Coagulation factors

The proteins of the coagulation cascade are pro-enzymes (serine proteases) and pro-cofactors, which are activated sequentially (Fig. 40.1). The cascade has been divided on the basis of laboratory tests into intrinsic, extrinsic and common pathways. This division is useful in understanding results of in vitro coagulation tests. In vivo, however, these pathways are closely interlinked. Coagulation begins in vivo when tissue factor is activated on the surface of injured cells and binds and activates factor VII; the complex activates factor X to Xa but also factor IX which, with activated cofactor VIII released from binding to von Willebrand factor (vWF), substantially amplifies activation of factor X to Xa.

The complex of Xa and Va, activated from factor V by thrombin, acts on prothrombin (factor II) to generate thrombin. Thrombin then converts fibrinogen into fibrin monomers, with release of fibrinopeptides A and B. The fibrin monomers combine to form a fibrin polymer clot. Factor XIII cross-links the polymer to form a more stable clot.

Platelets accelerate the coagulation process by providing membrane phospholipids which act as ‘docking’ stations for the coagulation factors.

Thrombin has a number of key roles in the coagulation process.

Coagulation inhibitory factors

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