Chapter 3 second half Flashcards

1
Q

deficiency of GPI anchor leads to what

A

can’t link CD59 and DAF to PM

-paroxysmal nocturnal hemoglobinuria

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2
Q

platelet activating factor function

A

platelet aggregation
vasoconstriction and bronchoconstriction
-low concentration = vasodilation and venular permeability

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3
Q

function of bradykinin

A

increase vascular permeability
contraction of SM
dilation of BVs
pain when injected into skin

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4
Q

substance P fnct

A

pain signals
regulate BP
increase vascular perm

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5
Q

serous inflammation is marked by what and where

accumulation called what

A

exudation of cellpoor fluid into peritoneium, pleura, or pericardium
called effusion
blister from burn or viral infection

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6
Q

fibrinous inflammation

A

increased vascular permeability of large molecules lke firbinogen get into extavascular space

  • meninges, lining of body cavities, pericardium, pleura
  • scarring
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7
Q

purulent inflammation

caused by what and this is called what

A

also called suppurative, abscess

  • production of pus
  • bacteria can cause this (pyogenic)
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8
Q

abscess morphology

A

central region with mass of necrotic leukocytes and tissue cells
-preserved neutrophils around necrotic focus

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9
Q

causes of chronic inflammation

A

persistent infections
hypersensitivity disease
prolonged exposure to toxic agents

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10
Q

morphology of chronic inflammation

A

lymphocytes, macrophages, plasmas cells
-fibrosis
tissue destruction

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11
Q

1/2 life of blood monocyte

lifespan of tissue macrophage

A

1 day

several months or years

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12
Q

classical activation of macrophages induced by

A

endotoxins and IFN-y from lymphocytes

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13
Q

alternative macrophage activation induced by

A

IL-4,IL-13

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14
Q

tissue repair
anti-inflammatory

cytokines

A

GF, TGF-B

TGF-B,IL-10

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15
Q

what recruits lymphocytes

A

TNF and IL-1 from macrophages

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16
Q

Th1 cells secrete

A

INF-y

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17
Q

TH2 cells secrtete

A

IL-4,5,13

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18
Q

Th17 secretes and role

A

IL-17, which induces secretion of chemokines responsible for recruiteing neutrphils

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19
Q

macrophages display antigen to T lymphocytes and secrete ____ which activates lymphocytes to secrete ___

A

IL-12, IFN-y

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20
Q

granulomatous inflammation cells

A

collection of activated macrophages often with T lymphocytes
central necrosis

activated macrophages can develop abundant cytoplasm = epitheloid cels

some activated macrophages fuse = giant cells

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21
Q

2 types of granulomas

A

foreign body: no T cells
-epitheloid and giant cells apposed to surface of foreign body susch as talc, sutures, fibers

immune granulomas
-t cell mediatged, when agent hard to get rid of

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22
Q

morphology of granulomas

A

activated macrophages have pink granular cytoplasm
giant cells
central cell nuecrosis in tuberculosis: caseous necrosis

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23
Q

granulomas in crohn disease, sarcoidosis, and foreign body reactions don’t have what

A

necrotic centers

-noncaseating

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24
Q

acute phase repsonse (5)

A
fever
acute phase proteins
leukocytosis
septic shock in severe infections
other manifestations: increased pulse and BP, decreased swet, anorexia
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25
fever path to prostaglandin
LPS-->leukocyte release TNF and IL-1 which increases COX which leads to PGE2
26
acute phase proteins
CRP, fibrinogen, serum amyloid A
27
what stimulates CRP and fibrinogen
IL-6
28
what stimulates serum amyloid A
IL-1 and TNF
29
elevated CRP marker for
risk of myocardial infarction
30
too much hepcidin in acute phase resonse can cause
anemia
31
fibrinogen binds ___ and causes them to make stacks, this is called
red cells | erythrocyte sedimentation
32
leukocytosis from where and from what stim
post mitotic reserve pool in bone marrow TNF and IL-1 proliferation of precursors in bone marrow from CSF
33
septic shock is induced by high
TNF and IL-1
34
repair of damaged tissue occurs by 2 types of rxns
regeneration of proliferation of uninured cells | maturation of tissue stem cells and deposition of CT to form scar
35
cells that proliferate during tissue repair
injured tissue vascular endothelial cells fibroblasts
36
tissues of body in 3 groups for regeneration
labile: continuosly lost and replaced: epithelial cells stable tissues: divide in response to injury: liver, kidney, pancreas permanent tissue: neurons, cardiac m, and skeletal m
37
liver regeneration steps
proliferation of remaining hepatocytes | repopulation from progenitor cells
38
priming in proliferation of hepatocytes
TNF acts on kuppfer cell which releases IL-6 IL-6 acts on hepatocyte which changes from G0 to G1 EGFR now on cell surface which binds TGFa and EGF MET now on surface and binds HGF ligands bind = proliferation
39
repair of tissue by CT deposition steps
angiogenesis -formation of new BV with VEGF, causes edema formation of granulation tissue -fibroblasts migrate and proliferate, lay down Type III collagen remodeling of CT
40
angiogenesis steps
vasodilation from NO, increased vasc perm VEFG separation of pericytes from abluminal surface and breakdown of BM migration of endothelial cells toward area of tissue injury prolif endothelial cells behind lead tip migrating cells remodeling cap tubes recruitment of periendothelial celsl from mature vessels suppression endothelial prolif and migration and depostion of BM
41
structural maturation of new vessels | recruitment pericytes and SM cells and deposition of CT
angiopoietins 1 and 2
42
___ cross talks with VEGF to regulate sprouting and brancheing of new vessels
Notch
43
matrix metalloproteinases require what for activity
zinc
44
what inactivates MMPs
TIMPs from mesenchymal cells
45
healing by first intention | layer involved
only epithelial layer involved
46
process of healing by first intention first step
1) wounding causes coag pathway and blood clot with proteins, acts as scaffold for migrating cells, release VEGF
47
within 24 hours first intention
neutrophils arrive and release enzyme to clrear debris | basal cells increase mitotic activity
48
24-48 hours first intention
epithelial cells from both edges migrate and proliferate along dermis depositing BM along way until meat beneath surface of scab = close wond
49
day 3 first intention
macrophages replace neutrophils granulation tissue invades space collagen and epthelial cell prolif
50
day 5 first intention
neovascularization reaches peak edema through vessels fibroblasts migrate adn proliferate
51
second week first intention
continued collagen accumulation | edema and leukocytes down
52
end of first month first intention
scar mainly Ct | devoid of inflammatory cells
53
healing by second intetion
tissue loss more extensive type III collagen at first then collagen I after 2 weeks wound contraction from myofibroblasts
54
wound ulceration from
inadequate vascularization during healing
55
rupture of wound occurs when most commonly
after abdominal surgery
56
hypertrophic scar
scar tissue grows beyond boundaries of original wound and called keloid
57
keloid
in individuals with predisposition | african americans
58
exuberant granulation
excessive granulation tissue blocks reepitheliazation proud flesh
59
desmoids or aggressive fibromatoses
between benign and malignant
60
contraction in size of wound abnormality
exaggeration gives rise to contracture and results in deformities of wound surround tssue -after serious burn