Principles of Inflammation 2 Flashcards

1
Q

what can apmplify a reaction?

A

mediators

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2
Q

what induces cell necrosis?

A

C5 - 9 MAC (membrane attack complex)

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3
Q

what effects are > than C3a

A

C5a, chemotactic for polys

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4
Q

Hageman factor

A

triggers kinin system cascade

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5
Q

plasmin

A

activates hageman factor, cleaves c3 + c5

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6
Q

what increases vascular permeability

A

when fibrin split products

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7
Q

fibrin is formed –>

A

vascular occlusion which may lead to ischemia

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8
Q

IL-6 fever

A

^ CRP production by liver

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9
Q

Endothelial damage

A

during wbc adhesion to endothelium

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10
Q

anti-oxidants

A

superoxide dismutase

catalase

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11
Q

sources of free radical

A

radition
phagocytosis, inflammation
mitochondria

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12
Q

free radicals especially bind to

A

thymine –> DNA breaks

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13
Q

free radicals on protein cross-linking

A

leads to enhanced degradation

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14
Q

managment system to deal with free raidcals

A

SOD converts

O2 ->H2O2 + O2

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15
Q

what can purines bind to?

A

receptors of platelets for activation and aggregation

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16
Q

what can be released from polys?

A

purines ATP and ADP

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17
Q

what reverses inflammtion? (5)

A
chalones
hemostasis
reducing swelling (lymphatics drain edema fluid from site)
mediators
anti-oxidants
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18
Q

eNO reduces?

A

rollng + adhesion

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19
Q

Lipoxins (reverse of inflammation)

A

part of lipo-oxygenase pathway

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20
Q

what stops IL-1 production

A

pyrin (marenostrin)

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21
Q

what triggers formation of inflammasome

A

bacterial endotoxins, cell necrosis and cytkines

22
Q

what activates IL-1

23
Q

what blocks activation of caspase1

24
Q

antiinflammatory drugs

A

antihistamins
corticosteroids
nsaids
leukotreine drugs

25
vasoactive amines (histamine)
released from mast cells induced by injury reorient WP bodies (p-selection
26
lysomal constiuents (enz)
released from polys, macrophage | tissue destruction and permeabiltiy
27
IL-8
chemotaxis for polys
28
acute-short duration of inflammation
polys predominate
29
subacute-intermiedaite duration of inflammation
polys, granulation tissue + round cells
30
chornic-long duration of inflammation
no polys, -->healing with collagen | lympcotes, macrophages and plasma cells
31
chronic-granuomatous | features:
localized, replaces normal tissue | giant cells, necrosis
32
chronic-granulomatous | general causes:
delated hypersensivity, foriegn material
33
chronic-granulomatous | specific causes:
TB, fungus, syphilis, sutures
34
what is a ganuloma
macrophages fused together forming giant cells
35
what influences grnaulomas
IL-4 made by Th2 cells
36
what does granuloma cause?
E-caderin expression on cell surface and fusion
37
serous
watery blister
38
effusion
serous fluid in body cavity
39
catarrhal
water + mucous
40
fibrinous
fibrin on surfaces
41
purulent
pus with polys abcess
42
hemorrhagic
vascular damage-bacteria
43
pseudomembranous
dead cells + polys
44
increased pmns in blood
leukocytosis
45
Esoinophilic leukocytosis
allergic reactions, parasiic infections
46
acute phase reactants include
fibrinogen, glibulins, C-reactive protein and protein SAA
47
Elevated CRP
post op, after acute MI, infections, inflammatory disease
48
CRP rises in serum after
4-6 hours
49
stimulant of increased hapatic CRP production
IL-6
50
ESR elevated in patients with inflammation
system inflammatory disease, infection