Platelet

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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.
Thrombocytes

WikiDoc Resources for

Platelet

Articles

Most recent articles on Platelet

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Review articles on Platelet

Articles on Platelet in N Eng J Med, Lancet, BMJ

Media

Powerpoint slides on Platelet

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Evidence Based Medicine

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Clinical Trials on Platelet at Google

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

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.

Histology

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 the granules are released upon activation of the platelet.

Production and degradation

Platelets are produced in hematopoiesis by budding off from megakaryocytes. Each megakaryocyte produces 5,000 and 10,000 platelets.

They circulate for approximately one week, and are then destroyed by the spleen and by Kuppfer cells in the liver.

Function

Functions of Platelets can be generalised into a number of categories:

  • Adhesion
  • Aggregation
  • Clot retraction
  • Pro-coagulation
  • Cytokine signalling
  • Phagocytosis[1]

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. 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

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 abundant 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).

Platelet aggregation is stimulated by 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 mediators[2] [3] [4] [5].

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 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.

Medications

Oral agents, often used to alter/suppress platelet function:

Intravenous agents, often used to alter/suppress platelet function:

Diseases

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

  • 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:

Discovery

Brewer[8] 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[9]. 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[10].

Additional images

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 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.

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.[11] Volume reduced platelets have a shelf life of only four hours.[12]

References

  1. Movat H.Zet al (1965). "Platelet Phagocytosis and Aggregation". Journal of Cell Biology 27: 531-543.
  2. Weyrich A.S. et al (2004). "Platelets: signaling cells in the immune continuum.". Trends Immunol 25: 489-495.
  3. Wagner D.D. et al (2003). "Platelets in inflammation and thrombosis.". Thromb Vasc Biol 23: 2131-2137.
  4. Diacovo T.G. et al (1996). "Platelet-mediated lymphocyte delivery to high endothelial venules.". Science 273: 252-255.
  5. Iannacone M. et al (2005). "Platelets mediate cytotoxic T lymphocyte-induced liver damage". Nat Med 11: 1167-1169.
  6. http://www.informaworld.com/smpp/content~content=a770733890~db=all~jumptype=rss
  7. 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.
  8. Brewer DB. Max Schultze (1865), G. Bizzozero (1882) and the discovery of the platelet. Br J Haematol 2006;133:251-8. PMID 16643426.
  9. Schultze M. Ein heizbarer Objecttisch und seine Verwendung bei Untersuchungen des Blutes. Arch Mikrosc Anat 1865;1:1-42.
  10. 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.
  11. Schoenfeld H, Spies C, Jakob C (2006). "Volume-reduced platelet concentrates". Curr. Hematol. Rep. 5 (1): 82–8. PMID 16537051.
  12. http://www.cbbsweb.org/enf/2001/pltwashvol.html

See also


Cost Effectiveness of Platelet

| group5 = Clinical Trials Involving Platelet | list5 = Ongoing Trials on Platelet at Clinical Trials.govTrial results on PlateletClinical Trials on Platelet at Google


| group6 = Guidelines / Policies / Government Resources (FDA/CDC) Regarding Platelet | list6 = US National Guidelines Clearinghouse on PlateletNICE Guidance on PlateletNHS PRODIGY GuidanceFDA on PlateletCDC on Platelet


| group7 = Textbook Information on Platelet | list7 = Books and Textbook Information on Platelet


| group8 = Pharmacology Resources on Platelet | list8 = AND (Dose)}} Dosing of PlateletAND (drug interactions)}} Drug interactions with PlateletAND (side effects)}} Side effects of PlateletAND (Allergy)}} Allergic reactions to PlateletAND (overdose)}} Overdose information on PlateletAND (carcinogenicity)}} Carcinogenicity information on PlateletAND (pregnancy)}} Platelet in pregnancyAND (pharmacokinetics)}} Pharmacokinetics of Platelet


| group9 = Genetics, Pharmacogenomics, and Proteinomics of Platelet | list9 = AND (pharmacogenomics)}} Genetics of PlateletAND (pharmacogenomics)}} Pharmacogenomics of PlateletAND (proteomics)}} Proteomics of Platelet


| group10 = Newstories on Platelet | list10 = Platelet in the newsBe alerted to news on PlateletNews trends on Platelet</small>


| group11 = Commentary on Platelet | list11 = Blogs on Platelet

| group12 = Patient Resources on Platelet | list12 = Patient resources on PlateletDiscussion groups on PlateletPatient Handouts on PlateletDirections to Hospitals Treating PlateletRisk calculators and risk factors for Platelet


| group13 = Healthcare Provider Resources on Platelet | list13 = Symptoms of PlateletCauses & Risk Factors for PlateletDiagnostic studies for PlateletTreatment of Platelet

| group14 = Continuing Medical Education (CME) Programs on Platelet | list14 = CME Programs on Platelet

| group15 = International Resources on Platelet | list15 = Platelet en EspanolPlatelet en Francais

| group16 = Business Resources on Platelet | list16 = Platelet in the MarketplacePatents on Platelet

| group17 = Informatics Resources on Platelet | list17 = List of terms related to Platelet


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