are associated
with the use of antiepileptic drugs?
A.
B.
C.
D.
E.
Confusion, ataxia, dizziness
Allergic reaction
GI symptoms
Blood dyscriaisis
AH the above
78. Which o f the following antiepileptic
drugs are associated with arrhythmias and
gingival hyperplasia?
A.
B.
C.
D.
E.
Carbamazepine
Hydantoins
Barbiturates
Valproic acid
Succinimides
79. Which antiepileptic drug is associated
with the birth defects, neural tube defects,
which is caused as a result of
administration o f the drug during
pregnancy?
A.
B.
C.
D.
E.
Carbamazepine
Phenytoin
Valproic acid
A and B only
All the above
80. What is the prototypical dopaminergic
antiparkinsonian agent?
A.
B.
C.
D.
Benztropine
Levodopa
Bromocriptine
Pramipexole
81 .Which o f the following increases the
efficiency o f levodopa by inhibiting the
degradation o f levodopa derived dopamine
in the brain?
A.
B.
C.
D.
E.
Carbidopa
Tolcapone
Selegiline
A and B
Band C
82. All o f the following antiparkinsonian
agents act by binding directly and
activating dopaminergic receptors
mimicking the activity o f striatal dopamine
EXCEPT
A.
B.
C.
D.
E.
amantadine
bromocriptine
ropinirole
pergolide
pramipexole
83.The anticholinergic agents act as
antiparkinsonians because
A. They stimulate the release o f
dopamine in the caudate-putamen
B. They inhibit the degradation of
dopamine in the brain
C. They act as agonists at the
dopaminergic receptors
D. They block the excitatory
cholinergic system
E. All but B
84. Amantadine is indicated for the
treatment o f all o f the following EXCEPT
A.
B.
C.
D.
E.
Idiopathic parkinsonism
Tardive dyskinesia
postencephalitic parkinsonism
Arteriosclerosis parkinsonism
None
85. Which o f the following should NOT be
used in the treatment o f extrapyramidal
effects that result from the use o f
neuroleptic drugs?
A.
B.
C.
D.
E.
Selegiline
Anticholinergics
Antihistamines
Levodopa
None
8 6 .Which o f the following adverse effects
is NOT associated with the use o f
levodopa?
A. Nausea, vomiting, anorexia
B. Tachycardia, orthostatic
hypotension
C. Dyskinesia
D. Delusion, hallucination, confusion
E. Livedo reticularis
87. All the following are adverse effects o f
amantadine EXCEPT
A.
B.
C.
D.
E.
Drowsiness, dizziness, insomnia
Urinary retention and ankle edema
Dyskinesia
Hallucination, confusion
None
.Which o f the following phenanthrenes
have enhanced oral bioavailability but
decreased agonist potency?
88
A.
B.
C.
D.
E.
Codeine
Hydromorphone
Hydrocodone
Oxycodone
All but B
89. Which o f the following is NOT correct
about the structure activity relationship o f
opioid agonists and antagonists?
A. M orphine’s phenolic hydroxyl
group is extremely important for
activity
B. The methyl group in morphine can
be changed without significant
change in the agonist property
C. Agents that have a free phenolic
hydroxyl group and a tertiary amine
function are chemically amphoterics
with erratic oral absorption
D. The analgesic activity depends on a
p-phenyl-N-alklypiperidine moiety
E. A and D
90. Which o f the following opioids is a
strong agonist as well as has high oral
bioavailability?
A. Methadone
B. Propoxyphene
C. Levorphanol
D. Meperidine
E. A and C
91 .All the following are mixed agonistantagonist opioids EXCEPT
A.
B.
C.
D.
Naloxone
Nalbuphine
Betorphanol
Pentazocine
92. Which o f the following is NOT correct
about tramadol?
A. It is structurally unrelated to natural,
semisynthetic, or synthetic opioids
B. It has no clear benefits over opiates
C. Its metabolite rather than the parent
drug itself appears to be the active
agent
D. It is an analogue o f the endogenous
opioid peptides
E. B and C
93.Which o f the following is the action o f
opioid agonists?
A.
B.
C.
D.
E.
