Thrombocytes, or platelets, are the smallest cellular component of blood. They circulate inactivated, about 250,000 per cubic mm of blood, until they come into contact with a damaged blood vessel. At this point, the platelets form a clump, adhering to each other and to the blood vessel wall. They secrete chemicals that alter a blood-borne protein, fibrinogen, so that it forms a mesh of fibers at the damage site. A clot forms when platelets and red and white blood cells become trapped in the fibers. Blood clotting begins within seconds of injury. The same process can produce unwelcome clots in undamaged blood vessels.
The smallest cells in the blood are the platelets, which are designed for a single purpose—to begin the process of coagulation, or forming a clot, whenever a blood vessel is broken. As soon as an artery or vein is injured, the platelets in the area of the injury begin to clump together and stick to the edges of the cut. They also release messengers into the blood that perform a variety of functions: constricting the blood vessels to reduce bleeding, attracting more platelets to the area to enlarge the platelet plug, and initiating the work of plasma-based clotting factors, such as fibrinogen. Through a complex mechanism involving many steps and many clotting factors, the plasma protein fibrinogen is transformed into long, sticky threads of fibrin. Together, the platelets and the fibrin create an intertwined meshwork that forms a stable clot. This self-sealing aspect of the blood is crucial to survival.