TERM REVIEW
INTRODUCTION TO PHARMACOLOGY
Why Study Pharmacology?
• Medical Errors – top 3 cause of death
in US (next to heart disease and
cancer)
• Medication error is the leading type of
medical error, causing 134 million
adverse events and
• 2.6 million deaths each year.
• Outside
documentation
and
communication, medication-related
task took most of the nurse’s
• time in a shift.
• Medication administration is the last
task involved in pharmacotherapy.
Medication Errors Originate & are
Intercepted
Prescribing
Origination 39%
Interception 48%
Transcribing
Origination 12%
Interception 33%
Dispensing
Origination 11%
Interception 34%
Administration
Origination 38%
Interception 2%
Drug Development
Agonist- a drug that binds to and stimulates
the activity of one or more receptors in the
body
Bioavailability-a measure of the extent of
drug absorption for a given drug and route
(from 0% to 100%)
Dependence-a state in which there is a
compulsive or chronic need, as for a drug
Idiosyncratic reaction- an abnormal and
unexpected response to a medication, other
than an allergic reaction, that is peculiar to
an individual patient
Adverse drug event-any undesirable
occurrence related to administering or
failing to administer a prescribed medication
Adverse drug reaction-any unexpected,
unintended, undesired, or excessive response
to a medication given at therapeutic dosages
Teratogenesis- the development of
congenital anomalies or defects in the
developing fetus
First pass effect-the initial metabolism in
the liver of a drug absorbed from the
gastrointestinal tract before the drug reaches
systemic circulation
Pharmaceutics- the science of preparing
and dispensing drugs, including dosage form
design
Half life- the time required for half of an
administered dose of a drug to be eliminated
by the body
Orphan drugs-a special category of drugs
that have been identified to help treat
patients with rare disease
Synergistic effects-drug interactions in
which the effect of a combination of two or
more drugs with similar actions is greater
than the sum of the individual effects
Tolerance-reduced response to a drug after
prolonged use
Trade name or propriety- the commercial
name given to a drug product by its
manufacturer
Trough level- the lowest concentration of
drug reached in the body
Steady state- the physiologic state in which
the amount of drug removed via elimination
is equal to the amount of drug absorbed with
each dose
Pharmacodynamics-the study of the
biochemical and physiologic interactions of
drugs at their sites of activity
Pharmacokinetics- the study of what
happens to a drug form the time it is put into
the body until the parent drug and all
metabolites have left the body.
Pharmacotherapeutics- the treatment of
pathologic conditions through the use of
drugs
Iatrogenic Effects- unintentional adverse
effects that are caused by the actions of a
prescriber, other health care professional, or
by a specific treatment
PHARMACOTHERAPEUTICS
- Is the branch of pharmacology
that uses drugs to treat, prevent
and diagnose.
PHARMACODYNAMICS
- Study of biochemical and
physiological effects of drugs;
study of drugs mechanism of
action.
PHARMACOKINETICS
- Study
of
the
absorption,
distribution,
and
biotransformation (metabolism)
and excretion of drugs.
PHARMACOGNOSY
- Study of drugs derived from
herbal and other natural sources.
TOXICOLOGY
- Study of poisons and poisoning.
SOURCES OF DRUGS
• Plants
• Animals
• Minerals
• Synthetic chemical
•
DRUG CLASSIFICATIONS
Drugs are classified according to
their effects on particular body
systems, their therapeutic uses.
A. PRESCRIPTION DRUGS
- Are those that have on their labels the
prescription legend.
- May be prescribed by the physicians,
dentists, veterinarians, or other
legally authorized health
- practitioner as part of their specific
practice.
B. NON-PRESCRIPTION DRUGS
- The drugs that may be legally
acquired by the client without the
prescription order.
- Also known as over the counter drugs
(OTC)
C. INVESTIGATIONAL DRUGS
- A new drug which a manufacturer
wishes to market.
- Must fulfill the requirements of FDA.
D. ORPHAN DRUG
- Are drugs that have been discovered
but are not financially viable and
therefore have not been “adopted” by
any drug company.
E. ELLICIT DRUG
- a.k.a. “street” drugs are those which
are used and/or distributed illegally.
Legal Regulation of Drugs
A. FDA Pregnancy Categories
B. Controlled Substances
A. FDA Pregnancy Categories
Category A
- Adequate studies in pregnant women
have NOT demonstrated a risk in the
fetus in the first trimester of
pregnancy and there is no evidence
of risk in later trimester.
Category B
- Animal
studies
have
NOT
demonstrated a risk for the fetus but
there are No adequate studies in
pregnant women, or animal studies
have shown an adverse effect, but
adequate studies in pregnant women
have not demonstrated a risk to the
fetus during the first trimester, and
there is no evidence of risk on later
trimester.
Category C
- Animal studies have shown an
adverse effect on the fetus but there
are no adequate studies in humans,
the benefits from the use of the drug
in pregnant women may be
acceptable despite the potential
risks, or there are no animal
reproduction
studies
and
no
adequate studies in humans.
Category D
- There is evidence of human fetal risk,
but the potential benefits from the use
of the drug in pregnant women may
be acceptable despite of its potential
risks.
B. Controlled Substances
Schedule I
- Drugs that are not approved for
medical use and have high abuse
potentials: heroin, lysergic acid
diethylamide
(LSD),
peyote,
mescaline,
tetrahydrocannabinol,
marijuana.
Schedule II
- Drugs that are used medically and
have high abuse potentials: opioid
analgesics
(eg,
codeine,
hydromorphone,
methadone,
meperidine, morphine, oxycodone,
oxymorphone),
central
nervous
system (CNS) stimulants (eg,
cocaine,
methamphetamine,
methylphenidate), and barbiturate
sedative-hypnotics
(amobarbital,
pentobarbital, secobarbital).
Schedule III
- Drugs with less potential for abuse
than those in Schedules I and II, but
abuse may lead to psychological or
physical dependence: an- drogens
and anabolic steroids, some CNS
stimulants (eg, benzphetamine), and
mixtures containing small amounts of
controlled substances (eg, codeine,
barbiturates not listed in other
schedules).
Schedule IV
- Drugs with some potential for abuse:
benzodiazepines (eg, diazepam,
lorazepam,
temazepam),
other
sedative
hypnotics
(eg,
phenobarbital, chloral hydrate), and
some
prescription
appetite
suppressants
(eg,
mazindol,
phentermine).
Schedule V
- Products
containing
moderate
amounts of controlled substances.
They may be dispensed by the
pharmacist without a physician’s
prescription
but
with
some
restrictions regarding amount, record
keeping, and other safeguards.
Included are antidiarrheal drugs,
such as diphenoxylate and atropine
(Lomotil).
CLASSIFICATIONS
Two Systems:
1. Anatomical Therapeutic Chemical
(ATC) Classification System
2. American Hospital Formulary System
(AHFS) Pharmacologic Therapeutic
Classification System®
Anatomical Therapeutic Chemical (ATC)
Classification System
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-
The
GENERIC
NAME
(eg,
amoxicillin) is related to the chemical
or official name and is independent of
the manufacturer.
Differentiated from Trade Name by
initial
lowercase
letter;
NOT
CAPITALIZED...
The TRADE NAME is designated and
patented by the manufacturer.
- CAPITALIZED FIRST LETTER
- For
example,
amoxicillin
is
manufactured
by
several
pharmaceutical companies, some of
which assign a specific trade name
(eg, Amoxil, Trimox)
CHEMICAL NAME is the exact molecular
formula of the drug; usually a long, very
difficult name to pronounce and of a little
concern to the health care worker.
OFFICIAL NAME is the name of the drug as
it appears in the official reference, the
USP/NF; generally, the same as the generic
name.
•
DRUG NAMES
Individual drugs may have several
different names, but the two most
commonly used are the
GENERIC NAME and the TRADE NAME
(also called the brand or proprietary name).
PRESCRIPTION AND
NONPRESCRIPTION DRUGS
• Legally, consumers have two routes
of access to therapeutic drugs.
•
•
One route is by PRESCRIPTION or
order from a licensed health care
provider, such as a physician, dentist,
or nurse practitioner.
The other route is by OVER-THECOUNTER (OTC) purchase of drugs
that do not require a prescription.
•
PHILIPPINE NATIONAL DRUG
FORMULARY
•
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DRUG APPROVAL PROCESSES
The FDA (Food and Drug
Administration) is responsible for
assuring that new drugs are safe and
effective before approving the drugs
and allowing them to be marketed.
DRUG DEVELOPMENT
Testing and Clinical Trials
The testing process begins with
animal studies to determine potential
uses and effects.
In Phase I, a few doses are given to
a few healthy volunteers to determine
safe
dosages,
routes
of
administration,
absorption,
metabolism, excretion, and toxicity.
In Phase II, a few doses are given to
a few subjects with the disease or
symptom for which the drug is being
studied,
and
responses
are
compared with those of healthy
subjects.
In Phase III, the drug is given to a
larger and more representative group
of subjects.
In phase IV, after a drug is approved
for marketing, it enters a phase of
continual evaluation.
TERMS INDICATING DRUG ACTION
INDICATIONS
- A list of medical conditions or
diseases for which the drug is meant
to be used.
ACTIONS
- A description of the cellular changes
that occur as a result of the drug.
CONTRAINDICATIONS
- A list of conditions for which the drug
should not be given.
SIDE EFFECTS and ADVERSE
REACTIONS
- A list of possible unpleasant or
dangerous effects, other than the
desired effects,
INTERACTIONS
- A list of other drugs or foods that may
alter the effects of the drug and
usually should not be given during
the same course of therapy.
