Fiser.13.Inflammation Flashcards Preview

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Flashcards in Fiser.13.Inflammation Deck (111):
1

what three processes occur with endothelial injury?

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

2

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

PDGF (platelet-derived growth factor) is released

3

what cells are recruited by endothelial release of PDGF?

recruits PMNs and macrophages

4

What cell type has the dominant role in wound healing?

macrophages

5

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

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

6

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

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

7

what effect does PDGF have on blood vessels?

causes angiogenesis

8

what effect does PDGF have on epithelial cells?

causes epithelialization

9

what effect does PDGF have on smooth muscle cells?

chemotactic for smooth muscle cells

10

what effect does PDGF have on wound healing?

shown to accelerate wound healing

11

name three effects of epidermal growth factor (EGF)

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

12

name three effects of fibroblastic growth factor (FGF)

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

13

what type of molecule is platelet-activating factor?

its a phospholipid

14

where is platelet-activating factor generated?

it is generated by phospholipase in the endothelium

15

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

chemotactic for inflammatory cells; increases adhesion molecules

16

name six chemotactic factors for inflammatory cells

PDGF, IL8, LTB4, C5a, C3a, PAF

17

name three chemotactic factors for fibroblasts

PDGF, EGF, FGF

18

name five angiogenesis factors

PDGF, EGF, FGF, IL8, hypoxia

19

name three epithelialization factors

PDGF, EGF, FGF

20

how long do PMNs last in tissues

PMNs last 1-2 days in tissue

21

how long do PMNs last in blood?

PMNs last 7 days in blood

22

How long do platelets last in blood?

last 7-10 days in blood

23

what type of lymphocyte is involved in chronic inflammation?

T-cells

24

what type of lymphocyte is involved in antibody production?

B cells

25

Which WBC is involved in type I hypersensitivity reaction

eosinophils

26

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

IgE receptors that bind to allergen

27

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

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

28

in what type of infection are eosinophils increased?

increased in parasitic infections

29

what is the major source of histamine in the blood?

basophils

30

are basophils present in tissue?

nope

31

what is the primary cell in type I hypersensitivity reactions?

mast cells

32

what is the major source of histamine in tissue?

mast cells

33

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

vasodilation, tissue edema, postcapillary leakage

34

what is the primary effector in type I hypersensitivity reactions?

histamine

35

Name four systemic effects of bradykinin

peripheral vasodilation, increased permeability, pain, pulmonary vasoconstriction

36

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

ACE inactivates bradykinin and is located in the lungs

37

what is the amino acid precursor for nitric oxide?

arginine

38

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

nitric oxide synthase converts arginine to nitric oxide

39

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

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

40

what is an alternative name for nitric oxide?

endothelium-derived relaxing factor

41

how does endothelin affect the vascular system?

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

42

name the two main initial cytokine response to injury and infection

TNF alpha and IL-1

43

what cell is the largest producer of TNF-alpha

macrophages

44

what is the effect of TNF alpha on adhesion molecules?

increases adhesion molecules

45

what is the effect of TNF-alpha on coagulation?

procoagulant

46

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

causes cachexia in patients with cancer

47

what is the effect of TNF alpha on other WBCs?

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

48

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

causes circulatory collapse and multisystem organ failure

49

what is the major source of IL-1?

macrophages

50

what does IL-1 synergize with?

synergizes with TNF-alpha

51

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

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

52

which interleukin causes fever?

IL-1

53

how does IL-1 cause fever?

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

54

What is the MOA of antipyretic NSAIDs?

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

55

What is the MOA of fever with atelectasis?

alveolar macrophages cause fever with atelectasis by releasing IL-1

56

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

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

57

what cell type releases interferons and why?

released by lymphocytes in response to viral infection

58

what are the three cell types activated by interferons?

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

59

how do interferons affect viruses?

inhibits viral replication

60

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

IL6

61

what is the function of C-reactive protein?

opsonin, activates complement

62

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

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

63

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

albumin, pre-albumin, transferrin

64

where are L-selectins located?

located on leukocytes

65

where are E-selectins located?

endothelium

66

where are P-selectins located?

platelets

67

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

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

68

where are beta-2 integrins located?

on leukocytes

69

what is the function of beta-2 integrins?

bind ICAMs and function in anchoring adhesion

70

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

on endothelial cells

71

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

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

72

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

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

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73

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

C1, C2, C4

74

how is the classic complement pathway activated?

IgG or IgM with antigen-antibody complex activation

75

what are the two stimuli for the alternative complement pathway

endotoxin or bacteria

76

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

factors B, D, and P (properdin)

77

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

C3

78

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

Magnesium

79

name three complement anaphylatoxins

C3a, C4a, C5a

80

what are the four systemic effects of complement anaphylatoxins

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

81

what complement factors create the membrane attack complex?

C5b-9b

82

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

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

83

define opsonization

targets antigen for immune response

84

name two complement factors that act as opsonins

C3b and C4b

85

name two complement factors that cause chemotaxis for inflammatory cells

C3a and C5a

86

what is the precursor for prostaglandins

produced from arachidonic precurosrs

87

name four systemic effects of PGI2

vasodilation, increased vascular permeability, bronchodilation, inhibit platelets

88

name four systemic effects of PGE2

vasodilation, increased vascular permeability, bronchodilation, inhibit platelets

89

what is the MOA of NSAIDs anti-inflammatory action?

reversible COX (cyclooxygenase) inhibitor

90

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

irreversible COX (cyclooxygenase) inhibitor

91

what is the MOA of platelet inhibition by aspirin?

inhibits platelet adhesion by decreasing TXA2

92

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

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

93

what is the precursor for leukotrienes?

produced from arachidonic precurosrs

94

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

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

95

what is the effect of LTB4 (leukotriene)

chemotactic for inflammatory cells

96

when do catecholamines peak after injury?

peak 24-48 hours after injury

97

where is norepinephrine released from?

released from sympathetic postganglionic neurons

98

where are epinephrine and norepinephrine released from?

released from adrenal medulla (neural response to injury)

99

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

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

100

what role do thyroid hormones play in injury/inflammation

no major role in injury or inflammation

101

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

chemotaxis, angiogenesis, wound healing

102

name two CXC chemokines

IL8, platelet factor 4

103

what does the "C" in CXC chemokines stand for?

cysteine

104

what does the "X" in CXC chemokines stand for?

another amino acid

105

what process results in oxidant generation?

inflammation (from main producer oxidase)

106

what enzyme produces the superoxide anion radical (O2-)

NADPH oxidase

107

what enzyme produces hydrogen peroxide (H2O2)?

xanthine oxidase

108

what is the cellular defense against superoxide anion radicals?

superoxide dismutase converts it to hydrogen peroxide

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109

what enzyme protects against hydrogen peroxide

glutathione peroxidase / catalse

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110

what cells are the primary mediator of reperfusion injury?

PMNs

111

what is the pathophysiology of chronic granulomatous disease?

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