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Pathology > Inflammation II > Flashcards

Inflammation II Flashcards

1
Q

What are the two major processes of phagocytosis?

A
  1. Recognition and attachments via complement

2. Engulfment

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2
Q

What is the function of complement?

A

Attach to microbes and macrophages

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3
Q

What is the process of engulfment?

A

Pseudopods surround object, forming, phagosome fusing with lysosome

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4
Q

Phagosome + lysosome = ?

A

Phagolysosome

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5
Q

What are the two types of mechanisms of microbe killing?

A
  1. Oxygen dependent

2. Oxygen independent

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6
Q

What are the three steps of oxygen dependent killing?

A
  1. Oxygen is reduced to superoxide via NADPH oxidase
  2. Superoxide is then converted to H2O2 by superoxide dismutase
  3. Myelo-peroxidase from PMNs granules catalyzes rxn b/t Cl and H2O2, forming HOCl
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7
Q

What are the oxygen-independent ways to kill microbes? (2)

A

Leukocytes granule proteins, and enzymes

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8
Q

What are the four outcomes of leukocyte activation?

A
  1. Production of arachidonic acid metabolites
  2. Degranulation and secretion of lysosomal enzymes
  3. Secretion of cytokines
  4. Modulation of leukocyte adhesion molecules
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9
Q

Where do mediators come from? What is their function?

A

plasma or granules of cells

Bind to specific receptors on target cells to stimulate other cell response

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10
Q

What are the three sequential phases of chemical mediators that leukocytes express?

A
  1. Initiation
  2. Amplification
  3. Termination
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11
Q

Why are mediators short lived?

A

To prevent over reaction, since most have potential to cause harm

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12
Q

What are the two major vasoactive amines? What are their functions (3)?

A

Histamine and serotonin

  1. arteriolar dilation
  2. constriction of large arteries
  3. Increase permeability of postcapillary venules
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13
Q

Where are vasoactive amines stored?

A

Preformed granules of mast cells or others

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14
Q

What are the first mediators likely to be released in response to damage?

A

Vasoactive amines

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15
Q

What stimulates mast cells? (5)

A 
Trauma
Platelet aggregation
IgE activation
Complement
Cytokines
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16
Q

What are the three plasma protein systems?

A

Complement
Kinin
Clotting

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17
Q

What activates the classical pathway of complement activation?

A

binding of an IgG or IgM complex to C1 (“GM makes C1assic cars”)

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18
Q

What activates the alternate pathway of complement activation?

A

C3 directly activated by bacterial endotoxins, or aggregated IgA

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19
Q

What activates the lectin pathway of complement activation?

A

C1 activation by binding of mannose-binding lectin to carbs on microbes

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20
Q

What is the essential pathway of complement activation (where all three pathways converge)?

A

C3 activation (cleavage)

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21
Q

What is the function of C3a, C4a, and C5a?

A

Stimulate histamine release from mast cells

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22
Q

What is the function of C5a specifically?

A

chemotaxis of monocytes and granulocytes via increased expression of leukocytes CAM which activates lipoxygenase pathway

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23
Q

What is the function of C3b specifically?

A

Opsonization with recognition by receptors on PMNS

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24
Q

What is the function of C5-9?

A

Membrane attack complex

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25
Q

What is the function of Factor XII (Hageman factor)? How is it activated?

A

Triggers the kinin system, fibrinolytic system, and the clotting cascade

Activated by direct contact with endotoxins, collagen, or basement membrane

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26
Q

Activated Hageman factor (XII) does what in the kinin system, specifically?

A

Converts prekallikrein to Kallikrein

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27
Q

What is the function of Kallikrein after it is activated via Hageman factor (XII)?

A

amplifies hageman factors activation

Cleaves kinins, including bradykinin

Converts plasminogen to plasmin

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28
Q

What is bradykinin?

A

A short lived vasoactive peptide that increases vascular permeability, andcauses pain

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29
Q

What inactivates bradykinin?

A

Plasma kininase

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30
Q

What is the coagulation-fibrinolytic system?

A

Cascade of reaction resulting in a fibrin clot which is then dissolved by the fibrinolytic system

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31
Q

What is the function of thrombin?

A

Cleaves fibrinogen to insoluble fibrin

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32
Q

Why is thrombin significant in terms of the inflammatory system?

A

Links the coagulation system and the inflammatory system

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33
Q

What is the function of plasmin? (2)

A

Lyses fibrin clots to form fibrin split products

Cleaves C3 to C3a

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34
Q

What activates Hageman factor (XII)?

A

Collagen, basement membrane, activated platelets

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35
Q

What is arachidonic acid?

A

Lipid normally bound to cell membrane phospholipids and is released by the action of cellular phospholipases

36
Q

What are the two pathways that activate arachidonic acid?

A

COX

LOX

37
Q

What are the AA metabolites produced in the COX pathway?

A 
TXA2
PGI2
PGE2
PGD2
PGF2
PGE
38
Q

What is the function of TXA2? (2)

A

Potent platelet aggregator and vasoconstrictor

39
Q

What is the function of ASA in treating an MI specificalLy?

A

inhibits production of TXA2, thus inhibits platelet aggregation and vasoconstriction

40
Q

What is the function of PGI2?

