Hemostatic

Hemostatic refers to the process that causes bleeding to stop, which is the first stage of wound healing. This involves coagulation, blood changing from a liquid to a gel. Intact blood vessels are central to moderating blood's tendency to form clots. The endothelial cells of intact vessels prevent blood clotting with a heparin-like molecule and thrombomodulin and prevent platelet aggregation with nitric oxide and prostacyclin. When endothelial injury occurs, the endothelial cells stop secretion of coagulation and aggregation inhibitors and instead secrete von Willebrand factor 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 fibrin clot. These processes seal the hole until tissues are repaired.

Vasoconstriction[edit | edit source]

Vasoconstriction is the first response as the blood vessels constrict to allow less blood to be lost. In addition, the endothelial cells become sticky due to the secretion of von Willebrand factor to help the platelets adhere to the damaged site.

Platelet plug formation[edit | edit source]

Platelets create a plug that fills in the broken part of the vessel. Platelets, or thrombocytes, are small, irregularly shaped clear cell fragments, 2–3 µm in diameter, which are derived from fragmentation of precursor megakaryocytes. The platelets are activated when they come into contact with collagen, a protein that makes up the walls of blood vessels. Activated platelets will release the contents of stored granules into the blood plasma.

Coagulation[edit | edit source]

Coagulation begins almost instantly after an injury to the blood vessel has damaged the endothelium lining the vessel. Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelian tissue factor to plasma Factor VII, which ultimately leads to fibrin formation. Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously: Additional coagulation factors or clotting factors beyond Factor VII (listed below) respond in a complex cascade to form fibrin strands, which strengthen the platelet plug.

See also[edit | edit source]

Hemostatic Resources
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