Basic Concepts and Processes
• How do systemic drugs reach,
interact with, and leave body cells?
• How do people respond to drug
actions?
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•
CELLULAR PHYSIOLOGY
Cells are dynamic, busy, “factories”
That is, they take in raw materials,
manufacture
various
products
required to maintain cellular and
bodily functions, and deliver those
products
to
their
appropriate
destinations in the body.
DRUG TRANSPORT THROUGH CELL
MEMBRANES
• Most drugs are given for effects on
body cells that are distant from the
sites of administration (ie, systemic
effects). To move through the body
and reach their sites of action,
metabolism, and excretion drug
molecules must cross numerous cell
membranes.
•
I.
-
PHARMACOKINETICS
Pharmacokinetics involves drug
movement through the body (ie,
“what the body does to the drug”) to
reach sites of action, metabolism,
and excretion.
ABSORPTION
Absorption is the process that occurs
from the time a drug enters the body
to the time it enters the bloodstream
to be circulated.
PHYSICAL FACTORS INFLUENCING
ABSORPTION
1. BLOOD FLOW to the absorption site:
-
blood flow to the intestine is much
greater than the flow to the stomach;
thus absorption from the intestine is
favored over that from the stomach.
2. TOTAL SURFACE AREA available
for absorption:
- because the intestine has a surface
rich in microvilli, it has a surface area
about 1,000 times that of the
stomach, thus absorption of the drug
across the intestine is more efficient.
3. CONTACT TIME at the absorption
surface:
- anything that delays the transport of
the drug from the stomach to the
intestine delays the rate of absorption
of the drug.
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BIOVAILABILITY
- Is the fraction of administered drug
that reaches the systemic circulation.
- Ex: if 100mg of drug is administered
orally and 70mg of this drug is
absorbed
- unchanged, the bioavailability is 70
%.
II.
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DISTRIBUTION
Distribution involves the transport of
drug molecules within the body.
Once a drug is injected or absorbed
into the bloodstream, it is carried by
the blood and tissue fluids to its sites
of pharmacologic action, metabolism,
and excretion
Distribution depends largely on the
adequacy of blood circulation.
Drugs are distributed rapidly to
organs receiving a large blood
supply, such as the liver, heart, and
kidneys.
Distribution to other internal organs,
muscle, fat, and skin is usually
slower.
Protein binding allows part of a drug
dose to be stored and released as
needed.
III.
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Some drugs also are stored in
muscle, fat, or other body tissues and
released gradually when plasma drug
levels
fall.
These
storage
mechanisms maintain lower, more
even blood levels and reduce the risk
of toxicity
Drug distribution into the central
nervous system (CNS) is limited
because the blood–brain barrier,
which is composed of capillaries with
tight walls, limits movement of drug
molecules into brain tissue
Drug distribution during pregnancy
and lactation is also unique.
During pregnancy, most drugs cross
the placenta and may affect the fetus.
During lactation, many drugs enter
breast milk and may affect the
nursing infant.
METABOLISM
Metabolism is the method by which
drugs are inactivated or bio
transformed by the body.
Most often, an active drug is changed
into one or more inactive metabolites,
which are then excreted.
Some active drugs yield metabolites
that are also active and that continue
to exert their effects on body cells
until they are metabolized further or
excreted.
Most drugs are lipid soluble, a
characteristic
that
aids
their
movement across cell membranes.
However, the kidneys, which are the
primary excretory organs, can
excrete
only
water
soluble
substances. Therefore, one function
of metabolism is to convert fatsoluble drugs into water- soluble
metabolites.
When drugs are given orally, they are
absorbed from the GI tract and
carried to the liver through the portal
circulation.
Some
drugs
are
extensively
metabolized in the liver, with only part
of a drug dose reaching the systemic
•
IV.
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circulation for distribution to sites of
action. This is called the first-pass
effect or presystemic metabolism.
The LIVER is the major site of
metabolism, but specific drugs may
undergo biotransformation in other
tissues.
•
EXCRETION
Excretion refers to elimination of a
drug from the body.
Effective excretion requires adequate
functioning of the circulatory system
and of the organs of
excretion (kidneys, bowel, lungs, and
skin).
Most drugs are excreted by the
kidneys and eliminated unchanged or
as metabolites in the urine.
Some drugs or metabolites are
excreted in bile, then eliminated in
feces; others are excreted in bile,
reabsorbed from the small intestine,
returned to the liver (called
enterohepatic recirculation),
The lungs mainly remove volatile
substances, such as anesthetic
gases.
The skin has minimal excretory
function.
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•
Toxic concentrations may stem from
a single large dose, repeated small
doses, or slow
metabolism that allows the drug to
accumulate in the body.
For most drugs, serum levels indicate
the onset, peak, and duration of drug
action.
The drug level continues to climb as
more of the drug is absorbed, until it
reaches its highest concentration and
peak drug action occurs. Then, drug
levels decline as the drug is
eliminated (ie, metabolized and
excreted) from the body.
RENAL ELIMINATION OF DRUG
1. GLOMERULAR FILTRATION
- Drugs enter the kidney
through renal arteries, which
divide to form a glomerular
capillary plexus.
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Serum Drug Levels
A serum drug level is a laboratory
measurement of the amount of a drug
in the blood at a
particular time.
It reflects dosage, absorption,
bioavailability, half-life, and the rates
of metabolism and excretion.
A toxic concentration is an
excessive level at which toxicity
occurs.
•
Serum Half-Life
Serum half-life, also called
elimination half-life, is the time
required for the serum concentration
of a drug to decrease by 50%. It is
determined primarily by the drug’s
rates of metabolism and excretion. A
drug with a short half-life requires
more frequent administration than
one with a long half-life.
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PHARMACODYNAMICS
Pharmacodynamics involves drug
actions on target cells and the
resulting alterations in cellular
biochemical reactions and functions
(ie, “what the drug does to the body”).
As previously stated, all drug actions
occur at the cellular level.
•
MINIMUM DOSE – a smallest
amount of a drug that will produce a
therapeutic effect.
•
MAXIMUM DOSE – largest amount
of a drug that will produce a desired
effect without producing symptoms of
toxicity.
LOADING DOSE – initial high dose
used to quickly elevate the level of
the drug in the blood (often followed
by a series of lower doses)
MAINTENANCE DOSE – dose
required to keep the drug blood level
at a steady state in order to maintain
the desired effect.
TOXIC DOSE – amount of drug that
will produce harmful effects or
symptoms of toxicity.
LETHAL DOSE – dose that can
cause death.
THERAPEUTIC DOSE- dose that is
customarily
given;
adjusted
according to variations from the
norm.
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VARIABLES THAT AFFECT DRUG
ACTIONS
• Expected responses to drugs are
largely based on those occurring
when a particular drug is given to
healthy adult men (18 to 65 years of
age) of average weight (150 lb [70
kg]).
• However, other groups of people (eg,
women, children, older adults,
different ethnic or racial groups, and
clients with diseases or symptoms
that the drugs are designed to treat)
receive drugs and respond differently
than healthy adult men.
Drug-Related Variables
• Dosage
- dose indicates the amount to be given at
one time and dosage refers to the
frequency, size, and number of doses.
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•
Dosage is a major determinant of
drug actions and responses, both
therapeutic and adverse.
If the amount is too small or
administered
infrequently,
no
pharmacologic
action
occurs
because the drug does not reach an
adequate concentration at target
cells.
If the amount is too large or
administered too often, toxicity
(poisoning) may occur.
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ROUTE OF ADMINISTRATION
There are two major routes of drug
administration:
• ENTERAL
• PARENTERAL
ENTERAL
1. ORAL
- The most common route of drug
administration
- The oral route usually produces
slower
drug
action
than
parenteral routes.
•
FIRST PASS metabolism by the
intestine or LIVER limits the efficacy
of many drugs when taken orally.
•
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2. SUBLINGUAL
- placement under the tongue
•
3. RECTAL
- both the sublingual and the rectal
have the additional advantage that
they prevent the destruction of the
drug by intestinal enzymes or low pH
in the stomach.
•
PARENTERAL
1. For rapid drug action and response,
the IV (Intravenous) route is most
effective because the drug is injected
directly into the bloodstream
2. For
some
drugs,
the
IM
(Intramuscular) route also produces
drug action within a few minutes
because muscles have a large blood
supply.
3. SUBCUTANEOUS
- It requires absorption and is
somewhat slower than the IV route
OTHERS
1. INHALATION
2. INTRANASAL
3. INTRATHECAL
4. VAGINAL
5. TRANSDERMAL
6. TOPICAL
•
Absorption and action of topical
drugs vary according to the drug
formulation, whether the drug is
applied
to
skin
or
mucous
membranes, and other factors.
Drug–Diet Interactions
•
•
Food may alter the absorption of oral
drugs. In many instances, food slows
absorption by slowing gastric
emptying time and altering GI
secretions and motility.
When tablets or capsules are taken
with or soon after food, they dissolve
more
slowly;
therefore,
drug
molecules are delivered to absorptive
sites in the small intestine more
slowly
Food also may decrease absorption
by combining with a drug to form an
insoluble drug–food complex.
In other instances, however, certain
drugs or dosage forms are better
absorbed with certain types of meals.
Drug–Drug Interactions
The action of a drug may be
increased or decreased by its
interaction with another drug in the
body. Most interactions occur
whenever the interacting drugs are
present in the body; some, especially
those affecting the absorption of oral
drugs, occur when the interacting
drugs are given at or near the same
time.
