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Path Gen 1 > Inflammatory Mediators > Flashcards

Inflammatory Mediators Flashcards

1
Q

most mediators have multiple functions, and most functions mediated by multiple factors (central to function of inflammatory mediators)

A

functional redundancy

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2
Q

kind of mediators for initiation

A

pre-formed

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3
Q

plasma-derived mediators needed for this stage of inflammation

A

initiation and augmentation

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4
Q

arachidonic acid derived mediators and chemokines serve this time period of inflammation

A

hours to days

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5
Q

mediators that must be synthesized before action…takes days to weeks

A

cytokines and growth factors

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6
Q

preformed mediators….needed for initiation

A

histamine, serotonin, lysozymes

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7
Q

preformed mediators involved with these early events in inflammation (initiate response)

A

vasodilation and vascular permeability

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8
Q

histamine receptor that mediates inflammatory reactions and increased vascular permeability

A

H1

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9
Q

histamine receptor that increases gastrointestinal secretions (anti-histamine causes block of acid production)

A

H2

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10
Q

histamine receptor in CNS (causes drowsiness in anti-histamine)

A

H3

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11
Q

histamine receptor in bone marrow and WBC

A

H4

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12
Q

do ACE inhibitors increase or decrease bradykinin levels? what is side effect?

A

increase; dry cough

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13
Q

how many C does arachidonic acid have? how many DB?

A

20, 4 (eicosatetraenoic acid)

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14
Q

these all derived from arachidonic acid

A

prostaglandins, thromboxanes, leukotrienes

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15
Q

what position is arachidonic acid normally located in phospholipid?

A

2nd

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16
Q

these enzymes responsible for release of arachidonic acid when phospoinositol is removed first

A

phospholipase C and diacylglycerol lipase

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17
Q

enzyme responsible for direct release of arachidonic acid

A

phospholipase A2

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18
Q

low dose aspirin only inhibits these mediators (good for pt who is at risk of heart attack)

A

thromboxane

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19
Q

do you want prostaglandins high or low in patient with risk for heart attack?

A

high

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20
Q

leukotriene primarily made by PMNs..cause PMN chemotaxis and secretion (effect is to enhance neutrophil chemotaxis and activity)

A

LTB4

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21
Q

binds to cys-LT receptor and acts as antagonist blocking LTC/LTD/LTE activity (eicosanoid derivate of arachidonic acid)

A

lipoxin

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22
Q

lipoxins formed as product of this (as seen in aspirin therapy)

A

acetylated cyclooxygenase

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23
Q

chemotactic molecule with adjacent cysteines

A

chemokine

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24
Q

TF for synthesis of inflammatory proteins

A

NFkB

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25
Q

chief source of cytokines and chemokines during inflammation

A

MP and monocytes

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26
Q

what makes IL-2?

A

T cells

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27
Q

what makes IL-1 (most important cytokine)?

A

MP

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28
Q

what synthesizes IL 1, IL 6, TNF

A

activated MP

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29
Q

purpose of CXCL8 (IL-8)

A

neutrophil chemotaxis

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30
Q

three molecules that are responsible for PMN chemotaxis

A

C5a, LTB4, CXCL8

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31
Q

these synthesize IL-12

A

MP, dendritic cells

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32
Q

nitric oxide synthesized from this; by what enzyme?

A

L-arginine; nitric oxide synthase

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33
Q

induced in inflammation resulting in increased levels of NO at sites of inflammation

A

iNOS

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34
Q

makes prostaglandins in hypothalamus (responsible for fever/increase in set point)

A

COX3

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35
Q

characterized by red streaks….inflammation of lymphatic channel (fluctuant…can squeeze)

A

lymphangitis

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36
Q

examples of acute phase proteins made by liver

A

fibrinogen, CRP, C3, haptoglobin, serum amyloid A

37
Q

differential for % neutrophils

A

40-80%

38
Q

differential for % bands

A

0-5%

39
Q

differential for % lymphocytes

A

15-50%

40
Q

differential for % basophils

A

2-10%

41
Q

differential for % eosinophils

A

1-5%

42
Q

increase in bands signifies this

A

acute bacterial infection

43
Q

length of time needed to develop primary immune response to first exposure to antigen

A

7-10 days

44
Q

length of time needed to develop secondary immune response when exposed to antigen again

A

3 days

45
Q

anti-inflammatory mediators produced for programmed dampening of inflammatory response

A

lipoxins, resolvins, protectins, acute phase proteins

46
Q

chief sources of cytokines and chemokines during inflammation…orchestrate cell migration/activation/proliferation after first 24-48 hours

