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Path Gen 1 > Inflammatory Mediators > Flashcards

Inflammatory Mediators Flashcards

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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
chief source of cytokines and chemokines during inflammation
MP and monocytes
26
what makes IL-2?
T cells
27
what makes IL-1 (most important cytokine)?
MP
28
what synthesizes IL 1, IL 6, TNF
activated MP
29
purpose of CXCL8 (IL-8)
neutrophil chemotaxis
30
three molecules that are responsible for PMN chemotaxis
C5a, LTB4, CXCL8
31
these synthesize IL-12
MP, dendritic cells
32
nitric oxide synthesized from this; by what enzyme?
L-arginine; nitric oxide synthase
33
induced in inflammation resulting in increased levels of NO at sites of inflammation
iNOS
34
makes prostaglandins in hypothalamus (responsible for fever/increase in set point)
COX3
35
characterized by red streaks....inflammation of lymphatic channel (fluctuant...can squeeze)
lymphangitis
36
examples of acute phase proteins made by liver
fibrinogen, CRP, C3, haptoglobin, serum amyloid A
37
differential for % neutrophils
40-80%
38
differential for % bands
0-5%
39
differential for % lymphocytes
15-50%
40
differential for % basophils
2-10%
41
differential for % eosinophils
1-5%
42
increase in bands signifies this
acute bacterial infection
43
length of time needed to develop primary immune response to first exposure to antigen
7-10 days
44
length of time needed to develop secondary immune response when exposed to antigen again
3 days
45
anti-inflammatory mediators produced for programmed dampening of inflammatory response
lipoxins, resolvins, protectins, acute phase proteins
46
chief sources of cytokines and chemokines during inflammation...orchestrate cell migration/activation/proliferation after first 24-48 hours
MP and monocytes
47
transcription factor for inflammatory cytokines
NF-kB
48
synthesize/release systemic cytokines
activated MP
49
increase in WBC due to systemic inflammatory reaction (increases release/delivery and synthesis)
leukocytosis
50
systemic effect of inflammation...swelling of lymph nodes
lymphadenitis
51
these synthesize IL-1a and IL-1B
activated MP, monocytes, dendritic cells
52
TNFa activates this portion of apoptotic death domain
TNF-R1 and TRADD signal
53
monoclonal Ab to this cytokine are used to treat chronic inflammation (in rheumatoid arthritis, Chron's)
TNF
54
local production of this cytokine by osteoblasts causes increased osteoclast activity and bone loss
IL-6
55
chemokines have this conserved structure
two cysteines
56
these synthesize chemokine IL-8
MP and endothelial cells
57
IL-8 binds to this receptor (7 spanning transmembrane GPCR)
CXCR-1
58
inflammatory chemokine from MP...chemotactic for monocytes and induces histamine release from mast cells
MCP-1
59
inflammatory chemokines for eosinophil chemotaxis
RANTES, MIP-1
60
7 spanning transmembrane GPCR...chemokine receptors for HIV
CXCR4 and CCR5
61
early GPCR on monocytes in HIV
CCR5
62
late infection HIV GPCR on T cells
CXCR4
63
actions of IFN-g (from T cells and NK cells)
activates MP, induces MHC I/II, inhibits TH2, enhances leukocyte-endothelial adherence
64
these secrete IFN-g (lymphokine)
T and NK cells
65
lymphokines that induce resistance to viral replication in all cells, increase MHC I expression, activates NK cells (to kills virus-infected)
Type 1 interferons (a and B)
66
these synthesize IL-12 (cytokine)
MP, dendritic cells
67
actions of IL-12 (important in cell mediated immune response)
induces TH1, inhibits Th2
68
these stimulate fibroblasts in healing/regeneration, cause fibrosis in chronic inflammation
FGF, TNFa
69
these are angiogenic, inflammatory growth factors
VEGF, FGF, PDGF
70
colony-stimulating factors that promote differentiation of granulocytes in bone marrow...also stimulates PMNs, eosinophils, and MP
GM-CSF
71
when LPS (from gram-neg bacteria) binds this receptor pro-inflammatory cytokine synthesis is stimulated (*causes septic shock*)
TLR4
72
two main sources of NO in inflammatory reaction
endothelial cells and activated MP
73
actions of NO during inflammatory reaction
vasodilation, platelet aggregation, bactericidal, inhibits leukocyte migration
74
pre-formed mediators in inflammatory reaction
histamine, serotonin, lysozymes
75
this activates Hagemann factor (XII)
plasmin
76
this cleaves complement components, creating C3a and C5a (also cleaves fibrin)
plasmin
77
this system increases vascular permeability, contraction smooth muscle, dilation blood vessels, causes pain (activated by XIIa)
kallikrein/kinin
78
these primarily produce new, larger cytokines (in latter phases of inflammation...18-72 hours)
endothelial cells, monocytes/MP, lymphocytes, fibroblasts
79
time it takes to see synthesis of new cytokines
18-72 hours
80
what is formed by lipoxygenase from arachidonic acid
leukotriene A
81
arachidonic acid derivatives released by MP; what is their function?
PGE, PGF; vasodilation, increased vascular permeability
82
arachidonic acid derivatives released by mast cells; what is their function?
LTC/D/E; bronchoconstriction
83
arachidonic acid derivatives released by endothelial cells; what is its function?
prostacyclin (PGI2); anti-thrombotic
84
what is produced by cyclo-oxygenase
prostanoic acid
85
made by mast cells....major mediators of bronchoconstriction...*slow reacting substances of anaphylaxis (SRS-As)*
LTC/D/E
86
this inhibits prostaglandin synthesis and promotes lipoxin synthesis
aspirin
87
structure of platelet-activating factor
acetylated lysophospholipid
88
sources of platelet-activating factor
mast cells, basophils, neutrophils, MP
89
this induces platelet aggregation/degranulation, enhances release of histamine and serotonin, increased vascular permeability and leukocyte adhesion, chemotaxis
platelet-activating factor

Path Gen 1 (6 decks)

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