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pharmacology

Quiz yourself by thinking what should be in each of the black spaces below before clicking on it to display the answer.
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Question
Answer
primary hemostasis   platelet plug formation  
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secondary hemostasis   fibrin formation  
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drugs that infere with thrombus formation   antithrombotics  
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drugs that promote degradatio of existing thrombi   thrombolytics/fibrinolytics  
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thrombi that form in arteries   white thrombi  
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thrombi w/more platelets and less fibrin   white thrombi  
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thrombi that form in veins   red thrombi  
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thrombi w/more fibrin and less platelets   red thrombi  
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types of antithrombotic drugs   antiplatelets and anticoagulants  
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drugs that interfere w/platelet plug formation   antiplatelets  
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test(s) used to measure antiplatelet effectiveness   bleeding time  
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drugs that interfere w/fibrin formation   anticoagulants  
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test(s) used to measure anticoagulant effectiveness   PT, INR, and PTT  
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site of von Willebrand factor binding   glycoprotein Ib receptors  
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1st step of platelet plug formation   platelet adhesion  
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2nd step of platelet plug formation   platelet activation/secretion  
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3rd step of platelet plug formation   platelet aggregation  
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needed to anchor platelets to BV wall   von Willebrand factor  
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5HT, ADP, and PDGR are secreted via   platelet cytoplasmic granules  
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TXA2 is secreted via   de novo synthesis/secretion  
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undergoes conformation change during platelet activation   glycoprotein IIb/IIIa receptors  
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platelet activation allows this to bind   fibrinogen molecules  
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instrinc and extrinsic pathways converge here   factor X  
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measures integrity of extrinsic and common pathways   PT  
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measures integrity of intrinsic and common pathways   PTT  
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usually ordered w/PT   INR  
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test(s) ordered to check warfarin's efficacy   PT & INR  
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test(s) ordered to check unfractionated heparin's efficacy   PTT  
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test(s) ordered to check LMW heparin's efficacy   factor Xa inhibition assay  
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MOA = irreversibly acetylates COOX, inhibiting production of TXA2   ASA  
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cardioprotective dose of ASA   75-325 mg/day  
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avoid in pts w/asthma and nasal polyps   ASA  
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tinnitus may indicate   ASA toxicity  
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AE = GI sx, hemorrhagic strokes   ASA  
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MOA = inhibit ADP-mediated platelet activation by irreversibly binding to ADP receptors   thienopyridines  
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ticlopidine   thienopyridines  
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clopidogrel   thienopyridines  
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prasugrel   thienopyridines  
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AE = dyspepsia, diarrhea, neutropenia   thienopyridines  
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AE = thombotic thrombocytopenic purpura, severe neutropenia   ticlopidine  
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dosing = twice daily   ticlopidine, ticagrelor  
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used w/ASA following coronary stenting and for acute corony syndromes   clopidogrel  
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dosing = once daily   clopidogrel  
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metabolized by CYP-2C19   clopidogrel  
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30% are "poor responders"   clopidogrel  
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used w/ASA following PCI   prasugrel  
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CI= elderly, TIA/CVA hx, small frame   prasugrel  
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MOA = reversibly binds to platelet ADP receptors   ticagrelor  
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used w/ASA for acute coronary syndromes   ticagrelor  
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most effective antiplatelet drugs   GP IIb/IIIa inhibitors  
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MOA = prevent fibrinogen-mediated platelet aggregation   GP IIb/IIIa inhibitors  
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MOA = monoclonal AB against GPIIb/IIIa receptors   abciximab  
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MOA = peptide antagonist   eptifibatide  
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MOA = nonpeptide antagonist   tirofiban  
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MOA = inc cAMP in platelets, decreasing cystolic Ca++ and inhibiting platelet aggregation   dipyridamole  
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AE = thrombocytopenia   abciximab  
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not usually given alone, but may enhance effect of other antithrombotics   dipyridamole  
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needs at least 18 saccharide residues to produce effect   heparin  
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selectively inhibits factor Xa   LMW heparin  
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has equal inhibitory activity against factor Xa and thrombin   UF heparin  
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AE = bleeding, thrombocytopenia, osteoporosis, skin necrosis, alopecia, hypoaldosteronism   heparin  
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lower incidence of heparin-induced thrombocytopenia   LMW heparin  
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given when severe bleeding complications occur w/heparin   protamine sulfate  
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most common type of HIT   non-immune mediated  
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life-and-limb threatening thrombosis can occur with this   immune-mediated HIT  
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IgG + heparin + PF4 =   platelet activation/aggregation  
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given when immune-mediated HIT occurs   direct thrombin inhibitors  
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MOA= inhibit thrombin activity independent of antithrombin III   direct thrombin inhibitors  
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lepirudin   direct thrombin inhibitors  
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bivalirudin   direct thrombin inhibitors  
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argatroban   direct thrombin inhibitors  
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AE = BLEEDING   direct thrombin inhibitors  
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MOA = synthetic heparin analog, bind to antithrombin III   fondaparinux  
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inhibits factor Xa without causing HIT   fondaparinux  
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dosing = subQ injection once daily   fondaparinux  
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used for DVT prophylaxis in ortho surgery, and to treat DVT/PE   fondaparinux  
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MOA = inhibits formation of reduced Vit K   warfarin  
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necessary for activation of coagulation factors II, VII, IX, and X   Vit K  
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delayed onset of anticoagulation   warfarin  
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Vit K protein w/shortest half life   Protein C  
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avoid large loading doses   warfarin  
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given to avoid transient paradoxical hypercoagulable state   warfarin and heparin together  
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AE = bleeding, teratogenic, skin necrosis   warfarin  
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associated w/protein C or S deficiency & warfarin use   skin necrosis  
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given when bleeding complications occur with warfarin   vit K or fresh frozen plasma transfusion  
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used for DVT, atrial fib, mechanical heart valve, and STEMI   warfarin  
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used for unstable angina/NSTEMI, STEMI, DVT, and PCI   UF heparin  
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used for unstable angina/NSTEMI, STEMI, and DVT   LMW heparin  
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used for PIC and HIT   direct thrombin inhibitors  
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used for chronic angina, unstable angina/NSTEMI, STEMI, and PCI   ASA  
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used for unstable angina/NSTEMI and STEMI   thienopyridines  
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used for PCI and unstable angina/NSTEMI   GP IIb/IIIa inhibitors  
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given if pt is unable to take warfarin for mechanical heart valve or a fib   UF heparin  
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