A minute, nonnucleated, disklike cytoplasmic body found in the blood plasma of mammals that is derived from a megakaryocyte and functions to promote blood clotting. Also called blood platelet, thrombocyte.
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A minute, nonnucleated, disklike cytoplasmic body found in the blood plasma of mammals that is derived from a megakaryocyte and functions to promote blood clotting. Also called blood platelet, thrombocyte.
Platelets are small fragments of cellular material in the blood. They originate by splitting off from large cells in the bone marrow. Platelets have essential functions. They are necessary for the process of clotting when blood vessels are damaged, both by providing crucial chemical substances and by physically plugging the hole — hence their other name: thrombocytes. That they have also a continuous rather than only an emergency function is shown by the effects of an abnormal shortage, known as thrombocytopenia; this leads to multiple tiny bleeds into the skin (purpura).
— Stuart Judge
See blood.
A disk found in the blood of mammals that is concerned in the coagulation and clotting of blood.
For more information on platelet, visit Britannica.com.
A small disk or platelike structure, the smallest of the formed elements in blood. Blood platelets (called also thrombocytes) are disk-shaped, non-nucleated blood elements with a very fragile membrane; they tend to adhere to uneven or damaged surfaces. They average about 250,000 per cubic millimeter of blood and are formed in the red bone marrow by fragmentation of megakaryocytes, the largest of the bone marrow cells. Platelet production is controlled by a hormone, thrombopoietin, and regulatory lymphocytes acting at the stem cell level. At any given time about one-third of the total blood platelets can be found in the spleen; the remaining two-thirds are in the circulating blood.
The functions of platelets are related to the clotting of blood. Because of their adhesion and aggregation capabilities platelets can occlude small breaks in blood vessels and prevent the escape of blood. Platelets which have adhered to exposed collagen in damaged vessels release ADP in milliseconds which in turn initiates the synthesis of thromboxane A2, a very potent prostaglandin which causes platelet aggregation and localized vasoconstriction. Fibrinogen, factors V and VIII, calcium ions, platelet phospholipid (PF-3), associated with the platelet membrane are also released. Substances contained within the platelet granules such as thromboglobulin, heparin neutralizing activity (PF-4) mitogens such as platelet derived growth factor, thrombospondin, ADP, serotonin and calcium ions are also released by aggregated platelets.
Platelets, or thrombocytes, are the cell fragments circulating in the blood that are involved in the cellular mechanisms of primary hemostasis leading to the formation of blood clots. 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 thrombocytopathy.
Like red blood cells, platelets in mammals are anuclear (no cell nucleus) and discoid (disc shaped); they measure 1.5–3.0 μm in diameter. The body has a very limited reserve of platelets, so they can be rapidly depleted. They contain RNA, mitochondria, a canalicular system, and several different types of granules; lysosomes (containing acid hydrolases), dense bodies (containing ADP, ATP, serotonin, histamine, 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.
Functions of Platelets can be generalised into a number of categories:
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
A normal platelet count in a healthy person is between 150,000 and 400,000 per mm³ of blood (150–400 x 109/L). 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; normal platelet function may not return until the aspirin has ceased and all 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.
Oral agents, often used to alter/supress platelet function:
Intravenous agents, often used to alter/supress platelet function:
Disorders leading to a reduced platelet count:
Alloimmune disorders
Disorders leading to platelet dysfunction or reduced count:
Disorders featuring an elevated count:
Disorders of platelet adhesion or aggregation:
Disorders of platelet metabolism
Disorders that indirectly compromise platelet function:
Disorders in which platelets play a key role:
Brewer[6] 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[7]. 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
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 from a donor 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 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.
| Blood | |
|---|---|
| General | |
| Lymphoid - WBC | T cells:
|
| Myeloid - WBC | Granulocytes
( Dendritic cells (Langerhans cells, Follicular dendritic cells) Monocytes/Macrophages (Histiocytes, Kupffer cells, Langhans giant cells, Microglia, Osteoclasts) Megakaryoblast - Megakaryocyte - Platelets |
| Myeloid - RBC | |
|
Proteins: |
|
|---|---|
| Coagulation factors | intrinsic pathway (FXII, FXI, FIX, FVIII) - extrinsic pathway (Tissue factor, FVII) - common pathway (FX, FV, (Pro)thrombin / FII, Fibrin / FI, FXIII) - HMWK - vWF - Kallikrein |
| Inhibitors | Antithrombin - Protein C - Protein S - Protein Z - ZPI - TFPI |
| Fibrinolysis | Plasmin - tPA/urokinase - PAI-1/2 - α2-AP - α2-macroglobulin - TAFI |
| 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 - Landsteiner-Weiner - Lewis - Lutheran - MNS - OK - P - Raph - Rh - Scianna - T-Tn - Xg - Yt |
| Blood products | Blood donation -
Blood substitutes - Cryoprecipitate -
Platelets - |
This entry is from Wikipedia, the leading user-contributed encyclopedia. It may not have been reviewed by professional editors (see full disclaimer)
Nederlands (Dutch)
bloedplaatje
Français (French)
n. - plaquette
Deutsch (German)
n. - Blutplättchen
Ελληνική (Greek)
n. - (βιολ.) αιμοπετάλιο, θρομβοκύτταρο
Português (Portuguese)
n. - plaqueta (f) (Anat.)
Русский (Russian)
тромбоцит, пластинка
Español (Spanish)
n. - plaqueta
Svenska (Swedish)
n. - blodplätt
中文(简体) (Chinese (Simplified))
血小板, 小板, 小盘
中文(繁體) (Chinese (Traditional))
n. - 血小板, 小板, 小盤
العربيه (Arabic)
(الاسم) صفيحه, اللويحه : إحدى لوحات الدم
עברית (Hebrew)
n. - טסית דם, תא עגול בקריש-דם
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