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Z.Fiser > Fiser.13.Inflammation > Flashcards

Fiser.13.Inflammation Flashcards

1
Q

what three processes occur with endothelial injury?

A

exposed collagen; platelet-activating factor release; tissue factor release

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2
Q

what substance is released from the endothelium when platelets bind to collagen

A

PDGF (platelet-derived growth factor) is released

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3
Q

what cells are recruited by endothelial release of PDGF?

A

recruits PMNs and macrophages

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4
Q

What cell type has the dominant role in wound healing?

A

macrophages

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5
Q

what three substances are released by macrophages that causes its dominant role in wound healing?

A

growth factors (PDGF), cytokines (IL-1, TNF-alpha)

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6
Q

what two cell types are attracted by PDGF and what do they cause?

A

PDGF is chemotactic and activates inflammatory cells (PMNs and macrophages) and fibroblasts (causing collagen and ECM proteins)

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7
Q

what effect does PDGF have on blood vessels?

A

causes angiogenesis

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8
Q

what effect does PDGF have on epithelial cells?

A

causes epithelialization

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9
Q

what effect does PDGF have on smooth muscle cells?

A

chemotactic for smooth muscle cells

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10
Q

what effect does PDGF have on wound healing?

A

shown to accelerate wound healing

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11
Q

name three effects of epidermal growth factor (EGF)

A

chemotactic and activates fibroblasts (collagen and ECM proteins); angiogenesis; epithelialization

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12
Q

name three effects of fibroblastic growth factor (FGF)

A

chemotactic and activates fibroblasts (collagen and ECM proteins), angiogenesis, epithelialization

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13
Q

what type of molecule is platelet-activating factor?

A

its a phospholipid

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14
Q

where is platelet-activating factor generated?

A

it is generated by phospholipase in the endothelium

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15
Q

what is the effect of platelet-activating factor (2)?

A

chemotactic for inflammatory cells; increases adhesion molecules

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16
Q

name six chemotactic factors for inflammatory cells

A

PDGF, IL8, LTB4, C5a, C3a, PAF

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17
Q

name three chemotactic factors for fibroblasts

A

PDGF, EGF, FGF

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18
Q

name five angiogenesis factors

A

PDGF, EGF, FGF, IL8, hypoxia

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19
Q

name three epithelialization factors

A

PDGF, EGF, FGF

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20
Q

how long do PMNs last in tissues

A

PMNs last 1-2 days in tissue

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21
Q

how long do PMNs last in blood?

A

PMNs last 7 days in blood

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22
Q

How long do platelets last in blood?

A

last 7-10 days in blood

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23
Q

what type of lymphocyte is involved in chronic inflammation?

A

T-cells

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24
Q

what type of lymphocyte is involved in antibody production?

A

B cells

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25
Q

Which WBC is involved in type I hypersensitivity reaction

A

eosinophils

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26
Q

what type of receptors are on eosinophils and how does it affects its ability to take part in allergic reactions / type I hypersensitivity reactions?

A

IgE receptors that bind to allergen

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27
Q

what chemical is released by eosinophils and how does this stimulate the immune system?

A

eosinophils release major basic protein, which stimulates basophils and mast cells to release histamine

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28
Q

in what type of infection are eosinophils increased?

A

increased in parasitic infections

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29
Q

what is the major source of histamine in the blood?

A

basophils

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30
Q

are basophils present in tissue?

A

nope

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31
Q

what is the primary cell in type I hypersensitivity reactions?

A

mast cells

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32
Q

what is the major source of histamine in tissue?

A

mast cells

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33
Q

name three effects of histamine on tissues and capillaries (3)?

A

vasodilation, tissue edema, postcapillary leakage

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34
Q

what is the primary effector in type I hypersensitivity reactions?

A

histamine

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35
Q

Name four systemic effects of bradykinin

A

peripheral vasodilation, increased permeability, pain, pulmonary vasoconstriction

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36
Q

what is the function of angiotensin-converting enzyme and where is it located?

A

ACE inactivates bradykinin and is located in the lungs

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37
Q

what is the amino acid precursor for nitric oxide?

A

arginine

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38
Q

what is the enzyme that catalyzes the synthesis of nitric oxide and what is its substrate?

