Haemostasis Steps

Expansion

1. Vascular spasm: immediate local vasoconstriction
2. Primary haemostasis: platelet adhesion to exposed collagen via von Willebrand factor and GPIb, activation with release of ADP and thromboxane A2, then aggregation via GPIIb/IIIa and fibrinogen, forming a soft plug
3. Secondary haemostasis: the coagulation cascade generates thrombin, which converts fibrinogen to fibrin, stabilising the plug
4. Fibrinolysis: plasmin, generated from plasminogen by tissue plasminogen activator, dissolves the clot as healing proceeds

The clinical pattern of bleeding localises the defect:

• Primary (platelets, von Willebrand disease): mucocutaneous bleeding, petechiae, epistaxis, menorrhagia, immediate bleeding after injury
• Secondary (haemophilia, warfarin): deep bleeding into joints and muscles, large haematomas, delayed bleeding after initial haemostasis

Drug targets map onto the steps: aspirin blocks thromboxane, clopidogrel blocks ADP receptors, abciximab blocks GPIIb/IIIa, heparin and direct oral anticoagulants act on the cascade, and alteplase drives fibrinolysis.