Hemostase

Hemostasis, or hemostase, is the physiological process that stops bleeding following a blood vessel injury. It involves a rapid sequence of events that stabilize the damaged site and allow tissue repair: a local vascular constriction, formation of a platelet plug (primary hemostasis), activation of the coagulation cascade to generate a fibrin clot (secondary hemostasis), and eventually fibrinolysis to remove the clot as healing occurs.

Vasoconstriction reduces blood flow; platelets adhere to exposed subendothelial collagen via von Willebrand factor, become activated, release granule contents, and recruit additional platelets. These reactions form a reversible platelet plug that helps limit bleeding but is not sufficient for large vessel injuries.

The coagulation cascade consists of intrinsic and extrinsic pathways that converge on the activation of thrombin, which converts fibrinogen to fibrin. Fibrin threads stabilize the platelet plug into a firm thrombus. Factor XII initiates intrinsic; tissue factor from damaged tissue initiates extrinsic; common pathway includes factors X, V, II (thrombin), and I (fibrin).

Endothelial cells regulate hemostasis by releasing antiplatelet and anticoagulant factors, such as nitric oxide, prostacyclin, thrombomodulin, protein C, and antithrombin. Fibrinolysis dissolves clots: plasminogen is activated to plasmin by tPA/uPA, and plasmin cleaves fibrin. The system is balanced to prevent excessive bleeding or thrombosis; markers such as D-dimers reflect fibrin turnover.

Disorders include bleeding disorders (hemophilia A and B, von Willebrand disease) and thrombotic conditions (antithrombin deficiency, Factor V Leiden). Diagnosis relies on coagulation tests (PT/INR, aPTT), platelet counts, and specific assays; management may involve desmopressin, factor concentrates, antifibrinolytics, or platelet transfusions, depending on the defect.