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cell injury and inflammation > Mediators of inflammation > Flashcards

Mediators of inflammation Flashcards

1
Q

examples of 2 preformed granules -

A

vasoactive amines

Lysosomal constituents of leukocytes

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2
Q

2 vasoactive amines

A

Histamine

Serotonin

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3
Q

Where is histamine stored?

A

In connective tissue mast cells

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4
Q

What causes degranulation of histamine?

A
  • physical injury
  • Binding of IgE to mast cell
  • binding of C3a and C5a (anaphylatoxins)
  • cytokines - IL-1 and IL-8
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5
Q

What receptor does histamine activate

A

Activates H1 receptor of microvasculature

  • leads to VASODILATION
  • endothelial CONTRACTION
  • increased permeability
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6
Q

Where is serotonin stored?

A

In platelets and neuroendocrine cells

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7
Q

What causes release of serotonin?

A

Rapid degranulation of platelets

  • aggregation upon collagen or thrombin exposure
  • antigen antibody complexes
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8
Q

What receptor does serotonin activate

A

Serotonin receptor on microvasculature

- leads to ENDOTHELIAL contraction - increased permeability

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9
Q

Where are the lysosomal constituents of leukocytes stored?

A

In neutrophils and macrophages

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10
Q

What do lysosomal constituents of leukocytes contain?

A
  • acid proteases
  • Neutral proteases
  • collagenases
    elastases
    Phospholipases
    Plasminogen activator
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11
Q

What activates C3 and C5

A

Neutral proteases
and
Plasminogen activator
- remember extracell space is neutral

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12
Q

What 3 mediators are synthesized de novo?

A

Arachidonic acid metabolites - eicosanoids
Nitric oxide
CYtokines

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13
Q

Where do eicosanoids get released from?

A

Leukocytes
and
Damaged cells

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14
Q

What causes the release of eicosanoids?

A
  • injury to the cell membrane

- C5a!!!!

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15
Q

Which enzymes convert membrane phospholipids to arachidonic acid?

A

Phospholipases

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16
Q

What happens when arachidonic acid is acted on by COX

A
  • produce Prostacyclin - vasodilation
  • TXA2 - vasoconstriction
    PGD2, PGE2 -> vasodilation and permeability

PRO-INFLAMMATORY

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17
Q

What happens when arachidonic acid is acted on by 5-Lipooxygense

A

Leukotriene B4 produced –> vasoconstriction, bronchospasm, increased permeability

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18
Q

Which proteins in eicosanoid cascade involved in vasodilation

A

prostacyclin (PGI)
PGE1
PGE2
PGD2

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19
Q

Which proteins in eicosanoid cascade involved in VASOCONSTRICTION

A

TXA2

Leukotrienes C4, D4, E4

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20
Q

Which proteins in eicosanoid cascade involved in vascular PERMEABILITY

A

Leukotrienes C4, D4, E4

21
Q

Which proteins in eicosanoid cascade involved in chemotaxis and leukocyte adhesion

A

Leukotriene B4!!!

5-HETE

22
Q

Where is nitric oxide released from?

A

Endothelium and

Macrophages

23
Q

What is the function of NO?

A

Microbial killing
Vasodilation
Anti-inflammatory (reduce leukocyte adhesion, inhibit platelet aggregation)

24
Q

2 main cytokines in the inflammatory cascade

A

IL-1

TNF-alpha

25
Q

IL-1 and TNF-a lead to systemic effects such as

A

Fever
Leukocytosis
more Acute phase reactants
—> can result in septic shock

26
Q

2 examples of Plasma protein-derived mediators of inflammation

A

1) complement system -

2) Coagulation and kinin systems -

27
Q

Which pathway involves direct activation of complement by microbes

A

Alternate pathway

28
Q

Which pathway involves antibody-mediated activation of complement?

A

Classical pathway

29
Q

Which pathway involves mannose-binding activation of compelement?

A

Lectin pathway

30
Q

Which part of the arachidonic acid pathway do C3a and C5a activate?

A

LIPOoxygenase –> anti-inflammatory

pro and anti-

31
Q

What are the effector functions of C3a and C5a

A

Inflammatory

  • chemoattractants
  • recruit and activate white blood cells - release neutral proteases
32
Q

What are the effector functions of C3b

A

Phagocytosis

33
Q

What are the effector functions of MAC

A

Lysis of microbes

34
Q

which complement helps form mac

A

C5a

35
Q

What factor is involved in the Coagulation and Kinin systems?

A

Hageman Factor 12

  • activates intrinsic clotting pathway
  • activates Kinin cascade
36
Q

Thrombin activation by factor 12 leads to

A

Activation of COX-2 -> proinflammatory state
AND
Kalikrein production and production of Bradykinin - as well as C5 activation causing pain and complement activation

37
Q

Activation of COX2 leads to

A

Production of PGglandins and TXA2

-> inflammation - vasodilation - increased perm -> platelet aggregation -> increased APRs from the liver

38
Q

3 mediators involved in vasodilation

A
  1. Prostaglandins
  2. Nitric oxide (early acute)
  3. Histamine (early acute)
39
Q

3 mediators involved in vascular permeability

A
  1. Histamine and serotonin
  2. Leukotrienes
  3. C3a and C5a
40
Q

Mediators involved in chemotaxis and activation

A
  1. TNF
  2. IL-1
  3. C3a and C5a
  4. Leukotriene B4
41
Q

3 morphological hallmarks of acute inflammation

A
  1. Dilation of blood vessels
  2. Engorgement of vessels
  3. Exudation of leukocytes and fluid
42
Q

3 PATTERNS of acute inflammation

A
  1. Serous
  2. Fibrinous
  3. Supparative/Purulent
43
Q

Pattern of acute inflammation depends on

A
  1. Nature of injury
  2. Site of injury
  3. Severity
44
Q

Features of Serous inflammation

A

1 - mild injury (mild burn/infection)

  1. Minimal vascular permeability
  2. Fluid»»> Leukocytes
45
Q

Features of Fibrinous inflammation

A
  1. Marked vascular permeability (leakgage of fibrinogen
  2. Local procoagulant stimulus - cancer cells
  3. Typically in serous cavities - pleura
46
Q

Features of Suppurative inflammation

A
  • leukocyte recruitment&raquo_space;»fluid extrvasation
  • A collection of neutrophils
  • Related to Pyogenic organisms
47
Q

Steroids are

A

Non specific inhibitors of formation of eicosanoid metaboloties block phospholipases

48
Q

When you inhibit platelet aggregation

A

Can inhibit inflammation via inhibiting serotonin release

cell injury and inflammation (9 decks)

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