koagulatsioonijada

The term koagulatsioonijada refers to the sequential biochemical process through which blood plasma transforms into a stable fibrin clot in response to injury. This cascade involves a series of tightly regulated proteolytic activations of plasma proteins, collectively called coagulation factors, that culminate in the conversion of fibrinogen to fibrin by thrombin. The cascade is traditionally divided into three interrelated pathways: the intrinsic, the extrinsic, and the common pathway. The intrinsic pathway is initiated by contact activation of factor XII on negatively charged surfaces, while the extrinsic pathway is triggered by tissue factor exposure following vascular damage. Both pathways converge on the activation of factor X, also known as the prothrombinase complex formation, which then activates prothrombin to thrombin. Thrombin not only converts fibrinogen to fibrin but also amplifies the cascade by activating additional factors and recruiting platelets. A coagulation diathesis occurs when one or more factors are deficient or dysfunctional, leading to increased bleeding risk, or when hyperactive, promoting unwanted thrombosis.

The scaffold of the koagulatsioonijada is compensated by natural anticoagulant mechanisms such as antithrombin III, protein C, and protein S, which help to prevent excessive clot formation. The balance between pro‑ and anticoagulant forces is essential for maintaining haemostasis. Clinically, assays of individual coagulation factors, activated partial thromboplastin time (APTT), and prothrombin time (PT) are employed to evaluate the integrity of this cascade. Prognosis and therapy for a variety of bleeding disorders, such as hemophilia and von Willebrand disease, as well as anticoagulant treatments for arterial and venous thrombosis, are fundamentally linked to the understanding of the koagulatsioonijada.