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49 Cards in this Set

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  • Back
How are microbes immobilized prior to phagocytosis?
bound by IgG, mannose receptors, or C3b
they are immobilized on phagocyte surface
Where is histamine released from?
basophils, mast cells, platelets
What biochemical shunt process does phagocytosis intiate?
HMP --> oxidative burst that gives electors to NADPH oxidase in phagosome membrane
ROI reactions
O2 ---> (catalyzed by NADPH) O2- --> H2O2 --> OH* or H2O2 --> HOCl (MPO catalyzes)
Where are acute inflammatory proteins synthesized?
what stimulates their release?
liver
IL1, TNF
What leads to histamine release?
C3a/C5a binding to mast cells
binding of allerins to IgE bound to mast cells
heat/cold
trauma
IL1
factors from neutrophils, monocytes, and platelets
what activates C3?
when is it constitutively activated?
C3 convertase
MPGN, AB stabilizes C3 convertase --> decreased C3
what cells are present in chronic inflammation?
Monos, plasma cells, macrophages (mononuclear infiltrate)
Clinical presentation of chronic granulomatous dz of childhood
which infx are they susceptible to?
Catalase + orgs can survive b/c they break down their own H2O2
Catalase - orgs produce H2O2 and don't break it down
Pts are susceptible to staph infetions (but not strep)
what is the cause of chronic granulomatous dz of childhood
inheritance
defective NADPH oxidase
X linked
What makes up epithelioid cells
aggregation fo activatd macrophages
Serous inflammation
mesothelial surface with fluid containing little cellular material/protein
Fibrinous inflammation
mesothelial surface --> outpouring of protein rich fluid
What is LTB4
neutrophil chemotactic factor
LAD type 1 deficiency
recurrent bacterial infx, B2 integrin deficiency
LAD type 2 deficiency
recurrent bacterial infx --> abnormal synth of sialyl Lewis X on neutrophils
Pathophysiology of CHF/Mitral stenosis
Morphology
chronic, passive congetsion of lung due to "backup"
Capillaries get distended, and RBC leak out into alveoli, they get degraded by phagocytosis
--> intra-alveolar hemosiderin laden macrophages
what are heart failure cells
hemosiderin laden macrophages
What causes brown induration
long-standing congestion and fibrosis of interstitium, and hemosiderin deposition
where are white infarcts?
where are red infarcts?
heart, spleen, liver
lung, GI
GPIa?
GP IIb/IIIa
platelets adhere to collagen
plts attach to VWF (impt for plt adhesion), and act as fibrinogen receptor (impt for plt-plt aggregation)
wVF fxn
where is it stored?
platelet adhesion
Weibel-Palade bodies in endothelial cells and some granules of plts
AT III - fxn, source
inactivates factors IX, X, and thrombin
EC
Thrombomodulin
binds thrombin --> conformational change in thrombin, which activates protein C
protein C
activated by thrombomodulin
inactivates Va and VIIIa
requires protein S as cofactor
protein S
cofactor
Tissue factor
activates factor VII
which steps in the coag cascade require Ca
VIII, X, V, II, I, XIII
which pathway is PT
VII, X, V, II, I, XIII
which pathway is PTT
XII, XI, IX, VIII, X, V, II, I, XIII
which steps in coag require PL
V, VIII
what is the #1 cause of thrombophilia
where are the clots
factor V leiden --> venous clots
clinical features of methylene tetrahydrofolage reductase mutation

treatment?
increased serum homocysteine --> arterial and venous clots

B12, folate
clinical features of anti-phospholipid syndrome
AB against protein, complexed with PL --> arterial and venous clots, fetal loss, neurologic probs
increased PTT b/c AB work against PL in vitro
morphology of arterial thrombi
non-occlusive, dark gray, alternates with fibrin = Lines of Zahn
morph of venous thrombi
on fibrin, so no lines of Zahn
Pathophys of decompression sickness
N2 comes out of skin and obstructs circulation --> muscle pains (bends) and can enter brain (caisson dz)
N2 has increased affinity for adipose tissue, so obese ppl are at higher risk
Why does reduced CO --> HTN
decreased CO --> low RBF --> RAS activation --> Na retention
SG of transudate?
Exudate?
<1.012 (decreased protein content)
>1.020 (increased protein and cellular content)
when do sx occur in fat embolism
cerebral edema?
1-3 days after trauma
1 week
pathophys of acute LV heart failure
(exudate/transudate)
venous congestion in pulm capillary beds --> increased hydrostatic pressure --> pulm edema via transudation into alveolar space
what causes gangrene
arterial occlusion
what causes shock lung
diffuse alveolar damage
what is PF4?
found in alpha granules
leads to plt aggregation during coag
what is the main cause of decreaesd plasma oncotic pressure
hypoalbuminemia
what is complication of mural thrombosis
embolization
clot breaks off and occludes popliteal artery (enters arterial circulation)
APC in neoplasia
normally: if not stimulated by WNT, it binds B-katenin and destroys it --> NO cell prolif
if stim by WNT, no destruction of B-katenin, B-katenin enters nucleus --> transcription
In APC mutation, no stim by WNT, no binding to B-katenin, so it enters nucleus --> cell prolif
RAS pathway in neoplasia
when RAS is inactive, bound to GDP
If GF binds cell receptor, RAS binds GTP and becomes activated, it recruits RAF-1 and begins transcription in nucleus
gets degraded by GTPase when done and RAS become inactive again (this last step doesn't occur in RAS mutation)
p53 in neoplasia
normally when there is damage to DNA during replication, p53 upregulates the transcription of p21
p21 inhibits the cyclin D, CD4 complex and cell cycle stops
also inhibits Rb phosphorylation and bax transcription