hemostaasis

Hemostasis is the physiological process that stops bleeding after vascular injury and promotes vessel repair. It involves a coordinated interaction of blood vessels, platelets, and plasma coagulation proteins to form a stable plug and restore integrity of the circulatory system. The term hemostaasis is a common misspelling of hemostasis found in some sources, but the standard spelling is hemostasis.

Primary hemostasis begins with immediate vascular responses to injury, including vasoconstriction and exposure of subendothelial collagen. Platelets adhere to the damaged surface via von Willebrand factor and become activated, releasing granules that recruit additional platelets. These activated platelets aggregate to form a temporary platelet plug, providing initial hemostasis while the coagulation cascade strengthens the clot.

Secondary hemostasis or coagulation involves a cascade of plasma proteins that culminates in the conversion of fibrinogen to fibrin by thrombin. This fibrin mesh stabilizes the platelet plug and reinforces the clot. The coagulation system is organized into intrinsic and extrinsic pathways that converge on a common pathway, leading to robust thrombin generation and fibrin formation.

Regulation and resolution of hemostasis ensure balance. Anticoagulant mechanisms, including protein C and protein S systems and antithrombin, limit clot growth. Fibrinolysis, primarily mediated by plasmin activated by tissue plasminogen activator, dissolves the clot after vessel repair.

Clinical relevance includes inherited or acquired bleeding disorders (such as von Willebrand disease or hemophilia) and thrombotic conditions. Laboratory assessment typically uses platelet count, coagulation screens (PT/INR, aPTT), and specific tests for platelet function or factor deficiencies. Treatment targets the specific defect and may involve replacement therapy, antifibrinolytics, or antiplatelet or anticoagulant medications.