Chapter 3 second half Flashcards
deficiency of GPI anchor leads to what
can’t link CD59 and DAF to PM
-paroxysmal nocturnal hemoglobinuria
platelet activating factor function
platelet aggregation
vasoconstriction and bronchoconstriction
-low concentration = vasodilation and venular permeability
function of bradykinin
increase vascular permeability
contraction of SM
dilation of BVs
pain when injected into skin
substance P fnct
pain signals
regulate BP
increase vascular perm
serous inflammation is marked by what and where
accumulation called what
exudation of cellpoor fluid into peritoneium, pleura, or pericardium
called effusion
blister from burn or viral infection
fibrinous inflammation
increased vascular permeability of large molecules lke firbinogen get into extavascular space
- meninges, lining of body cavities, pericardium, pleura
- scarring
purulent inflammation
caused by what and this is called what
also called suppurative, abscess
- production of pus
- bacteria can cause this (pyogenic)
abscess morphology
central region with mass of necrotic leukocytes and tissue cells
-preserved neutrophils around necrotic focus
causes of chronic inflammation
persistent infections
hypersensitivity disease
prolonged exposure to toxic agents
morphology of chronic inflammation
lymphocytes, macrophages, plasmas cells
-fibrosis
tissue destruction
1/2 life of blood monocyte
lifespan of tissue macrophage
1 day
several months or years
classical activation of macrophages induced by
endotoxins and IFN-y from lymphocytes
alternative macrophage activation induced by
IL-4,IL-13
tissue repair
anti-inflammatory
cytokines
GF, TGF-B
TGF-B,IL-10
what recruits lymphocytes
TNF and IL-1 from macrophages
Th1 cells secrete
INF-y
TH2 cells secrtete
IL-4,5,13
Th17 secretes and role
IL-17, which induces secretion of chemokines responsible for recruiteing neutrphils
macrophages display antigen to T lymphocytes and secrete ____ which activates lymphocytes to secrete ___
IL-12, IFN-y
granulomatous inflammation cells
collection of activated macrophages often with T lymphocytes
central necrosis
activated macrophages can develop abundant cytoplasm = epitheloid cels
some activated macrophages fuse = giant cells
2 types of granulomas
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
morphology of granulomas
activated macrophages have pink granular cytoplasm
giant cells
central cell nuecrosis in tuberculosis: caseous necrosis
granulomas in crohn disease, sarcoidosis, and foreign body reactions don’t have what
necrotic centers
-noncaseating
acute phase repsonse (5)
fever acute phase proteins leukocytosis septic shock in severe infections other manifestations: increased pulse and BP, decreased swet, anorexia
fever path to prostaglandin
LPS–>leukocyte release TNF and IL-1 which increases COX which leads to PGE2
acute phase proteins
CRP, fibrinogen, serum amyloid A
what stimulates CRP and fibrinogen
IL-6
what stimulates serum amyloid A
IL-1 and TNF
elevated CRP marker for
risk of myocardial infarction
too much hepcidin in acute phase resonse can cause
anemia
fibrinogen binds ___ and causes them to make stacks, this is called
red cells
erythrocyte sedimentation
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
septic shock is induced by high
TNF and IL-1
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
cells that proliferate during tissue repair
injured tissue
vascular endothelial cells
fibroblasts
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
liver regeneration steps
proliferation of remaining hepatocytes
repopulation from progenitor cells
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
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
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
structural maturation of new vessels
recruitment pericytes and SM cells and deposition of CT
angiopoietins 1 and 2
___ cross talks with VEGF to regulate sprouting and brancheing of new vessels
Notch
matrix metalloproteinases require what for activity
zinc
what inactivates MMPs
TIMPs from mesenchymal cells
healing by first intention
layer involved
only epithelial layer involved
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
within 24 hours first intention
neutrophils arrive and release enzyme to clrear debris
basal cells increase mitotic activity
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
day 3 first intention
macrophages replace neutrophils
granulation tissue invades space
collagen and epthelial cell prolif
day 5 first intention
neovascularization reaches peak
edema through vessels
fibroblasts migrate adn proliferate
second week first intention
continued collagen accumulation
edema and leukocytes down
end of first month first intention
scar mainly Ct
devoid of inflammatory cells
healing by second intetion
tissue loss more extensive
type III collagen at first then collagen I after 2 weeks
wound contraction from myofibroblasts
wound ulceration from
inadequate vascularization during healing
rupture of wound occurs when most commonly
after abdominal surgery
hypertrophic scar
scar tissue grows beyond boundaries of original wound and called keloid
keloid
in individuals with predisposition
african americans
exuberant granulation
excessive granulation tissue
blocks reepitheliazation
proud flesh
desmoids or aggressive fibromatoses
between benign and malignant
contraction in size of wound abnormality
exaggeration gives rise to contracture and results in deformities of wound surround tssue
-after serious burn
