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20-September-2008 09:55:54 - Platelet Human blood smear: platelets. This slide has been stained with MayGrunwald Giemsa, and observed with a 100x objective in oil immersion. Human blood smear: platelets. This slide has been stained with MayGrunwald Giemsa, and observed with a 100x objective in oil immersion. A 250 ml bag of newly collected platelets. A 250 ml bag of newly collected platelets. Thrombocytes Thrombocytes Platelets, or thrombocytes, are the cells circulating in the blood that are involved in the cellular mechanisms of primary hemostasis leading to the formation of blood clots. In strict sense, the term platelet should be reserved for anucleated thrombocytes of mammals. Nucleated thrombocytes of nonmammalian vertebrates differ from the mammalian plates not only in having a nucleus and thus resembling B lymphocytes, but also these nucleated thrombocytes do not aggregate in response to ADP, serotonin and adrenaline they do aggregate with thrombin, of course. 1. Dysfunction or low levels of platelets predisposes to bleeding, while high levels, although usually asymptomatic, may increase the risk of thrombosis. An abnormality or disease of the platelets is called a thrombocytopathy2 which could be either a decrease in number ie thrombocytopenia, decrease in function ie thrombasthenia or an increase in number ie thrombocytosis. Contents 1 Production and degradation 2 Function 2.1 Activation 2.2 Adhesion and aggregation 2.3 Cytokine signalling 3 Role in disease 3.1 High and low counts 3.2 Medications 3.3 Diseases 4 Discovery 5 Additional images 6 In transfusion medicine 7 References 8 See also Production and degradation Platelets are produced in hematopoiesis by budding off from megakaryocytes. Each megakaryocyte produces between 5,000 and 10,000 platelets. They circulate for approximately one week, and are then destroyed by the spleen and by Kupffer cells in the liver. Function Functions of Platelets can be generalised into a number of categories: Adhesion Aggregation Clot retraction Pro-coagulation Cytokine signalling Phagocytosis3 Activation 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 receptors P2Y1 and P2Y12 expressed on platelets, a negatively charged surface e.g. glass, or several other activating factors. Once activated, they release a number of different coagulation factors and platelet activating factors. These substances are normally stored in one of two cytoplasmic granules: either the dense granules containing ADP or ATP, calcium and serotonin or the α-granules containing platelet factor 4, PDGF, fibronectin, B-thromboglobulin, vWF, fibrinogen, and coagulation factors V and XIII. 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. Adhesion and aggregation Platelet aggregation is the clumping of platelets together, using fibrin as the connecting agent. Activated platelets have fibrin receptors on their surfaces. Platelet adhesion is the process of platelets sticking to the damaged inner surface of the vessel wall. Adhesion can occur because collagen in the vessel wall is exposed when the endothelial surface lining the vessel is breached, and activated platelets have collagen receptors on their surfaces. Aggregation and adhesion act together to form the platelet plug. The high concentration of myosin and actin filaments in platelets are stimulated to contract during aggregation, further reinforcing the plug. The most abundant platelet aggregation 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. Platelet aggregation is stimulated by ADP, thromboxane and α2 receptor-activation, but inhibited by other inflammatory products like PGI2 and PGD2. Cytokine signalling Besides being the chief cellular effector of hemostasis, platelets are rapidly deployed to sites of injury or infection and potentially modulate inflammatory processes by interacting with leukocytes and by secreting cytokines, chemokines and other inflammatory mediators4 5 6 7. It also secretes e.g. platelet-derived growth factor PDGF. Role in disease High and low counts A normal platelet count in a healthy person is between 150,000 and 400,000 per mm³ microlitre of blood 150-400 x 109/L.8 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 thrombocytopenic 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 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; Platelets have no DNA and are unable to produce new cyclooxygenase. Normal platelet function will not return until the aspirin has ceased and enough of the affected platelets have been replaced by new ones, which can take over a week. Similarly, uremia a consequence of renal failure leads to platelet dysfunction that may be ameliorated by the