Flashcards in 283b thrombophilia Deck (11):
1
thrombodulin
activates TAFI --I plasmin
activates Protein C --I thrombus formation
2
arteria thrombis
artery - platelet driven; wall atherosclerosis --> MI, stroke, gangrene
risks - htn, lipids, DM, hyperhomocysteinemia
3
adiponectin
blocks platelet aggregation and increased insulin sensitivity
fat people has low adiponectin --> thromus and inflammation --> atherothbombosis
4
venous thromosis
fat, OCP, older age, cancer, trauma, surgery
5
genetic factors for VTE
gain of function - factor V leiden, prothrombin 20210A
loss of fxn - Ptn C, S, antithrombin
6
Factor V Leiden - cause? who gets it?
mutant factor V --> resistant to degradation by activated protein C.
Most common cause of inherited hypercoagulability in whites.
7
FV leiden and OCPs
dramatically increases risk, but still low prevalence
8
Prothrombin G20210A gene mutation? who gets it?
Mutation in 3′ untranslated region --> increases production of prothrombin --> increase plasma levels and venous clots
hispanics
9
Antithrombin deficiency
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.
10
Protein C or S deficiency
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.”
11