hemostaasista

Hemostasis is the physiological process that stops bleeding at the site of vascular injury while preserving normal blood flow elsewhere. It integrates vascular responses, platelets, and coagulation factors to form a stable clot and begin tissue repair.

The process is typically described as having three overlapping phases: vascular spasm, primary hemostasis, and secondary hemostasis. Vascular spasm quickly reduces blood loss by constricting damaged vessels. In primary hemostasis, platelets adhere to exposed collagen via von Willebrand factor, become activated, release granules, and aggregate to form a temporary platelet plug. Secondary hemostasis involves the coagulation cascade, where coagulation factors generate thrombin, which converts fibrinogen to fibrin and stabilizes the platelet plug into a durable clot.

Clot stabilization is followed by clot retraction and remodeling to strengthen the vessel and restore flow. Finally, fibrinolysis dissolves the clot once healing is underway, primarily through plasmin-mediated breakdown of fibrin. Hemostasis is tightly regulated by procoagulant and anticoagulant pathways, including natural inhibitors such as antithrombin, protein C and S, and tissue factor pathway inhibitor, to balance clot formation and dissolution.

Dysfunction in hemostasis can lead to bleeding disorders or thrombosis. Bleeding disorders include hemophilia A or B (factor deficiencies) and von Willebrand disease. Thrombotic conditions include deep vein thrombosis and pulmonary embolism. Clinical assessment involves platelet counts and coagulation tests such as PT/INR and aPTT, along with factor-specific assays when indicated. Management depends on the defect and may involve replacement therapy, antifibrinolytics, platelet support, or anticoagulation to prevent or treat pathological clots.