•
Chemically, lipid include compounds that yield------------- fatty acids on hydrolysis
and -------------------------- that can combine with fatty acid to form --------protein, --- complex alcohols------ carbohydrate
fatty acids, --- complex alcohols------ ester
Carbohydrate, --- complex alcohols------ protein
All of the above are corrects.
None of the above is correct.
2- Apolipoproteins differ:
in their primary, secondary, and tertiary structure.
Physiochemical behavior
Their function and distribution
All of the above
None of the above
A.
B.
C.
D.
E.
•
A.
B.
C.
D.
E.
F.
• 3- Which of the following is corrects for HDL Apolipoproetin ?
A. Apolipoproetin A form the major proteins found in HDL
B. They originate on liver or intestine or both.
C. Apo B is the major protein found inHDL.
D. A and B
E.
B and C
• 4- which of the following is/are correct/s for VLDL
A.
VLDL synthesized in and released from the liver.
B.
VLDL transports hepatic-synthesized triglycerides and cholesterol which called endogenous lipids.
C.
VLDL is absorbed from plant sources in the intestine.
D.
A and B
E.
A, B and C
•
• 8- Wilson’s disease is an inherited condition characterized by
A.
low blood level of the copper-binding protein ceruloplasmin
B.
low blood level of the iron-binding protein ceruloplasmin
C.
High blood level of the cholesterol-binding protein ceruloplasmin
D.
A and B
E.
A and C
•
• The pathological stage of the echinococcus species is
A.
Larva
B.
Egg
C.
Adult
D.
A and b
E.
B and C
•
• Echinococcus body composed of
A. Scolex, Neck, 3 segments
B. Scolex, Neck, 10 segments
C. Scolex, Neck, 1 segments
D. Scolex, Neck, 30 segments
E.
None of the above
•
• Echinococcus granulosus Definitive Host include/s:
A. Carnivores including dogs, wolves
B. Intermediate Host: Herbivores sheep and mice
C. Human
D. A and B
E.
B and C
•
• Echinococcus granulosus infection through
A. Insect bite such as fly
B. Animal bites such as dogs
C. ingestion of eggs
D. A and B
• Mycobacteria pathogenic for humans can be
differentiated
A. speed of growth (all are slower than most other
pathogens)
B. production of chromogenic pigments (in light, in dark, or
none)
C. speed of growth (all are faster than most other
pathogens)
D. A and B
E. B and C
•
• Different forms of Apo B protein is found in humans:
A. Large B or B-100 synthesized in Liver
B. Small B or B-48 synthesized in intestine.
C. Medium B or B-75 synthesized in heart
D. A and B
E. A,B and C
Q#
Answer
Statements
300. of plant sterols is ingested but poorly absorbed
Almost 90% of the body cholesterol is synthesized by the liver and gut
from simpler molecules particularly acetate.
Synthesized cholesterol is releazed into circulation for transport with
specific apolipoproteins in complexes known as lipoproteins.
Polyunsaturated fatty acids have more than one double bond
F
LDL form from the hepatic depletion of IDL by hepatic lipoprotein lipase
in the liver
F
HDL accumulates cholesterol and Apo E is rapidly transferred to IDL
F
IDL is catabolized to VLDL.
T
Chylomicrons
F
VLDL synthesized in and released from the stomach
T
Familial Hybercholesrolemia is an inherited autosomal dominant gene.
T
An apolipoprotein E variant is the only unequivocal genetic risk factor
Responsible for transporting dietary fat
Essay Questions
•
1.
Observation of more than or equal to (≥) 5mm reactivity of PPD
test mean________
2.
WHat is the difference between Intermediate host, Definitive
host, and Paratenic host
3.
Infection can be acquired by various routes, mention five routes
with example
4.
The development of the Mycobacteria disease depends on the
outcome of the battle between the TB and the specific cellular
immune defenses.
Q1 - PPD Tuberculosis Skin Test Criteria
PPD = Purified Protein Derivative from M. tuberculosis
Q2 Answer
• Symbiosis: A parasitic relationship which results in
great advantage to each other as compared to
disadvantage.