A

Vasodilator and inhibitor of platelet aggregation

41
Q

What is the function of PGE2?

A

Sensitizes skin to painful stimuli and fever

42
Q

What is the function of PGD2, PGF2, and PGE2?

A

Vasodilation/edema

43
Q

What are the metabolites of the LOX pathway?

A

LTB4

LTC4, D4, E4

44
Q

What is the KEY function of LTB4?

A

Potent chemoattractant causing PMN aggregation and adhesion to endothelial cells

45
Q

What are the functions of LTC4, D4, and E4?

A

Causes intense vasoconstriction and bronchospasm

46
Q

What are lipoxins?

A

Endogenous negative regulators of Leukotriene action

47
Q

What is the function of lipoxin A4 and B4?

A

Inhibit PMN adhesion to endothelium and PMN chemotaxis

48
Q

What is the function of steroids in treating asthma?

A

Inhibit phospholipases that produce AA

49
Q

What are the two pathways that AA can go down?

A

Cyclooxygenase (COX)

Lipoxygenase (LOX)

50
Q

What is the MOA of ASA?

A

Inhibits Cyclooxygenase

51
Q

What generates platelet activating factors (PAF)?

A

basophils, PMNs, etc

52
Q

What is the main function of PAF? What is this dependent on?

A

Vaso/bronchoconstriction at high[C], BUT opposite at low [C]

53
Q

What is the other, more minor functions of platelet activating factor (PAF) mentioned in class?

A

Stimulates prostaglandin & leukotriene synthesis

54
Q

What are cytokines and chemokines?

A

Polypeptide which function as “cellular hormones”, that participate in intricate networks to achieve their effects

55
Q

What are the key cytokines?

A

IL-1 IL-8 and TNF-alpha

56
Q

What produces IL-1 and TNF-alpha? (or cytokines in general)

A

activated macrophages

57
Q

What are the acute phase effects of IL-1 and TNF-alpha?

A

Fever, sleep, shock, neutrophilia and hemodynamic effects

58
Q

What are the three endothelial effects of IL-1 and TNF-alpha?

A
  1. Increase leukocyte adherence
  2. Produces IL-1
  3. Increases Procoagulant activity
59
Q

What is the major fibroblastic effects of IL-1 and TNF-alpha?

A

Increased collagen synthesis

60
Q

What are the leukocyte effects of IL-1 and TNF-alpha?

A

Increase cytokine secretion (IL-1, IL-6)

61
Q

What is the function of chemokines?

A

Stimulates leukocyte recruitment in inflammation

62
Q

Almost all chemokines are what type of molecule?

A

Cysteine residues with some other amino acids in there somewhere

63
Q

What is the function of C-X-C (or alpha) chemokines?

A

Act primarily on PMNs

IL-8

64
Q

What is the function of C-C (or beta) chemokines?

A

Attract cells BESIDES neutrophils

65
Q

What is the function of C or Gamma-chemokines?

A

Specific fo lymphocytes

66
Q

What is the function of CX3C chemokines?

A

Strong attractant for monocytes and T cells

67
Q

What are the two functions of NO?

A

Vasodilation

Reduces platelet aggregation

68
Q

What are the two places that NO are prodced?

A

Endothelial cells

Macrophages

69
Q

What are the effects of ROS? (3)

A
  1. Endothelial cell damage
  2. Inactivation of antiproteases
  3. Injury to other cells
70
Q

What is substance P? Neurokinin A?

A

Both are neuropeptides, and act to cause pain, increases vascular permeability

71
Q

Vasodilation is caused by what two chemicals?

A

PG, NO

72
Q

Vascular permeability is produced by what?

A

Vasoacive amines,

C3a, C5a Leukotrienes (C4 D4 and E4) substance P

73
Q

Chemotaxis and leukocyte activation is produced by what?

A

C5a, leukotriene B4, chemokines

74
Q

Fever is produced by what?

A

IL-1, IL-6, TNF-alpha, and PG

75
Q

Pain is produced by what?

A

PG and bradykinin

76
Q

What produces tissue damage?

A

Lysosomal enzymes
Oxygen metabolites
NO

77
Q

Why is it that you do not develop a severe allergic reaction to a substance upon first exposure?

A

Because IgE needs to bind to mast cells (via Fc region) and “prime” it for next time

78
Q

What is the main constituent of bee venom? What does this cause?

A

Bradykinin= pain

79
Q

What are the three systems that activation of the Hageman factors sets in motion (4)

A
  1. Kinin cascade
  2. Fibrinolytic system
  3. Complement cascade
  4. Clotting cascade
80
Q

What is the cause of the bronchoconstriction seen in an allergic reaction?

A

Production of LTC4, D4, and E4

81
Q

What are the endogenous inhibitors of leukotrienes?

A

Lipoxins

82
Q

What are the major chemicals that inhibit neutrophil adhesion to the endothelium and neutrophil chemotaxis?

A

Lipoxin A4 and B4

83
Q

What does the COX pathway produce?

A

Prostaglandins

84
Q

What does the LOX pathway produce?

A

Leukotrienes

85
Q

What is the really general function of lysosomal enzymes of leukocytes? Why is this bad if left unchecked?

A

Destroy stuff, and that’s bad

Pathology (32 decks)

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