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Pathology > 2.6 Termination of inflammation > Flashcards

2.6 Termination of inflammation Flashcards

1
Q

inflammation termination mediators

A

TGF beta, IL10

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2
Q

lipid mediators

A

lipoxins,
resolvins, and
protectins

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3
Q

discharge of

A

Ach_..cholinergic discharge

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4
Q

steps

A

resolution,
fibrosis (scar),
abscess,
chronic inflammation

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5
Q

areas that do not have capacity to undergo resolution

A

brain and heart - so you only see scar or worse

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6
Q

when you cannot dilute you under go

A

chronic inflammation

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7
Q

chronic inflammation occurs

A

when acute response is unsuccessful and may occur initially in many situations -

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8
Q

chronic inflammation involves

A

mononuclear cells,
scarring ,
tissue destruction

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9
Q

persistent infectious agens that avoid acute inflammation

A 
TB, 
fungi, 
treptonemes, 
autoimmunity, 
foreign bodies, 
parasites
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10
Q

activated macrophages lead to

A

epitheliod cells,
giant cells,
granuloma formation

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11
Q

differntiated macrophages

A

microglia,
kupffer cells,
alveolar macrophages,
osteoclasts

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12
Q

macrophages are very plastic cells meaning that

A

they can activate and deactivate functions when needed

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13
Q

alveolar macrophages have a downregulated

A

ability to make free readicals bc they are constantly responding to particulate matter and don_t’ want to squirt out radicals all the time

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14
Q

what kills alveolar macs

A

TB – causes some infalmmation, t cells come in, pump up gamma getting macs activated to kill intracellular target

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15
Q

products released by macrophages

A 
enzymes, 
neutral proteases, 
elastase, 
collagenase, 
plasminogen activator, 
acid hydrolases, 
phosphatases, 
lipases,
 plasmaproteins, 
complement, 
coagulation factors, 
reactive metabolites of oxygen, 
eicosanoids, 
cytokines and chemokines (TNF IL1, IL8) , 
growthfactors (PDGF, EGF, FGF, TGFbeta), 
nitric oxide
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16
Q

cross over cells from innate to adaptive immunity

A

macrophages

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17
Q

Eosinophils associated with

A

allergic (TH2) types of reactions involved in parasitic infections

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18
Q

Eosinophils are recruited by

A

eotaxin a C-C chemokine that binds to CCR3 found only on eosinophils

19
Q

Eosinophil granules contain

A

major basic protein that lyses parasites but also epithelial cells

20
Q

granulomatous inflammation

A

type of chronic inflammation mediated by mactivated macrophages

21
Q

granulmatous inflammation is seen in

A 
TB, 
leprosy, 
foreign bodies, 
sarcoid, 
cat scratch disease
22
Q

granulomas contain

A

epitheliod cells,
plasma cells,
lymphocytes, and
fibroblasts

23
Q

sarcoid granulomas

A

autoimmune,

cat scratch

24
Q

caseous necrosis

A

TB

25
Q

non caseous

A

foreign bodies and other things

26
Q

why do you see anthrocotic pigment around caseous necrosis

A

bc anthrocotic pigment lives inside macrophages

27
Q

how to diagnose caseating necrosis

A

acid fast cuz it would be TB

28
Q

serous transudat/effusion

A

proteinless fluid

29
Q

fibrinous inflammation

A

deposition of plasma proteins mainly fibrin

30
Q

suppurative/purulent inflammation

A

pus

31
Q

ulcers

A

erosion or defect in epithelial surface

32
Q

systemic effects of inflammation

A 
fever, 
leukocytosis, 
inc sedimentation rate, 
shunting of blood flow, 
increased BP and pulse rate (esp if you have pain), 
rigor, 
chills, 
malaise, 
anorexia, 
somnolence, 
acute phase reactants
33
Q

increased sed rate at 1 g means

A

suffering inflammatory response - acute phase reactions causing cells to aggregate like fibrinogen

34
Q

fibrinogen induced by

A

il6

35
Q

fibrinogen causes

A

inc sed rate

36
Q

c reactive protein induced by

A

il6

37
Q

CRP - c reactive protein binds

A

microbes and chromatin, and

fixes complement

38
Q

serum amyloid protein (SAA) induced by

A

Il1

TNF

39
Q

SAA causes

A

inc sed rate and

replaces ApoA in HDL target to macrophages

40
Q

if you have constant CRP for no apparent reason

A

this is a predictor of cardiovascular disease

41
Q

amyloidosis

A

in ppl who suffer arthritis because of chronic secretion of acute phase proteins they have amyloidosis

42
Q

acute phase proteins

A

fibrinogen,
CRP,
SAA

43
Q

aspiration pnemonea on the way down

A

see in an old person –> granulomatous

44
Q

aspiration pneumonia on the way up

A

see in a young person –>hcl and other stuff deposits so massive necrosis

Pathology (26 decks)

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