• Obligate parasite: A parasite which is completely
dependent upon the host.
• Pathogen: a parasite which is able to produce
disease.
• Intermediate host: a host in which the intermediate
stage of the parasite develops.
• Definitive host: a host is which sexual reproduction
takes place or the adult form of the parasite resides.
• Paratenic host: a host which acts as a transporting
agent for the parasite and in which parasites dose
not undergo any development.
• Infection: refer to the presence of parasite in or on
the tissue of the host.
• Infestation: presence of arthropods on the skin of
the host.
• Incubation period: the time interval between the
entrance of the parasite into host and the beginning
of disease.
Q3, Answer- Mode of infection in
parasite disease
•
Infection can be acquired by various routes.
1. Through animals :
A. pig : e.g. porktapeworm
B. Cat : e.g. toxoplasmosis
2.
3.
4.
5.
6.
7.
Autoinfection: threadworm
Water-borne: e.g. Amoebiasis, giardisis.
Vector borne: e.g. mosquito (malaria)
Contaminated food: Ascaris, Amoebiasis
Vertical transmission: malaria, toxoplasmosis
Penetration through skin: Hookworm, Schistosomiasis
Q4, Answer- Pathogenesis and clinical
picture
• It is necessary to differentiate between primary and
secondary tuberculosis (reactivation or postprimary
tuberculosis)
• The clinical symptoms are based on reactions of the
cellular immune system with TB antigens.
• Primary tuberculosis: In the majority of cases, the
pathogens enter the lung in droplets, where they are
phagocytosed by alveolar macrophages.
• TB bacteria are able to reproduce in these macrophages due to their
ability to inhibit formation of the phagolysosome.
• Within 10–14 days a reactive inflammatory the TB bacteria move into
the regional hilar lymph nodes, where they reproduce and stimulate a
cellular immune response, which in turn results in clonal expansion of
specific T lymphocytes and attendant lymph node swelling.
• The Ghon’s complex (primary complex, PC) develops between six and
14 weeks after infection.
• At the same time, granulomas form at the primary infection site and in
the affected lymph nodes, and macrophages are activated by the
cytokine MAF (macrophage activating factor).
• A tuberculin allergy also develops in the macroorganism.
• The development of the disease depends on the outcome of the
battle between the TB and the specific cellular immune
defenses.
• Postprimary dissemination: development of local tissue defect
foci at other localizations, typically the apices of the lungs.
• Mycobacteria may also be transported to other organs via the
lymph vessels or bloodstream and produce dissemination foci
there.
• The host eventually prevails in over 90% of cases: the
granulomas and foci fibrose, scar, and calcify, and the infection
remains clinically silent.
Secondary tuberculosis
• About 10% of infected primary tuberculosis persons the reactivates to
become an organ tuberculosis, either within months (5 %) or after a
number of years (5 %).
• Exogenous reinfection is rare in the populations of developed
countries.
• Reactivation begins with a caseation necrosis in the center of the
granulomas (also called tubercles) that may progress to cavitation
(formation of caverns).
• Tissue destruction is caused by cytokines, among which tumor necrosis
factor a (TNFa) appears to play an important role.
• This cytokine is also responsible for the cachexia (wasting syndrome is
loss of weight, muscle atrophy) associated with tuberculosis.
Reactivation frequently stems from old foci in the lung apices.
Secondary tuberculosis
• About 10% of infected primary tuberculosis persons the reactivates to
become an organ tuberculosis, either within months (5 %) or after a
number of years (5 %).
• Exogenous reinfection is rare in the populations of developed
countries.
• Reactivation begins with a caseation necrosis in the center of the
granulomas (also called tubercles) that may progress to cavitation
(formation of caverns).
• Tissue destruction is caused by cytokines, among which tumor necrosis
factor a (TNFa) appears to play an important role.
• This cytokine is also responsible for the cachexia (wasting syndrome is
loss of weight, muscle atrophy) associated with tuberculosis.
Reactivation frequently stems from old foci in the lung apices.