Path Ch 4

Front 1

55 yr old male presents SOB, orthopnea, severe peripheral edema. Hypertension. pitting edema. DD?

Back 1

MI, CHF, COPD, emphysema.

Front 2

pitting edema, or subcutaneous edema often points to

Back 2

cardiac or renal disorders

Front 3

pulmonary edema often points to

Back 3

LEFT ventricular failure and is a set up for bacterial infection of lung

Front 4

nutmeg pattern of congestion in liver usually in

Back 4

chronic passive congestion of liver

Front 5

intrinsic pathway of coagulation cascade

Back 5

factors 12,11,9,8 (12 IN PTT+3) then 10-5-2-1

Front 6

extrinsic pathway of coagulation cascade

Back 6

factors 7 then 10-5-2(thrombin)-1(fibrinogen)

Front 7

virchows triad

Back 7

endothelial injury, abnormal blood flow, hypercoagulability leads to thrombosis

Front 8

common primary genetic factors that lead to hypercoagulability

Back 8

factor V mut, prothrombin def, inc F8,9,11,fibrinogen

Front 9

rare genetic hypercoagulability

Back 9

antithrombin def, protein C,S def, fibrinolysis defects, homozygous homocysteinuria

Front 10

acquired high risk for thrombosis

Back 10

prolonged bed rest, MI, atrial fibrillation, tissue injury(surgery,fracture,burn), cancer, prosthetic cardiac valves, heparin induced thombocytopenia

Front 11

acquired low risk for thrombosis

Back 11

cardiomyopathy, nephrotic syndrome, hyperestrogen states, oral contraceptives, sickle cell anemia, smoking

Front 12

possible outcomes for thrombus

Back 12

propagate, embolize, dissolve, organize/recanalate

Front 13

if see hemosiderin-laden macrophages, think

Back 13

heart failure cells

Front 14

pitting edema more specifically suggests

Back 14

RIGHT heart failure, sudden death

Front 15

where is the area of most injury from deoxygenation in liver?

Back 15

centilobular areas

Front 16

cause of hemosiderin laden macrophages and small hemorrhages commonly seen in chronically congested tissue? Stain?

Back 16

capillary rupture in long standing congestion. Prussian blue to stain iron in hemosiderin

Front 17

is hyperemia active/passive? Why?

Back 17

active due to increased blood flow commonly from inflammation

Front 18

where do arterial or cardiac thrombi usually begin? Venous?

Back 18

at sites of turbulence of endothelial injury. Site of stasis

Front 19

which direction do arterial/venous thrombi tend to grow from point of attachment?

Back 19

arterial thrombi grow retrograde, venous extend in direction of bloow flow (both propagate toward heart)

Front 20

most common sites of arterial thrombi

Back 20

coronary, cerebral, femoral arteries. Occlusive.

Front 21

gelatinous clots with a dark red dependent portion where RBC have settled and a yellow chicken fat upper portion. Firmer

Back 21

postmortem clots

Front 22

red, enmeshed red cells clot. Relatively few platelets

Back 22

venous thrombosis(phlebothrombosis)

Front 23

venous thrombi can be the source of

Back 23

congestion, edema due to outflow reduction. Cause emboli

Front 24

characteristic of true thrombi

Back 24

attached to vascular wall at some point

Front 25

may have lines of Zahn visible from layering effect of flowing blood, usually occlusive

Back 25

arterial thrombi

Front 26

thrombi composed of infectious agents(fungi, bacteria) present on heart valves

Back 26

vegetations

Front 27

when do marrow emboli occur?

Back 27

after fracture of large bones, extensive injury to fatty tissue, or severe burns

Front 28

ischemic necrosis of tissue cause by occlusion of an artery or vein

Back 28

infarction

Front 29

where do clinically significant infarct occur in?

Back 29

heart,brain, lungs, kidneys

Front 30

what do nearly all infarcts occur from?

Back 30

thrombotic, embolic events

Front 31

what kind of tissue do red infarcts occur in

Back 31

dual blood supply, with venous occlusions and in loose tissue

Front 32

what kind of tissue do white infarcts occur in

Back 32

end arterial circulation in solid organs-limitation to the slow of blood between adjourning capillary circulations

Front 33

dominant morphology of infarcts

Back 33

ischemic coagulative necrosis

Front 34

major factors that determine cliniical and pathological outcome of an infarction

Back 34

nature of vascular supply, rate of occlusion, tissue resistance to hypoxia, O2 content of blood

Front 35

mechanisms of developing red infarcts

Back 35

venous occlusions, loose tissue, dual circulation-blood flow into necrosis, previously congested, flow reestablished of previous occlusion

Front 36

hemorrhagic infarction of small intestine is usually due to? Presents with?

Back 36

volvulus. Severe abdominal pain

Front 37

62 yr old with rheumatic heart disease, onset fever, malaise. Petechiae. Hypertension. Dad died of MI. DD?

Back 37

heart valve infection(endocarditis), transietn bacteremia, INFARCTION.

Front 38

25 yr old femaile has menorrhagia. Frequent nose bleeds. Petechiae, purpura over arms/legs. PTT,PTT normal. DD?

Back 38

coagulopathy, vWF, factor V def

Front 39

common inherited bleeding disorder usually mild

Back 39

von willebrand disease

Front 40

vWF disease often presents with

Back 40

mild bleeding, menorrhagia or epistaxis

Front 41

important adhesion molecule between subendothelial collagen and Gp1b

Back 41

von willebrand factor

Front 42

26 yr old female has swelling, pain, tenderness beneath R calf. Several Episodes of thrombosis occurred. DD

Back 42

thrombus, factor V, ATIII, protein C,S

Front 43

most common inherited cause of hypercoagulation

Back 43

factor V mut, prothrombin def, inc F8,9,11,fibrinogen

Front 44

red thrombi which occlude the vessel, occur in low flow. Many RBC. Make break off as emboli.

Back 44

DVT deep vein thrombosis