Inflammation Flashcards

1
Q

What 3 things happen in acute inflammation

A
  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
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2
Q

What is the dominant cell type in acute inflammation

A

PMN

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3
Q

What is the aim of acute inflammation

A

To get PMN into the site of need and activation

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4
Q

How long does acute inflammation last for once stimulus is withdrawn

A

<2 days

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5
Q

Outline the vascular changes that occur in acute inflammation

A

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

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6
Q

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

A
  1. Endothelial gap widening
  2. Cellular damage
  3. Increased transyctosis across endothelium
  4. Angiogenesis (leaky new vessels)
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7
Q

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

A
  1. platelet activating factor (PAF)
  2. bradykinin
  3. histamine
  4. leuokotrienes
  5. Substance P
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8
Q

In what 3 situations might vascular permeability account for oedema in

A
  1. acute anaphylaxis
  2. adult respiratory distress syndrome
  3. serum sickness
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9
Q

What mediates arteriolar dilatation in early stages of acute inflammation

A
  1. prostacyclin (PGI2)
  2. nitric oxide (NO)
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10
Q

How does endothelial gap widening occur

A
  • mediated by histamine, bradykinin, PAF, leukotrienes, substance P ! only involves venules; capillaries & arterioles unaffected
  • cytoskeletal reorganization ! mediated by IL-1 and TNF-a
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11
Q

How does cell damage contribute to increased permeability

A
  • From direct injury > cell dies > release above mediators > affect the entire microcirculation
  • From leukocytes aggregating and releasing toxic oxygen free radicals and proteolytic enzymes
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12
Q

How does transcytosis increase vascular permability

A

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

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