Final Exam (Antiplatelet & Anticoagulant) Flashcards
Aspirin
Antiplatelet
COX inhibitor
MOA: blocking conversion of AA to TXA2, decreases platelet aggregation
Dazoxiben
Antiplatelet
Thromboxane A2 synthetase inhibitor
MOA: blocks the enzyme (synthetase) that would normally convert prostaglandin to thromboxane thereby decreasing platelet aggregation
Clopidogrel (Plavix), Ticlopidine (Ticlid), Prasugrel, Ticagrelor
Antiplatelet
ADP inhibitors
MOA: irreversibly binds to ADP receptors on platelets which prevents the activation of the ADP-mediated glycoprotein GPIIb/IIIa complex which is necessary for platelet aggregation
Abciximab
Antiplatelet
Glycoprotein IIB/IIIA inhibitor
MOA: blocks the GP IIB/IIIA receptor on activated platelets which prevents fibrinogen from attaching. Fibrinogen is unable to be converted to fibrin which results in the absence of the structural framework that holds platelets together
Eptifibatide, Tirofiban
Antiplatelet
Glycoprotein IIB/IIIA inhibitor
MOA: blocks the GP IIB/IIIA receptor on activated platelets which prevents fibrinogen from attaching. Fibrinogen is unable to be converted to fibrin which results in the absence of the structural framework that holds platelets together
Cilostazol, Dipyridamole
Antiplatelet
PDE inhibitor
MOA: inhibiting the breakdown of cAMP so more cAMP is able to inhibit the release of ADP thereby reducing platelet aggregation
Warfarin
Vitamin K antagonist
MOA: prevents reduced vitamin K regeneration by inhibiting vitamin K epoxide reductase, thereby slowing coagulation.
Notes: Vitamin K is a necessary cofactor for conversion of prothrombin into thrombin. A carboxylate enzyme requires reduced vitamin K to carboxylate (activate) prothrombin from its inactive (decarboxylated) form.
Compared to heparin: slower onset of action, contraindicated in pregnant women
Drugs that INCREASE effects:
Broad spectrum ABO, statins, alcohol, NSAID, metronidazole (increases time for clotting)
Drugs that DECREASE effects:
Vitamin K, barbiturates, cholestyramine, glutethimide
Heparin
Anticoagulant
Thrombin inhibitor
MOA: binds directly to Anti-thrombin III, increasing its affinity for thrombin, decreasing thrombin’s activity of converting fibrinogen to fibrin and thus slowing the rate of coagulation. With anti-thrombin III
Indications: pulmonary embolism, MI, anticoagulant for pregnant women (doesn’t cross placenta)
SE: excessive bleeding, hypersensitivity reactions
Enoxaparin
Anticoagulant
Thrombin inhibitor
MOA: binds directly to Anti-thrombin III, increasing its affinity for thrombin, decreasing thrombin’s activity of converting fibrinogen to fibrin and thus slowing the rate of coagulation. With anti-thrombin III
Notes: compared to heparin, increased bioavailability, less frequent dosing, less frequent bleeding
Dabigatran (Pradaxa)
Anticoagulant
Oral thrombin inhibitor
Indications: stroke prevention in non-valvular AFib
Rivaroxaban
Anticoagulant
Oral thrombin inhibitor
Indications: stroke prevention in non-valvular AFib and DVT prophylaxis
Alteplase
MOA: Directly converts plasminogen to plasmin. Plasmin attacks and erodes fibrin strands which breaksdown clots
Indications: acute MI, pulmonary embolism, stroke
SE: hemorrhage
Notes: contraindicated in pregnancy and pts with history of stroke
Streptokinase
MOA: Forms complex with plasminogen which then converts plasminogen to plasmin. Plasmin attacks and erodes fibrin strands which breaksdown clots
Indications: acute MI, pulmonary embolism, stroke
SE: hemorrhage
Notes: contraindicated in pregnancy and pts with history of stroke
Anistreplase
MOA: Directly converts plasminogen to plasmin. Plasmin attacks and erodes fibrin strands which breaksdown clots
Indications: acute MI, pulmonary embolism, stroke
SE: hemorrhage
Notes: contraindicated in pregnancy and pts with history of stroke
Dicumarol
Vitamin K antagonist
MOA: prevents reduced vitamin K regeneration by inhibiting vitamin K epoxide reductase, thereby slowing coagulation.