A

MP and monocytes

47
Q

transcription factor for inflammatory cytokines

A

NF-kB

48
Q

synthesize/release systemic cytokines

A

activated MP

49
Q

increase in WBC due to systemic inflammatory reaction (increases release/delivery and synthesis)

A

leukocytosis

50
Q

systemic effect of inflammation…swelling of lymph nodes

A

lymphadenitis

51
Q

these synthesize IL-1a and IL-1B

A

activated MP, monocytes, dendritic cells

52
Q

TNFa activates this portion of apoptotic death domain

A

TNF-R1 and TRADD signal

53
Q

monoclonal Ab to this cytokine are used to treat chronic inflammation (in rheumatoid arthritis, Chron’s)

A

TNF

54
Q

local production of this cytokine by osteoblasts causes increased osteoclast activity and bone loss

A

IL-6

55
Q

chemokines have this conserved structure

A

two cysteines

56
Q

these synthesize chemokine IL-8

A

MP and endothelial cells

57
Q

IL-8 binds to this receptor (7 spanning transmembrane GPCR)

A

CXCR-1

58
Q

inflammatory chemokine from MP…chemotactic for monocytes and induces histamine release from mast cells

A

MCP-1

59
Q

inflammatory chemokines for eosinophil chemotaxis

A

RANTES, MIP-1

60
Q

7 spanning transmembrane GPCR…chemokine receptors for HIV

A

CXCR4 and CCR5

61
Q

early GPCR on monocytes in HIV

A

CCR5

62
Q

late infection HIV GPCR on T cells

A

CXCR4

63
Q

actions of IFN-g (from T cells and NK cells)

A

activates MP, induces MHC I/II, inhibits TH2, enhances leukocyte-endothelial adherence

64
Q

these secrete IFN-g (lymphokine)

A

T and NK cells

65
Q

lymphokines that induce resistance to viral replication in all cells, increase MHC I expression, activates NK cells (to kills virus-infected)

A

Type 1 interferons (a and B)

66
Q

these synthesize IL-12 (cytokine)

A

MP, dendritic cells

67
Q

actions of IL-12 (important in cell mediated immune response)

A

induces TH1, inhibits Th2

68
Q

these stimulate fibroblasts in healing/regeneration, cause fibrosis in chronic inflammation

A

FGF, TNFa

69
Q

these are angiogenic, inflammatory growth factors

A

VEGF, FGF, PDGF

70
Q

colony-stimulating factors that promote differentiation of granulocytes in bone marrow…also stimulates PMNs, eosinophils, and MP

A

GM-CSF

71
Q

when LPS (from gram-neg bacteria) binds this receptor pro-inflammatory cytokine synthesis is stimulated (causes septic shock)

A

TLR4

72
Q

two main sources of NO in inflammatory reaction

A

endothelial cells and activated MP

73
Q

actions of NO during inflammatory reaction

A

vasodilation, platelet aggregation, bactericidal, inhibits leukocyte migration

74
Q

pre-formed mediators in inflammatory reaction

A

histamine, serotonin, lysozymes

75
Q

this activates Hagemann factor (XII)

A

plasmin

76
Q

this cleaves complement components, creating C3a and C5a (also cleaves fibrin)

A

plasmin

77
Q

this system increases vascular permeability, contraction smooth muscle, dilation blood vessels, causes pain (activated by XIIa)

A

kallikrein/kinin

78
Q

these primarily produce new, larger cytokines (in latter phases of inflammation…18-72 hours)

A

endothelial cells, monocytes/MP, lymphocytes, fibroblasts

79
Q

time it takes to see synthesis of new cytokines

A

18-72 hours

80
Q

what is formed by lipoxygenase from arachidonic acid

A

leukotriene A

81
Q

arachidonic acid derivatives released by MP; what is their function?

A

PGE, PGF; vasodilation, increased vascular permeability

82
Q

arachidonic acid derivatives released by mast cells; what is their function?

A

LTC/D/E; bronchoconstriction

83
Q

arachidonic acid derivatives released by endothelial cells; what is its function?

A

prostacyclin (PGI2); anti-thrombotic

84
Q

what is produced by cyclo-oxygenase

A

prostanoic acid

85
Q

made by mast cells….major mediators of bronchoconstriction…slow reacting substances of anaphylaxis (SRS-As)

A

LTC/D/E

86
Q

this inhibits prostaglandin synthesis and promotes lipoxin synthesis

A

aspirin

87
Q

structure of platelet-activating factor

A

acetylated lysophospholipid

88
Q

sources of platelet-activating factor

A

mast cells, basophils, neutrophils, MP

89
Q

this induces platelet aggregation/degranulation, enhances release of histamine and serotonin, increased vascular permeability and leukocyte adhesion, chemotaxis

A

platelet-activating factor

Path Gen 1 (6 decks)

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