Analgesia
Euphoria
Sedation
Nausea and vomiting
All the above
94.Opioids may be used as
.Preanesthetic medicaments
II.
Adjunct to anesthetic agents
III. Primary anesthetic agents
I
A.
B.
C.
D.
E.
I only
I and II only
I and III only
II and III only
L 11 and III
95. Which of the following opioids are used
as antidiarrheals?
I.Codeine
II.
Loperamide
III. Diphenoxylate
IV. Dextromethrophan
A.
B.
C.
D.
E.
I and II only
II and III only
Ill and IV only
I, II and IV only
II, III and IV only
ANSW ERS
Nervous System and Drugs
1.
Answer: C. I and II
^Explanation:
Direct-acting adrenergic agonists interact directly with adrenergic receptors to elicit a response.
Two o f the direct-acting adrenergic agonists, norepinephrine and epinephrine, are endogenous
cathecholamines, which are biosynthesized from tyrosine.
D opam ine
2. Answer: B. Replacing the meta (3) hydroxyl group will result in loss o f direct-acting property
Explanation:
Although the meta (3) hydroxyl group is nccessary for direct a - and p-receptor activity, this is not
always the case because drugs in which the meta hydroxyl is replaced by a sulfonamide or a
hydroxymethyl group retain their activity.
3. Answer: C. I and II are correct
Explanation:
Cathecholamines are inactivated by methylation of the Meta hydroxyl group, which is catalyzed
i and by oxidative deamination, which is catalyzed by
monoamine oxidase (MAO). N-substitutibn with large groups makes the drugs to be (3-receptor
selective.
ch
I
4
gh
I
•N H -C H
3
OH I
HO
Adrenaline (Epinephrine):
M ore info:
Catecholamines (epinephrine, norepinephrine, and dopamine) cause general physiological
changes that prepare the body for phys cal activity (fight-or-flight response). Some typical
effects are increases in heart rate, blood pressure, blood glucose levels, and a general reaction^of
the sympathetic nervous system.
4. Answer: C. Their structure is very different from that o f the direct-acting adrenergic agonists
Explanation:
Indirect-acting adrenergic agonists ha^e structures that are similar to that o f catecholamines, but
they do not interact directly with adrenergic receptors. Their actions depend on the release o f
endogenous catecholamines either by displacement o f stored catecholamines from the adrenergic
nerve ending or inhibiting the reuptake o f catecholamines already released.
5.
Answer: B. Circular muscles o f tljie iris; constriction o f the pupil
Explanation:
j
Postjunctional alpha] adrenergic receptors are found in most vascular smooth muscles, radial
smooth muscles o f the iris, pilomotoi: smooth muscles o f the hair follicle, in the heart and in the
sphincter o f the GI tract. The effect o f agonists on these receptors is excitatory as a result o f
which they cause contraction o f the iris sphincter muscle. This causes mydriasis (i.e., widening of
the pupil).
More Info:
The adrenergic receptors (or adrenoceptors) are targets of the catecholamines adrenaline and
noradrenaline (called epinephrine and norepinephrine in the USA), and are activated by these.
There are several types of adrenergic receptors, but there are two main groups: a-Adrenergic and
|3-Adrenergic.
Receptor location andfunction:
a receptors
a l : Smooth muscles. In blood vessels the principal effect is vasoconstriction. Blood vessels with
a l receptors are present in the skin and the gastrointestinal system, and during the fight-or-flight
response vasoconstriction results in the decreased blood flow to these organs. This accounts for
an individual's skin appearing pale when frightened. In the GI tract, the effect is relaxation.
a2 are located in Pre- and postsynaptic nerve terminals and mediates synaptic transmission.
fS receptors
pi:
Heart and cerebral cortex.
In heart, agonists enhance myocardial contractility and increase heart rate. Also found on
juxtaglomerular cells, activation results in renin release.
P2:
Lungs, smooth muscle, cerebellum, and skeletal muscle.
•
•
In lung, agonists cause bronchiole dilation (useful in asthma treatment).
In smooth muscle, relaxes walls. Relaxes uterine muscle and promotes
release o f insulin.
