Random Path Facts

Front 1

How are microbes immobilized prior to phagocytosis?

Back 1

bound by IgG, mannose receptors, or C3b
they are immobilized on phagocyte surface

Front 2

Where is histamine released from?

Back 2

basophils, mast cells, platelets

Front 3

What biochemical shunt process does phagocytosis intiate?

Back 3

HMP --> oxidative burst that gives electors to NADPH oxidase in phagosome membrane

Front 4

ROI reactions

Back 4

O2 ---> (catalyzed by NADPH) O2- --> H2O2 --> OH* or H2O2 --> HOCl (MPO catalyzes)

Front 5

Where are acute inflammatory proteins synthesized?
what stimulates their release?

Back 5

liver
IL1, TNF

Front 6

What leads to histamine release?

Back 6

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

Front 7

what activates C3?
when is it constitutively activated?

Back 7

C3 convertase
MPGN, AB stabilizes C3 convertase --> decreased C3

Front 8

what cells are present in chronic inflammation?

Back 8

Monos, plasma cells, macrophages (mononuclear infiltrate)

Front 9

Clinical presentation of chronic granulomatous dz of childhood
which infx are they susceptible to?

Back 9

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)

Front 10

what is the cause of chronic granulomatous dz of childhood
inheritance

Back 10

defective NADPH oxidase
X linked

Front 11

What makes up epithelioid cells

Back 11

aggregation fo activatd macrophages

Front 12

Serous inflammation

Back 12

mesothelial surface with fluid containing little cellular material/protein

Front 13

Fibrinous inflammation

Back 13

mesothelial surface --> outpouring of protein rich fluid

Front 14

What is LTB4

Back 14

neutrophil chemotactic factor

Front 15

LAD type 1 deficiency

Back 15

recurrent bacterial infx, B2 integrin deficiency

Front 16

LAD type 2 deficiency

Back 16

recurrent bacterial infx --> abnormal synth of sialyl Lewis X on neutrophils

Front 17

Pathophysiology of CHF/Mitral stenosis
Morphology

Back 17

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

Front 18

what are heart failure cells

Back 18

hemosiderin laden macrophages

Front 19

What causes brown induration

Back 19

long-standing congestion and fibrosis of interstitium, and hemosiderin deposition

Front 20

where are white infarcts?
where are red infarcts?

Back 20

heart, spleen, liver
lung, GI

Front 21

GPIa?
GP IIb/IIIa

Back 21

platelets adhere to collagen
plts attach to VWF (impt for plt adhesion), and act as fibrinogen receptor (impt for plt-plt aggregation)

Front 22

wVF fxn
where is it stored?

Back 22

platelet adhesion
Weibel-Palade bodies in endothelial cells and some granules of plts

Front 23

AT III - fxn, source

Back 23

inactivates factors IX, X, and thrombin
EC

Front 24

Thrombomodulin

Back 24

binds thrombin --> conformational change in thrombin, which activates protein C

Front 25

protein C

Back 25

activated by thrombomodulin
inactivates Va and VIIIa
requires protein S as cofactor

Front 26

protein S

Back 26

cofactor

Front 27

Tissue factor

Back 27

activates factor VII

Front 28

which steps in the coag cascade require Ca

Back 28

VIII, X, V, II, I, XIII

Front 29

which pathway is PT

Back 29

VII, X, V, II, I, XIII

Front 30

which pathway is PTT

Back 30

XII, XI, IX, VIII, X, V, II, I, XIII

Front 31

which steps in coag require PL

Back 31

V, VIII

Front 32

what is the #1 cause of thrombophilia
where are the clots

Back 32

factor V leiden --> venous clots

Front 33

clinical features of methylene tetrahydrofolage reductase mutation

treatment?

Back 33

increased serum homocysteine --> arterial and venous clots

B12, folate

Front 34

clinical features of anti-phospholipid syndrome

Back 34

AB against protein, complexed with PL --> arterial and venous clots, fetal loss, neurologic probs
increased PTT b/c AB work against PL in vitro

Front 35

morphology of arterial thrombi

Back 35

non-occlusive, dark gray, alternates with fibrin = Lines of Zahn

Front 36

morph of venous thrombi

Back 36

on fibrin, so no lines of Zahn

Front 37

Pathophys of decompression sickness

Back 37

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

Front 38

Why does reduced CO --> HTN

Back 38

decreased CO --> low RBF --> RAS activation --> Na retention

Front 39

SG of transudate?
Exudate?

Back 39

<1.012 (decreased protein content)
>1.020 (increased protein and cellular content)

Front 40

when do sx occur in fat embolism
cerebral edema?

Back 40

1-3 days after trauma
1 week

Front 41

pathophys of acute LV heart failure
(exudate/transudate)

Back 41

venous congestion in pulm capillary beds --> increased hydrostatic pressure --> pulm edema via transudation into alveolar space

Front 42

what causes gangrene

Back 42

arterial occlusion

Front 43

what causes shock lung

Back 43

diffuse alveolar damage

Front 44

what is PF4?

Back 44

found in alpha granules
leads to plt aggregation during coag

Front 45

what is the main cause of decreaesd plasma oncotic pressure

Back 45

hypoalbuminemia

Front 46

what is complication of mural thrombosis

Back 46

embolization
clot breaks off and occludes popliteal artery (enters arterial circulation)

Front 47

APC in neoplasia

Back 47

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

Front 48

RAS pathway in neoplasia

Back 48

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)

Front 49

p53 in neoplasia

Back 49

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