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cell injury and inflammation > Mediators of inflammation > Flashcards

Mediators of inflammation Flashcards

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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

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A

Leukotrienes C4, D4, E4

21
Q

Which proteins in eicosanoid cascade involved in chemotaxis and leukocyte adhesion

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A

Leukotriene B4!!!

5-HETE

22
Q

Where is nitric oxide released from?

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A

Endothelium and

Macrophages

23
Q

What is the function of NO?

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A

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

24
Q

2 main cytokines in the inflammatory cascade

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A

IL-1

TNF-alpha

25
IL-1 and TNF-a lead to systemic effects such as
Fever Leukocytosis more Acute phase reactants ---> can result in septic shock
26
2 examples of Plasma protein-derived mediators of inflammation
1) complement system - | 2) Coagulation and kinin systems -
27
Which pathway involves direct activation of complement by microbes
Alternate pathway
28
Which pathway involves antibody-mediated activation of complement?
Classical pathway
29
Which pathway involves mannose-binding activation of compelement?
Lectin pathway
30
Which part of the arachidonic acid pathway do C3a and C5a activate?
LIPOoxygenase --> anti-inflammatory | pro and anti-
31
What are the effector functions of C3a and C5a
Inflammatory - chemoattractants - recruit and activate white blood cells - release neutral proteases
32
What are the effector functions of C3b
Phagocytosis
33
What are the effector functions of MAC
Lysis of microbes
34
which complement helps form mac
C5a
35
What factor is involved in the Coagulation and Kinin systems?
Hageman Factor 12 - activates intrinsic clotting pathway - activates Kinin cascade
36
Thrombin activation by factor 12 leads to
Activation of COX-2 -> proinflammatory state AND Kalikrein production and production of Bradykinin - as well as C5 activation causing pain and complement activation
37
Activation of COX2 leads to
Production of PGglandins and TXA2 | -> inflammation - vasodilation - increased perm -> platelet aggregation -> increased APRs from the liver
38
3 mediators involved in vasodilation
1. Prostaglandins 2. Nitric oxide (early acute) 3. Histamine (early acute)
39
3 mediators involved in vascular permeability
1. Histamine and serotonin 2. Leukotrienes 3. C3a and C5a
40
Mediators involved in chemotaxis and activation
1. TNF 2. IL-1 3. C3a and C5a 4. Leukotriene B4
41
3 morphological hallmarks of acute inflammation
1. Dilation of blood vessels 2. Engorgement of vessels 3. Exudation of leukocytes and fluid
42
3 PATTERNS of acute inflammation
1. Serous 2. Fibrinous 3. Supparative/Purulent
43
Pattern of acute inflammation depends on
1. Nature of injury 2. Site of injury 3. Severity
44
Features of Serous inflammation
1 - mild injury (mild burn/infection) 2. Minimal vascular permeability 3. Fluid>>>>> Leukocytes
45
Features of Fibrinous inflammation
1. Marked vascular permeability (leakgage of fibrinogen 2. Local procoagulant stimulus - cancer cells 3. Typically in serous cavities - pleura
46
Features of Suppurative inflammation
- leukocyte recruitment >>>>fluid extrvasation - A collection of neutrophils - Related to Pyogenic organisms
47
Steroids are
Non specific inhibitors of formation of eicosanoid metaboloties block phospholipases
48
When you inhibit platelet aggregation
Can inhibit inflammation via inhibiting serotonin release

cell injury and inflammation (9 decks)

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