P3:
Adipose tissue.
Agonists enhance lipolysis (breakdown o f fat stored in fat cells).
6.
Answer: B. II and III
Explanation:
Stimulation o f beta adrenoceptors causes relaxation o f most kind o f smooth muscles by
increasing cAMP formation. Bronchial smooth muscles contain beta2 receptors that cause
relaxation. Activation o f these receptors thus results in bronchodilation. In the vascular system,
there is beta2 mediated vasodilation, which is mainly endothelium dependent and mediated by
nitric oxide release. It occurs in many vascular beds and is especially marked in skeletal muscle.
7. Answer: D. Isoproterenol
Explanation:
Direct acting adrenergic agonists are those, which primarily act by direct stimulation o f
adrenergic receptors. They may be selective to a particular receptor subtype or they may be
nonselective in that they can activate a variety o f receptor subtypes. Examples o f those which are
selective, include clonidine (alpha2), dobutamine (betal), phenylephrine (alphal) and terbutaline
(beta2). Examples o f nonselective agonists include, norepinephrine (all but especially alphal,
alpha2, and betal), epinephrine (alp h al, alpha2, b e ta l, and beta2). Isoproterenol a nonselective
beta activator has no effect on alpha receptors.
8. Answer: A. Phenylephrine
Explanation:
Phenylephrine is direct acting alpha! agonist, which is given systemically to treat nasal
decongestion. Oxymetazoline and xylometazoline, which are also alpha 1 agonists, are used as
topical decongestants because o f their ability to promote constriction o f nasal mucosa.
9. Answer: B. Alpha 2 selective
Explanation:
Alpha2 selective agonists have a paradoxical ability to reduce blood pressure through actions in
local application may cause vasoconstriction. These
agents, which include drugs like clonidine, methyldopa, guanfacine, guanabenz. etc, are used as
antihypertensives.
10.Answer: B. Dobutamine; systemic bronchodilator
Explanation:
!
Dobutamine is a betal selective agonist (and thus does not have effect on the lung) and is used to
improve myocardial function in CHF n emergency situations. Isoproterenol is a nonselective
beta agonist, which can be used as a bronchodilator and as a cardiac stimulant in shock and
cardiac arrest. Epinephrine is nonseleittive alpha and beta adrenergic agonist. It is the preferred
agent for treating anaphylactic reactions (because o f its great efficiency at alpha, betal and beta2
rcceptors, since stimulation o f all three is helpful in reversing the pathophysiologic process) and it
is also used to treat hypersensitivity reactions. Terbutaline, like the other beta2 selective agonist
has both systemic and local bronchodilation effect as a result o f which they have achieved a
special place in the treatment o f asthma.
11 .Answer: C. Epinephrine
Explanation:
Because o f their ability to constrict bjlood vessels and thus reduce blood flow, epinephrine (and
also phenylephrine) is used to reduce the diffusion o f local anesthetics away from the site o f
administration. This way they can be used to prolong the activity o f local anesthetics and reduce
the total dose. Epinephrine has also the ability to decrease intraocular pressure by enhancing the
outflow o f aqueous humor and decreasing the production of aqueous humor through
vasoconstriction. Hence, it is used in the treatment o f glaucoma.
12. Answer: E. To lower intraocular pressure during surgery
Explanation:
Apraclonidine is an alpha2 selective agonist that is used to lower intraocular pressure during
surgery.
13.Answer: B. Propranolol is beta2-selective adrenergic antagonist
Explanation:
Propranolol is a nonselective beta adrenergic antagonist.
14.Answer: E. Timolol
Explanation:
Timolol, which is a nonselective beta-blocker has the ability to decrease ciliary body production
o f aqueous humor and thus can be used in the topical treatment o f glaucoma.
15.Answer: A. Prazosin
Explanation:
Prazosin causes the relaxation of both arterial and venous smooth muscle, which makes it
effective in the management o f hypertension. It is also used to relieve prostatic obstruction and
increase urine flow in patients with benign prostatic hyperplasia.
16.
