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Hemostasis or haemostasis (from the Ancient Greek: αἱμόστασις haimóstasis "styptic (drug)") is a complex process which causes the bleeding process to stop. It refers to the process of keeping blood within a damaged blood vessel (the opposite of hemostasis is hemorrhage). Most of the time this includes the changing of blood from a fluid to a solid state. Intact blood vessels are central to moderating blood's tendency to clot. The endothelial cells of intact vessels prevent blood coagulation by secretion of heparin like molecule and thrombomodulin and prevent platelet aggregation by the secretion of nitric oxide and prostacyclin. When endothelial injury occurs, the endothelial cells cease secretion of coagulation and aggregation inhibitors and instead secrete von Willebrand factor and tissue thromboplastin which initiate the maintenance of hemostasis after injury. Hemostasis has three major steps: 1) vasoconstriction, 2) temporary blockage of a break by a platelet plug, and 3) blood coagulation, or formation of a clot that seals the hole until tissue are repaired.

[edit] Overview

Hemostasis is maintained in the body via three mechanisms:

• Vascular spasm - Damaged blood vessels constrict.
• Platelet plug formation - Platelets adhere to damaged endothelium to form platelet plug (primary hemostasis) and then degranulate.
• Blood coagulation - Clots form upon the conversion of fibrinogen to fibrin, and its addition to the platelet plug (secondary hemostasis).

[edit] Steps

• The first step is immediate constriction of damaged vessels caused by vasoconstrictive paracrine released by the endothelium. Vasoconstriction temporarily decreases blood flow and pressure within the vessel. When you put pressure on a bleeding wound, you also decrease flow within the damaged vessel.
• Vasoconstriction is rapidly followed by the second step,mechanical blockage of the hole by a platelet plug. The plug forms as platelets stick to the exposed collagen(platelet adhesion) and become activated, releasing cytokines into the area around the injury. Platelet factors reinforce local vasoconstriction and activate more platelets which stick to one another( platelet aggregation) to form a loose platelet plug.
• Simultaneously, exposed collagen and tissue factor (a protein-phospholipid mixture) initiate the third step, a series of reactions known as the coagulation cascade. The cascade is a series of enzymatic reactions that ends in the formation of a fibrin protein fiber mesh that stabilizes the platelet plug. The reinforced platelet plug is called a clot. Some chemical factors involved in the coagulation cascade also promote platelet adhesion and aggregation in the damaged region.

Eventually, as the damaged vessel repairs itself, the clot retracts and is slowly dissolved by the enzyme plasmin.

[edit] External links

• MeSH Hemostasis

v • d • e Myeloid physiology Hematopoiesis Myelopoiesis (CFU-GEMM) CFU-GM Granulopoiesis (Myeloblast, Promyelocyte, Myelocyte, Metamyelocyte, Band cell) Monocytopoiesis (Monoblast, Promonocyte) MEP Thrombopoiesis (Megakaryoblast, Promegakaryocyte) Erythropoiesis (Proerythroblast, Normoblast, Reticulocyte) General Extramedullary hematopoiesis Hemostasis Coagulation (Fibrinolysis) · Clot retraction · Platelet adhesiveness myeloid navs: cells/physio, disease of RBCs+megakaryocytes/monocytes+granulocytes/neoplasia, symptoms+signs/eponymous

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