A

nitric oxide synthase converts arginine to nitric oxide

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39
Q

name the two reactions that occur in the endothelium that causes nitric oxide to vasodilate

A

NO activates guanylate cyclase, increases cGMP, resulting in vascular smooth muscle dilation

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40
Q

what is an alternative name for nitric oxide?

A

endothelium-derived relaxing factor

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41
Q

how does endothelin affect the vascular system?

A

causes vascular smooth muscle constriction (opposite effect of nitric oxide)

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42
Q

name the two main initial cytokine response to injury and infection

A

TNF alpha and IL-1

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43
Q

what cell is the largest producer of TNF-alpha

A

macrophages

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44
Q

what is the effect of TNF alpha on adhesion molecules?

A

increases adhesion molecules

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45
Q

what is the effect of TNF-alpha on coagulation?

A

procoagulant

46
Q

what is the effect of TNF-alpha on cancer patients?

A

causes cachexia in patients with cancer

47
Q

what is the effect of TNF alpha on other WBCs?

A

activates neutrophils and macrophages –> more cytokine production and cell recruitment

48
Q

name two systemic effects of high levels of TNF-alpha?

A

causes circulatory collapse and multisystem organ failure

49
Q

what is the major source of IL-1?

A

macrophages

50
Q

what does IL-1 synergize with?

A

synergizes with TNF-alpha

51
Q

what are the effects of IL-1? (3)

A

similar to TNF-alpha: increased adhesion molecules, procoagulant, activates neutrophils and macrophages

52
Q

which interleukin causes fever?

A

IL-1

53
Q

how does IL-1 cause fever?

A

mediated by PGE2 in the hypothalamus by raising the thermal set point

54
Q

What is the MOA of antipyretic NSAIDs?

A

reduces PGE2 synthesis, which is responsible for increasing the thermal set point in the hypothalamus

55
Q

What is the MOA of fever with atelectasis?

A

alveolar macrophages cause fever with atelectasis by releasing IL-1

56
Q

what proteins are stimulated for release by IL-6 (2)?

A

IL-6 stimulates increased hepatic acute phase proteins (C-reactive protein and amyloid A)

57
Q

what cell type releases interferons and why?

A

released by lymphocytes in response to viral infection

58
Q

what are the three cell types activated by interferons?

A

activates macrophages, natural killer cells, and cytotoxic T-cells

59
Q

how do interferons affect viruses?

A

inhibits viral replication

60
Q

what is the most potent stimulus for hepatic acute phase response proteins?

A

IL6

61
Q

what is the function of C-reactive protein?

A

opsonin, activates complement

62
Q

name 7 hepatic acute phase response proteins that are increased with IL6

A

CRP, amyloid A, amyloid P, fibrinogen, haptoglobin, ceruloplasmin, alpha-1 antitrypsin, C3 (complement)

63
Q

name 3 hepatic acute phase response proteins that are decreased with IL6

A

albumin, pre-albumin, transferrin

64
Q

where are L-selectins located?

A

located on leukocytes

65
Q

where are E-selectins located?

A

endothelium

66
Q

where are P-selectins located?

A

platelets

67
Q

how do L-selectins, E-selectins, and P-selectins interact to allow for rolling adhesion

A

L-selectins on leukocytes bind to E-selectins on endothelium and P-selectins on platelets, causing rolling adhesion

68
Q

where are beta-2 integrins located?

A

on leukocytes

69
Q

what is the function of beta-2 integrins?

A

bind ICAMs and function in anchoring adhesion

70
Q

where are ICAM, VCAM, PECAM, and ELAM located?

A

on endothelial cells

71
Q

what is the function of ICAM, VCAM, PECAM, and ELAM? (2)

A

bind to beta-2 integrin molecules located on leukocytes and platelets. Also involved in transendothelial migration.

72
Q

**PHOTO** describe the four steps of leukocyte recruitment

A

1) circulating leukocytes express integrins in low-affinity conformation; 2) exposure to activated endothelium leads to rolling mediated by L-selecting/P-selectin on neutrophils and E-selectin on endothelium; 3) leukocyte exposure to cytokines released by macrophages phagocytosing pathogens induces high-affinity integrin conformation –> tight lieukocyte-nedothelial adhesion withintegrin; 4) exposure to chemokines leads to diapedesis mediated by beta1 and beta2 integrins

73
Q

what are the three complement factors are present only in the classic pathway?