Answer: E. I, II and III are correct
Explanation:
Labetolol is a reversible adrenoreceptor antagonist available as a racemic mixture o f two pairs o f
chiral isomers. The SS and RS isomers are inactive, SR is a potent alphal —selective blocker,
and the RR isomer is a potent beta blocker. Labetalol is used in the management o f
hypertension.
MO
OH
17. Answer: C. It can be used safely in patients with asthma. ( NOT True)
Explanation:
Propranolol is a nonselective beta adi energic blocker. Therefore, beta-2-receptor blockade
associated with the use o f such as agent commonly causes worsening o f preexisting asthma and
other forms o f airway obstruction with 3ut having these consequences in normal individuals. In
fact, a relatively trivial asthma may bee<ome severe after beta blockade.
18. Answer: E. AH o f the above
Explanation:
All the given choices are the therapeut c applications o f phenoxybenzamine and phentolamine.
19. Answer: D. It is long acting cholin :rgic agonist
Explanation:
After relaying a nerve impulse, acetylicholine is rapidly broken down by the enzyme
cholinesterase. Therefore, it is extremiely short acting, which makes it not suitable to be used as a
therapeutic agent.
20.Answer: A. Methacholine
Explanation:
The direct acting cholinergic agonists bind and activate muscarinic or nicotinic receptors. They
are produced by replacing the acetyl giftoup o f acetylcholine with a carbamoyl group or by
substituting a methyl group o f the beta ■carbon. This renders them more tolerant to the action o f
acetylcholinesterase and thus long actin:g agents.
Examples include methacholine and thanechol. By inhibiting acetlycholinesterase, the indirect
acting drugs increase the concentration o f endogenous acetylcholine in the synaptic clefts and
neuroeffector junctions, and the excess acetylcholine in turn stimulates cholinergic receptors to
evoke increased response. Examples in elude the long acting, irreversible agents, such as
isoflurophate and echothiophate, and th e short acting, reversible agents such as physostigmine
and neostigmine.
21. Answer: C. Parasympathetic postganglionic neuroeffector sites
Explanation:
Peripheral nervous system muscarinic receptors are present at parasympathetic postganglionic
neuroeffector sites. Peripheral nervous system nicotinic receptors are present at the ganglia o f
parasympathetic nervous system, neuromuscular junctions o f somatic nervous system, at the
ganglia o f sympathetic nervous system.
22.Answer: B. Both direct-acting and indirect-acting cholinergic agonist are used to cause
mydriasis to aid in eye examination
Explanation:
Muscarinic agonists, both direct acting and indirect-acting, instilled into the conjunctival sac
causes contraction o f the smooth muscle o f the iris sphincter (which results in miosis) and o f the
ciliary muscle (which results in accommodation). As a result, the iris is pulled away from the
angle o f the anterior chamber, and the trabecular meshwork at the base o f ciliary muscle is
opened up. Both effects facilitate the outflow o f aqueous humor into the canals o f Schlemm,
which drains the anterior chamber. This makes them useful in the treatment o f glaucoma.
23.Answer: C. the quaternary ammonium antimuscarinic agents are designed to produce more
central effect
Explanation:
The presence o f quaternary or tertiary nitrogen in these agents determines the spectrum o f
activity, in that the quaternary ammonium antimuscarinic drugs have more peripheral effect with
reduced central nervous system effect. The tertiary ammonium analogues are used for their effect
on the eye and central nervous system since they can cross lipid barriers.
24.Answer: B. Scopolamine
Explanation:
Certain vestibular disorders respond to antimuscarinic drugs. Scopolamine, an antimuscarinic
agent, is one o f the oldest remedies for motion sickness and is still as effective as any other more
recently introduced agents. It can be given by injection, mouth or by means o f a transdermal
patch.
25.
Answer: E. All o f the above
Explanation:
All the given choices are the correct matches.
26. Answer: D. diarrhea
Explanation:
Blockade o f muscarinic receptors he.s dramatic effects on the motility and some o f the secretory
functions o f the gut. Motility o f GI smooth muscles is affected from the stomach to the colon.
In general, the walls o f the viscera are relaxed, and both tone and propulsive movements are
diminished. Therefore, cholinergic E.ntagonist could be used to treat diarrhea and may cause
constipation as an adverse effect.
