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8 Cards in this Set
- Front
- Back
Aspirin
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1. MECHANISM:
- irreversibly acetylates COX, which leads to decreased TXA2 production, thereby decreasing platelet aggregation - at low doses, inhibits TXA2 production, but does not affect PGI2 - does not inhibit other platelet aggregation factors (ADP) so it is not a complete antithrombotic 2. CLINICAL: - very effective in pts. with CVD - not proven to be a good source of primary prevention 3. ADVERSE: - dyspepsia and nausea GI bleeding, hemorrhagic strokes, allergic rxn, asthma exacerbation - may exacerbate gout |
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Thienopyridines: clopidogrel
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1. MECHANISM:
- inhibit ADP-mediated activation of platelets - irreversibly block P2Y12, which is needed for ADP activation 2. CLINICAL: - used in pts allergic to aspirin. also to prevent thrombotic complications following percutaneous soronary stenting 3. ADVERSE: - dyspepsia and diarrhea |
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glycoprotein IIb/ IIIa receptor antagonists: abciximab
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1. MECHANISM:
- monoclonal Ab that inhibits the binding of activated platelet to fibrinogen and von Willebrand factor - platelets cannot "stick together" inhibiting the formation of plug 2. CLINICAL: - for pts undergoing percutaneous coronary interventions and high risk ACS - must be given IV 3. ADVERSE: - bleeding and thrombocytopenia |
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unfractioned Heparin (UFH)
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1. MECHANISM:
- positively associates with antithrombin III (ATIII) - reduces thrombin's ability to generate fibrin from fibrinogen - also inhibits activated factor X - antiplatelet activities by binding to von Willebrand factor 2. CLINICAL: - parenteral administration - unstable angina, non-STEMI, acute MI, PE or DVT 3. ADVERSE: - bleeding - heparin induced thrombocytopenia (HIT): most common type is direct heparin induced platelet aggregation. Rarer and more lethal is immune mediated. Abs are formed against heparin-platelet complex, causing thrombosis |
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low molecular weight heparins: enoxaparin
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1. MECHANISM:
- preferentially inhibits factor Xa - also inhibits thrombin via association with ATIII, but not as well as UFH - have more prominent anticoagulation abilites v. UFH, fewer complications, less HIT 2. CLINICAL: - prophylaxis against DVT following leg sx - tx for DVT - tx for ACS 3. ADVERSE: - do not give to pts with a history of HIT |
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Fondaparinux
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1. MECHANISM:
- binds to ATIII with very high affinity, thereby inhibiting factor Xa - does not inactivate formed thrombin, does not affect platelet activity, or cause HIT - long half life - subQ 2. CLINICAL: - prevention of DVT - tx for DVT and PE |
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vitamin K antagonist: warfarin
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1. MECHANISM:
- antagonizes vit K epoxide reductase, which inhibits vit K metabolism - vit K needed for carboxylation of coagulation factors. these are inactive with warfarin - vit K also activates coagulation inhibitors (protein C and S) so that warfarin aslo inactivates these factors 2. CLINCAL: - long-term anticoagulation 3. ADVERSE: - reduced dose in liver and hepatic dysfunction - teratogenic. do not give during pregnancy, especially first trimester |
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fibrinolytics: alteplase (tPA)
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1. MECHANISM:
- stimulates natural fibrinolytic system, transforming plasminogen into plasmin, thereby lysing fibrin clots - bind preferentially to fibrin in a formed thrombus 2. CLINICAL: - for use in acute STEMI. best to give within 30mins - not effective in UA or NSTEMI 3. ADVERSE: - contraindicated in pts with necessary fibrin clots (active peptic ulcer dx, hx of CVA, recovery from recent sx) |