Increased Drug Effects
Interactions that can increase the
therapeutic or adverse effects of
drugs are as follows:
Additive effects
• Additive effects occur when two
drugs with similar pharmacologic
actions are taken.
• Example: ethanol + sedative drug
→increased sedation
Synergism or potentiation
• Synergism or potentiation occurs
when two drugs with different sites or
mechanisms of action produce
•
greater effects when taken together
than either does when taken alone.
Example:
acetaminophen
(nonopioid analgesic) + codeine (opioid
analgesic) →increased analgesia
Interference
• Interference by one drug with the
metabolism or elimination of a
second drug may result in intensified
effects of the second drug.
• Example: cimetidine inhibits CYP 1A,
2C, and 3A drug-metabolizing
enzymes in the liver and therefore
interferes with the metabolism of
many drugs
• When these drugs are given
concurrently with cimetidine, they are
likely to cause adverse and toxic
effects.
Displacement
• Displacement of one drug from
plasma protein - binding sites by a
second drug increases the effects of
the displaced drug. This increase
occurs because the molecules of the
displaced drug, freed from their
bound
form,
become
pharmacologically active.
• Example: aspirin (anti-inflammatory/
analgesic/ antipyretic agent) +
warfarin
(an
anticoagulant)
→increased anticoagulant effect
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Decreased Drug Effects
• Interactions in which drug effects are
decreased are grouped under the
term antagonism.
• Examples of such interactions are as
follows:
•
•
In some situations, a drug that is a
specific antidote is given to
antagonize the toxic effects of
another drug.
Example: naloxone (a narcotic
antagonist) + morphine (a narcotic or
opioid analgesic) →relief of opioid
•
•
induced respiratory depression.
Naloxone
molecules
displace
morphine molecules from their
receptor sites on nerve cells in the
brain so that the morphine molecules
cannot continue to exert their
depressant effects.
Decreased intestinal absorption of
oral drugs occurs when drugs
combine to produce nonabsorbable
compounds.
Example: aluminum or magnesium
hydroxide
(antacids)
+
oral
tetracycline (an antibiotic) →binding
of tetracycline to aluminum or
magnesium, causing decreased
absorption and decreased antibiotic
effect of tetracycline
Activation
of
drug-metabolizing
enzymes in the liver increases the
metabolism rate of any drug
metabolized primarily by that group of
enzymes. Several drugs (eg,
phenytoin, rifampin), ethanol, and
cigarette smoking are known enzyme
inducers.
Example:
phenobarbital
(a
barbiturate)
+
warfarin
(an
anticoagulant) →decreased effects of
warfarin
Increased excretion occurs when
urinary pH is changed and renal
reabsorption is blocked.
Example: sodium bicarbonate +
phenobarbital → increased excretion
of phenobarbital. The sodium
bicarbonate alkalinizes the urine,
raising the number of barbiturate ions
in the renal filtrate.
Client-Related Variables
Age
The effects of age on drug action are
most pronounced in neonates,
infants, and older adults. In children,
drug action depends largely on age
and developmental stage. During
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pregnancy, drugs cross the placenta
and may harm the fetus.
Drug distribution, metabolism, and
excretion differ markedly in neonates,
especially
premature
infants,
because their organ systems are not
fully developed.
Older infants (1 month to 1 year)
reach approximately adult levels of
protein binding and kidney function,
but liver function and the blood–brain
barrier are still immature.
Children (1 to 12 years) experience a
period of increased activity of drugmetabolizing enzymes so that some
drugs are rapidly metabolized and
eliminated.
After approximately 12 years of age,
healthy children handle drugs
similarly to healthy adults.
In older adults (65 years and older),
physiologic changes may alter all
pharmacokinetic processes.
Changes in the GI tract include
decreased gastric acidity, decreased
blood flow, and decreased motility.
Despite these changes, however,
there is little difference in absorption.
Body Weight
Body weight affects drug action
mainly in relation to dose. The ratio
between the amount of drug given
and body weight influences drug
distribution and concentration at sites
of action.
In general, people heavier than
average need larger doses, provided
that their renal, hepatic, and
cardiovascular
functions
are
adequate. Recommended doses for
many drugs are listed in terms of
grams or milligrams per kilogram of
body weight.
TOLERANCE AND CROSS-TOLERANCE
• Drug tolerance occurs when the body
becomes accustomed to a particular
drug over time so that larger doses
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must be given to produce the same
effects.
Tolerance may be acquired to the
pharmacologic action of many drugs,
especially opioid analgesics, alcohol,
and other CNS depressants.
Tolerance
to
pharmacologically
related drugs is called crosstolerance.
For example, a person who regularly
drinks large amounts of alcohol
becomes able to ingest even larger
amounts
before
becoming
intoxicated— this is tolerance to
alcohol. If the person is then given
sedative-type drugs or a general
anesthetic, larger-than-usual doses
are
required
to
produce
a
pharmacologic effect—this is crosstolerance.
ADVERSE EFFECTS OF DRUGS
The term adverse effects refers to
any undesired responses to drug
administration, as opposed to
therapeutic effects, which are desired
responses.
• Most drugs produce a mixture of
therapeutic and adverse effects; all
drugs can produce adverse effects.
Adverse effects may produce
essentially any sign, symptom, or
disease process and may involve any
body system or tissue.
• Some adverse effects occur with
usual therapeutic doses of drugs
(often called side effects); others are
more likely to occur and to be more
severe with high doses.
• Common or serious adverse effects
include the following:
•
1. CNS effects
- CNS effects may result from CNS
stimulation (eg, agitation, confusion,
delirium,
disorientation,
hallucinations, psychosis, seizures)
2.
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3.
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4.
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5.
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or CNS depression (dizziness,
drowsiness, impaired level of
consciousness, sedation, coma,
impaired respiration and circulation).
Gastrointestinal effects
Gastrointestinal effects (anorexia,
nausea,
vomiting,
constipation,
diarrhea) are among the most
common adverse reactions to drugs.
Diarrhea occurs with drugs that
cause local irritation or increase
peristalsis.
More serious effects include bleeding
or ulceration (most often with aspirin
and nonsteroidal anti-inflammatory
agents) and severe diarrhea/colitis
(most often with antibiotics).
Hematologic effects
Hematologic
effects
(blood
coagulation
disorders,
bleeding
disorders, bone marrow depression,
anemias,
leukopenia,
agranulocytosis, thrombocytopenia)
are relatively common and potentially
life threatening. Excessive bleeding
is most often associated with
anticoagulants and thrombolytics;
bone marrow depression is usually
associated with antineoplastic drugs.
Hepatotoxicity
Hepatotoxicity
(hepatitis,
liver
dysfunction or failure, biliary tract
inflammation or obstruction) is
potentially life threatening. Because
most drugs are metabolized by the
liver, the liver is especially
susceptible to drug induced injury.
Drugs that are hepatotoxic include
acetaminophen (Tylenol), isoniazid
(INH),
methotrexate
(Mexate),
phenytoin (Dilantin), and aspirin and
other salicylates.
Nephrotoxicity
Nephrotoxicity
(nephritis,
renal
insufficiency or failure) occurs with
several antimicrobial agents (eg,
gentamicin
and
other
aminoglycosides),
nonsteroidal
antiinflammatory
agents
(eg,
ibuprofen and related drugs), and
others.
6. Hypersensitivity
- Hypersensitivity or allergy may occur
with almost any drug in susceptible
clients. It is largely unpredictable and
unrelated to dose. It occurs in those
who have previously been exposed
to the drug or a similar substance
(antigen) and who have developed
antibodies
7. Drug fever
- Drug fever is a fever associated with
administration of a medication. Drugs
can cause fever by several
mechanisms,
including
allergic
reactions, damaging body tissues,
increasing body heat or interfering
- with its dissipation, or acting on the
temperature regulating center in the
brain.
8. Drug dependence
- Drug dependence may occur with
mind- altering drugs, such as opioid
analgesics,
sedative-hypnotic
agents, antianxiety agents, and CNS
stimulants.
9. Carcinogenicity
- Carcinogenicity is the ability of a
substance to cause cancer. Several
drugs are carcinogens, including
some hormones and anticancer
drugs. Carcinogenicity apparently
results from drug-induced alterations
in cellular DNA.
10. Teratogenicity
- Teratogenicity is the ability of a
substance to cause abnormal fetal
development
when
taken
by
pregnant women. Drug groups
considered
teratogenic
include
analgesics, diuretics, antiepileptic
drugs, antihistamines, antibiotics,
antiemetics, and others.
11. Toxic Effects of Drugs
- Drug toxicity (also called poisoning,
overdose, or intoxication) results
from excessive amounts of a drug
and may cause reversible or
irreversible damage to body tissues.
- In some cases, the patient or
someone accompanying the patient
may know the toxic agent (eg,
accidental overdose of a therapeutic
drug, use of an illicit drug, a suicide
attempt).
RIGHTS OF DRUG ADMINISTRATION
• RIGHT DRUG
- Generic Name – Brand Name
•
-
RIGHT DOSE
g/mg/mcg
Units
•
-
RIGHT TIME
Preparation
Administration
12H/24H format
Window time if dose is missed
•
-
RIGHT ROUTE
Integrity
Client’s ability
Drug form
Equipment
•
-
RIGHT PATIENT
At least 2 identifiers
o Full name
o Date of birth
o Medical ID number
Pharmacology of Antipyretics, Analgesic
Medications, Anesthetics and NonPharmacological Treatment
Outline:
Clinical Pharmacology of:
• Paracetamol (Acetaminophen)
• Non-steroidal
anti-inflammatory
drugs (NSAIDS)/COX-2 specific
inhibitors
- Opioids / Narcotics
• Ketamine
- Drugs used for neuropathic pain
• Local Anesthetic agents
• Others - Steroids
(2) Non-drug treatments
•
DRUG CLASSIFICATIONS
Analgesics - agents that are used
relieve pain
•
•
•
Anesthetics-agents that are used to
produce local or systemic loss of
sensation.