27.Answer: D. The principal active ajlkaloid in curare is metocurine
Explanation:
Curare is an alkaloid extract from the bark o f South American tree (Strychnos and
Chondodendron species) that relaxes and paralyzes voluntary muscles. The principal active
alkaloid in curare is tubocurarine. Me ocurine is the trimethyl derivative o f tubocurarine. Their
most important structural feature is th 5 presence o f a tertiary-quaternary amine in which the
distance between the two cations is fix ed at about 14 angstroms twice the length o f the critical
receptor binding moiety o f acetylchol me.
28. Answer: C. It has a long duration o f action
Explanation:
Succinylcholine has extremely brief d uration o f action since it is rapidly hydrolysed by
pseudocholinesterase (butyrylcholine:sterase), an enzyme o f the liver and plasma.
29.Answer: A. To cause total unconsiciousness o f the body
Explanation:
The main aim o f using neuromuscular blocking agents is to cause only skeletal muscle paralysis
while the patient remains conscious and capable o f sensation. Before the introduction of
neuromuscular blocking drugs, adequate skeletal muscle relaxation could only be achieved by
deep anesthesia that was often associated with hazardous depressant effect on various organ
systems, especially cardiorespiratory system. The neuromuscular blocking agents have made it
possible to achieve adequate muscle relaxation for all surgical requirements without the
depressant effects o f deep anesthesia. Therefore, neuromuscular drugs are used not to cause total
unconsciousness o f the body but rather to avoid it.
30.Answer: C. Decreased intraocular pressure
Explanation:
Administration o f succinylcholine is followed by an increase in intraocular pressure that is
manifested 1 minute after injection, nlaximum at 2-4minutes, and subsides after 5 minutes. The
mechanism for this effect has not bee n clearly defined, but it may involve contraction o f tonic
myofibrilis or transient dilation o f ch aroidal blood vessels.
31 .Answer: E. All o f the above
Explanation:
Tubocurarine causes all o f the given adverse effects.
32. Answer: E. All o f the above
Explanation:
In addition to the above, general anesthetics can cause skeletal muscle relaxation in many cases.
33. Answer: E. All o f the above
Explanation:
An ideal anesthetic drug would induce anesthesia rapidly and smoothly.
34.Answer: A. I only
Explanation:
Volatile general anesthetics act by interacting with the lipid bilayer o f cell membranes, causing
depressed excitability. Therefore, in order to interact with the cell membrane, they must be
lipophilic in nature. Volatile general anesthetics include the inorganic agents such as nitrous
oxide, and the nonflammable halogenated hydrocarbons (e.g., halothane), and ethers (e.g.,
methoxyflurane, isoflurane).
35.Answer: B. Thiopental
Explanation:
In general, the water-soluble intravenous anesthetics, which include the barbiturates (e.g.,
thiopental), cyclohexylamines (e.g., ketamine), benzodiazepines (e.g., diazepam), butyrophenones
(e.g., droperidol), and opioid analgesics (e.g., morphine), are short acting. However, the
barbiturates are even ultra-short acting. For example, following intravenous administration,
thiopental rapidly crosses the blood brain barrier, and if given in sufficient dosage, produces
hypnosis in one circulation time.
36.Answer: C. Propofol
Explanation:
Propofol, a dialkylphenol, which is prepared as an emulsion, should not be mixed with other
therapeutic agents before administration.
37.Answer: C. The lungs
Explanation:
Because they are volatile gases, inhalation anesthetics are absorbed and primarily excreted
through the lungs.
38.
Answer: D. Analgesics
Explanation:
Usually the inhalation anesthetics are administered along with other therapeutic agents that serve
different purposes. For example, adminislration o f analgesics allows the reduction in the
concentration o f the inhalation anesthetics required to produce anesthesia. Skeletal muscle
relaxants are added to cause adequate muscle relaxation during surgery, and antimuscarinic
agents to decrease bronchiolar secretions
39.Answer: C. Ketamine
Explanation:
In general, nonvolatile anesthetics are administered intravenously (e.g., thiobarbiturates,
benzodiazepines). However, there are some agents such as ketamine that are administered
intramuscularly.
