Koagulaatioon

Koagulaatioon, or coagulation, is the biological process by which blood forms a clot to seal injuries and prevent excessive bleeding. In many species, it occurs in two coupled stages: primary hemostasis, which forms a platelet plug, and secondary hemostasis, which strengthens the plug with a fibrin mesh. The process is tightly regulated to confine clots to the site of injury and to restore normal blood flow once healing begins.

During primary hemostasis, damaged vessels constrict and expose subendothelial structures. Platelets adhere via von Willebrand factor, become activated, release granules, recruit additional platelets, and form a temporary platelet plug.

Secondary hemostasis involves a coagulation cascade that converts soluble fibrinogen into insoluble fibrin, stabilizing the plug. The cascade is traditionally divided into intrinsic and extrinsic pathways, both generating thrombin, which converts fibrinogen to fibrin and activates factor XIII to cross-link fibrin. The extrinsic pathway is initiated by tissue factor released from injured tissue; the intrinsic pathway is activated by contact with negatively charged surfaces.

Regulation and dissolution: Antithrombin, protein C and protein S, and tissue factor pathway inhibitor limit clot formation. Fibrinolysis dismantles clots through plasmin, activated from plasminogen by tissue plasminogen activator, allowing removal of the clot as healing proceeds.

Clinical relevance: Defects in coagulation cause bleeding disorders such as hemophilia A or B and von Willebrand disease; excessive clotting in conditions like factor V Leiden raises thrombosis risk. Laboratory testing includes prothrombin time (PT) for the extrinsic pathway and activated partial thromboplastin time (aPTT) for the intrinsic pathway. Treatments range from factor concentrates and antifibrinolytics to anticoagulants such as heparin, warfarin, or direct oral anticoagulants (DOACs), depending on the disorder.