Plasmatic coagulation - intrinsic system

Slowly running part of the plasmatic coagulation cascade (see also fast running coagulation = extrinsic coagulation), which begins after an endothelial lesion with the contact activation of factors XI and XII.

The intrinsic system got its name because it was observed that coagulation factors could be activated by contact with glass surfaces.

The intrinsic system is introduced at the negatively charged membrane surface. Together with the high molecular weight kininogen, factor XII is activated to form XIIa. This is a membrane-bound factor. It is absorbed at the negative surface, for example collagen. The binding alters the configuration of factor XII, making it up to 500 times more sensitive to the proteolysis of the kallikrein kininogen system. Kallikrein partially denatures factor XII and thus causes the activation of factor XII in XIIa. The product of this proteolysis activates from the complex prekallikrein-HMWK, the prekallikrein to kallikrein. This activates F-XII again until the substrate is exhausted.

The activated factor XII activates factor XI to Xia. Factor XI is not only activated by factor XIIa, but also by a platelet factor, which is localized on the platelet membrane. Because of this additional activation of F-XI, there is no more severe bleeding in people with a factor XII deficiency.
Together with cofactor VIIIa, calcium ions and phospholipids, factor IXa forms an enzymatically active complex called tenase. F-Xia activates F-IX to form IXa, which together with F-VIIIa, phospholipids and calcium forms the enzyme complex Tenase. This enzyme complex activates factor X to Xa.

When factor X is activated, the extrinsic and intrinsic systems join in a common pathway: together with factors Xa, Va, calcium ions and phospholipids, an enzymatically active complex is formed, called prothrombinase. The prothrombinase activates the prothrombin= F-II to F-IIa.

1. HA Neumann (2014) The coagulation system. ABW-Wissenschaftsverlag GmbH Berlin S. 77f.