Platelets and Hemostasis
Platelets (thrombocytes) are formed elements necessary to the process of hemostasis, the cessation of bleeding.
Platelets result from fragmentation of certain large cells, called megakaryocytes, that develop in red bone marrow. Platelets are produced at a rate of 200 billion per day, and the blood contains 150,000-300,000 per mm3. Because platelets have no nucleus, they last at most ten days, assuming they are not used sooner than that in hemostasis.
Hemostasis Hemostasis is divided into three events: vascular spasm, platelet plug formation, and coagulation (Fig. 11.5).
Vascular spasm, the constriction of a broken blood vessel, is the immediate response to blood vessel injury. Platelets release serotonin, a chemical that prolongs smooth muscle contraction.
Platelet plug formation is the next event in hemostasis.
Platelets don’t normally adhere to damaged blood vessel walls, but when the lining of a blood vessel breaks, connective tissue, including collagen fibers, is exposed. Platelets adhere to collagen fibers and release a number of substances, including one that promotes platelet aggregation so that a so-called platelet plug forms. As a part of normal activities, small blood vessels often break, and a platelet plug is usually sufficient to stop the bleeding.
Coagulation, also called blood clotting, is the last event to bring about hemostasis. As you will see, two plasma proteins, called fibrinogen and prothrombin, participate in blood clotting. Vitamin K, found in green vegetables and also formed by intestinal bacteria, is necessary for the production of prothrombin. If, by chance, vitamin K is missing from the diet, hemorrhagic bleeding disorders develop.
Figure 11.5 Hemostasis requires three events: vascular spasm, platelet plug formation, and coagulation. Coagulation is further broken down into four steps.
Coagulation requires many clotting factors and enzymatic reactions that are preliminary to the few we will consider. One important preliminary step that occurs in the body is the release of tissue thromboplastin, a clotting factor that interacts with platelets, other clotting factors, and calcium ions (Ca2+). Figure 11.5 breaks down the subsequent clotting process into four steps: 1 After thromboplastin is released, prothrombin activator is formed. 2 Prothrombin activator then converts prothrombin to thrombin. 3 Thrombin, in turn, severs two short amino acid chains from each fibrinogen molecule, and these activated fragments join end-to-end, forming long threads of fibrin.
4 Fibrin threads wind around the platelet plug in the damaged area of the blood vessel and provide the framework for the clot. Red blood cells also are trapped within the fibrin threads; these cells make a clot appear red.
Clot retraction follows, and the clot gets smaller as platelets contract. A fluid called serum (plasma minus fibrinogen and prothrombin) is squeezed from the clot. A fibrin clot is present only temporarily. As soon as blood vessel repair is initiated, an enzyme called plasmin destroys the fibrin network and restores the fluidity of the plasma.
Disorders of Hemostasis
Among the many possible disorders of hemostasis, we will mention but a few. Thrombocytopenia, a low platelet count, can be due to any impairment of the red bone marrow. Despite the presence of anticoagulants in the blood, sometimes a clot forms in an unbroken blood vessel.
Such a clot is called a thrombus if it remains stationary. Should the clot dislodge and travel in the blood, it is called an embolus. If thromboembolism is not treated, a heart attack can occur.
Hemophilia is an inherited clotting disorder caused by a deficiency in a clotting factor. (So-called hemophilia A is due to the lack of clotting factor VIII.) The slightest bump can cause bleeding into the joints. Cartilage degeneration in the joints and resorption of underlying bone can follow. Bleeding into muscles can lead to nerve damage and muscular atrophy. The most frequent cause of death is bleeding into the brain with accompanying neurological damage.