administration of desmopressin. Medications Oral agents, often used to alter/suppress platelet function: aspirin clopidogrel cilostazol ticlopidine Intravenous agents, often used to alter/suppress platelet function: abciximab eptifibatide tirofiban Diseases Disorders leading to a reduced platelet count: Thrombocytopenia Idiopathic thrombocytopenic purpura - also known as immune thrombocytopenic purpura ITP Thrombotic thrombocytopenic purpura Drug-induced thrombocytopenia, e.g. heparin-induced thrombocytopenia HIT Gaucher's disease Aplastic anemia Alloimmune disorders Fetomaternal alloimmune thrombocytopenia Some transfusion reactions Disorders leading to platelet dysfunction or reduced count: HELLP syndrome Hemolytic-uremic syndrome Chemotherapy Dengue Alpha-Delta platelet storage pool deficiency αδSPD is a rare inherited bleeding disorder.9 Disorders featuring an elevated count: Thrombocytosis, including benign essential thrombocytosis elevated counts, either reactive or as an expression of myeloproliferative disease; may feature dysfunctional platelets Disorders of platelet adhesion or aggregation: Bernard-Soulier syndrome Glanzmann's thrombasthenia Scott's syndrome von Willebrand disease Hermansky-Pudlak Syndrome Disorders of platelet metabolism Decreased cyclooxygenase activity, induced or congenital Storage pool defects, acquired or congenital Disorders that indirectly compromise platelet function: Haemophilia Disorders in which platelets play a key role: Atherosclerosis Coronary artery disease, CAD and myocardial infarction, MI Cerebrovascular disease and Stroke, CVA cerebrovascular accident Peripheral artery occlusive disease PAOD Cancer 10 Discovery Brewer11 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 Anatomie12. He describes spherules 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. 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 coagulation13. Additional images Blood cell lineage In transfusion medicine Platelets are either isolated from collected units of whole blood and pooled to make a therapeutic dose or collected by Apheresis, sometimes concurrently with plasma or red blood cells. The industry standard is for platelets to be tested for bacteria before transfusion to avoid septic reactions, which can be fatal. Pooled whole blood platelets, sometimes called random platelets, are made by taking a unit of whole blood that has not been cooled and placing it into a large centrifuge in what is referred to as a soft spin. This splits the blood into three layers: the plasma, a buffy coat layer which includes the platelets, and the red blood cells. These are expressed into different bags for storage. From four to six of these are typically pooled into a single bag for a therapeutic dose, though individual components can also be used. Apheresis platelets are collected using a mechanical device which draws blood from the donor and centrifuges the collected blood to separate out the platelets and other components to be collected. The remaining blood is returned to the donor. The advantage to this method is that a single donation provides at least one therapeutic dose, as opposed to the multiple donations for whole blood platelets. This means that a recipient is not exposed to as many different donors and has less risk of transfusion transmitted disease and other complications. Sometimes a person such as a cancer patient who requires routine transfusions of platelets will receive repeated donations from a specific donor to further minimize the risk. Platelets are not crossmatched unless they contain a significant amount of RBCs, which results in a reddish-orange color to the product. This is usually associated with whole blood platelets, as apheresis methods are more efficient than soft spin centrifugation at isolating the specific components of blood. An effort is usually made to issue type specific platelets, but this is not as critical as it is with red blood cells. Platelets collected by either method have a very short shelf life, typically five or seven days depending on the system used. This results in frequent problems with short supply, as testing the donations often uses up a full day of this time. Since there are no effective preservative solutions for platelets, they lose potency quickly and are best when fresh. Platelets, either apheresis or random donor platelets, can be processed through a volume reduction process. In this process, the platelets are spun in a centrifuge and the excess plasma is removed, leaving 10 to 100 ml of platelet concentrate. Volume reduced platelets are normally only transfused to neonatal and pediatric patients when a large volume of plasma could overload the child's small circulatory system. The lower volume of plasma also reduces the chances of an adverse transfusion reaction to plasma proteins.14 Volume reduced platelets have a shelf life of only four hours.15 References ^ Nature 220, 509 - 510 02 November 1968; doi:10.1038/220509a0 ADP is not Involved in Thrombin-induced Aggregation of Thrombocytes of a Non-mammalian Vertebrate FRANK A. BELAMARICH, DAVID SHEPRO MARJA KIEN Biology Department, Boston University, Massachusetts. 