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

25
non caseous
foreign bodies and other things
26
why do you see anthrocotic pigment around caseous necrosis
bc anthrocotic pigment lives inside macrophages
27
how to diagnose caseating necrosis
acid fast cuz it would be TB
28
serous transudat/effusion
proteinless fluid
29
fibrinous inflammation
deposition of plasma proteins mainly fibrin
30
suppurative/purulent inflammation
pus
31
ulcers
erosion or defect in epithelial surface
32
systemic effects of inflammation
``` 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
increased sed rate at 1 g means
suffering inflammatory response - acute phase reactions causing cells to aggregate like fibrinogen
34
fibrinogen induced by
il6
35
fibrinogen causes
inc sed rate
36
c reactive protein induced by
il6
37
CRP - c reactive protein binds
microbes and chromatin, and | fixes complement
38
serum amyloid protein (SAA) induced by
Il1 | TNF
39
SAA causes
inc sed rate and | replaces ApoA in HDL target to macrophages
40
if you have constant CRP for no apparent reason
this is a predictor of cardiovascular disease
41
amyloidosis
in ppl who suffer arthritis because of chronic secretion of acute phase proteins they have amyloidosis
42
acute phase proteins
fibrinogen, CRP, SAA
43
aspiration pnemonea on the way down
see in an old person --> granulomatous
44
aspiration pneumonia on the way up
see in a young person -->hcl and other stuff deposits so massive necrosis