Professional Documents
Culture Documents
1. In acute inflammation
a. A hallmark is reduced vascular permeability
b. Vasodilation is a late manifestation
c. Extravasation involves movement of leukocytes from interstitial tissue to the vessel lumen
d. Chemotaxis is migration of leukocytes along a chemical gradient
e. Selectins have a minor role
6. Chronic inflammation is
a. Always preceded by acute inflammation – no, can result from low-grade persistent insult
b. Characterized by hyperaemia, oedema and leukocyte infiltration
c. Most frequently results in resolution
d. The factors underlying monocyte infiltration are the same as for acute inflammation
e. ?
7. In the triple response the reactive hyperaemia is due to:
- something wrong with the question, reactive hyperaemia is due to an increase in blood flow after re-
establishment after occlusion. The redness in the triple response is erythema.
a. Blushing
b. Exercise
c. Arteriolar dilation – true (if the question read initial then it would be incorrect, the initial is due to
capillary dilation)
d. Inflammatory mediators
e. Still present after sympathectomy – true
Tripple response = normal response to injury w/ red reaction, wheal and flare. Reddening in 10sec
due to capillary dilation, then oedema due to permeability, then flare due to arterioloar dilation.
Because it is an axon reflex with antidromic conduction sympathectomy or higher nerve block doesn’t
effect (although local block will prevent flare)
17. With regard to the acute inflammatory response, which is the most common mechanism of
vascular leakage?
a. Endothelial cell contraction
b. Junctional retraction
c. Direct injury
d. Leukocyte-dependent leakage
e. Regeneration indothelium
18. With regard to the role of complement in the acute inflammatory response, which is
INCORRECT?
a. C5a is a powerful chemotactic agent for neutrophils, monocytes and eosinophils
b. C5a increases leukocyte adhesion to endothelium by activating leukocytes
c. C3a and C5a are called anaphylatoxins because they cause mast cell degranulation
d. C3a activated the lipooxygenase pathway in leukocytes – C5a does…
e. C3 and C5 can be activated in inflammatory exudates by lysosomal enzymes
21. Cellular events in acute inflammation include all of the following EXCEPT:
a. Redistribution of preformed adhesion molecules to the cell surface of leukocytes
b. Adhesion and transmigration of leukocytes to endothelium
c. Leukocyte activation
d. Margination of macrophages to vessel walls
e. Extracellular release of lysosomal enzymes and products of arachidonic acid metabolism
28. In chronic inflammation the life span of tissue macrophages is closest to:
a. 4-8 hours
b. 1 day
c. 8 days
d. 2-4 weeks
e. 2 months
33. In acute inflammation, which is the correct sequence of events with regard to vascular
flow and caliber?
a. Vasodilation, margination, stasis, vasoconstriction
b. Vasoconstriction, stasis, margination, vasodilation
c. Vasodilation, stasis, vasoconstriction, marginaiton
d. Vasoconstriction, vasodilation, stasis, margination
e. Vasodilation, vasoconstriction, stasis, margination
38. With regard to the leukocyte extravasation of the acute inflammatory response, which of
the following is INCORRECT?
a. ELAM-1 is a selectin found on endothelium – aka E-selectin
b. E and P-selectins bind to oligosaccharides found on neutrophils and monocytes
c. L-selectin is found on neutrophils, monocytes and lymphocytes
d. ICAM-1 belongs to the immunoglobulin family of molecules, and is found on leukocytes – ICAM is
an intergrin ligand found on endolthelial cells
e. VCAM-1 binds to integrins
39. Phagocytosis
a. Occurs in 2 steps – 3 steps: recognition, engulfment and killing
b. C5a is an opsonin – C3b and iC3b
c. IgM is a potent opsonin
d. Bacterial killing occurs by mainly O2 dependent mechanisms
e. Doesn’t occur without opsonisation