Blood clotting

The process of blood solidification. Clotting is important in stemming bleeding from damaged blood vessels. However, unwanted blood clotting can occur inside major blood vessels and cause a myocardial infarction (heart attack) or stroke (see thrombosis). When a blood vessel is damaged, it constricts immediately to reduce blood flow to the area. The damage sets off a series of chemical reactions that lead to the formation of a clot to seal the injury. First, platelets around the injury site are activated, becoming sticky and adhering to the blood-vessel wall. Then, the activated platelets release chemicals, which, in turn, activate blood clotting factors. These factors, together with vitamin K, act on fibrinogen and convert it to fibrin. Strands of fibrin form a meshwork, which traps red blood cells to form a clot. There are several anticlotting mechanisms to prevent the formation of unwanted clots. These include prostacyclin (a prostaglandin), which prevents platelet aggregation, and plasmin, which breaks down fibrin (see fibrinolysis). Blood flow washes away active coagulation factors; and the liver deactivates excess coagulation factors. Defects in blood clotting may result in bleeding disorders. Excessive clotting (thrombosis) may be due to an inherited increase or defect in a coagulation factor (see factor V), the use of oral contraceptives, a decrease in the level of enzymes that inhibit coagulation, or sluggish blood flow through a particular area. Treatment is usually with anticoagulant drugs such as heparin or warfarin.


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