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88 Cards in this Set

  • Front
  • Back
what is the hallmark of the acute response?
the vascular response: increased permeability
what are the main components of the acute inflamm response?
increased blood flow
changes in microvasculature structure with delivery of plasma proteins and cells
emigration, accumulation and activation of these cells
what are the main cells of acute inflamm?
what is the lewis triple response?
run key down arm:
initial vasoconstriction (white)
aterioles dilate (red)
fluid loss and stasis (slower blood flow due to fluid loss and incr viscosity of blood)-(wheal,edema)
what occurs as a result of stasis in the blood?
PMNs can accumulate along vascular endothelium to extravasate
what vessles are involved in acute inflamm and the vascular response?
venules: complete BL; layers of pericytes
capillaries: complete BL; scattered pericytes
lymphatics: loose endothelium; indistinct BL; valve-like strcutures
what are pericytes?
cells that share BL with endothelial cells
contract to change permeability
who has a longer lifespan: PMNs or monocytes? significance?
PMNs live for hours; monocytes for days
PMNs first to arrive
what causes the edema formation?
endothelial cells contract and separate intercellular jxns
increase blood flow (incr cap hydrostatic P)
leakage of plasma proteins (decr cap osmotic pressure)
what contributes to incr permeability of vessels? (6)
gap formation
durect injury
leukocyte dep injury
incr transcytosis
new bld vessel formation
what forms endothelial gaps in venules?
histamine, bradykinin, serotonin (premade; immediate, transient)
IL-1, TNF, IFN-gamma: delayed, long-lived effects
direct injury
leads to endothelial cell necrosis and detachment
ex: severe burns, lytic bacterial infection
immediate, sustained
affects all microcirc: venules, caps, arterioles
delayed, prolonged leakage
ex: late-appearing sunburn
also Xrays
affects caps and venules
2-12 after; can last days
leukocyte-mediated enodthelial injury
leukocytes adhere to endothelium and rel ROIs and proteolytic enzymes to damage vessels
venules, pulm and glomerular caps
increased transcytosis
VEGF induces channel formation in venules
cellular events in acute inflamm
margination- stasis->tether, rolling and adhesion, activation (pavementing)
diapedesis-ACTIVE process using filopods
migration to area of damage
what are 3 types of selectins?
cytokine activated(TNF, IL-1) expression on endothelial cells
binds sialylated carb on WBCs
P- Selectins
cytokine activated (histamine, thrombin, platelet activating factor, PAF)
expressed on endothelial cells and platelets
bind sialylated carbs on WBCs
on lymphocytes, PMNs and other leukocytes
binds CD34 on endothelial cells
TNF, IL-1 activated expression on endothelial cells
bind integrins on WBCs
types of integrins
LFA-1, Mac-1, VLA-4
on many cells including WBCs
bind ICAM-1 on endothelial cells
high affinity
on many cells including WBCs
bind VCAM-1 on endothelial cells
high affinity
what are weibel-palade bodies?
secretory granules of P-selectin in endothelial cells
stimulation by histamine, thrombin rel P-selectin to surface
where does diapedesis occer? exception? receptors?
at intercellular jxns
exception: pulmonary and glomerular capillaries
R: PECAM-1, CD99
what is the difference between chemotaxis and chemokinesis?
taxis- unidirectional, active migration; resp to diffusion gradient
kinesis- incr velocity of WBC movement
what are ex of chemoattractants?
exogenous: bacterial
endogenous: C' (C3a, C5a)
leukotrienes, cytokines (IL-8 chemokine)
how do chemoattractants work?
bind transmbr G-coupled R
polymerization of actin on leading edge
"front wheel drive"
leukocyte activation
induced degranulation, rel of cytokines via binding of subst to TLRs
why does adding serum to a mix of bacteria and phagocytes increase phagocytosis?
addn of opsonins (ex: C')
phagocytic killing by PMNs
most PMN killing is O2 dependent
myeloperoxidase imp to convert mild H2O2 to HOCL (hypochlorite)
what are the preformed cell-derived mediators? what cells?
histamine (mc, basophils, platelets)
serotonin (platelets)
lysosomal enzymes MPh, PMN)
what are the newly syn cell-derived mediators? cells?
PG (WBCs, platelets, ECM)
Leukotrienes (WBCs)
NO (MPh)
cytokines (lymphocytes, MPh, ECM)
plasma-derived mediators
Hageman (kinin and coagulation) and C' (anaphylatoxins and MAC) activation
mc, basophils, platelets
binds H1 receptors on endothelial cells
constrict lg a.
dilate arterioles
incr venule permeability
in platelets and enterochromaffin cells of GI
rel stim by platelet aggregation
due to collagen, thrombin, ADP, PAF, ICs
what plasma protein pathways act in inflammation?
what does hageman factor initiate? what activates it? what does it become? what paths can it take?
hageman initiates clotting and kinin cascades
activated by HMWK, BM, col 4, activated platelets and kallikrein
becomes XIIa which goes into EITHER the clotting or kinin path
describe the clotting cascade
hageman-> factor XIIa
XIIa converts XI->XIa
XIa converts X->Xa
Xa converts prothrombin->thrombin (IIa)
thrombin converts fibronogen->fibrin plus fibrinopeptides
what component of the clotting cascade activates acute inflamm?
thrombin plus protease activated receptors stim acute inflamm
what can fibrin form? what are they important in?
fibrin split products
imp in DIC
what is the kinin cascade?
