Blood coagulation

Abstract

Blood coagulation can be initiated by two pathways: the extrinsic pathway, which is triggered by release of tissue factor from the site of injury, and the intrinsic system, which is stimulated by contact with a negatively charged surface. Following initial triggering, a series of serine proteases are sequentially activated, culminating in the formation of thrombin, the enzyme responsible for the conversion of soluble fibrinogen to the insoluble fibrin clot. Activation of coagulation is tightly regulated. Initiation by tissue factor is inhibited by tissue factor pathway inhibitor. Antithrombin can inactivate many of the serine proteases, including thrombin, by forming stable complexes which are rapidly cleared from the circulation. Protein C and protein S combine to inactivate coagulation factors V and VIII. The deposition of excess fibrin is prevented by the fibrinolytic system which can lyse fibrin into fibrin degradation products. Both genetic and environmental factors can influence the activation of coagulation and may predispose affected individuals to thrombosis.

Viscoelasticity and Ultrastructure in Coagulation and Inflammation: Two Diverse Techniques, One Conclusion

“…Cross-links between fibrin strands lead to the formation of a network that covers the platelet plug. It seals the injury site and forms the stable, secondary haemostatic plug [ 7 ].…”

“…This potent system therefore needs to be carefully regulated to ensure that clot formation is not augmented or propagated, which can result in thrombotic complications. Several anti-coagulant factors are set in place to prevent pathological clotting [ 7 ].…”

“…Vessel damage exposes TF, which activates the coagulation system, and within seconds, fibrin is produced at the injury site [ 7 ]. Rapid activation of the haemostatic system is due to the specific interactions of coagulation factors.…”

“…Along with this pro-coagulant process of fibrin formation, the fibrinolytic system is also triggered to ensure that fibrin deposition is limited to the injury site. In addition, the anti-coagulant system ensures negative feedback to the coagulation cascade to block any further activation of the system [ 7 ].…”

“…Fibrin strands act as a plug to seal the injury site and thus protects the damaged tissue while the wound heals [ 7 ]. A number of steps are involved in this closely controlled process of fibrin formation.…”