Inflammation

Question 1

What 3 things happen in acute inflammation

Answer 1

1. vascular changes
   - increased flow
   -increased permeability
2. cellular reactions
   - extravasation of leukocytes
   - migration of leukocytes to target area > recognition and phagocytosis
3. orchestration of chemical mediators of acute inflammation

Question 2

What is the dominant cell type in acute inflammation

Answer 2

PMN

Question 3

What is the aim of acute inflammation

Answer 3

To get PMN into the site of need and activation

Question 4

How long does acute inflammation last for once stimulus is withdrawn

Answer 4

<2 days

Question 5

Outline the vascular changes that occur in acute inflammation

Answer 5

Increased flow
1. initially, transient vasoconstriction of arterioles occurs
2. vasodilation follows, causing increased flow > accounts for heat and redness
* this is mediated by PGI2 & NO
3. eventually this slows down because of increased vascular permeability > leading to stasis > oedema
4. 4. with slowing, leukocytic margination appears, a prelude to the cellular events

Question 6

What are the 4 main reasons there is an increase in permeability in acute inflammation

Answer 6

1. Endothelial gap widening
2. Cellular damage
3. Increased transyctosis across endothelium
4. Angiogenesis (leaky new vessels)

Question 7

What 5 chemical mediators are involved in increasing permeability of venules during the acute inflammatory reaction

Answer 7

1. platelet activating factor (PAF)
2. bradykinin
3. histamine
4. leuokotrienes
5. Substance P

Question 8

In what 3 situations might vascular permeability account for oedema in

Answer 8

1. acute anaphylaxis
2. adult respiratory distress syndrome
3. serum sickness

Question 9

What mediates arteriolar dilatation in early stages of acute inflammation

Answer 9

1. prostacyclin (PGI2)
2. nitric oxide (NO)

Question 10

How does endothelial gap widening occur

Answer 10

• mediated by histamine, bradykinin, PAF, leukotrienes, substance P ! only involves venules; capillaries & arterioles unaffected
• cytoskeletal reorganization ! mediated by IL-1 and TNF-a

Question 11

How does cell damage contribute to increased permeability

Answer 11

• From direct injury > cell dies > release above mediators > affect the entire microcirculation
• From leukocytes aggregating and releasing toxic oxygen free radicals and proteolytic enzymes

Question 12

How does transcytosis increase vascular permability

Answer 12

via vesicles and vacuoles of the vesiculovacuolar organelle
* some growth factors, e.g. vascular endothelial growth factor may cause vascular leakage by increasing number and size of these channels