40. Answer: A. Chloroform
Explanation:
Chloroform is no more used because of its toxicity while cyclopropane and diethylether are not
used because o f their flammable and ex “>losive properties.
41 .Answer: B. For rapid penetration o f biological membranes
Explanation:
The cationic form o f the drug is the active form o f the drug that blocks generation o f action
potentials at the membrane receptor co(mpIex (cationic drugs cannot readily leave closed
channels). This site o f anesthetic actioiji is found on the inner surface o f the membrane. So it is not
accessible from the external side o f the cell membrane. Therefore, the anesthetic agent must be
able to cross the cell membrane, and tile lipophilic form o f the drug allow diffusion across
connective tissue and cell membranes. Once inside the cell, the drug becomes ionized to a
chargcd ammonium cation, which is the active form. Moreover, this charged form of the drug is
not able to penetrate cell membrane aijid thus remains trapped inside the cell, thereby enhancing
the duration o f action.
42.Answer: B. Loss o f consciousnes
Explanation:
Local anesthetics are capable o f reveitsibly blocking nerve impulse conduction and thus produce a
reversible loss o f sensation at the site o f administration as well as a temporary but complete
analgesia o f well-defined parts o f the body. However, they do not cause loss o f consciousness.
43.Answer: E. A and B
Explanation:
Epinephrine is a vasoconstrictor and when included in local anesthetic preparations, it reduces
vascular blood flow at the administration site. This reduces systemic absorption, and hence
prolongs the duration o f action and reduces systemic toxicity.
44. Answer: B. Injected into the epidural space or the subarachnoid space o f the spinal chord
Explanation:
The effect o f local anesthetic agents on a particular body part depends up on the site of
application o f the agent. When injected close to the innervating nerve, they produce regional
nerve block for relief o f pain; when infiltrated around the tissue, they provide anesthesia for
minor operations; when applied locally, they provide anesthesia o f the skin and mucous
membrane. And in order to provide anesthesia for surgery o f the lower limbs and pelvis, the local
anesthetics should be injected into the epidural space or the subarachnoid space o f the spinal
chord.
45. Answer: D. Thioxanthenes
Explanation:
Thioxanthenes (e.g., thiothixene) lack the ring nitrogen o f phenothiazines and have a side chain
attached by a double bond. In general, these compounds are slightly less potent than their
phenothiazine analogues. Butyrophenones, o f which haloperidol is the most widely used, has a
very different structure from those o f thioxanthene and phenothiazines. Clozapine, pimozide, and
molindone are examples o f newer drugs that have varied structures.
Haloperidol
O
I!
.
C — (CH-,)-,— N
HALPER1DOL
46.Answer: D. A and B only
Explanation:
Antipsychotic drugs block dopamine rec|eptors in cortical and limbic areas o f the brain to elicit
antispychotic action.The blockade o f dopamine receptors in the basal ganglia by these agents
results in the adverse extrapyramidal effects such as parkinsonism- like syndrome, akathisia and
acute dystonic reactions.
47.Answer: C. Dopamine receptors
Explanation:
The majority o f the antipsychotic drugs! have effects other than their main action, which are
related to their interaction with muscarinic receptors, seretonin receptors, H]-histamonergic
receptors, Alphar adrenergic receptors.) The strong antiemetic effect is, however, related to the
blockade o f dopamine receptors both centrally (in the chemoreceptor trigger zone o f the medulla)
and peripherally (on receptors in the stomach).
48.Answer: A. They are very weak antagonists at the serotonin receptors.
Explanation:
The atypical antipsychotic agents are strong antagonists at the serotonin receptors in addition to
their blockade o f dopamine receptors
49.Answer: E. Poikilothermy
Explanation:
Poikilothermy is the inability to reguljate body temperature, which can fluctuate according to the
temperature o f the surroundings. It is also centrally mediated adverse effect o f antipsychotic
drugs.
50.Answer: C. Weight loss
Explanation;^
Increased appetite and weight gain (not weight loss) are common adverse effects associated with
antipsychotic drugs, which require close monitoring o f food intake.
