100114 anti thrombotic pharm Flashcards
STEMI treatment
immediate reperfusion therapy
antiplatelet/antithrombotic agents, statin, aspirin, beta adrenergic blockers, nitrates
NSTEMI and UA treatment
antiplatelet/antithrombotic agents, statin, aspirin, beta adrenergic blockers, nitrates
alteplase MOA
plasminogen activator
adverse effects of fibrinolytic therapy
bleeding
contraindications to thrombolytic therapy
about 30% of pts unsuited for thrombolytics
situations where drug therapy could impair necessary fibrin clots within circulation
active peptic ulcer, recent stroke, recovering from recent surgery
anticoagulants’ goals
inhibit activation of thrombin by Xa
directly inhibit thrombin
decrease production of functional prothrombin
unfractionated heparin MOA
catalyzes antithrombin’s actions on Xa and thrombin
low molecular weight heparin MOA
catalyzes antithrombin’s action on Xa
enoxaparin, dalteparin
fondaparinux
catalyzes antithrombin’s action on Xa
unfractionated heparin, LMWHs, fondaparinux are all administered how?
parenterally
side effects of unfractionated heparin
heparin induced thrombocytopenia
LMWH and fondaparinux have an advantage over UFH how?
they have longer half lives and more predictable bioavailability (less bleeding, less risk of thrombocytopenia)
direct thrombin inhibitor
bivalirudin
inhibits independently of antithrombin
acts on both circulating and clot bound thrombin
no thrombocytopenia
unstable angina pts undergoing PCI
MOA of thienopyridines
prevent ADP and P2Y12/P2Y1 interaction so that platelet cannot have increased Ca and be activated
GP IIb/IIIa receptor antagonists MOA
prevent fibrinogen binding in the GP IIb/IIIa
aspirin MOA
irreversibly actylates COX-1 in platelet. blocks production of thromboxane, which activates platelets and helps with platelet aggregation
platelets lack nuclei so permanent effect of aspirin
endothelial cells (which produce prostacyclin downstream of COX) do not experience loss of prostacyclin like platelets experience loss of thromboxane because endothelial cells have nuclei
aspirin uses
UA, acute MI, history of MI
chronic stable angina without history of MI
pts who’ve had minor stroke or transient cerebral ischemia
pts who have undergone coronary artery bypass
should not be used for primary prevention to completely healthy ppl
which thienopyridines are irreversible
clopidogrel, prasugrel
advantage of reversible platelet inhibitor
if pt requires surgery (like coronary bypass) and is taking drug like clopidogrel or aspirin, you have to wait for platelet fxn to return to normal (platelet life span is 7-10 days)
side effects of thienopyridines
bleeding
GI related symptoms
clopidogrel is metabolized by
CYP2C19
effectiveness of thienopyridines compared to aspirin
as monotherapy, are modestly superior to aspirin in reducing risk of MI
glycoprotein IIb/IIIa receptor antagonists examples
abciximab, eptifibatide
glycoprotein IIb/IIIa inhibition is reversible or irrev?
reversibly inhibit the final common pathway of platelet aggregation-binding of GPIIb/IIIa receptor to fibrinogen and vWF. so platelets cannot stick to each other and you don’t get formation of the hemostatic plug
rivaroxaban MOA
inhibits Xa
dabigatran MOA
inhibits thrombin