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MOD 1 > Chapter 3 second half > Flashcards

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
Q

fever path to prostaglandin

A

LPS–>leukocyte release TNF and IL-1 which increases COX which leads to PGE2

26
Q

acute phase proteins

A

CRP, fibrinogen, serum amyloid A

27
Q

what stimulates CRP and fibrinogen

A

IL-6

28
Q

what stimulates serum amyloid A

A

IL-1 and TNF

29
Q

elevated CRP marker for

A

risk of myocardial infarction

30
Q

too much hepcidin in acute phase resonse can cause

A

anemia

31
Q

fibrinogen binds ___ and causes them to make stacks, this is called

A

red cells

erythrocyte sedimentation

32
Q

leukocytosis from where and from what stim

A

post mitotic reserve pool in bone marrow
TNF and IL-1

proliferation of precursors in bone marrow from CSF

33
Q

septic shock is induced by high

A

TNF and IL-1

34
Q

repair of damaged tissue occurs by 2 types of rxns

A

regeneration of proliferation of uninured cells

maturation of tissue stem cells and deposition of CT to form scar

35
Q

cells that proliferate during tissue repair

A

injured tissue
vascular endothelial cells
fibroblasts

36
Q

tissues of body in 3 groups for regeneration

A

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
Q

liver regeneration steps

A

proliferation of remaining hepatocytes

repopulation from progenitor cells

38
Q

priming in proliferation of hepatocytes

A

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
Q

repair of tissue by CT deposition steps

A

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
Q

angiogenesis steps

A

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
Q

structural maturation of new vessels

recruitment pericytes and SM cells and deposition of CT

A

angiopoietins 1 and 2

42
Q

___ cross talks with VEGF to regulate sprouting and brancheing of new vessels

A

Notch

43
Q

matrix metalloproteinases require what for activity

A

zinc

44
Q

what inactivates MMPs

A

TIMPs from mesenchymal cells

45
Q

healing by first intention

layer involved

A

only epithelial layer involved

46
Q

process of healing by first intention first step

A

1) wounding causes coag pathway and blood clot with proteins, acts as scaffold for migrating cells, release VEGF

47
Q

within 24 hours first intention

A

neutrophils arrive and release enzyme to clrear debris

basal cells increase mitotic activity

48
Q

24-48 hours first intention

A

epithelial cells from both edges migrate and proliferate along dermis depositing BM along way until meat beneath surface of scab = close wond

49
Q

day 3 first intention

A

macrophages replace neutrophils
granulation tissue invades space
collagen and epthelial cell prolif

50
Q

day 5 first intention

A

neovascularization reaches peak
edema through vessels
fibroblasts migrate adn proliferate

51
Q

second week first intention

A

continued collagen accumulation

edema and leukocytes down

52
Q

end of first month first intention

A

scar mainly Ct

devoid of inflammatory cells

53
Q

healing by second intetion

A

tissue loss more extensive
type III collagen at first then collagen I after 2 weeks
wound contraction from myofibroblasts

54
Q

wound ulceration from

A

inadequate vascularization during healing

55
Q

rupture of wound occurs when most commonly

A

after abdominal surgery

56
Q

hypertrophic scar

A

scar tissue grows beyond boundaries of original wound and called keloid

57
Q

keloid

A

in individuals with predisposition

african americans

58
Q

exuberant granulation

A

excessive granulation tissue
blocks reepitheliazation
proud flesh

59
Q

desmoids or aggressive fibromatoses

A

between benign and malignant

60
Q

contraction in size of wound abnormality

A

exaggeration gives rise to contracture and results in deformities of wound surround tssue
-after serious burn

MOD 1 (6 decks)

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