• Anti-platelet drugs

• Heparins and protamine

• Oral anticoagulants

• Drugs affecting the fibrinolytic system

Physiology

Haemostasis is complicated. Two models are currently used to explain what is thought to occur.

The classical model

This has three elements: platelets, the coagulation cascade and fibrinolysis. The first two are involved in preventing haemorrhage by thrombus formation, while fibrinolysis is an essential limiting mechanism.

Thrombus formation is initially dependent on platelet adhesion, which is triggered by exposure to subendothelial connective tissue. The von Willebrand factor, which is part of the main fraction of factor VIII, is essential in this process. Subsequent platelet aggregation and vasoconstriction is enhanced by the release of thromboxane A2 (TXA2) from platelets. Adjacent undamaged vascular endothelium produces prostacyclin (PGI2), which inhibits aggregation and helps to localize the platelet plug to the damaged area. The localized primary platelet plug is then enmeshed by fibrin converting it to a stable haemostatic plug.

The coagulation cascade is formed by an intrinsic and extrinsic pathway, which converge to activate factor X and the final common pathway (Figure 23.1). The intrinsic pathway is triggered by the exposure of collagen, thereby activating factor Ⅻ, while the extrinsic pathway is triggered by leakage of tissue factors, activating factor VII.

Venous thrombus consists mainly of a fibrin web enmeshed with platelets and red cells. Arterial thrombus relies more on platelets and less on the fibrin mesh.

A crucial part of this process is its limitation to the initial site of injury.