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Image from a light microscope (500 ×) from a Giemsa-stained peripheral blood smear showing platelets (blue) surrounded by red blood cells
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Image from a light microscope (500 ×) from a Giemsa-stained peripheral blood smear showing platelets (blue) surrounded by red blood cells

Platelets are biconvex discs, fragments of cytoplasm 2–3 µm in diameter,[1] found only in the blood of mammals. Platelets form by budding off from megakaryocytes[2] in the bone marrow, and then entering the circulation. They help stop bleeding.

On a stained blood smear, platelets appear as dark purple spots, about 20% the diameter of red blood cells. The smear is used to examine platelets for size, shape, qualitative number, and clumping.

The main function of platelets is to contribute to hemostasis: the process of stopping bleeding at the site of interrupted endothelium. First, platelets stick to substances outside the interrupted endothelium: adhesion. Second, they change shape, turn on receptors and secrete chemical messengers: activation. Third, they stick to each other: aggregation.[3] Formation of this platelet plug (primary hemostasis) is followed by activation of the coagulation cascade with resultant fibrin deposition and linking (secondary hemostasis). These processes may overlap: the spectrum is from a predominantly platelet plug, or "white clot" to a predominantly fibrin clot, or "red clot" or the more typical mixture. The final result is the clot.

Low platelet concentration is thrombocytopenia and is due to either decreased production or increased destruction. Elevated platelet concentration is thrombocytosis and is either congenital, reactive (to cytokines), or due to unregulated production: one of the myeloprolerative neoplasms. A disorder of platelet function is a thrombocytopathy.

Normal platelets can respond to an abnormality on the vessel wall rather than to hemorrhage, resulting in inappropriate platelet adhesion/activation and thrombosis. These arise by different mechanisms than a normal clot. Examples are: extending the fibrin clot of venous thrombosis; extending an unstable or ruptured arterial plaque, causing arterial thrombosis; and microcirculatory thrombosis. An arterial thrombus may partially obstruct blood flow, causing downstream ischemia; or completely obstruct it, causing downstream infarction.

Discovery, early observations, and naming[edit]

George Gulliver in 1841 drew pictures of platelets shortly after Lister improved the resolution of the microscope sufficiently that it was possible to see them. William Addison in 1842 drew pictures of a platelet-fibrin clot. Lionel Beale in 1864 was the first to publish a drawing showing platelets.[4] Max Schultze in 1865 described what he called "spherules", which he noted were much smaller than red blood cells, occasionally clumped, and were sometimes found in collections of fibrin material[5] Giulio Bizzozero in 1882 studied the blood of amphibians microscopically in vivo.   He named Schultz's spherules (It.) piastrine: little plates.[6][7] William Osler observed them and, in published lectures in 1886, called them a third corpuscle and a blood plaque and described them as a colorless protoplasmic disc.(ref) James Wright examined blood smears using the stain named for him, and used the term plates in his 1906 publication[8] but changed to platelets in his 1910 publication[9] which has become the universally accepted term.

The term thrombocyte (clot cell) arose in the early 1900s and is sometimes used as a synonym for platelet; but not generally in the scientific literature, except as a root word for other terms related to platelets. This is partly due to the discovery in non-mammalian vertebrates of nucleated cells that have a hemostatic function and were given the name thrombocyte.

In some contexts, the word thrombus is used interchangeably with the word clot, regardless of its composition (white, red, or mixed). In other contexts it is used to contrast a normal from an abnormal clot: thrombus arises from physiologic hemostasis, thrombosis arises from a pathologic and excessive quantity of clot.[10] In a third context it is used to contrast the result from the process: thrombus is the result, thrombosis is the process.


Platelet concentration is measured either manually using a hemacytometer or by placing blood in an automated analyzer, the Coulter counter.[11] The normal range (95% of population) for platelets is 150,000 to 400,000 per cubic millimeter, (the same as per microliter).[12]  or 150–400 × 109/L. This normal range varies slightly in different laboratories.

The platelet concentration is often referred to informally as the platelet count without stating the units.

Symptoms of platelet disorders[edit]

Spontaneous bleeding can be caused by deficient numbers of platelets, dysfunctional platelets, or very excessive numbers of platelets: over 1.5 million/microliter. The bleeding from a skin cut such as a razor nick is prompt and excessive, but can be controlled by pressure. Spontaneous bleeding into the skin causes a purplish stain named by its size: petechiae, purpura, ecchymoses; bleeding into mucous membranes causes bleeding gums, nose bleed, and gastrointestinal bleeding. Intraretinal bleeding and intracranial bleeding can also occur.

Excessive numbers of platelets, and normal platelets responding to abnormal vessel walls, can result in venous thrombosis and arterial thrombosis. The symptoms depend on the site of thrombosis.


Platelets derive from blood stem cells


3D Rendering of Platelets

The separation of platelet dynamics into three stages is useful, but artificial. In fact, each stage is initiated in rapid succession, and each continues until the trigger for that stage is no longer present, so there is overlap.

Thrombus formation on an intact endothelium is prevented by nitric oxide,[14] prostacyclin,[15] and CD39.[16]


Endothelial cells are attached to the subendothelial collagen by von Willebrand factor (vWF) which these cells produce. vWF is also stored in endothelial cells and secreted constitutively into the blood. Platelets store vWF in their granules.

