Structure
Structurally the platelet can be divided into four zones, from peripheral to innermost:
Peripheral zone – is rich in glycoproteins required for platelet adhesion, activation and aggregation. For example, GPIb/IX/V; GPVI; GPIIb/IIIa. Sol-gel zone – is rich in microtubules and microfilaments, allowing the platelets to maintain their discoid shape. Organelle zone – is rich in platelet granules. Alpha granules contain clotting mediators such as factor V, factor VIII, fibrinogen, fibronectin, platelet-derived growth factor, and chemotactic agents. Delta granules, or dense bodies, contain ADP, calcium and serotonin, which are platelet-activating mediators. Membranous zone – contains membranes derived from megakaryocyte smooth endoplasmic reticulum organized into a dense tubular system which is responsible for thromboxane A2 synthesis. This dense tubular system is connected to the surface platelet membrane to aid thromboxane A2 release. Development
Megakaryocyte and platelet production is regulated by thrombopoietin, a hormone produced in the kidneys and liver. Each megakaryocyte produces between 1,000 and 3,000 platelets during its lifetime. An average of 1011 platelets are produced daily in a healthy adult. Reserve platelets are stored in the spleen and are released when needed by splenic contraction induced by the sympathetic nervous system. The average life span of circulating platelets is 8 to 9 days. Life span of individual platelets is controlled by the internal apoptotic regulating pathway, which has a Bcl-xL timer. Old platelets are destroyed by phagocytosis in the spleen and liver. Hemostasis
An overview summarizing platelet dynamics, the complex process of converting inactive platelets into a platelet plug, is essential.
These processes may overlap: the spectrum is from a predominantly platelet plug, or "white clot" to a predominantly fibrin, or "red clot" or the more typical mixture. Some would add the subsequent retraction and platelet inhibition as fourth and fifth steps to the completion of the process and still others would add a sixth step, wound repair. Platelets also participate in both innate and adaptive intravascular immune responses. The platelet cell membrane has receptors for collagen. Following the rupture of the blood vessel wall, the platelets are exposed and they adhere to the collagen in the surrounding connective tissue. Low platelet concentration is called thrombocytopenia, and is due to either decreased production or increased destruction. Elevated platelet concentration is called thrombocytosis, and is either congenital, reactive (to cytokines), or due to unregulated production: one of the myeloproliferative neoplasms or certain other myeloid neoplasms. A disorder of platelet function is called a thrombocytopathy or a platelet function disorder. Normal platelets can respond to an abnormality on the vessel wall rather than to hemorrhage, resulting in inappropriate platelet adhesion/activation and thrombosis: the formation of a clot within an intact vessel. This type of thrombosis arises by mechanisms different from those of a normal clot: namely, extending the fibrin of venous thrombosis; extending an unstable or ruptured arterial plaque, causing arterial thrombosis; and microcirculatory thrombosis. An arterial thrombus may partially obstruct blood flow, causing downstream ischemia, or may completely obstruct it, causing downstream tissue death.