Anti-inflammatory—agents that are
used to reduce inflammation
Disease Modifying Anti-Rheumatic
Drugs/agents (DMARDs)- agents
that alter disease process rather than
manifestations
•
•
Gold Compounds - used for
conditions unresponsive to usual
anti-inflammatory treatment
DMARDSs
INFLAMMATORY RESPONSE
ANALGESICS
Types:
• Narcotic
- also called as opioids; stimulates
opiate receptors in the CNS; high risk
for dependence and addiction
- Example:
Morphine,
Codeine,
Meperidine
• Non-narcotic
- also called non-opioids
o Non-steroidal anti-inflammatory
drug (NSAIDS)
- Also has antipyretic and antiplatelet
(aspirin) properties
o Acetaminophen/Paracetamol
- Has antiseptic property; no antiinflammatory effects
•
•
➢
➢
➢
➢
ANESTHETICS
General - administered to achieve
analgesia, unconsciousness, and
amnesia through CNS depression
Local - loss of sensation to specific
body parts
Topical
Infiltration
Field block
Nerve block
ANTI-INFLAMMATORY
• NSAIDS
• Corticosteroids - agents used to
suppress immune system and
inflammatory process
➢ Androgens
➢ Glucocorticoids
➢ Mineralocorticoids
•
•
•
•
•
Clinical Pharmacology includes
Mechanism of Action
Absorption / Elimination of the drug
Indication for use / dosage
Adverse / side effects
Any special precautions that should
be taken
Paracetamol
- AKA acetaminophen
➢ has been in use for more than a
century
- It has both anal esic and anti retic
action
- However, the exact mechanism of its
action is unclear
Absorption / Elimination from the body:
- It is well tolerated when taken orally.
- On oral administration it is absorbed
from the intestine (70%), stomach
and colon (30^4)
-
-
-
The rate of absorption is rapid and
depends on the dose
The time taken to reach maximum
plasma concentration (Tmax) is 1530 minutes depends on the
preparation
It is available as tablets (adults),
suspension or syrup for children and
suppositories
Tmax is 2 - 3 hours with suppositories
Bioavailability ranges from 6o-90%
Elimination
• Paracetamol is metabolized in the
liver and only 2 - 596 is excreted
unchanged
Indications and Dosages
Indications:
- It is used as an anal esic dru for mild
to moderate
➢ E.g. Tooth ache / teething pain in
children, backpain, joint and muscle
pain, headache, dysmenorrhoea
- ReIief of fever in adults and children
Hepatotoxicity with an overdose of
paracetamol:
- This can occur when a patient does
not get adequate relief with
paracetamol and decides to take
more than the prescribed dose of a
maximum of 4g/day (8 - 10 g / day)
- Intentional overdose (Paracetamol
overdose / poisoning is the leading
cause of acute liver failure in the US,
UK and Australia)
- Overdose causes acute liver failure,
as the elimination pathways are
saturated resulting in elevated levels
of toxic metabolites
Adverse Effects
- N-acetylcysteine (NAC) is the
antidote for paracetamol poisoning
and it is most effective when
administered within 8 - 10 hours after
ingestion
- Renal toxicity —Overdose can cause
severe kidney necrosis
- Allergic reactions are rare
Dosage:
- Adults - Up to1goral / rectal, every
6hours (4g should not be exceeded /
day)
- Children - Oral / rectal 20 mg / kg every 6 hours
Side Effects:
- Paracetamol is well tolerated and has
no side effects at therapeutic doses
- It has good hematological tolerability
and does not alter hemostasis
Caution
- Since itis metabolized in the liver it
must be used with caution or omitted
in the presence of liver impairment.
- In patients with renal impairment, the
dose of paracetamol should be
reduced.
- Do not exceed 4g/day in adults and
125 mg/kg in children
Adverse effects
NSAIDS
Non-Steroidal
Anti-inflammatory
Drugs
History of Aspirin
- Salicylate from the bark of the willow
tree and was used to treat fever and
rheumatism for centuries
- In the late 19th century, salicylic acid
and later acetyl salicylic acid was
synthesized and called aspirin.
- Aspirin was widely used to treat fever
and pain till the availability of other
drugs with similar mechanisms
- of action. It continues to be used in
many parts of the world
Non-Steroidal Anti-inflammatory Drugs
(NSAIDs)
-
-
-
-
-
-
They
are
diverse
group
of
compounds which were
later
synthesized, with actions similar to
that of aspirin
and became known as NSAIDs
The mechanism of action of aspirin
/NSAIDs
was
discovered
in
the1960’s by Prof Vane, who was
awarded a Nobel prize in Medicine
in1982
NSAIDs are widely used to treat pain
and inflammation
They act through inhibition of the 2
isoforms
of
the
enzyme
cyclooxygenase (COX) - i.e. COX-1
and COX-2
NSAIDs that act on bath the enzymes
are known as non-selective NSAIDs
(ns-N5AIDs)
NSAIDs which act predominantly on
the COX-2 enzyme are known as
specific/selective COX-2inhibitors
(also referred to as Coxibs)
Cyclo-oxygenase (COX)
- Exists in the tissue as constitutive
isoform (COX-1).
- At site of inflammation, cytokines
stimulate the induction of the 2nd
isoform (COX-2).
- Inhibition of COX-2 is thought to be
due to the anti
The Two Isoforms of COX:
• COX-1 is a normal constituent in the
body for homeostasis, such as in:
- Gastric
mucosa-gastric
cyto
protection
- Kidney-Sodium
and
water
balance/renal perfusion
- Platelets-for aggregation
• COX-2 is induced in the presence if
injury and inflammation.
COX-2 is also a normal constituent in
the many organs such as: Kidney,
brain, endothelium, ovary and uterus.
What happens when there is tissue
injury?
Mediators of inflammation
• Prostaglandins
• Bradykinin
• Serotonin
• Histamine
• Interleukins- 2 — 6, 10, 12,13
• Platelet activating factor
• Gamma-interferon
• Tumor Necrosis Factor
• Transforming GrowthFactor
• Lymphotoxin
Arachidonic Acid Cascade
The role of some prostaglandins in the
body
• PGE
2
(ProstaglandinE2)
—
Endoperoxide synthase
- vasodilation,
bronchodilation,
inhibition of gastric acid secretion,
stimulation
of
gastric
mucus
secretion, sensitization of pain
receptors
to
chemical
and
mechanical stimuli, promotion of
anterior pituitary hormones release.
• TXA2 (Thromboxane), produced by
platelets, - induction of platelet
aggregation, vasoconstriction;
Nonsteroidal Anti-Inflammatory Drugs
(NSAIDs)
Nonselective COX inhibitors:
1. Salicylates
- Acetylsalicylic acid (aspirin)
- Salicylamide
2. Pyrazolone derivatives
- Phenylbutazone
- Metamizole (analginum)
3. Indole deerivatives
- Indomethacin
4. Propionic acid derivatives
- Naproxen and ibuprofen
5. Antranilic acid derivatives
- Mefenamic acid
6. Aryl – acetic acid derivatives
- Diclophenac sodium
7. Oxicam derivatives
- Piroxicam
8. Dihydropyrrolizine Carboxylic acid
derivative
- Ketorolac
Selective COX inhibitors
Preferential COX-2 inhibitors
- Nimesulide
- Meloxicam
- Nabumeton
Selective COX-2 inhibitors (“coxibs”)
- Celecoxib (oral capsules)
- Parecoxib (parenteral)
- Etoricoxib (oral tablets)
NOTE! These drugs cause little gastric
mucosa damage, they do not inhibit platelet
aggregation!!!
Anti-Pyretics / NSAIDs on the WHO
essential drug list:
- Acetylsalicylic acid (aspirin)
- tablet 100 mg to 500 mg
- suppository 50 mg to 150 mg
-
Ibuprofen > 3 months in age
tablet 200 mg; 400 mg
oral liquid: 200 mg/5 ml
Absorption and Elimination
- When administered orally, aspirin,
ns-NSAIDs and Coxibs are well
absorbed and reach therapeutic
- levels within 30 to 60 minutes
Indications
- Both the ns-NSAIDs and Coxibs have
the same efficacy in postoperative
analgesia
- sole analgesia for day surgery
- along with opioid for major surgery
-
Musculoskeletal pain – e.g. back
pain, joints, muscle sprains etc.
Osteoarthritis
Rheumatoid arthritis
Not indicated for neuropathic pain
(Chronic nerve pain, distinguished by
+ or – symptom)
Side effects / Adverse effects
Gastrointestinal effects
- The risk of erosions, ulcers and
bleeding is higher with ns-NSAIDs
compared to COxibs
- This risk with ns-NSAIDs is also
variable with some being less than
others
- Risk is greater in elderly patients
those who are also taking aspirin
- Risk can be reduced by adding a
proton-pump
inhibitor
(e.g.
omeprazole) to ns-NSAIDs.
