Flashcards in 283b thrombophilia Deck (11):
activates TAFI --I plasmin
activates Protein C --I thrombus formation
artery - platelet driven; wall atherosclerosis --> MI, stroke, gangrene
risks - htn, lipids, DM, hyperhomocysteinemia
blocks platelet aggregation and increased insulin sensitivity
fat people has low adiponectin --> thromus and inflammation --> atherothbombosis
fat, OCP, older age, cancer, trauma, surgery
genetic factors for VTE
gain of function - factor V leiden, prothrombin 20210A
loss of fxn - Ptn C, S, antithrombin
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.
FV leiden and OCPs
dramatically increases risk, but still low prevalence
Prothrombin G20210A gene mutation? who gets it?
Mutation in 3′ untranslated region --> increases production of prothrombin --> increase plasma levels and venous clots
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.
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.”