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Hemostasis

ClassDrugsMechanismAdverse effectsIndications
Anti-coagulants - inhibit active factors Heparin Very acidic (antidote is basic) - very quick acting (IV admin) - activated ATIII (1000X) and inactivates factor Xa (HIT) heparin-induced thrombocytopenia, osteoporosis, allergic, pregnancy
Anti-coagulants - inhibit factor synthesis Warfarin (oral) Vit K antagonist (can't get reduced/recycled) - a week to start and a week to stop - CYP2C9 slow metab VKORC fast metab bleeding, hypersensitivity, TONS of drug interactions pregnancy, liver or kidney disease (metab/excrete)CYP2C9
Anti-coagulants - direct thrombin inhibitors Hirudin Inhibits fibrin activation, (blank) (blank)
Anti-coagulants - inhibit active factors LMW Heparin LMWHeparin inhibits Xa, Subcut admin, Don't have to monitor levels like others (blank) (blank)
Anti-coagulants - inhibit active factors Fundaparinux Inhibits Xa, Not assoc with HIT or Heparin induced osteoporosis (blank) (blank)
Anti-coagulants - direct thrombin inhibitors AT III (blank) (blank) used for hereditary ATIII deficiency
Anti platelet - prevent aggregation ticlopidine, clopidogrel, dipyridamole Inhibits ADP-induced aggregation, irreversible, decreased adhesion. (ticlopidine, clopidogrel bind ADP receptor, dipyridamole inhibits ADP uptake) statistically significant (but not really clinically significant) elevation in lever fxn, (ticlopidine - TPP, aplastic anemia), bleeding (dipyridamole) post-op clot prevention - can replace exercise in heart stress test (vasodilator)
Anti platelet - prevent adhesion Abciximab(monoclonal Ab), tirofiban (peptide), eptifibatide (synthetic non-peptide- oral bioavailability) block IIa/IIIb receptor - no platelet binding. Abciximab has shortest half-life (10min) and highest affinity (longest for platelet fxn to return to normal), tirofiban next, eptifibatide next bleeding (blank)
Anti-Platelet - COX inhibitors Aspirin Irreversibly acetylates COX - inhibits platelet-induced vasoconstriction (blank) (blank)
Thrombolytic - main Streptokinase, alteplase (synthetic streptokinase) activates plasminogen to plasmin. (streptokinase is antigenic so can only be used once or twice) - short half life bleeding - can be reversed with aminocaproic acid (blank)
Thrombolytic - others anistreplase, urokinase activates plasminogen bleeding (blank)
Anti-fibrinolytic (prevent clot dissolution) Epsilon-Aminocaproid acid activates plasminogen to plasmin, then sits in active site of plasmin (blank) (blank)
Drug-eluting stent sirolimus, paclitaxel Don't prevent clots, just inhibit growth of endothelium over stents and forming next clots. Doesn't seem to work quite as well as we think (blank)
Recombinant protein C recombinant protein C Inactivated Va and IIIa to prevent bleeding bleeding sepsis
Created by: milletbrock
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