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Questions and Answers
Which natural anticoagulant inactivates the serine protease IIa?
Which factor is responsible for the initial activation of factor X to Xa?
In what condition is a systemic lytic state created with an attendant increase in bleeding risk?
What causes resistance to inactivation by the protein C, protein S mechanism?
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Which regulatory system is overwhelmed by therapeutic doses of plasminogen activators?
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What is a clinically useful inhibitor of fibrinolysis?
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What is the ideal goal of anticoagulant drugs?
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How do indirect thrombin inhibitors exert their antithrombotic effect?
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Which drug binds to antithrombin and enhances its inactivation of factor Xa?
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What is the principle toxicity of anticoagulants and fibrinolytic drugs?
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Which phase of the clotting mechanism does unfractionated heparin (UFH) enhance?
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What is the main interaction of indirect thrombin inhibitors for exerting their antithrombotic effect?
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What is the effect of unfractionated heparin and to a lesser extent LMW heparin on antithrombin?
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What is the role of thromboxane A2 (TXA2) in platelet function?
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Which of the following substances is released from platelet granules and is a powerful inducer of platelet aggregation?
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What is the main initiator of blood coagulation in vivo?
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What is the function of the glycoprotein (GP) IIb/IIIa receptor on platelets?
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In paVents with defects in primary hemostasis, such as von Willebrand disease, where do they typically bleed from?
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What regulates the TF-factor VIIa-catalyzed activation of factor Xa in blood coagulation cascade?
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What is the primary function of hemostasis?
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What are common causes of dysregulated hemostasis?
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What is atrial fibrillation associated with?
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What is the normal relationship between the vascular endothelial cell layer and circulating blood platelets and clotting factors?
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What are the risk factors considered in the CHA2DS2-VASC score for the use of oral anticoagulants?
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Which condition represents a breakdown of the hemostatic mechanism?
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What is the peak therapeutic level of enoxaparin for twice-daily dosing?
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What is the primary risk associated with long-term heparin therapy?
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What is a major adverse effect of heparin?
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How are patients who develop HIT (heparin-induced thrombocytopenia) treated?
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What is the therapeutic range for treatment of venous thromboembolic disease with heparin?
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How is low-dose prophylaxis of heparin achieved?
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What is the molecular weight range of unfractionated heparin (UFH)?
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How do LMW heparins such as ENOXAPARIN, DALTEPARIN, and TINZAPARIN compare with UFH in terms of dosing requirements?
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Which factor does unfractionated heparin (UFH) inhibit to a greater extent than thrombin?
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How is the biologic activity of heparin dependent upon antithrombin?
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In patients receiving UFH, which monitoring test is necessary for close monitoring of its effect?
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How does heparin function as a cofactor for the antithrombin-protease reaction without being consumed?
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What is the mechanism of action of fondaparinux?
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How is excessive anticoagulant action of heparin treated?
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What is the role of protamine sulfate in neutralizing heparin's anticoagulant activity?
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Why must excess protamine be avoided when used to neutralize heparin?
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What effect does protamine have on LMW heparin?
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What is the effect of protamine on fondaparinux?
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What is the advantage of fondaparinux's long half-life of 15 hours?
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In what situation is administration of protamine sulfate indicated?
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What is the mechanism of action of warfarin in preventing blood clot formation?
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Which drug interaction mechanism causes an increased anticoagulant effect and risk of bleeding when combined with warfarin?
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How does warfarin affect the fetal proteins with γ-carboxyglutamate residues found in bone and blood?
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Which drug inhibits the metabolic transformation of S-warfarin, leading to an increased anticoagulant effect?
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What is the recommended international normalized ratio (INR) range for prophylaxis and treatment of thrombotic disease?
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How does cholestyramine affect warfarin's absorption and bioavailability?
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What is the main adverse effect associated with cutaneous necrosis during the first weeks of warfarin therapy in patients with inherited deficiency of protein C?
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What was the initial use of warfarin and its congeners?
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What is the main mechanism of action of coumarin anticoagulants?
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How does warfarin's binding to plasma albumin contribute to its characteristics?
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What is the specific function of vitamin K in the context of coumarin anticoagulants?
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What is the oral bioavailability of racemic warfarin?
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How do coumarin anticoagulants affect coagulation factor molecules?
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What contributes to the long half-life of racemic warfarin in plasma?
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How can the excessive anticoagulant effect and bleeding from warfarin be reversed?
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What is the mechanism of action of rivaroxaban, apixaban, and edoxaban?
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What is the recommended prophylactic dosage of rivaroxaban for prevention of venous thromboembolism following hip replacement?
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Why do rivaroxaban, apixaban, and edoxaban not require monitoring?
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Which factor influences the drug half-life of rivaroxaban?
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What is the recommended dosage of apixaban for prevention of venous thromboembolism following hip or knee surgery?
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What makes edoxaban a once-daily Xa inhibitor with a 62% oral bioavailability?
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Which oral direct thrombin inhibitor is approved for the reduction of risk of stroke and systemic embolism with nonvalvular atrial fibrillation?
