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cardio exam 3
drug list
| drug name | class/MOA | SOA | ADRs/side effects | contraindications | DDI | key information |
|---|---|---|---|---|---|---|
| Aspirin | - COX-1 inhibitor - irreversibly binds to and inhibits COX-1, inhibits formation of thromboxane A2 (TXA2) | - platelets | - aspirin-induced asthma - CV: inc preload - GI: epigastric distress, nausea, vomiting, gastric ulceration, and hemorrhage - ototoxicity - reye syndrome | - alcohol (inc bleeding) - other antiplatelet, anticoagulants | - can give w/NSAIDs but take aspirin first | |
| Dipyridamole | - antiplatelet agent - MOA: decreases the degradation of cAMP via PDE inhibition (weak antiplatelet drug), coronary vasodilator | - GI distress, angina, headache, dizziness, and rash | ||||
| Clopidogrel (Plavix) | - antiplatelet agent - irreversible P2Y12 inhibitor, coupled to Gi (inc cAMP) - cAMP inhibits platelet glycoprotein receptors, and reduces fibrinogen binding and platelet aggregation | - bleeding, neutropenia, and thrombocytopenia | - PPIs and CYP2C19 inhibitors (dec potency of clopidogrel, inc clotting) | |||
| Prasugrel (Effient) | - antiplatelet agent - irreversible P2Y12 inhibitor, which leads to prevention of GPIIb/IIIa complex formation | - fatal and life-threatening bleeding | - CYP3A4 - other antiplatelets and anticoagulants | |||
| Ticagrelor | ||||||
| Cangrelor | ||||||
| Eptifibatide (Integrilin) | - antiplatelet agent - cyclic peptide inhibitor of IIb/IIIa binding site | |||||
| Tirofiban (Aggrastat) | - antiplatelet agent - non-peptide small molecule that inhibits IIb/IIIa binding site | - inc risk of bleeding | ||||
| Nitroglycerin | - nitrovasodilator - relax smooth muscle by releasing NO which stimulates production of cGMP - inc oxygen supply, dec ventricular wall stress - dec oxygen demand | - headache and flushing - postural hypotension - tolerance develops rapidly | - PDE5 inhibitors - Vericiguat (direct agonist to sGC) | |||
| Isosorbide dinitrate/mononitrate | - nitrovasodilator - relax smooth muscle by releasing NO which stimulates production of cGMP - inc oxygen supply, dec ventricular wall stress - dec oxygen demand | |||||
| Ranolazine | - antagonist to the late phase of the inward Na channel, reducing Ca overload during myocardial ischemia - prevents inc workload of heart w/o major changes in HR and BP | - headache, nausea, and constipation - CNS (Na channel blocker): dizziness, diplopia (double vision), and confusion | - CYP3A4 inducers. inhibitors, and substrates - P-gp transport inhibitors (inc ranolazines absorption) | |||
| Heparin | - Anticoagulant - increases the rate of thrombin-antithrombin III reactions by making the reactive site more accessible to the protease, thrombin inactivation - forms complex with antithrombin III and inhibits factors IIa or Xa | antithrombin III | - HIT: development of IgG antibodies against platelet factor 4 (PF4) - hemorrhage - hyperkalemia - osteoporosis | - existing bleeding condition or bleeding tendency | - drugs that inc risk of bleeding (other anticoagulants, antiplatelets, and thrombolytics) | - Antidote: protamine sulfate - glycosaminoglycan produced by mast cells |
| Enoxaparin (Lovenox) | - low MW heparin - inhibits factor Xa, less effect on IIa | - HIT less likely - osteoporosis less likely - bleeding less likely | ||||
| Bivalirudin | - direct thrombin (IIa) inhibitor - synthetic compound that is reversible by thrombin cleavage | |||||
| Warfarin (Coumadin) | - anticoagulant, vit K antagonist - inhibits vit K epoxide reductase | - hemorrhage, skin necrosis, blue-tinged discoloration of plantar surfaces | - pregnancy | - CYP2C9 inhibitors inc warfarin toxicity CYP2C9 inducers dec warfarin efficacy | - antidote: vit K - racemic mixture (S-isomer is more potent) - peak effect: 5-7 days | |
| Dabigatran (Pradaxa) | - anticoagulant, direct thrombin inhibitor - selective and reversible inhibitor of thrombin (free and fibrin-bound) - directly binds to factor IIa and blocks conversion of cofactor I to Ia (fibrinogen to fibrin) | - bleeding - dyspepsia | - P-gp inducers and inhibitors | - prodrug - hydrolyzed by esterases; gluronidation | ||
| Apixaban (Eliquis) | - factor Xa inhibitor - reversible antagonist | - CYP3A4/5 | - P-gp substrate | |||
| Rivaroxaban (Xarelto) | - factor Xa inhibitor - reversible antagonist | |||||
| Fondaparinux (Anixtra) | - synthetic heparin - only inhibits Xa | - HIT and osteoporosis are unlikely | - synthetic pentasaccharide anticoagulant | |||
| Alteplase (Cathflo, Activase) | - fibrinolytic - serine protease which activates plasminogen (bound to fibrin) and increases plasmin levels (clot specific and must bind to fibrin | - hemorrhage | ||||
| Tenecteplase | - fibrinolytic - serine protease which activates plasminogen (bound to fibrin) and increases plasmin levels (clot specific and must bind to fibrin | - hemorrhage | ||||
| Urokinase | - fibrinolytic - enzyme obtained from urine - directly activates plasminogen; isolated from human kidney (less chance of allergic reaction) | |||||
| Argatroban | - direct thrombin (IIa) inhibitor - synthetic compound based on the structure of L-arginine that binds reversibly to the catalytic site of thrombin | - S-isomer is more potent - metabolized by CYP3A4: hydroxylation and aromatization | ||||
| Vorapaxar (Zonitivity) | - antiplatelet agent - competitive antagonist to the PAR-1 receptors, inhibits thrombin-induced platelet aggregation | - bleeding | - CYP3A4 inhibitors and inducers - other antiplatelets/coagulants | |||
| Streptokinase | - fibrinolytic - protein obtained from streptocci - combines with plasminogen to form an active complex that converts plasminogen to plasmin to dissolve the fibrin |
Created by:
Marrufoj