51 .Answer: A. Chlorpromazine
Explanation:
Chlopromazine is phenothiazine, which is used in the treatment o f Psychosis. The element
lithium, in the form o f carbonate salt, is used to treat depression and dipolar disease, so do the
organic compounds Valproic acid and carbamazepine.
52.Answer: A. Tricyclic antidepressants
Explanation:
By blocking the amine reuptake pumps, tricyclic antidepressants reduce CNS neuronal reuptake
o f the biogenic amine and thus prolonging the synaptic availability o f the biogenic amines and
hence their action at central aminergic receptors.
53.Answer: D. bupropion
Explanation:
Bupropion is an antidepressant drug, which is approved for clinical use but its mechanism o f
action remains unclear.
54.Answer: B. MAO inhibitors
Explanation:
MAO inhibitors block the major degradative pathway for the amine neurotransmitters, which
permit more amines to accumulate in presynaptic stores and more to be released.
55.Answer: C. selective serotonin reuptake inhibitors
Explanation:
As their name indicates selective serotonin reuptake inhibitors inhibit serotonin reuptake into the
nerve terminals, thus prolonging the synaptic activity o f the amine.
56.
Answer: D. ]I and III only
Explanation:
Tricyclic and atypical antidepressants are the agents o f choice in the treatment o f endogenous
depression. MAO inhibitors are indicated to treat depression, phobic anxiety and narcolepsy that
have not responded to other treatments. Their adverse effects limit their use.
57.Answer: B. Imipramine
Explanation:
In addition to their use in the treatment of endogenous depression, many individual tricyclic and
atypical antidepressants may be used to treat various disorders. For example, imipramine is used
to treat enuresis; clomipramine, fluoxeti ne, and fluvoxamine are used in obsessive-compulsive
disorder; and doxepin for anxiety.
58.Answer: E. All the above
Explanation:
MAO inhibitors, by increasing stores o f cathecholamines, sensitize the patient to indirectly acting
sympathomimetics such as tyramine, Which is found in some fermented foods and beverages
(such as wine, cheese, sausage), and to sympathomimetic drugs that may be administered
therapeutically. Such sensitization can result in dangerous hypertensive crisis.
59.Answer: E. All but B
Explanation:
Dry mouth, bone marrow depression, and urinary retention are all symptoms o f
antimuscarinic activity, which is sho wn by all the three classes o f antidepressants. Bone marrow
depression is the adverse effect o f onH some tricyclic antidepressants.
60.Answer: C. barbiturates
Explanation:
Anxiolytics and sedative-hypnotic agients in current use include the highly effective
benzodiazepines and the atypical azas pirodecanediones and imidazopyridines. Other classes of
drugs, which were used previously su<eh as the barbiturates, meprobamate and hydroxyzine are no
longer used due to some o f their limitaitions, which include liability to produce tolerance, physical
dependence, severe withdrawal reactions,, and serious toxicity with over dosage.
61.Answer: C. I, II, and III only
Explanation:
Benzodiazepines with 3-hydroxyl grolup (e.g., temazepam, lorazepam, and oxazepam) are
susceptible to metabolism by phase II glucuronidation and thus, are short acting. Benzodiazepines
that lack a 3-hydroxyl group (e.g., diazepam) must first undergo phase 1 metabolism, which
include N-dealkaylation and 3-hydroxylation. Therefore, these drugs are long acting.
Moreover, many long acting benzodiazepines can form phase-I metabolites that are active, with
half-lives greater than that o f the pare nt drugs.
CH3
o
OH
Cl
c 6h 5
TEMAZEPAM
CH 3
Cl
OXAZEPAM
LORAZEPAM
0
Cl
C 6H5
DIAZEPAM
62.Answer: B. Diazepam is insoluble in aqueous solutions
Explanation:
Some benzodiazepines that lack an amino side chain, such as diazepam, are not basic enough to
form water-soluble salts with acids. Therefore, IV solutions o f diazepam are prepared by using
propylene glycol as a solvent.
63.
Answer: C. decreasing the urinary pH, increases the excretion o f barbiturates
Explanation:
Barbiturates and many o f their metabolites ar