- H2 receptor blockers are not very
effective
Renal Effects
• Both COX-1 & 2 are constituent
enzymes in the kidney
• maintain renal perfusion and
sodium/water balance
•
•
•
Both ns-NSAIDS and Coxibs can
cause:
Hypertension, edema
decrease in creatinine clearance
that may be significant in patients
with impaired renal function or
transient
hypotension
/
hypovolemia in the postoperative
period
Cardiovascular effects
•
•
•
Some studies have shown that
there was a higher risk of
thrombotic cardiovascular events
(stroke,heartattack) when on
Coxibs when compared to nsNSAIDs such as naproxen
Other studies have shown that
the cardiovascular events are
similar
Nevertheless,
,current
recommendations
are
that
Coxibs should not be used in
patients
with
active
cardiovascular disease and a
known thrombotic condition
Effect on platelets
• ns-NSAIDs are able to prevent
platelet aggregation as platelets do
not have COX-2. There is therefore a
potential for bleeding with ns-NSAIDs
• Coxibs do not prevent platelet
aggregation
• ns-NSAIDs should be used with
caution in patients who are already
on aspirin
Others Effects:
• Some ns-NSAIDs can precipitate
asthma is aspirin sensitive asthmatic
patients.
• Coxibs are well tolerated by patients
who have aspirin sensitive asthma
➢ Non-opioids/Non-narcotics
➢ Acetaminophen and NSAIDS
➢ Opioids/Narcotics
•
•
•
•
•
Antipyretic
Anti-inflammatory (NSAIDS)
Non CNS Depression
No anti-inflammatory or antipyretic
effects
Causes CNS depression (think and
Low and Slow); sedation
ANALGESICS
C - Celebrex
N - Naproxen
S
A - Advil (ibuprofen) I - Indomethacin
D
N - Not Good for the entire body
GI bleeding - BAD for ulcers
Lungs - BAD for asthma
Heart - HTN & Heart Failure
Kidney clogging - increased Ceat & BUN
Blood clots
Key points:
NEVER TAKE 2 NSAIDS simultaneously
Use lowest dose for shortest time possible
S - Sticky blood “clots”
Increased risk for thrombosis
A - Asthma worsening
Asthma and nasal polyps - CLARIFY
ORDER
Acetaminophen is used instead
I - Increased bleed risk
Notify HCP Bleeding
Key words
- Easy bruising
- Tarry stool & coffee-ground
Emesis = GI Bleed
- Avoid - “peptic ulcer” (GI Bleeding)
- Take medicine with food
- NEVER EMPTY STOMACH
Key points
AVOID EGGO vitamins
E - Vitamin E
G - Gingko, Garlic
O - Omega 3 oils
“Increased bleed risk”
D - Dysfunctional kidneys
Renal injury = Long term used
Memory tricks:
Creatine over 1.3 = BAD KIDNEY
Urine output 30ml/hr or LESS = KIDNEYS
in destress
Ketorolac - KILLS the jneys
S - Swelling heart
CHF (heart failure) & HTN worsening
Key words
Clients with long term Hypertension or
Cardiovascular disease
NO NSAIDS – notify HCP
Respiratory System Drugs
Adrenergic Agonists
Definition
- Called
sympathomimetic
drugs
because they mimic the effects of
sympathetic nervous system (SNS)
Therapeutic and Adverse Effects
- related to their stimulation
adrenergic receptor sites
of
Uses
- Varies from ophthalmic preparations
for dilating pupils to systemic
preparations for shock
Physiological Responses of Adrenergic
Agonists
Alpha and Beta Adrenergic Agonists and
their Indications
• Epinephrine (Adrenalin, Sus-Phrine):
Shock; glaucoma; prolongs effects of
regional anesthetic
• Norepinephrine (Levophed): Treat
shock or during cardiac arrest to get
sympathetic activity
• Dopamine (Intropin): Shock
• Dobutamine (Dobutrex): Congestive
heart failure
• Ephedrine
(Pretz-D):
Seasonal
rhinitis; hypotensive episodes
• Metaraminol (Aramine): Synthetic
agent that is similar to norepinephrine
Alpha and Beta Adrenergic Agonists
• Actions
- the effects of these drug are
mediated by the adrenergic receptors
in target organs; heart rate increases;
bronchi
dilate;
vasoconstriction
occurs;
intraocular
pressure
decreases, glycogenolysis occurs
throughout the body
• Indications
- treatment of hypotensive shock,
bronchospasm, and some types of
asthma
• Pharmacokinetics
- rapidly absorbed after injection or
passage through mucous
membranes
- metabolized in the liver and excreted
in the urine
• Contraindications
- Pheochromocytoma
- tachyarrhythmias or ventricular
fibrillation
- hypovolemia
- halogenated hydrocarbon general
anesthetics
Caution should be used with peripheral
vascular disease
• Caution
- PVD
• Adverse reactions
- arrhythmias, hypertension,
palpitations, angina, dyspnea
•
-
nausea and vomiting
headache and sweating
Drug to drug interaction
tricyclic antidepressants and MAOI’s
Alpha-Specific Adrenergic Agonists (AlphaAgonists)
• Definition
- drugs that bind primarily to alphareceptors rather than to betareceptors
•
•
•
-
•
•
•
•
•
-
Drugs in this Class
Phenylephrine
(Neo-Synephrine,
Allerest, AK-Dilate, and others)
Midodrine (ProAmantine)
Clonidine (Catapres)
Actions
therapeutic effects come from the
situation of alpha-receptors within the
SNS
Indications
Hypertension, constriction of topical
vessels in nose
Pharmacokinetics
well absorbed and reach peak levels
in a short period-20 to 45 minutes
widely distributed in the body
metabolized in the liver and excreted
in the urine
Contraindications
allergy to drug
severe hypertension or tachycardia
narrow-angle glaucoma
pregnancy
Caution
CVD or vasomotor spasm
Thyrotoxicosis or diabetes
Adverse Reactions
anxiety, restlessness, depression,
fatigue, blurred vision
ECG changes, arrhythmias, blood
pressure changes
nausea, vomiting
decreased urinary output
Drug-to-drug Interaction
MAOIs and TCAs
Digoxin and beta-blockers
QUESTION AND ANSWER
True – Another name for an adrenergic
agonist drug is a sympathomimetic drug
Rationale: An adrenergic agonist is also
called a sympathomimetic drug because it
mimics the effects of the sympathetic
nervous system (SNS)
Beta- Specific Adrenergic Agonists and
Their Indication
• Isoproterenol (Isuprel)
- treatment of shock, cardiac standstill,
and heart block in transplanted
hearts; prevention of bronchospasm
during anesthesia; inhaled to treat
bronchospasm
• Ritodrine (Yutopar)
- management of preterm labor
Beta-Specific Adrenergic Agonists
• Actions
- effect is related to its stimulation of
the beta-adrenergic receptors
- increase heart rate, conductivity, and
contractibility,
bronchodilation,
increase blood flow to skeletal
muscles and splanchnic bed, and
relaxation of uterus
• Pharmacokinetics
- Rapidly distributed after injection
- metabolized in the liver and excreted
in the urine
- T ½ less than 1 hour
• Contraindications
- Allergy
- Pulmonary Hypertension
- Eclampsia, uterine hemorrhage, and
intrauterine death
- pregnancy and lactation
• Caution
- diabetes, thyroid disease
- vasomotor problems
- heart disease and stroke
• Adverse Reactions
- restlessness, anxiety, and fear
- tachycardia,
angina,
MI,
and
palpitations
•
-
difficulty breathing, cough, and
bronchospasm
nausea, vomiting, and anorexia
Drug-to-drug interaction
increase with other sympathomimetic
drugs
decrease with beta adrenergic
blockers
Nursing Considerations for Alpha- and BetaAdrenergic Agonists
• Assessment: History and Physical
Exam
• Nursing Diagnosis
• Implementation
• Evaluation
Nursing Considerations for Alpha-Agonists
• Assessment: History and Physical
Exam
• Nursing Diagnosis
• Implementation
• Evaluation
Nursing Considerations for Beta-Specific
Adrenergic Agonists
• Assessment: History and Physical
Exam
• Nursing Diagnosis
• Implementation
• Evaluation
Q AND A
When providing care for a patient receiving
alpha and beta adrenergic agonists, which of
the following would be important to assess in
order to prevent the systemic overload of
catecholamines?
A. Hypotension
B. Pheochromocytoma
C. Hypovolemia
D. Allergic Rhinitis
Rationale:
Assess for contraindications or cautions
including pheochromocytoma which could
lead to fatal reactions due to systemic
overload of catecholamines.
•
-
•
•
•
-
Adrenergic Blocking Antagonists
Definition
called sympatholytic drugs because
they lyse, or block, the effect of the
SNS
Therapeutic
related to their ability to react with
specific adrenergic receptors sites
without activating them
Action
prevent
•
•
-
•
•
•
-
•
Alpha and Beta Adrenergic Blocking Agents
and Their Indications
• Carvedilol (Coreg): Hypertension,
congestive heart failure (Adult)
• Guanadrel (Hylorel): hypertension in
adults not responding to thiazide
diuretics
• Labetalol (Normodyne, Trandate):
hypertension, pheochromocytoma,
clonidine withdrawal
• Phentolamine (regitine)
- diagnosis of pheochromocytoma
- management of severe hypertension
during
- pheochromocytoma surgery
- prevention of cell death with IV
infiltration of
- norepinephrine or dopamine
Alpha and Beta Adrenergic Blocking
Agents
-
Actions
Competitively block the effects of
norepinephrine at the alpha and beta
receptors throughout the SNS
prevents the signs and symptoms
associated with sympathetic stress
reaction and results in lower blood
pressure,
slower
pulse,
and
increased renal perfusion with
decreased renin levels
Indications
essential hypertension
Pharmacokinetics
well absorbed and distributed and
throughout the body metabolized in
the liver and excreted in feces and
urine
Contraindications
bradycardia or heart block
shock or CHF
Caution
Bronchospasm
Adverse Reactions
dizziness, insomnia, fatigue, nausea,
vomiting, arrhythmias, hypotension,
CHF,
pulmonary
edema,
Bronchospasm
Drug-to-drug Interaction
Enflurance, halothane, or isoflurane
anesthethics
diabetes agents
calcium channel blockers
Nursing Considerations for Alpha- and Beta
Adrenergic Blocking Agents
• Assessment: History and Physical
Exam
•
•
•
Nursing Diagnosis
Implementation
Evaluation
Q and A
What is an indication for use non-selective
adrenergic blocking agents?
