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Coagulation cascade: Introduction

The correct functioning of the hemostatic cascade is a vital function of the human body. It is an extremely complex process requiring the coordinated interaction of endothelial cells, platelets and plasma proteins, leading to well-ordered activation and deactivation between coagulation factors to retain the integrity of the blood vessel system and promote healing. This process has been described as taking place in four key phases: initiation, amplification, propagation and stabilization.

See here for more detailed information or choose one of the factors to learn more.

Detailed information:

The cascade illustrates the recruitment and activation of the various factors involved in the cascade, leading to the production of an insoluble fibrin net, which is key for mainte­nance of the platelet plug during the healing process.

The coagulation factors are numbered with Roman numerals (according to the order of their discovery), eg, Factor VIII. Some of these factors are better known by their original name, eg, prothrombin (now referred to as Factor II).

The process of initiation begins with the release of tissue factor (TF) from the injured endothelium and the collagen rich subendo­thelium, where it acts with other factors to promote the activation of small amounts of thrombin from prothrombin.

The central magnified area of the illustration shows the amplification phase and the key interaction between von Willebrand factor (VWF) and Factor VIII, which, among other roles, is involved in the recruitment and activation of platelets. In the amplification phase, the small amount of thrombin is able to activate Factor VIII and V, which act as accelerators, enabling a several thousand-fold increase of thrombin formation – the thrombin burst seen in the propagation phase. In the two final phases, propagation and stabilization, the large amount of thrombin catalyzes the production of fibrin from fibrinogen, as well as activating Factor XIII which further catalyzes the process of stabilizing the platelet plug by cross-linking the fibrin fibers, thus forming a fibrin net and rendering the fibrin insoluble.

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