Which drug is a GP IIb/IIIa inhibitor used to prevent reocclusion during PCI?

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Multiple Choice

Which drug is a GP IIb/IIIa inhibitor used to prevent reocclusion during PCI?

Explanation:
The key idea is that this drug blocks the final common pathway of platelet aggregation to keep the vessel open during a PCI. Abciximab is a GP IIb/IIIa receptor inhibitor; it binds to these receptors on activated platelets, preventing fibrinogen from cross-linking platelets. By doing so, it markedly reduces platelet aggregation at the intervention site and lowers the risk of reocclusion or stent thrombosis during and after PCI. It’s given IV around the procedure as a bolus followed by an infusion, and patients are monitored for bleeding and thrombocytopenia. Other agents described act through different mechanisms and aren’t GP IIb/IIIa inhibitors. Clopidogrel reduces platelet activation via P2Y12 receptor blockade, not GP IIb/IIIa inhibition. Warfarin is a vitamin K antagonist that prevents new clot formation by affecting coagulation factors, not immediate platelet aggregation. Streptokinase dissolves existing clots as a thrombolytic, rather than preventing reocclusion by inhibiting platelet aggregation.

The key idea is that this drug blocks the final common pathway of platelet aggregation to keep the vessel open during a PCI. Abciximab is a GP IIb/IIIa receptor inhibitor; it binds to these receptors on activated platelets, preventing fibrinogen from cross-linking platelets. By doing so, it markedly reduces platelet aggregation at the intervention site and lowers the risk of reocclusion or stent thrombosis during and after PCI. It’s given IV around the procedure as a bolus followed by an infusion, and patients are monitored for bleeding and thrombocytopenia.

Other agents described act through different mechanisms and aren’t GP IIb/IIIa inhibitors. Clopidogrel reduces platelet activation via P2Y12 receptor blockade, not GP IIb/IIIa inhibition. Warfarin is a vitamin K antagonist that prevents new clot formation by affecting coagulation factors, not immediate platelet aggregation. Streptokinase dissolves existing clots as a thrombolytic, rather than preventing reocclusion by inhibiting platelet aggregation.

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