A. Essential hypertension
B. Malignant hypertension
C. Secondary hypertension
D. Malignant Hyperthermia
Rationale: The alpha and beta adrenergic
blocking agents block all of the receptors
sites within the SNS, which results in lower
blood pressure, slower pulse, and increased
renal perfusion with decreased renin levels.
These drugs are indicated for the treatment
of essential hypertension.
•
•
•
•
•
-
Alpha-Adrenergic Blocking Agent
Actions
blocks postsynaptic alpha, receptors,
decreasing sympathetic tome in the
vasculature and causing vasodilation
Pharmacokinetics
absorbed after injection and is
excreted in the urine
Contraindications
Allergy
CAD or MI
Caution
pregnancy and lactation
adverse reactions
hypotension,
orthostatic
hypotension, angina, MI, CVA
Arrhythmia, weakness, and dizziness
Drug-to-drug interaction
ephedrine and epinephrine
alcohol
Alpha- selective adrenergic blocking agents
• Doxazosin (Cardura): used to treat
hypertension; also effective in the
treatment
of
benign prostatic
hypertrophy
• Prazosin (Minipress): used to treat
hypertension, alone or in combination
with other drugs
• Terazosin (Hytrin): used to treat
hypertension as well as BPH
• Tamsulosin (Flomax) and Alfuzosin
(Uroxatral): used only in the
treatment of BPH
• Actions
- blocks the postsynaptic alpha 1receptor sites
- this causes a decrease in vascular
tone and vasodilation
• Indications
- BPH and hypertension
• Pharmacokinetics
- well absorbed, undergo extensive
hepatic metabolism, excreted in the
urine
• Contraindications
- allergy, lactation
• Caution – CHF or renal failure
• Adverse Reaction
- dizziness, weakness, fatigue
- nausea, vomiting, abdominal pain,
diarrhea
- arrhythmias, hypotension, edema,
CHF, and angina
- Drug-to-drug interaction
- vasodilators or antihypertensive
drugs
Q and A
Alpha- selective adrenergic blocking agents
are to be used with cautio in what population
of patients?
A. Those with hepatic disease
B. Those with hypotension
C. Those with congestive heart failure
D. Those with respiratory distress
Rationale:
alpha-selective
adrenergic
blocking agents are used with caution in
patients who have CHF or renal failure.
Beta-adrenergicp blocking agents
Actions
competitive blocking of the betareceptors in the SNS
- blocking of beta receptors in the heart
and in the juxtaglomerular apparatus
of the nephron
- Indications
- treating cardiovascular problems
-
hypertension
angina
migraine headaches
preventing reinfarction after MI
Pharmacokinetics
absorbed from GI tract and undergo
hepatic metabolism
Contraindication
allergy
bradycardia, heart block, shock or
CHF
COPD, asthma
Caution
diabetes, hepatic dysfunction
Adverse reactions
fatigue, dizziness, depressions, sleep
disturbances
bradycardia,
heart
block,
hypotension
bronchospasm
nausea, vomiting, diarrhea
decrease libido
Drug-to-drug interaction
Clonidine
NSAIDs
insulin or anti- diabetic medications
•
-
Beta1 – selective adrenergic blocking
agents
- Advantage
- Do not usually block beta-receptor
sites, including the sympathetic
bronchodilation
- preferred for patients who smoke or
have asthma, obstructive pulmonary
disease, or seasonal or allergic
rhinitis
- Uses
- hypertension, angina, some cardiac
arrhythmias
- Actions
- selectively block beta 1 receptors in
the SNS
- Pharmacokinetics
- absorbed from GI tract
- metabolized in liver and excreted in
urine
- Contraindication
- allergy
- sinus bradycardia, heart block,
cardiogenic shock, CHF, and
hypotension
- Caution
- COPD, diabetes, thyroid disease
- Adverse Reactions
- FATIGUE, DIZZINESS, SLEEP
- DISTURBANCES
- bradycardia, heart block, CHF,
hypotension
- symptoms in respiratory tract range
from
- rhinitis to bronchospasm
- nausea, vomiting, diarrhea
- decreased libido and impotence
Drug-to-drug Interaction
NSAIDs
IV lidocaine
Q AND A
You are facing for a child who has been
diagnosed with a
heart problem. Protocol has been ordered for
this patient.
What would be considered in calculating a
child’s dose?
A. Child’s body weight and age
B. Child’s body mass
C. Child’s age in months and height
D. Child’s age and body mass index
Rationale: children are at greater risk for
complications associated bradycardia,
difficulty breathing, and changes in glucose
metabolism. The safety and efficacy for use
of these drugs has not been established for
children younger than 18 years of age. If one
of these drugs is used, the dosage for these
agents need to be calculated from the child’s
body weight and age.
CHAPTER 32: Cholinergic Agonists
Definition
Chemicals that act at the same site as the
neurotransmitter acetylcholine (ACh)
Action
- Often called parasympathomimetic drugs
because their action mimics the action of the
parasympathetic nervous system
- Not limited to a specific site; therefore
associated with many undesirable systemic
effects
Types of Cholinergic Agonists
• Direct-Acting Cholinergic Agonists
- Occupy receptor sites for ACh on the
membranes of the effector cells of the
postganglionic cholinergic nerves
- Cause increased stimulation of the
cholinergic receptor
• Indirect-Acting Cholinergic Agonists
React
with
the
enzyme
acetylcholinesterase and prevent it from
breaking down the ACh that was released
from the nerve
- Cause increased stimulation of the ACh
receptor sites
Pharmacodynamics of Cholinergic Drugs
Direct-Acting Cholinergic Agonists and Their
Indications
Bethanechol (Duvoid, Urecholine)
- Treat urinary retention; neurogenic
bladder atony
- Diagnose and treat reflux esophagitis
Carbachol (Miostat); Pilocarpine (Pilocar)
- Induce miosis or pupil constriction
- Relieve intraocular pressure of
glaucoma.
- Perform certain surgical procedures
Direct-Acting Cholinergic Agonists
• Actions
- Act at cholinergic receptors in the
peripheral nervous system to mimic
the
effects
of
ACh
and
parasympathetic stimulation
•
-
Indications
Increase the tone of the detrusor
muscle of the bladder and relax the
bladder sphincter
•
-
Pharmacokinetics
Well, absorbed and have relatively
short half-life (1-6 hours)
Metabolized and excretion of these
drugs is not known
•
-
-
Contraindications
Any condition that would be
exacerbated by parasympathetic
effects-bradycardia, hypotension
Peptic ulcer disease
Intestinal obstruction or recent GI
surgery
Asthma
Bladder obstruction
-
Epilepsy and parkinsonism
•
-
Caution
Pregnancy and lactation
•
-
-
Adverse Reactions
Nausea, vomiting, cramps, diarrhea,
increase salivation, and involuntary
defecation
Bradycardia,
heart
block,
hypotension
Urinary urgency
Flushing or increased sweating
•
-
Drug-to-Drug Interaction
Acetylcholinesterase
-
Question
Tell whether the following statement is true
or false.
An indication for the use of Duvoid is to
diagnose and treat esophageal varices.
False
Rationale: Bethanechol (Duvoid, Urecholine)
-
Treat urinary retention; neurogenic
bladder atony
Diagnose and treat reflux esophagitis
-
Autoimmune disease; patients make
antibodies to ACh receptors, causing
gradual destruction of them
Symptoms
- Progressive weakness and lack of
muscle control with periodic acute
episodes
Acetylcholinesterase Inhibitors Used to
Treat Myasthenia Gravis
- Neostigmine (Prostigmine): has a
strong
influence
at
the
neuromuscular junction
- Pyridostigmine
(Regonol,
Mestinon): has a longer duration of
action than neostigmine
- Ambenonium (Mytelase): available
only in oral form; cannot be used if
patient is unable to swallow tablets
- Endrophonium (Tensilon, Enlon):
diagnostic agent for myasthenia
gravis
•
•
•
-
Alzheimer's Disease
A progressive disorder involving
neural degeneration in the cortex
Leads to a marked loss of memory
and the ability to carry on activities of
daily living
Cause of the disease is not yet known
There is a progressive loss of AChproducing neurons and their target
neurons
Indirect-Acting Cholinergic Agonists
• Do Not React Directly with ACh
Receptor Sites
- React
chemically
with
acetylcholinesterase in the synaptic
cleft to prevent it from breaking down
Ach
- ACh released from the presynaptic
nerve accumulates, stimulating the
ACh receptors
- Bind
reversibly
to
acetylcholinesterase, so effects will
pass with time
Drugs Used to Treat Alzheimer's Disease
• Tacrine (Cognex) - First drug to treat
Alzheimer's dementia
o Galantamine (Reminyl) Used to stop progression of
Alzheimer's dementia.
