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Pathology

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Inflammation

Question
11 out of 13
 

In acute inflammation due to the contraction of endothelial cell cytoskeleton, which of the following results? (AIIMS May 2014)



A Delayed transient increase in permeability

B Early transient increase in permeability

C Delayed permanent increase in permeability

D Early permanent increase in permeability

Ans. B i.e., Early transient increase in permeability [Ref Robbin's 8th/e p. 47]

Increased vascular permeability

The hallmark of acute inflammation is increased vascular permeability

Mechanisms for increased permeability.

Mechanisms of increased vascular permeability

Mechanism

Caused by

Affected blood vessels

Properties of response

1. Formation of endothelial gaps (immediate transient response)

Vasoactive mediators like histamine, leukotrienes bradykinin and contraction of endothelial cell cytoskeleton

Venules

Rapid; Reversible; short lived (15 to 30 minutes)

2. Direct endothelial injury (immediate sustained response)

Toxins, infections, burns, chemicals causing endothelial cell necrosis and detachment

Venules, capillaries and arterioles

Fast and may be long lived

3. Delayed prolonged leakage

Thermal and radiation injury induced endothelial cell damage

Venules and capillaries

Delayed and long lived

4. Leukocyte mediated endothelial injury

Activated leukocytes causing endothelial injury or detachment

Venules (Mostly): Pulmonary and glomerular capillaries

Late and long lived

5. Increased transcytosis

Formation of vesiculopapular organelles near inter cellular junctions by histamine and VEGF

Venules

6. Leakage from new blood vessel

Mostly by vascular endothelial growth factor (VEGF) and less commonly by histamine and substance P

Sites of angiogenesis

Inflammation Flashcard List

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