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