• Rivastigmine (Exelon) - Available in
solution for swallowing ease
o Donepezil (Aricept) - Has
once-a-day dosing
Myasthenia Gravis
Definition
- Chronic muscular disease caused by
a
defect
in
neuromuscular
transmission
Indirect-Acting Cholinergic Agonists
• Actions
- Blocks acetylcholinesterase at the
synaptic cleft. This allows the
accumulation of ACh released from
the nerve endings and leads to
increased and prolonged stimulation
of ACh
•
-
Indications
Myasthenia gravis and Alzheimer's
disease
•
-
Pharmacokinetics
Well, absorbed and distributed
throughout the body
Metabolized in the liver and excreted
in the urine
-
•
•
-
-
•
-
Contraindications
Allergy
Bradycardia
Intestinal or urinary tract obstruction
Lactation
Caution
Any condition that could be
exacerbated
by
cholinergic
stimulation
Asthma, coronary disease, peptic
ulcer, arrhythmias, epilepsy, or
parkinsonism
-
Adverse Reactions
Bradycardia
Hypotension
Increased GI secretions and activity
Increased bladder tone
Relaxation of GI and genitourinary
sphincters
Bronchoconstriction
Pupil constriction
•
-
Drug-to-Drug Interaction
NSAIDS
Question
Which of the drugs used to treat Alzheimer's
disease is available in solution for swallowing
ease?
A. Cognex
B. Reminyl
C. Aricept
D. Exelon
Rationale: Rivastigmine (Exelon): Available
in solution for swallowing ease
Nerve Gas
Definition
- Irreversible
acetylcholinesterase
inhibitor
Action
- Leads to toxic accumulations of ACh
at cholinergic receptor sites
- Can cause parasympathetic crisis
and muscle paralysis
Use of Cholinergic Agonists Agents
Across Lifespan
Prototype Direct-Acting Cholinergic
Agonists
Prototype Summary: Bethanechol
Indications:
Acute
postoperative
or
postpartum nonobstructive urinary retention,
neurogenic atony of the bladder with
retention
Actions: Acts directly on cholinergic
receptors to mimic the effects of ACh,
increases tone f detrusor muscles and
causes emptying of the bladder
Pharmacokinetics:
Route: Oral
Onset: 30-90 min
Peak: 60-90 min
Duration: 1-6 h
T1/2: Metabolism and excretion unknown,
thought to be synaptic
Adverse Effects: Abdominal discomfort,
salivation, nausea, vomiting, sweating,
flushing
Prototype Summary: Pyridostigmine
Indications: Treatment of myasthenia
gravis,
antidote
for
nondepolarizing
neuromuscular junction blockers, increased
survival after exposure to nerve gas
Actions: Reversible cholinesterase inhibitor
that increases the levels of ACh, facilitating
transmission at the neuromuscular junction
Nursing Considerations for Direct-Acting
Cholinergic Agonists
• Assessment: History and Physical
Exam
• Nursing Diagnosis
• Implementation
• Evaluation
Nursing Considerations for Indirect-Acting
Cholinergic Agonists
• Assessment: History and Physical
Exam
• Nursing Diagnosis
• Implementation
• Evaluation
Pharmacokinetics:
Question
The nurse is providing patient education to a
patient taking an indirect-acting cholinergic
agonist. What drug-to-drug interaction would
the nurse include in the patient education?
A. NSAIDs
B. Direct-acting cholinergic agonist
C. Acetylcholinesterase inhibitors
D. Direct-acting cholinergic antagonist
Rationale:
Indirect-acting
cholinergic
agonists have a drug to-drug interaction with
NSAIDs.
Prototype Summary: Donepezil
Chapter 33: Anticholinergic Agents
Anticholinergic Drugs
• Action
- Used to block the effects of
acetylcholine
- Lyse, or block effects of the PNS;
also called parasympatholytic agents
• Uses (better drugs are available now)
- decrease G.I. activity and secretions
(treat ulcers)
- Decreased
parasympathetic
activities to allow the sympathetic
system to become more dominant
Anticholinergics/Parasympatholytics
• Derived from the plant Belladonna
•
•
•
-
Black only the muscarinic effectors in
the PNS and cholinergic receptors in
the SNS
Act by competing with acetylcholine
for the muscarinic acetylcholine
receptor sites
Do not block the nicotinic receptors
have little or no effect at the
neuromuscular junction
Effects of Blocking the Parasympathetic
System
• Increase in heart rate
• Decrease in G.I. activity
• Decrease in urinary bladder tone and
function
• Pupil dilation
• Cycloplegia
•
•
•
•
•
•
•
-
Pharmacodynamics of Anticholinergic Drugs
•
-
Anticholinergic Agents and Their Indications
• Atropine
blocks parasympathetic affects in
many situations
• Dicyclomine (Antispas, Dibent, ansd
others)
- Relaxes GI tract; treats hyperactive
or irritable bowel
• Glycopyrrolate (Robinul)
- Adjunct in the treatment of ulcers
• Propantheline (Pro-Banthine)
- Adjunct in the treatment of ulcers
•
•
•
Atropine
Depresses salivation and bronchial
secretion
Dilates the bronchi
Inhibits vagal responses in the heart
•
•
•
-
Relaxes the G.I. and genitourinary
tracts
Inhibits GI secretions
Causes mydriasis
Causes cycloplegia
Anticholinergic Drugs
Actions
Blocks the acetylcholine receptors at
the muscarinic cholinergic receptor
site
Indications
Decrease secretions
Restore cardiac rate and blood
pressure
Pylorospasm and hyperactive bowel
Relax uterine hypertonicity
Pharmacokinetics
Well absorbed
Widely distributed throughout the
body
Cross the blood brain barrier
T ½ varies based on route snd drug
Excreted in the urine
Contraindications
Allergy
Any condition that could be
exacerbated by blocking of the
parasympathetic nervous system
o Glaucoma
o Peptic ulcer disease
o Prostatic hypertrophy
o Bladder obstruction
Caution
Breast feeding
Spasticity and brain damage
Adverse Reactions
Blurred vision
Mydriasis
Cyclopegia
Photophobia
Palpitations, bradycardia
Dry mouth, altered taste perception
Urinary hesitency and retention
Decreased sweating; predisposition
to heat prostration
Drug-to-Drug Interaction
Any other drug with anticholinergic
activity
o Antihistamines
-
o Antiparkinson’s drugs
Phenothiazines
•
•
•
•
Drugs
Assessment: Hostory and Physical
Exam
Nursing Diagnosis
Implementation
Evaluation
Question
In which group ompatients would the
healthcare provider use caution in
prescribing anticholinergic medications?
A. Patients with spasticity
B. Patients with myasthenia gravis
C. Patients with Parkinson’s disease
D. Patients with hyperactive reflexes
Rationale: caution: Breast feeding; spasticity
snd brain damage
Chapter 21: Drugs Treating Parkinson
Disease and Other Movement Disorders
Physiology
The extrapyramidal system is
responsible for course control of
voluntary muscles.
This system is composed of basal
ganglia, cortical areas of the brain.
Motor activity requires integration of
the actions of the cerebral cortex,
basal ganglia, and cerebellum.
The basal ganglia are a group of
functionally related look like located
in prayer groups in each cerebral
hemisphere.
The regulatory neurotransmitter
document is produced in the
substantia nigra and adrenal glands
and is then transmitted to the basal
ganglia along in neural pathway.
•
•
•
•
•
•
•
•
•
•
•
Parkinson’s Disease
Parkinson disease is also called
idiopathic parkinsonism or paralysis
agitans.
This disease is naturally occurring
in that an external stimulus, such as
virus or trauma, does not trigger it.
Parkinson Disease generally a flex
patients age 50 years and older and
progressing slowly.
In Parkinson disease, degeneration
of the neurons that supply
dopamine to the striatum occurs,
resulting in reduced dopamine in
the nerve terminals of the
nigrostriatal tract.
Dopamine is the Nerotransmitter
that sends information to the parts
of the brain that control movement
and coordination.
As the disease progresses,
messages from the brain telling the
body how and when to move are
delivered more slowly.
Amyotrophic Lateral Sclerosis
ALS is a progressive neurologic
disorder that affects motor function.
The etiology of ALS is unknown.
ALS affects both the upper motor
neurons in the cerebral cortex and
the lower motor neurons in the brain
stem and spinal cord.
One of its classic features is that it
spears the entire sensory system.
The disease begins in the distal
neurons.
The loss of upper motor neuron‘s
results in spastic paralysis and
hyperreflexia.
The loss of lower motor neurons
results in decreased muscle tone and
reflexes and flaccid paralysis.
•
•
•
•
•
•
•
•
•
•
•
•
Multiple Sclerosis
MS is a major cost of neurologic
disability among young and middleaged adults.
There are four subtypes of MS:
relapsing-remitting,
primary
progressive,
secondary
progressive,
and
progressiverelapsing.
In MS, more than one area of
information and scarring of the
myelin in the brain and spinal cord
occurs.
When
myelin
is
damaged,
messages between the brain and
other parts of the body are affected.
The most common symptoms of MS
include
fatigue,
weakness,
spasticity,
balance
problems,
bladder and bowel problems,
numbness, vision loss, tremor, and
vertigo.
•
•
•
•
•
•
•
-
•
•
-
•
-
Antiparkinson Drugs
The relative lack of dopamine
combined with a relative excess of
excitatory acetylcholine causes the
symptoms of Parkinson disease.
The goal of therapy is the restore the
balance between dopamine and
acetylcholine.
Drugs used to treat Parkinson and
Disease and Increased dopamine
levels, stimulate dopamine receptors,
extend the action of dopamine in the
brain, or prevent the activation of
cholinergic receptors.
Prototype for the dopaminergic drug:
carbidopa-levodopa
(Sinemat,
Parcopa).