1 ^ Maton, Anthea; Jean Hopkins, Charles William McLaughlin, Susan Johnson, Maryanna Quon Warner, David LaHart, Jill D. Wright 1993. Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. ISBN 0-13-981176-1. ^ Movat H.Zet al 1965. Platelet Phagocytosis and Aggregation. Journal of Cell Biology 27: 531-543. doi:10.1083/jcb.27.3.531. PMID 4957257. ^ Weyrich A.S. et al 2004. Platelets: signaling cells inside the immune continuum.. Trends Immunol 25: 489-495. ^ Wagner D.D. et al 2003. Platelets in inflammation and thrombosis.. Thromb Vasc Biol 23: 2131-2137. ^ Diacovo T.G. et al 1996. Platelet-mediated lymphocyte delivery to high endothelial venules.. Science 273: 252-255. ^ Iannacone M. et al 2005. Platelets mediate cytotoxic T lymphocyte-induced liver damage. Nat Med 11: 1167-1169. ^ Lab Tests Online UK 2004-05-28. Platelet count aka thrombocyte count. Retrieved on 2008-05-22. ^ Alpha-delta platelet storage pool deficiency in three generations - Platelets ^ McCarty OJT. et al 2000. Immobilized platelets support human colon carcinoma cell tethering, rolling, and firm adhesion under dynamic flow conditions. Blood 96: 1789-1197. ^ Brewer DB. Max Schultze 1865, G. Bizzozero 1882 and the discovery of the platelet. Br J Haematol 2006;133:251-8. PMID 16643426. ^ Schultze M. Ein heizbarer Objecttisch und seine Verwendung bei Untersuchungen des Blutes. Arch Mikrosc Anat 1865;1:1-42. ^ Bizzozero J. Ãœber einen neuen Forrnbestandteil des Blutes und dessen Rolle bei der Thrombose und Blutgerinnung. Arch Pathol Anat Phys Klin Med 1882;90:261-332. ^ Schoenfeld H, Spies C, Jakob C 2006. Volume-reduced platelet concentrates. Curr. Hematol. Rep. 5 1: 82-8. PMID 16537051. ^ CBBS: Washed and volume-reduced Plateletpheresis units See also Hemostasis Plateletpheresis v d e Blood General Plasma - Hematopoietic stem cells Lymphoid - WBC T cells: Cytotoxic CD8+, Helper CD4+/Regulatory, γδ, Natural Killer T cell B cells: Plasma, Memory Natural killer cells Lymphokine-activated killer cell Null cell Myeloid - WBC Monocytes/Macrophages Histiocytes, Kupffer cells, Langhans giant cells, Microglia, Osteoclasts, Epithelioid cells Granulocytes Neutrophil, Eosinophil, Basophil - Mast cell precursors Dendritic cells Langerhans cells, Follicular dendritic cells Megakaryoblast - Megakaryocyte - Platelets Myeloid - RBC Reticulocyte - Normoblast v d e Proteins: coagulation Coagulation factors primary hemostasis: vWF intrinsic pathway: HMWK/Bradykinin - Kallikrein - Hageman / FXII - FXI - FIX - FVIII extrinsic pathway: Tissue factor / FIII - FVII common pathway: FX - FV - Prothrombin / FII, Fibrin / FI - FXIII Coagulation inhibitors Antithrombin inhibits II, IX, X, XI, XII - Protein C inhibits V, VIII/Protein S cofactor for protein C - Protein Z inhibits X - ZPI inhibits X, XI - TFPI inhibits III Fibrinolysis Plasmin - tPA/urokinase - PAI-1/2 - α2-AP - α2-macroglobulin - TAFI v d e Transfusion medicine General concepts Apheresis Plasmapheresis, Plateletpheresis, Leukapheresis - Blood transfusion - Coombs test - Cross-matching - Exchange transfusion - International Society of Blood Transfusion - Intraoperative blood salvage - ISBT 128 - Transfusion reactions Human blood group systems - Blood type ABO - Chido-Rodgers - Colton - Cromer - Diego - Dombrock - Duffy - Gerbich - GIL - Hh - Ii - Indian - JMH - Kell Xk - Kidd - Knops - LW - Lewis - Lutheran - MNS - OK - P - Raph - Rh - Scianna - T-Tn - Xg - Yt - Other Blood products Blood donation - Blood substitutes - Cryoprecipitate - Platelets - Plasma - Red blood cells - Whole blood Retrieved from http://en..org/wiki/Platelet Categories: Blood products | Coagulation system | Cell biology | Transfusion medicine | Human cells Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages العربية বাংলা Bosanski БългарÑ?ки Català Česky Dansk Deutsch Þ‹Þ¨ÞˆÞ¬Þ€Þ¨Þ„Þ¦Þ?Þ° Español Esperanto Euskara Français Frysk Galego í•œêµì–´ Hrvatski Bahasa Indonesia Interlingua Ã?slenska Italiano עברית Latina Lietuvių МакедонÑ?ки Nederlands 日本語 ‪Norsk bokmÃ¥l‬ Plattdüütsch Polski Português Runa Simi РуÑ?Ñ?кий Shqip Simple English SlovenÄ?ina SlovenÅ¡Ä?ina СрпÑ?ки / Srpski Basa Sunda Suomi Svenska தமிழà¯? Türkçe УкраїнÑ?ька ä¸æ–‡ This page was last modified on 18 August 2008, at 12:38
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