Anticoagulants
Mechanisms
- Anticoagulants act at different points in the coagulation cascade - vitamin K antagonists (warfarin, inhibiting synthesis of factors II, VII, IX, X), direct oral anticoagulants (direct factor Xa or thrombin inhibition), and heparins (antithrombin-mediated factor Xa/thrombin inhibition) - mechanism determines monitoring requirements, reversal options, and specific clinical use cases
- Warfarin inhibits hepatic vitamin K epoxide reductase, reducing synthesis of vitamin K-dependent clotting factors - its delayed onset (days, reflecting the half-life of existing clotting factors already in circulation) and narrow therapeutic index requiring INR monitoring are direct consequences of this mechanism
- DOACs directly inhibit a single specific clotting factor (Xa for apixaban/rivaroxaban, thrombin for dabigatran) - producing rapid onset, predictable pharmacokinetics, and generally no requirement for routine monitoring, though renal function must be checked given renal clearance dependence for several agents
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