283b thrombophilia

Question 1

thrombodulin

Answer 1

activates TAFI –I plasmin

activates Protein C –I thrombus formation

Question 2

arteria thrombis

Answer 2

artery - platelet driven; wall atherosclerosis –> MI, stroke, gangrene

risks - htn, lipids, DM, hyperhomocysteinemia

Question 3

adiponectin

Answer 3

blocks platelet aggregation and increased insulin sensitivity

fat people has low adiponectin –> thromus and inflammation –> atherothbombosis

Question 4

venous thromosis

Answer 4

fat, OCP, older age, cancer, trauma, surgery

Question 5

genetic factors for VTE

Answer 5

gain of function - factor V leiden, prothrombin 20210A

loss of fxn - Ptn C, S, antithrombin

Question 6

Factor V Leiden - cause? who gets it?

Answer 6

mutant factor V –> resistant to degradation by activated protein C.

Most common cause of inherited hypercoagulability in whites.

Question 7

FV leiden and OCPs

Answer 7

dramatically increases risk, but still low prevalence

Question 8

Prothrombin G20210A gene mutation? who gets it?

Answer 8

Mutation in 3′ untranslated region –> increases production of prothrombin –> increase plasma levels and venous clots

hispanics

Question 9

Antithrombin deficiency

Answer 9

Inherited deficiency of antithrombin: has no direct effect on the PT, PTT, or thrombin time but diminishes the increase in PTT following heparin administration.

Can also be acquired: renal failure/nephrotic syndrome –> antithrombin loss in urine –> increased factors II and X.

Question 10

Protein C or S deficiency

Answer 10

can’t inactivate factors V and VIII.

increased risk of thrombotic skin necrosis with hemorrhage following administration of warfarin.

Skin and subcutaneous tissue necrosis after warfarin administration–> think protein C deficiency. “Protein C Cancels Coagulation.”

Question 11

homocysteine-metabolism

Answer 11

homocysteine - methionine OR cystathionine

1- MTHF reductase
B12, folate

2- cystathionine synthase
B6

increased risk of thrombosis b/c damages endothelium