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Patho > Principles of Inflammation 2 > Flashcards

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

A

caspase 1

23
Q

what blocks activation of caspase1

A

pyrin

24
Q

antiinflammatory drugs

A

antihistamins
corticosteroids
nsaids
leukotreine drugs

25
Q

vasoactive amines (histamine)

A

released from mast cells
induced by injury
reorient WP bodies (p-selection

26
Q

lysomal constiuents (enz)

A

released from polys, macrophage

tissue destruction and permeabiltiy

27
Q

IL-8

A

chemotaxis for polys

28
Q

acute-short duration of inflammation

A

polys predominate

29
Q

subacute-intermiedaite duration of inflammation

A

polys, granulation tissue + round cells

30
Q

chornic-long duration of inflammation

A

no polys, –>healing with collagen

lympcotes, macrophages and plasma cells

31
Q

chronic-granuomatous

features:

A

localized, replaces normal tissue

giant cells, necrosis

32
Q

chronic-granulomatous

general causes:

A

delated hypersensivity, foriegn material

33
Q

chronic-granulomatous

specific causes:

A

TB, fungus, syphilis, sutures

34
Q

what is a ganuloma

A

macrophages fused together forming giant cells

35
Q

what influences grnaulomas

A

IL-4 made by Th2 cells

36
Q

what does granuloma cause?

A

E-caderin expression on cell surface and fusion

37
Q

serous

A

watery blister

38
Q

effusion

A

serous fluid in body cavity

39
Q

catarrhal

A

water + mucous

40
Q

fibrinous

A

fibrin on surfaces

41
Q

purulent

A

pus with polys abcess

42
Q

hemorrhagic

A

vascular damage-bacteria

43
Q

pseudomembranous

A

dead cells + polys

44
Q

increased pmns in blood

A

leukocytosis

45
Q

Esoinophilic leukocytosis

A

allergic reactions, parasiic infections

46
Q

acute phase reactants include

A

fibrinogen, glibulins, C-reactive protein and protein SAA

47
Q

Elevated CRP

A

post op, after acute MI, infections, inflammatory disease

48
Q

CRP rises in serum after

A

4-6 hours

49
Q

stimulant of increased hapatic CRP production

A

IL-6

50
Q

ESR elevated in patients with inflammation

A

system inflammatory disease, infection

Patho (9 decks)

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