Flashcards in Pharm: Anti Coag Anti Platelet Deck (62)
When do we use antithrombotic therapy?
prevent thrombosis in pts w/acute or symptomatic venous thromboembolism
3 subgroups of antithrombotic agents
Venous thrombosis thrombi?
Red thrombi, RBCs enmeshed in thrombi
Arterial thrombosis thrombi?
White thrombi, platelets with little fibrin or red cells
Venous thrombosis risk factors?
immobility, surgery, cancer, pregnancy, estrogen use
Arterial thrombosis risk factors?
smoking, HTN, DM, obesity, hyperlipidemia
Gain of function mutations associated with venous thrombosis?
factor V leiden
What causes primary hemostasis?
formation of a platelet monolayer over the subendothelial matrix
platelets are held in place by vWF
What receptor is necessary for platelet aggregation?
What do platelets synthesize from arachidonic acid?
What causes secondary hemostasis?
coagulation cascase (conversion of soluble fibrinogen to insoluble fibrin)
How to platelets activate the coagulation cascade?
surface phospholipids provide support on which the complexes of coag cascade are formed, allowing for calcium binding
no intrinsic anticoag activity
binds antithrombin and thrombin simultaneously
accelerates rate of interaction of antithrombin w/Xa
parenteral, immediate onset of action
What are the LMWHs?
potentiate factor Xa inhibition by antithrombin
(not as good at inhibiting thrombin)
parenteral, can accumulate in pts w/renal disease
lower risk of thrombocytopenia
What are the direct thrombin inhibitors?
binds tightly to catalytic site and extended substrate recognition site of thrombin
occupies catalytic site of thrombin
Direct thrombin inhibitors admin?
excreted by kidneys
What is the direct factor Xa inhibitor?
causes antithrombin mediated selective inhibition of Xa
Do NOT use in pts w/renal failure
Direct thrombin inhibitor SEs?
bleeding if they accumulate
much less likely to cause thrombocytopenia
inhibits vitamin K epoxide, which recycles vit K back to it's active form