How and why does blood clot?
All animals, including humans, have an inborn mechanism— called blood clotting (coagulation)— by which a possible leak at the site of blood vessel injury is plugged. endothelium, is exposed. The subendothelium is rough and sticky. As a consequence, platelets, which are the cells that prevent blood from leaking out of an injured blood vessel, stick or adhere to the subendothelium where it is exposed. In the process, the platelets change their shape from a disk to a globular shape (like an ameba). During this shape-changing process, certain internal structures or granules are disrupted and release substances that activate the platelets. Activated platelets have receptors on their surfaces that allow them to stick to one another (that is, aggregate). Aggregated platelets form a plug at the site of a possible leak. This plug remains just a clump of platelets until a mesh or net made of a substance called fibrin surrounds these cells. Fibrin is a solid that is formed from fibrinogen, a specialized protein or clotting factor that is found in blood. When a blood vessel is injured, the exposed subendothelium causes a protein known as tissue factor to be exposed to the blood. The tissue factor sets off a chain reaction, called the coagulation cascade, that activates a whole series of clotting factors. The last step of this chain reaction is the conversion of fibrinogen into fibrin, which forms the mesh that holds the platelets firmly in place. A clot (also known as a thrombus), therefore, is made up of fibrin, platelets, and other cells, particularly red blood cells that are trapped in the process. Besides blood vessel injury, two other factors are associated with the development of blood clots: interruption of blood flow (which results in slow, sluggish, or nonexistent blood flow) and an increased tendency within the blood to form clots. The identification of these three factors associated with the development of blood clots is attributed to a famous nineteenthcentury German pathologist, Rudolph Virchow (although he did not actually describe them). Blood vessel injury, interruption of blood flow, and the increased tendency toward blood clotting are, therefore, commonly called Virchow’s triad. Virchow did describe the process whereby some clots detach Fibrin A solid substance formed from fibrinogen, a specialized protein or clotting factor that is found in blood. Fibrin makes a clot more stable (harder to break up). It forms the mesh or net that holds blood platelets firmly in place. Fibrinogen A specialized protein or clotting factor that is found in blood. When a blood vessel is injured, another clotting factor, thrombin, is activated and converts fibrinogen to fibrin, which is the mesh or net that holds platelets firmly in place from the subendothelium, travel through larger blood vessels, and become lodged in smaller, remote blood vessels. Because clots are necessary to prevent blood from leaking out of blood vessels after injury, individuals who have too few platelets, abnormal platelets, platelets that do not function normally, or deficiencies of clotting factors may not form normal clots and may suffer from excessive bleeding. Conversely, when clots form when and where they should not, serious consequences—including death—may occur. For instance, if a clot forms in the arteries supplying the heart (the coronary arteries), blood flow is blocked, the oxygen supply is cut off, and the cells in the heart begin to die, resulting in a myocardial infarction (heart attack). If a clot forms in the arteries supplying the brain, blood flow is blocked, the oxygen supply is cut off, and the cells in the brain begin to die, resulting in a cerebrovascular accident (stroke).