Fibrinolytics and Antiplatelet Drugs
Start with the big picture
Fibrinolytics such as alteplase activate plasminogen to form plasmin, which breaks down fibrin. The lesson distinguishes fibrin-selective alteplase from agents such as streptokinase and outlines key indications, contraindications, and the serious risk of intracranial hemorrhage. Antiplatelet drugs act through several pathways: aspirin reduces thromboxane A₂ production; P2Y₁₂ inhibitors limit ADP-dependent platelet activation; GP IIb/IIIa antagonists prevent fibrinogen binding; and PDE-3 inhibitors increase cAMP. The topic also introduces PAR-1 blockade and clinical considerations such as bleeding risk, platelet monitoring, antiplatelet combinations, and pre-surgical drug holds. These distinctions provide a framework for comparing how the agents work and where their safety profiles require attention.
What you'll learn
- Explain how fibrinolytics convert plasminogen to plasmin and promote fibrin breakdown.
- Compare key fibrinolytic agents by selectivity, indications, and major safety concerns.
- Describe how aspirin and the major antiplatelet drug classes affect platelet function.
- Identify notable adverse effects and contraindications associated with selected antiplatelet agents.
- Summarize the lesson’s clinical considerations for monitoring, bleeding risk, and pre-surgical holds.
Continue your study
Work through the complete notes and reinforce the topic with the study tools available in the full lesson.