A

C1, C2, C4

74
Q

how is the classic complement pathway activated?

A

IgG or IgM with antigen-antibody complex activation

75
Q

what are the two stimuli for the alternative complement pathway

A

endotoxin or bacteria

76
Q

what are three factors only found in the alternate complement pathway?

A

factors B, D, and P (properdin)

77
Q

what is the complement factor that is common to both classic and alternative pathways and functions as its convergence point?

A

C3

78
Q

what chemical is required for both classic and alternative complement pathways?

A

Magnesium

79
Q

name three complement anaphylatoxins

A

C3a, C4a, C5a

80
Q

what are the four systemic effects of complement anaphylatoxins

A

C3a, C4a, C5a –> increased vascular permeability, bronchoconstriction, activate mast cells, basophils

81
Q

what complement factors create the membrane attack complex?

A

C5b-9b

82
Q

what is the function of the membrane attack complex created by complement?

A

cell lysis (usually bacteria) by creating a hole in cell membrane

83
Q

define opsonization

A

targets antigen for immune response

84
Q

name two complement factors that act as opsonins

A

C3b and C4b

85
Q

name two complement factors that cause chemotaxis for inflammatory cells

A

C3a and C5a

86
Q

what is the precursor for prostaglandins

A

produced from arachidonic precurosrs

87
Q

name four systemic effects of PGI2

A

vasodilation, increased vascular permeability, bronchodilation, inhibit platelets

88
Q

name four systemic effects of PGE2

A

vasodilation, increased vascular permeability, bronchodilation, inhibit platelets

89
Q

what is the MOA of NSAIDs anti-inflammatory action?

A

reversible COX (cyclooxygenase) inhibitor

90
Q

what is the MOA of aspirin’s anti-inflammatory action

A

irreversible COX (cyclooxygenase) inhibitor

91
Q

what is the MOA of platelet inhibition by aspirin?

A

inhibits platelet adhesion by decreasing TXA2

92
Q

what is the MOA of steroids’ anti-inflammatory action?

A

inhibit phospholipase (converts phospholipids to arachidonic acid) –> inhibits inflammation

93
Q

what is the precursor for leukotrienes?

A

produced from arachidonic precurosrs

94
Q

what are the systemic effects of LTC4, LTD4, and LTE4 (leukotrienes) (2)

A

slow-reacting substances of anaphylaxis; bronchoconstriction, vasoconstriction followed by increased permeability (wheal and flare)

95
Q

what is the effect of LTB4 (leukotriene)

A

chemotactic for inflammatory cells

96
Q

when do catecholamines peak after injury?

A

peak 24-48 hours after injury

97
Q

where is norepinephrine released from?

A

released from sympathetic postganglionic neurons

98
Q

where are epinephrine and norepinephrine released from?

A

released from adrenal medulla (neural response to injury)

99
Q

describe the pathophysiology of the neuroendocrine response to injury (6 hormones)

A

afferent nerves from site of injury –> stimulate CRF (corticotropin releasing factor), ACTH, ADH, growth hormone, epinephrine, and norepinephrine release

100
Q

what role do thyroid hormones play in injury/inflammation

A

no major role in injury or inflammation

101
Q

what is the role of CXC chemokines in inflammation (3)

A

chemotaxis, angiogenesis, wound healing

102
Q

name two CXC chemokines

A

IL8, platelet factor 4

103
Q

what does the “C” in CXC chemokines stand for?

A

cysteine

104
Q

what does the “X” in CXC chemokines stand for?

A

another amino acid

105
Q

what process results in oxidant generation?

A

inflammation (from main producer oxidase)

106
Q

what enzyme produces the superoxide anion radical (O2-)

A

NADPH oxidase

107
Q

what enzyme produces hydrogen peroxide (H2O2)?

A

xanthine oxidase

108
Q

what is the cellular defense against superoxide anion radicals?

A

superoxide dismutase converts it to hydrogen peroxide

109
Q

what enzyme protects against hydrogen peroxide

A

glutathione peroxidase / catalse

110
Q

what cells are the primary mediator of reperfusion injury?

A

PMNs

111
Q

what is the pathophysiology of chronic granulomatous disease?

A

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

Z.Fiser (22 decks)

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