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
What requires Vit K?
facotrs 2,7,9,10, protein C, protein S
Which enantiomer of warfarin ia most active?
What metabolizes warfarin?
Polymorphisms in which protein affects dosing?
affects the susceptibility of hte enzyme to warfarin induced inhibition
purple toe syndrome
What is the oral direct thrombin inhibitor?
Metab of dabigatran?
What drug should NOT be administered with dabigatran?
(both are Pgp substrates)
What is the orally available direct factor Xa inhibitor?
What does factor Xa do?
converts prothrombin to thrombin
How is rivaroxaban eliminated?
unchanged by kidneys or metabolized by liver
What are the thrombolytic agent?
Mechanism of alteplase?
bolus dose over 1 min followed by infusion
List the antiplatelet drugs
Mehcanism of aspirin
inhibits platelet aggregation by irreversibly inhibiting COX
block PG and TXA2 production
Where is aspirin absorbed?
upper GI tract
What are the ADP receptor blockers?
clopidogrel, ticlopidine, prasurgrel, ticagrelor
Mechansim of clopidogrel et al?
inhibit ADP from binding P2Y12
except for ticagrelor, irreversible antagonists
What metabolises Clopidogrel/ticlopidine?
prodrugs, activated by CYP2C19
What drug can potentially inhibit clopidogrel?
PPIs used to tx peptic ulcer (ie/ omeprazole)
What is the adenosine deaminase and phosphodiesterase inhibitor?
What is the end result of dipyridamole?
inhibits aggregation, may cause vasodilation, may also cause release of prostcyclin of PGD2, casues coronary vasodilation
headache, GI upset, dixxiness
How do abciximab and eptifibatide work?
prevent platetlet aggregation by binding to CPIIb/IIIa to prevent fibrinogen binding/crosslinking platelets
Is abciximab competitive?
Is eptifibatide competitive?