Information AboutPlatelet |
| CATEGORIES ABOUT PLATELET | |
| blood products | |
| coagulation system | |
| leukocytes | |
| cell biology | |
| transfusion medicine | |
| SHOPPER'S DELIGHT | |
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Platelets or '''thrombocytes''' are the Blood cell fragments that are involved in the cellular mechanisms that lead to the formation of Blood Clot s. Low levels or dysfunction predisposes for Bleeding , while high levels — although usually asymptomatic — may increase the risk of Thrombosis . ANATOMY Like Red Blood Cells , platelets are anuclear and discoid; they measure 1.5–3.0 μm in diameter. The body has a very limited reserve of platelets and so they can be rapidly depleted. They contain RNA , a Canalicular system, and several different types of granules; Lysosomes (containing Acid Hydrolases ), dense bodies (containing ADP , ATP Serotonin and Calcium ) and alpha granules (containing Fibrinogen , Factor V , Vitronectin , Thrombospondin and Von Willebrand Factor ), the contents of which are released upon activation of the platelet. These granule contents play an important role in both Hemostasis and in the inflammatory response. PHYSIOLOGY Production Platelets are produced in the Bone Marrow ; the progenitor cell for platelets is the Megakaryocyte . This large, multinucleated cell sheds platelets into the circulation. Thrombopoietin (''c-mpl ligand'') is a hormone, mainly produced by the Liver , that stimulates platelet production. It is bound to circulating platelets; if platelet levels are adequate, serum levels remain low. If the platelet count is decreased, more thrombopoeitin circulates freely and increases marrow production. Circulation The circulating life of a platelet is 9–10 days. After this it is sequestered in the Spleen . Decreased Function (or absence) of the spleen may increase platelet counts, while Hypersplenism (overactivity of the spleen, e.g. in Gaucher's Disease , Leukemia and Cirrhosis ) may lead to increased elimination and hence low platelet counts. Function Platelets are Activated when brought into contact with Collagen (which is exposed when the Endothelial blood vessel lining is damaged), Thrombin (primarily through PAR -1), ADP , with receptors expressed on White Blood Cells or the endothelial cells of the blood vessels, among other activators. Once activated, they release a number of different Coagulation Factor s and platelet activating factors. Platelet activation further results in the Scramblase mediated transport of negatively charged phospholipids to the platelet surface. These phospholipids provide a catalytic surface (with the charge provided by Phosphatidylserine and Phosphatidylethanolamine ) for the Tenase and Prothrombinase complexes. The platelets adhere to each other via adhesion receptors or Integrins , and to the endothelial cells in the wall of the blood vessel forming a haemostatic plug in conjunction with Fibrin . The high concentration of Myosin and Actin filaments in platelets are stimulated to contract during aggregation, further reinforcing the plug. The most common platelet adhesion receptor is Glycoprotein (GP) IIb/IIIa; this is a calcium-dependent receptor for fibrinogen, Fibronectin , vitronectin, thrombospondin and von Willebrand factor (vWF). Other receptors include GPIb-V-IX complex (vWF) and GPVI ( Collagen ) Activators There are many known platelet activators. They include
Inhibitors
ROLE IN DISEASE High and low counts A normal platelet count in a healthy person is between 150,000 and 400,000 per mm3 of blood. 95% of healthy people will have platelet counts in this range. Some will have statistically abnormal platelet counts while having no abnormality, although the likelihood increases if the platelet count is either very low or very high. Both Thrombocytopenia (or thrombopenia) and Thrombocytosis may present with coagulation problems. Generally, low platelet counts increase bleeding risks (although there are exceptions, e.g. 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 generally not corrected by transfusion unless the patient is bleeding or the count has fallen below 5 (x 109/ L ); it is contraindicated in thrombotic thrombocopenic purpura (TTP) as it fuels the coagulopathy. In patients having surgery, a level below 50 (x 109/ L ) is associated with abnormal surgical bleeding, and regional anaesthetic procedures such as Epidural s 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 and hence normal hemostasis; normal platelet function may not return until the aspirin is ceased and the affected platelets have been replaced by new ones, which may take over a week. Similarly, Uremia (a consequence of Renal Failure ) leads to platelet dysfunction that may be ameliorated by the administration of Desmopressin . Diseases Disorders leading to a reduced platelet count:
Disorders leading to platelet dysfunction or reduced count: Disorders featuring an elevated count:
Disorders of platelet adhesion or aggregation: Disorders of platelet metabolism
DISCOVERY BrewerBrewer DB. Max Schultze (1865), G. Bizzozero (1882) and the discovery of the platelet. ''Br J Haematol'' 2006;133:251-8. DOI 10.1111/j.1365-2141.2006.06036.x . traced the history of the discovery of the platelet. Although red blood cells had been known since . 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 ''. One of his findings was the fact that platelets clump at the site of blood vessel injury, which precedes the formation of a Blood Clot . This observation confirmed the role of platelets in Coagulation Bizzozero J. Über einen neuen Forrnbestandteil des Blutes und dessen Rolle bei der Thrombose und Blutgerinnung. ''Arch Pathol Anat Phys Klin Med'' 1882;90:261-332.. REFERENCES SEE ALSO > |