Carbidopa-Levodopa: Core Drug
Knowledge
Pharmacotherapeutics
combination drug use in treating
Parkinson Disease
Pharmacokinetics
administered:
oral.
Metabolism:
peripherally. Onset: 1 to 2 months. T
1/2 : 1 to 2 hours
Pharmacodynamics
diffuses levodopa into the central
nervous system (CNS), where it is
converted to dopamine
Carbidopa is administrated in
combination
to
prevent
the
conversion of levodopa to dopamine
in the periphery.
Contraindications and precautions
hypersensitivity and undiagnosed
pigment lesions
Adverse effects
nausea,
vomiting,
anorexia,
orthostatic hypotension, abnormal
movements, cardiac arrhythmias,
bruxism, and ballismus.
Drug interactions
Hydantoins, MAOIs, phenothiazines,
or tricyclic antidepressants
Carbido-Levodopa: Core Patient
Variables
• Health status
- Past medical/allergies and physical
assessment
• Life span and gender
- Pregnancy Category C drug
• Lifestyle, diet, and habits
- Protein can interefere with absorption
• Environment
- Usually given at home
• Culture and inherited traits
- The drug effective in those of
Chinese, Filipino, or Thai descent.
Carbido-Levodopa: Nursing Diagnoses and
Outcomes
• Disturbed thought processes related
to adverse CNS effects
- Desired outcome: the patient will
remain oriented and communicate
effectively.
- Desired outcome: the patient will
report alterations in sleep patterns
affecting activities of daily living.
• Impaired physical mobility related to
on-off effect.
- Desired outcome: The patient will
immediately report incidents of the
on-off effect to the prescriber.
• Risk for Injury related to drug-induced
orthostatic hypotension.
- Desired Outcome: The patient will
learn to change position slowly,
carefully, and safely to minimize
effects of orthostatic hypotension.
Carbidopa-Levodopa: Planning and
Interventions
• Maximizing therapeutic effcts
- take on an empty stomach
- Monitor diet for high protein and
pyridoxine
• Minimizing adverse effects
- administer carbidopa-levodopa at
evenly spaced intervals
- Titrate the dose.
Carbidopa-Levodopa: Teaching,
Assessment, and Evaluations
•
•
-
Patient and family education
Advise that palliative treatment is not
a cure
Advise about adverse reactions and
dietary restrictions.
Ongoing
assessment
and
evaluation
Monitor for the ability to perform
activities of daily living.
Question:
What is the rationale for giving levodopa and
carbidopa together?
A. The medications create a synergistic
effect.
B. The carbidopa facilitates peripheral
uptake of the levodopa.
C. The carbidopa prevents levodopa from
crossing into the brain.
D. The carbidopa prevents levodopa from
being broken down in the periphery.
Rationale: When carbidopa is administered
in combination with levodopa, it’s inhibiting
the conversion of levodopa the opening in
the periphery of the body, thereby increasing
the amount of levodopa available to diffuse
into the CNS.
Centrally Acting Anticholinergic Drugs
• The centrally acting anticholinergic
drugs work by blocking the access of
acetylcholine to cholinergic receptors
in the striatum.
• Centrally acting anticholinergic drugs
are less effective than carbidopalevodopa.
• Historically, there has not been
specific pharmacotherapy for treating
ALS.
• In December 1995, the FDA
approved riluzole (Rilutek), the first
drug for treatment of ALS.
Riluzole: Core Drug Knowledge
• Pharmacotherapeutics
- Indicate for treating ALS because it
shows
down
the
disease’s
progression
• Pharmacokinetics
•
•
•
•
•
•
•
•
•
-
Administered: oral. Metabolism: liver.
Excreted: urine and bile. Duration: 3
to 5 days
Pharmacodynamics
Unknown mechanism of action
Contraindications and precautions
Hypersensitivity
Adverse effects
Muscle fatigue, nausea, dizziness,
diarrhea,
anorexia,
vertigo,
somnolence, and hepatic injury
Drug interactions
Hepatotoxic drugs
Riluzole: Core Patient Variables
Health Status
Past medical (liver or kidney) and
physical assessment
Life span and gender
Monitor closely when given to elderly
patients.
Lifestyle, diet, and habits
Evaluate diet.
Environment
Drug most often given at home
Culture and inherited traits
Japanese descent affects clearance
of the drug.
Riluzole: Nursing Diagnoses and Outcomes
• Risk for injury related to hepatic
dysfunction, anemia, and CNS and
cardiovascular effects of riluzole
therapy.
- Desired outcomes: The patient will
immediately report any signs of
hepatic dysfunction, anemia, or CNS
or cardiovascular effects to the
prescriber.
• Disturbed thought processes related
to adverse CNS Effects
- Desired outcome: The patient will
remain oriented and able to
communicate effectively.
Riluzole: Planning and Interventions
• Maximize therapeutic effects
- Take with full glass of water on an
empty stoamch.
• Minimizing adverse effects
-
May cause dizziness or sedation
Teach patients not to drive until they
know the effects of the medication
Rilozule: Teaching, Assessment, and
Evaluations
• Patient and family education
- tell the patient with the drug will not
change the course of the disease.
- Elaborate on how to properly take the
medication.
- Discuss a adverse a Effects of
medication
• Ongoing assessment and evaluation
- Coordinate regular follow-up care.
- Contact the provider if experience
adverse effects.
Question:
In teaching a patient about riluzole, which of
the following statements would indicate the
need for addiitonal teaching?
A. “I should take my medication with
breakfast and dinner.”
B. “I will take my medication before meals.”
C. “I will take my medication with a full glass
of water
Rationale: taking riluzole with meals will
decrease the bioavailability of the drug, whk
will make the drug less effective.
•
•
•
-
•
Anti-Multiple Sclerosis Drugs
Although there is no cure for MS,
various drugs are available to modify
the deceased of course, three
exacerbations
and
manage
symptoms.
Pharmacotherapy for MS uses a
multilayered approach.
Drugs used to affect the pro green of
the disease are called “ABC therapy.”
These drugs are interferon beta-1a
(Avenox),
interferon
beta-1b
(Betaseron),
and
glatiramer
(Copaxone).
Proptoptype
drug:
glatiramer
(Copaxone)
Glatiramer: Core Drug Knowledge
Pharmacotherapeutics
Used to reduce the frequency of MS
attacks
• Pharmacokinetics
- Has not been studies
• Pharmacodynamics
- Synthetic chemical that is similar in
structure to myelin basin protein
- Action unclear
• Contraindications and precautions
- IV administration and hypersensitivity
to mannitol
• Adverse effects
- Chest pain or tightness, breathing
difficulties, hives, or sever rash,
pounding heartbeat, and unusual
muscle weakness or tiredness.
• Drug interactions
- Can alter the results of a
Papanicolaou test
•
-
Glatiramer: Core Patient Variables
Health status
Past medical/allergy to mannitol,
baseline function
• Life span and gender
- Pregnancy Category B drug
• Lifestyle, diet, and habits
- No known lifestyle interactions
• Environment
- Administered in home setting
•
-
Glatiramer: Nursing Diagnoses and
Outcomes
• Weakness related to glatiramer
injection
- Desired outcome: The patient will
recognize weakness and take
measures to decrease its impact on
activities of daily living
• Skin integrity, Impaired, related to
injection site reactions
- Desired outcome: The patient will
employ strategies to minimize
injection site reactions.
• Disturbed
Sensory
Perception
related to anxiety and dizziness
-
Desired outcome: The patient will
notify the provider if these adverse
effects occur.
•
•
Glatiramer: Planning and Interventions
• Maximizing therapeutic effects
- Store in the refrigerator.
- Administer at room temperature
• Minimizing adverse effects
- Use
correct
administration
procedure.
- Rotate injection sites.
Glatiramer: Teaching, Assessment, and
Evaluations
• Patient and family education
- Review
adverse
effects
of
medication.
- Review proper preparation and
administration of medication.
• Ongoing assessment and evaluation
- Evaluate the progression of the
disease at each visit.
- Effective should decrease the
intensity of baseline symptoms and
prolong the intervals between acute
exacerbations of MS.
Question:
Which of the following is the route of
administration of glatiramer?
A. Oral
B. SC
C. IM
D. IV
Rationale: Glatiramer
subcutaneously
•
•
is
administered
Mysasthenia Gravis
Myasthenia Gravis (MG) is an
autoimmune disorder that impair the
receptors for acetycholine at the
myoneural junction.
It occurs more frequently in men over
50 years of age.
•
•
•
•
•
•
•
•
•
•
•
The first symptoms of MG are usually
weakness of the eye muscles and
ptosis.
Diagnosis of MG is based on the
edrophonium (Tensilon).
Cholinesterase inhibitors are the
drugs of choice.
Huntington Disease
Huntington Disease (Chorea) is an
inherited disorder.
The two main symptoms of the
disease or progressive mental status
changes and choreiform movements.
The inhibitory neurotransmitter GABa
is depleted in the basal nuclei and
substantia nigra.
There is currently no effective
treatment to prevent or delay the
progression of Huntington disease.
Treatment of choreiform movements
includes anti-psychotic drugs.
Gilles de la Tourette Disease
Gilles de lan Tourette disease
(Tourette syndrome, TS) is an
automobile dominant inherited tic
disorder appearing in childhood.
Motor and vocal tics from this disease
may respond to haloperidol (Haldol).
Primozide (Orap) is another drug
used for TS.
Other phenothiazines, particularly
fluphenazine (Prolixin), may be an
effective treatment.
Another drug useful in treating TS is
clonidine (Catapres).