XIIa converts prekallikrein to kallikrein
kallikrein converts HMWK to bradykinin
kallikrein also converts plasminogen to plasmin
(kallikrein also activates hageman in pos feedback)
plasmin activates C' cascade (C3->C3a)
plasmin also goes to fibrin
what 3 things can kallikrein do?
activate hageman
form bradykinin (from HMWK)
convert plasminogen to plasmin
what is C5a assoc with?
anaphylatoxin with C3a
leukocyte activation
adhesion of leukocytes
action of bradykinin (3)
incr vascular permeability
smooth m. contraction
arteriolar dilation
what is the fxn of fibrinopeptides? (2)
increase vascular permeability
chemotactic for WBCs
fxn of fibrin split products? what forms them?
incr vascular permeability
plasmin acts on fibrin
what products does arachidonic acid prod?
prostaglandins (via COX 1 and 2) and leukotrienes (via 5-lipoxygenase)
what does prostaglandins produce?
prostacyclin (vasodilation; inhibits platelet aggegation)
thromboxane (vasoconstriction, promotes platelet aggregation)
PGE2- vasodilation, edema
fxn of leukotrienes
incr permeability
fxn lipoxin A4
inhibit PMN chemotaxis
stimulate mo adhesion
what are 2 general types of granules? which causes more damage?
specific granules and azurophilic granules (more damaging)
platelet activating factor: where derived from? how formed? fxn?
from membranes
rel by phospholipase A (also rel arachidonic acid)
activates and aggregates platelets, stim their rel of histamine and 5HT
can prod most signs of inflamm (ex: bronchoconstriction)
what are 2 main interleukins rel in acute inflamm? what do they do? (4 targets)
IL-1 and TNF
stim acute phase reactions
stim endothelium: WBC adhesion, pro and anticoagulant
stim fibroblasts: prolif, col syn and brkdown
stim WBC to rel IL1 and IL6
chemokines: 3 important ex
platelet factor 4
NO syn and fxn
relax sm mm, decr platelet aggregation, inhibit WBC adhesion
NO synthase (NOS, 3 forms): L arginine, O2, NADPH
endothelial NOS (eNOS), neuronal NOS (nNOS) and inducible NOS
diff b/w eNOS, nNOS, inducible NOS
eNOS and nNOS constituitively produced
inducible NOS induced by TNF and IL-1
what are some ex of diseases where we might see reduced NO syn? what happens?
->more platelet aggregation
ex of chemotactic factors and their targets
C5a: PMN, MPh
fibrin split prod: PMNs
elastin and collagen: mo, MPh
what is cellulitis?
inflamm between cells
diffuse edematous spreading b/w cells in sold tissues
fibrinous exudate
outpouring of fibrinogen and conversion to fibrin
whats another name for purulent?
catarrhal: defn
mucoid discharge
lymphangitic: defn
inflamm of lymphatics b/c of cells that enter
LN enlargement and tendernous
localized collection of pus (high PMNs)
assoc with tissue destruction
walled off; difficult to tx with antibiotics and may need to be surgically drained
difference b/w ulcer and erosion
erosion-loss of epithelium
ulcer-sloughing of necrotic tissue that also removes some underlying tissue in addn to epithelium
ACUTE inflamm
azurophilic (primary) and specific granules
O2 dep and indep
eotaxin chemoattractant
major basic protein in granules (parasites)
which type of WBC recirculates?
contents of basophils
granules with histamine and heparin
platelets: granules and contents
alpha granules: fibrinogen, platelet factor 4, platelet derived GF
delta granules: ATP, histamine, serotonin
chediak higashi vs. CGD
chediak- no phagolysosome
CGD- no NADPH oxidase (neg NBT)
what disease results in a defect in chemotaxis, adhesion, phagocytosis, and microbicidal activity?
4 possible outcomes of acute inflammation?
resolution- returns to normal
fibrosis- some loss of fxn
abscess- localized; pus
chronic inflammation- w/ or w/o acute
resolution after acute inflamm
clearance of injurious stimuli and mediators of inflamm
replace injured cells
return to normal fxn
healing after acute inflamm or abscess formation
results in some loss of fxn
chronic inflamm: charac
mononuclear cell infiltrates
fibrosis and scar
can occur w/o acute (ex: viral, bacterial infection, autoimmune disease)
how does resolution lead to return of fxn?
decr vessel permeability and incr lymphatic drainage -> reduces tumor
MPh clean up cells, debris
GF and fibroblasts stim repair
what occurs in chronic inflamm? why does it occur?
MPh, lymphocyte, plasma cells infiltrate
deposit extracellular matrix
fibrosis and destruction of tissue
due to: continued infection or stimulus (ex: pathogen) or autoimmune disease
what is the role of MPh in chronic inflamm?
fibrosis: GF, angiogenesis factors, remodeling via collagenesis

tissue injury: toxic metabolites, NO
charac of granulomatous inflamm
TYPE of chronic inflamm:
well circumscribed lesion
necrosis and repair simultaneously
accumulation of epitheloid MPh
3 systemic effects of inflamm
acute phase response
acute phase reactants
syn by liver; marker of inflamm
incr RBC sedimentation rate (due to fibrinogen?)
ex: CRP, SAA, C', coagulation proteins
IL-1,6, TNF, IFN
stim SNS
dermal vasoconstriction
LPS -> TNF, IL-1
induce: DIC (activation of coagulation and fibrinolysis at same time)
charac of septic shock
cardiovascular failure
adult respiratory distress syndrome
assoc with sepsis or major systemic insult (ex: burns, hypoxia, O2 toxicity)
high IL-1, TNF
*diffuse damage to alveoli capillaries
*incr in vascular permeability