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ABSITE > 13 Inflammation > Flashcards

13 Inflammation Flashcards

1
Q

what causes chronic granulomatous disease? what does it result in?

A

NADPH-oxidase system enzyme defect in PMNs. results in decreased superoxide radical formation

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2
Q

what is the primary mediator of reperfusion injury?

A

PMNs

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3
Q

what are the cellular defenses against oxidative species?

A
  • for superoxide anion radical, superoxide dismutase: converts to hydrogen peroxide.
  • glutathione peroxidase, catalase then break down hydrogen peroxide
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4
Q

what are the oxidants generated in inflammation and what are the enzymes that caused it?

A

superoxide anion radical produced by NADPH oxidase. hydrogen peroxide generated from xanthine oxidase

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5
Q

what does CXC chemokines stand for and what are they?

A

C = cysteine; X = another amino acid. IL-8 and platelet factor 4

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6
Q

what do cxc chemokines do?

A

chemotaxis, angiogenesis, wound healing

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7
Q

what does thyroid hormone do during injury or inflammation?

A

nothing

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8
Q

what is the neuroendocrine response to injury?

A

afferent nerves from site of injury stimulate CrF, ACTH, ADH, growth hormone, epinephrine, and norepinephrine release

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9
Q

where in the body are epinephrine and norepinephrine released?

A

adrenal medulla (neural response to injury)

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10
Q

where in the nerve is norepinephrine released?

A

from sympathetic postganglionic neurons

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11
Q

when do catecholamines peak after injury?

A

24-48h

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12
Q

what does LTB4 do?

A

chemotactic for inflammatory cells

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13
Q

what are the leukotrienes and what do they do?

A

LTC4, LTD4, LTE4. slow reacting substances of anaphylaxis. bronchoconstriction, vasoconstriction, followed by inc permeability (wheal and flare)

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14
Q

where do prostaglandins come from?

A

arachidonic precursors

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15
Q

where do leukotrienes come from?

A

produced from arachidonic precursors

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16
Q

what does phospholipase do?

A

converts phospholipids to arachidonic acid

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17
Q

how do steroids work?

A

inhibit phospholipase, which converts phospholipids to arachidonic acid –> inhibits inflammation.

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18
Q

what does aspirin do? is it irreversible?

A

inhibits cyclooxygenase (irreversible), inhibits platelet adhesion by decreasing TXA2

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19
Q

what do NSAIDs do? are they reversible?

A

inhibits cyclooxygenase (reversible)

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20
Q

what prostaglandins cause vasodilation, bronchodilation, inc permeability, and inhibits platelets?

A

PGI2 and PGE2

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21
Q

what factors are responsible for chemotaxis for inflammatory cells?

A

C3a and C5a

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22
Q

what does opsonization do? mediated by what?

A

targets antigen for immune response, C3b and C4b

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23
Q

what is the membrane attack complex and what does it do?

A

C5b-9b; causes cell lysis (usually bacteria) by creating a hole in the cell membrane

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24
Q

what are the anaphylatoxins? what do they do?

A

C3a, C4a, C5a.

  • Increase vascular permeability
  • bronchoconstriction
  • activate mast cells and basophils
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25
Q

what factors are activated in classic pathway?

A

C1, C2, C4 found only in classic pathway

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26
Q

what electrolyte is required for both pathways?

A

Mg

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27
Q

what factor is common to and is the convergence point for both common and alternative pathway?

A

C3

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28
Q

what factors are activated in alternate pathway?

A

B, D, P found only in the alternate pathway

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29
Q

what are the activators in alternative pathway?

A

endotoxin, bacteria, other stimuli

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30
Q

what are the major molecules in classic pathway?

A

IgG or IgM: antigen-antibody complex activates complement

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31
Q

can you illustrate leukocyte recruitment?

A

illustration

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32
Q

where are ICAM, VCAM, PECAM, ELAM located? what do they do?

A

located on endothelial cells, bind beta-2 integrin moecules located on leukocytes and platelets. Also involved in transendothelial migration

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33
Q

what CD molecules are beta-2 integrins? where are they located? where do they bind? what do they do?

A

CD11/18
located on leukocytes
bind ICAMs etc.
they anchor adhesion

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34
Q

where are L-, E-, and P- selectins located?

A

leukocytes, endothelial, platelets

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35
Q

what do selectins do? what is the process?

A

cause rolling adhesion. L-selectins bind to E and P selectins

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36
Q

what are the cell adhesion molecules?

A

selectins, beta-2 integrins, ICAM, VCAM, PECAM, ELAM

37
Q

what hepatic acute phase response proteins are decreased?

A

albumin, prealbumin, transferrin

38
Q

what hepatic acute phase response proteins are increased??

A 
CRP
amyloid A and P 
fibrinogen
haptoglobin
ceruloplasmin
alpha-1 antitrypsin
C3 (complement)
39
Q

what is the most potent stimulant of hepatic acute phase response proteins?

40
Q

what type of protein is CRP?