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What is the primary toxicity of dabigatran, the only oral direct thrombin inhibitor approved by the FDA?
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Which direct thrombin inhibitor has a short half-life with clearance that is 20% renal and the remainder metabolic, and has been FDA-approved for use in percutaneous coronary angioplasty?
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Which direct thrombin inhibitor is a small molecule thrombin inhibitor FDA-approved for use in patients with heparin-induced thrombocytopenia (HIT) with or without thrombosis?
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Which direct thrombin inhibitor requires no monitoring due to its predictable pharmacokinetics and bioavailability, allowing for fixed dosing and predictable anticoagulant response?
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Which direct thrombin inhibitor is excreted by the kidney and should be used with great caution in patients with renal insufficiency as no antidote exists?
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Which direct thrombin inhibitor inhibits platelet activation and has been FDA-approved for use in percutaneous coronary angioplasty?
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For which condition is Idarucizumab, a humanized monoclonal antibody Fab fragment that binds to dabigatran and reverses its anticoagulant effect, approved for use?
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What is the action of lepirudin, a specific, irreversible thrombin inhibitor from leech saliva?
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Which drug is synthesized by streptococci and combines with the proactivator plasminogen?
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What permits the clinical use of urokinase and the streptokinase-proactivator complex?
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What is the preferred target of tissue plasminogen activators (t-PAs) for activation of plasminogen?
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How is recombinant human t-PA manufactured?
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What prevents the effects of naturally occurring inhibitors (antiplasmins) on urokinase and the streptokinase-proactivator complex?
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What is the primary source of streptokinase?
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What converts plasminogen to active plasmin in the absence of inhibitors?
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What does recombinant human t-PA preferentially activate if bound?
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What is the primary clinical use of recombinant factor VIIa?
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What is the recommended dosage of tranexamic acid for congenital factor VII deficiency?
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What is the main clinical use of aminocaproic acid?
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What is the mechanism of action of aminocaproic acid?
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For which condition is recombinant factor VIIa not indicated?
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What is the mechanism of action of tranexamic acid?
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What is the primary clinical use of fresh frozen plasma?
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What is the role of a four-factor plasma replacement preparation containing vitamin K– dependent factors II, VII, IX, and X (4F PCC, Kcentra)?
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What adverse effect is most seriously associated with ticlopidine?
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Which drug is contraindicated in patients with a history of TIA or stroke due to increased bleeding risk?
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Which drug is rarely associated with neutropenia and is frequently preferred over ticlopidine due to its superior adverse effect profile?
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Which drug achieves maximum platelet inhibition with a maintenance dosage of 75 mg/d?
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Which drug is a peptidomimetic inhibitor with the RGD sequence motif?
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Which P2Y12 inhibitor is approved for IV use in coronary interventions in patients without previous ADP P2Y12 inhibitor therapy?
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What is the primary function of the platelet GP IIb/IIIa (integrin αIIbβ3) receptor?
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Which drug is a vasodilator that inhibits platelet function by inhibiting adenosine uptake and cGMP phosphodiesterase activity?
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Which vitamin confers biologic activity upon prothrombin and factors VII, IX, and X?
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What are the two natural forms of vitamin K?
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Which factor deficiency accounts for classic hemophilia, or hemophilia A?
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Which factor is Eloctate, a factor VIII-Fc domain conjugate, designed to treat?
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Which drug is used primarily to treat intermittent claudication?
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How is Alteplase (t-PA) administered?
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What is the recommended dose of recombinant t-PA for acute ischemic stroke?
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What is the dosing scheme for Reteplase?
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How does Aspirin inhibit platelet aggregation?
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How do Thienopyridines such as Ticlopidine, Clopidogrel, & Prasugrel reduce platelet aggregation?
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What is the main target for antiplatelet drugs that block GP IIb/IIIa receptors on platelets?
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What is the mechanism of action of Dipyridamole and Cilostazol as antiplatelet drugs?
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How do recombinant T-PA drugs differ from Reteplase and Tenecteplase in terms of dosing schemes?
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Match the fibrinolytic drug with its mechanism of action:
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Match the drug characteristic with the corresponding effect:
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Match the drug dosing scheme with the corresponding drug:
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Match the drug's inhibitor with the corresponding protection mechanism:
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Match the antiplatelet drug with its recommended dosage for patients with acute coronary syndromes:
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Match the antiplatelet drug with its adverse effects:
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Match the antiplatelet drug with its primary clinical use:
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Match the antiplatelet drug with its unique pharmacological characteristic:
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Match the following drugs with their primary mechanism of action:
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Match the following drugs with their clinical use:
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Match the following vitamin K forms with their characteristics:
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Match the following plasma coagulation factor products with their characteristics:
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Match the thrombolytic agent with its dosing scheme for administration:
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Match the antiplatelet drug with its mechanism of action:
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Match the factor with its association in the context of anticoagulant drugs:
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Match the drug with its clinical indication for use:
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Match the following inhibitors of fibrinolysis with their clinical uses:
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Match the following recombinant coagulation factors with their clinical uses:
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Match the following anticoagulants with their respective dosing schemes:
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