Platelet
Blood cell lineage
Platelets, or thrombocytes, are small, irregularly-shaped anuclear cells (i.e. cells that do not have a nucleus containing DNA), 2-3 µm in diameter[1], which are derived from fragmentation of precursor megakaryocytes. The average lifespan of a platelet is between 8 and 12 days. Platelets play a fundamental role in hemostasis and are a natural source of growth factors. They circulate in the blood of mammals and are involved in hemostasis, leading to the formation of blood clots.
If the number of platelets is too low, excessive bleeding can occur. However, if the number of platelets is too high, blood clots can form (thrombosis), which may obstruct blood vessels and result in such events as a stroke, heart attack, pulmonary embolism or the blockage of blood vessels to other parts of the body, such as the extremities of the arms or legs. An abnormality or disease of the platelets is called a thrombocytopathy[2], which could be either a low number of platelets (thrombocytopenia), a decrease in function (thrombasthenia), or an increase in the number of (thrombocytosis). There are disorders that reduce the number of platelets, such as heparin-induced thrombocytopenia (HIT) or thrombotic thrombocytopenic purpura (TTP) that typically cause thromboses, or clots, instead of bleeding.
Kinetics
- Platelets are produced in blood cell formation (thrombopoiesis) in bone marrow, by budding off from megakaryocytes.
- The physiological range for platelets is 150-400 x 109 per litre.
- Around 1 x 1011 platelets are produced each day by an average healthy adult.
- The lifespan of circulating platelets is 7 to 10 days.
- This process is regulated by thrombopoietin, a hormone usually produced by the liver and kidneys.
- Each megakaryocyte produces between 5,000 and 10,000 platelets.
- Old platelets are destroyed by phagocytosis in the spleen and by Kupffer cells in the liver.
High and low counts
A normal platelet count in a healthy individual is between 150,000 and 450,000 per μl (microlitre) of blood (150–450 x 109/L)[15]. Ninety-five percent of healthy people will have platelet counts in this range. Some will have statistically abnormal platelet counts while having no demonstrable abnormality. However, if it is either very low or very high, the likelihood of an abnormality being present is higher.
Both thrombocytopenia (or thrombopenia) and thrombocytosis may present with coagulation problems. In general, low platelet counts increase bleeding risks; however there are exceptions. For example, immune heparin-induced thrombocytopenia and thrombocytosis (high counts) may lead to thrombosis, although this is mainly when the elevated count is due to myeloproliferative disorder.
Low platelet counts are, in general, not corrected by transfusion unless the patient is bleeding or the count has fallen below 5 x 109/L. Transfusion is contraindicated in thrombotic thrombocytopenic purpura (TTP), as it fuels the coagulopathy. In patients undergoing surgery, a level below 50 x 109/L is associated with abnormal surgical bleeding, and regional anaesthetic procedures such as epidurals are avoided for levels below 80-100.
Normal platelet counts are not a guarantee of adequate function. In some states, the platelets, while being adequate in number, are dysfunctional. For instance, aspirin irreversibly disrupts platelet function by inhibiting cyclooxygenase-1 (COX1), and hence normal hemostasis. The resulting platelets have no DNA and are unable to produce new cyclooxygenase. Normal platelet function will not return until the use of aspirin has ceased and enough of the affected platelets have been replaced by new ones, which can take over a week. Ibuprofen, another NSAID, does not have such a long duration effect, with platelet function usually returning within 24 hours[16], and taking ibuprofen before aspirin will prevent the irreversible effects of aspirin[17]. Uremia, a consequence of renal failure, leads to platelet dysfunction that may be ameliorated by the administration of desmopressin.
HISTORY
Brewer[20] traced the history of the discovery of the platelet. Although red blood cells had been known since van Leeuwenhoek, it was the German anatomist Max Schultze (1825-1874) who first offered a description of the platelet in his newly-founded journal Archiv für mikroscopische Anatomie[21]. He describes “spherules” to be much smaller than red blood cells that are occasionally clumped and may participate in collections of fibrous material. He recommends further study of the findings.
Giulio Bizzozero (1846-1901), building on Schultze’s findings, used “living circulation” to study blood cells of amphibians microscopically in vivo. He is especially noted for discovering that platelets clump at the site of blood vessel injury, a process that precedes the formation of a blood clot. This observation confirmed the role of platelets in coagulation[22].
a minute colorless anucleate disklike body of mammalian blood that is derived from fragments of megakaryocyte cytoplasm, that is released from the bone marrow into the blood, and that assists in blood clotting by adhering to other platelets and to damaged epithelium—called also blood platelet, thrombocyte
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