Overview
Pathophysiology
The coagulation cascade converts fibrinogen to fibrin, forming a mesh that stabilises a platelet plug.
The coagulation cascade converts fibrinogen to fibrin, forming a mesh that stabilises a platelet plug. Anticoagulants interrupt key steps—warfarin blocks vitamin K–dependent clotting factors (II, VII, IX, X); heparin catalyses antithrombin‑mediated inactivation of thrombin and factor Xa; direct oral anticoagulants (DOACs) either bind thrombin (dabigatran) or inhibit factor Xa (apixaban, rivaroxaban, edoxaban). Thrombolytics (e.g., alteplase) accelerate plasmin generation, cleaving fibrin and dissolving an existing clot. The therapeutic goal is to tip the balance toward clot dissolution without overwhelming haemostasis, because the same pathways that clot protect against bleeding when inhibited.