A

an opsonin, activates complement

41
Q

what do interferons do?

A

activate macrophages, natural killer cells, cytotoxic T cells. they inhibit viral replication

42
Q

what releases interferons?

A

lymphocytes, in response to viral infections and other stimulants

43
Q

what does IL-6 do?

A

increase hepatic acute phase proteins via c-reactive protein, amyloid A

44
Q

how does atelectasis cause fever?

A

alveolar macrophages release IL-1

45
Q

how do NSAIDs decrease fever?

A

reduce PGE2 synthesis

46
Q

how does IL-1 cause fever?

A

through PGE2 mediated in hypothalamus, raising thermal set point, causing fever

47
Q

what are the effects of IL-1?

A

similar to TNF-a and synergizes TNF-a

responsible for fever

48
Q

what is the main source of IL-1?

A

macrophages

49
Q

what is the major producer of TNF-a?

A

macrophages

50
Q

is TNF-a a procoagulant or anticoaculant?

A

procoagulant

51
Q

what does TNF-a do to pts with cancer?

52
Q

what does high concentrations of TNF-a do?

A

cause circulatory collapse and multisystem organ failure

53
Q

what does TNF-a do?

A

recruits macrophages
increases adhesion molecules
activates neutrophils and macrophages –> more cytokine production, cell recruitment

54
Q

what cytokine are initially released to injury and infection?

A

TNF-a and IL1

55
Q

what substance causes the opposite effect of nitric oxide?

A

endothelin. (causes vascular smooth muscle constriction)

56
Q

what is the other name for nitric oxide?

A

endothelium-derived relaxing factor

57
Q

what does nitric oxide do?

A

activates guanylate cyclase and increases cGMP, resulting in vascular smooth muscle dilation

58
Q

what amino acid is the substrate in the nitric oxide precursor? what is the enzyme?

A

arginine. nitric oxide synthase

59
Q

what does angiotensin-converting enzyme (ACE) do? where is ACE located?

A

inactivates bradykinin. located in lung

60
Q

what does bradykinin do?

A

peripheral vasodilation, increased permeability, pain, pulmonary vasoconstriction

61
Q

what is the primary effector in type I hypersensitivity reactions?

62
Q

what does histamine do?

A

vasodilation, tissue edema, postcapillary leakage

63
Q

what is the primary cell type in type I hypersensitivity reactions?

A

mast cells

64
Q

where are basophils found?

A

blood. not tissue

65
Q

in what infections are eosinophils increased?

A

parasitic infections

66
Q

what does major basic protein do?

A

stimulate basophils and mast cells to release histamine

67
Q

how do eosinophils work?

A

have IgE receptors that bind to allergen, release basic science protein

68
Q

what cells are involved in type I hypersensitivity reactions?

A

eosinophils, basophils, mast cells, histamine, bradykinin, ACE

69
Q

what do TXA2 and PGI2 do?

A

what cells are involved in antibody production?

70
Q

what cells are involved in antibody production?

71
Q

what cells are involved in chronic inflammation?

72
Q

how long do platelets last?

73
Q

how long do PMNs last in the tissue? in blood?

A

1-2d. 7d in blood

74
Q

what are the chemotactic factors for fibroblasts?

A

PDGF
EGF
FGF

75
Q

what are the epithelialization factors?

76
Q

what are the angiogenesis factors?

A

PDGF
EGF
FGF
IL-8

77
Q

what are the chemotactic factors for inflammatory cells?

A 
PDGF
IL8
LTB-4
C5a, C3a
PAF
78
Q

what does FGF do?

A
  • fibroblastic growth factor
  • chemotactic and activates fibroblasts (collagen and ECM proteins).
  • angiogenesis, epithelialization
79
Q

what does EGF do?

A

epidermal growth factor
chemotactic, activates fibroblasts,angiogenesis
epithelialization

80
Q

what generates PAF? is it stored? what makes it? what type of molecule is it?

A

phospholipase in endothelium. not stored. is a phospholipid.

81
Q

what does PAF do?

A

platelet activating factor: chemotactic for inflammatory cells, increase of adhesion molecules

82
Q

what cells migrate toward pdgf using chemotaxis?

A

inflammatory cells, fibroblasts, smooth muscle cells

83
Q

what does PDGF do?

A

chemotacticm activates inflammatory cells, fibroblasts, angiogenesis, epithelialization, accelerates wound healing

84
Q

what happens during the macrophages phase?

A

release of important growth factors (PDGF) and cytokines (IL-1 and TNF-a)

85
Q

which cytokines are released during the macrophage phase?

A

IL-1 and TNFa

86
Q

what cell plays a the dominant role in wound healing?

A

macrophages

87
Q

what happens during the platelets bind collagen phase?

A

release growth factors (platelet-erived growth factor [PDGF]); leads to PMN and macrophage recruitment

88
Q

what happens during the injury phase?

A

leads to exposed collagen, platelet activating factor release, and tissue factor release from endothelium

89
Q

what are the inflammation phases?

A

injury, platelets bind collagen, macrophages

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