- Plural of platelet
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. 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.
Production and degradationPlatelets 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.
FunctionFunctions of Platelets can be generalised into a number of categories:
- Clot retraction
- Cytokine signalling
ActivationPlatelets 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 aggregationPlatelet 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 signallingBesides 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 mediators
It also secretes e.g. platelet-derived growth factor (PDGF).
Role in disease
High and low countsA normal platelet count in a healthy person is between 150,000 and 400,000 per mm³ (microlitre) 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; 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.
MedicationsOral agents, often used to alter/suppress platelet function:
Intravenous agents, often used to alter/suppress platelet function:
DiseasesDisorders leading to a reduced platelet count:
Disorders leading to platelet dysfunction or reduced count:
- HELLP syndrome
- Hemolytic-uremic syndrome
- Alpha–Delta platelet storage pool deficiency (αδSPD) is a rare inherited bleeding disorder.
Disorders featuring an elevated count:
Disorders of platelet adhesion or aggregation:
Disorders of platelet metabolism
- Decreased cyclooxygenase activity, induced or congenital
- Storage pool defects, acquired or congenital
Disorders that indirectly compromise platelet function:
Disorders in which platelets play a key role:
DiscoveryBrewer 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. 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 coagulation.
Image:Illu blood cell lineage.jpg|Blood cell lineage
In transfusion medicinePlatelets 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 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 protiens. Volume reduced platelets have a shelf life of only four hours.
platelets in Arabic: صفيحة دموية
platelets in Bengali: অণুচক্রিকা
platelets in Bulgarian: Тромбоцит
platelets in Catalan: Plaqueta
platelets in Czech: Krevní destička
platelets in Danish: Blodplade
platelets in German: Thrombozyt
platelets in Dhivehi: ޕްލޭޓްލިޓް
platelets in Spanish: Plaqueta
platelets in Esperanto: Trombocito
platelets in Basque: Plaketa
platelets in French: Thrombocyte
platelets in Western Frisian: Bloedplaatsjes
platelets in Galician: Plaqueta
platelets in Korean: 혈소판
platelets in Croatian: Trombociti
platelets in Indonesian: Keping darah
platelets in Interlingua (International Auxiliary Language Association): Plachetta
platelets in Icelandic: Blóðflaga
platelets in Italian: Piastrina
platelets in Hebrew: טסית דם
platelets in Latin: Thrombociti
platelets in Lithuanian: Trombocitas
platelets in Macedonian: Тромбоцит
platelets in Dutch: Bloedplaatje
platelets in Japanese: 血小板
platelets in Norwegian: Blodplate
platelets in Low German: Bloodplattken
platelets in Polish: Trombocyt
platelets in Portuguese: Plaqueta sanguínea
platelets in Quechua: Yawar llukllunacha
platelets in Russian: Тромбоциты
platelets in Albanian: Trombociti
platelets in Simple English: Platelet
platelets in Slovak: Krvná doštička
platelets in Slovenian: Trombocit
platelets in Serbian: Крвне плочице
platelets in Sundanese: Trombosit
platelets in Finnish: Verihiutale
platelets in Swedish: Trombocyt
platelets in Tamil: இரத்தத் தட்டு
platelets in Turkish: Trombosit
platelets in Ukrainian: Тромбоцити
platelets in Chinese: 血小板