When the endothelial layer is disrupted, collagen and vWF anchor platelets to the subendothelium. Platelet GP1b-IX-V receptor binds with vWF; and GPVI receptor binds with collagen.[17]


Scanning electron micrograph of blood cells. From left to right: human erythrocyte, activated platelet, leukocyte.


The intact endothelial lining inhibits platelet activation by producing nitric oxide, endothelial-ADPase, and PGI2.  Endothelial-ADPase degrades the platelet activator, ADP.


Platelet activation begins seconds after adhesion occurs. It is triggered when collagen from the subendothilium, and/or tissue factor from the media and adventitia[17] bind with their respective receptors on the platelet. These are G protein coupled receptors and they turn on cAMP mediated signaling pathways within the platelet. Families of three G proteins (Gi, Gq, G12) operate together for full activation.


Coagulation facilitation[edit]

One of the signaling pathways turns on scramblase, which moves negatively charged phospholipids from the inner to the outer platelet membrane surface. These phospholipids then bind the tenase and prothrombinase complexes, two of the sites of interplay between platelets and the coagulation cascade. Calcium ions are essential for the binding of these coagulation factors.

Morphology change[edit]

Mitochondrial hyperpolarization is a key event in initiating changes in morphology.[18] Intraplatelet calcium concentration increases, stimulating the interplay between circumferential microtubules and actin filaments , resulting in platelets becoming more spherical and with pseudopods on their surface.  Thus they assume a stellate shape: morphological evidence of the activated platelet.

Granule secretion[edit]
Diagram of the structure of a platelet showing the granules

Platelets contain dense granules, lambda granules and alpha granules. Activated platelets secrete the contents of these granules through their canalicular systems to the exterior.  Granule characteristics:

GPIIb/IIIa activation[edit]

Thromboxane A2 synthesis increases during activation: it is secreted and acts on both its own thromboxane receptors (the so-called "out-in" mechanism), and those of other platelets. These receptors trigger intraplatelet signaling, which converts GPIIb/IIIa receptors to their active form to initiate aggregation.[19]


Platelet clumps in a blood smear

Aggregation begins minutes after activation, and occurs as a result of turning on the GPIIb/IIIa receptor, which allows these receptors to bind with vWF or fibrinogen.[19] There are 50–100 of these receptors per platelet.[20] When any one or more of at least nine different platelet surface receptors are turned on during activation, intraplatelet signaling pathways cause existing GpIIb/IIIa receptors to change shape – curled to straight – and thus become capable of binding.[3]

Classically it was thought that this was the only mechanism involved in aggregation, but three new mechanisms have been identified which can initiate aggregation, depending on the velocity of blood flow (i.e. shear range).[21]

Ultrastructure and function[edit]

Platelet-coagulation factor interactions[edit]

In addition to interacting with vWF and fibrin, platelets interact with thrombin, Factors X, Va, VIIa, XI, IX, and prothrombin to complete clot formation via the coagulation cascade.[22][23] Six studies suggested platelets express tissue factor: the definitive study shows they do not.[22]

Wound repair[edit]

The blood clot is only a temporary solution to stop bleeding; tissue repair is needed. [24] The fibrin is slowly dissolved by the fibrinolytic enzyme, plasmin, and the platelets are cleared by phagocytosis.[25]

Clot formation in non-mammalian vertebrates[edit]

Non-mammalian vertebrates instead of having platelets have thrombocytes which have a nucleus and resemble B lymphocytes in morphology. They aggregate in response to thrombin (but not to ADP, serotonin, nor adrenaline, as platelets do).[26][27]

Role in inflammation[edit]

In addition to being the 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.[28][29][30][31][32]

Platelets also secrete platelet-derived growth factor (PDGF).

Disorders of platelets[edit]

Disorders associated with a reduced platelet count:

Alloimmune disorders

Disorders associated with platelet dysfunction or reduced count:

Disorders associated with an elevated platelet count:

Disorders of platelet adhesion or aggregation:

Disorders of platelet activation:

Disorders of platelet granule amount or release

Disorders of platelet metabolism

Disorders associated with compromised platelet signaling:

Drugs affecting platelets[edit]

Some drugs used to treat inflammation have the unwanted side effect of suppressing normal platelet function. These are the non-steroidal anti-inflammatory agents (NSAIDS). Aspirin irreversibly disrupts platelet function by inhibiting cyclooxygenase-1 (COX1), and hence normal hemostasis.  The resulting platelets are unable to produce new cyclooxygenase because they have no DNA.  Normal platelet function will not return until the use of aspirin has ceased and enough of the affected platelets have been replaced by new ones, which can take over a week.  Ibuprofen, another NSAID, does not have such a long duration effect, with platelet function usually returning within 24 hours,[37] and taking ibuprofen before aspirin prevents the irreversible effects of aspirin.[38] 

Uremia, a consequence of renal failure, leads to platelet dysfunction that may be ameliorated by the administration of desmopressin.

Drugs which suppress platelet function are used to prevent thrombus formation. The oral agents are aspirin, clopidogrel, cilostazol, ticlopidine, ticagrelor and prasugrel. The intravenous agents are abciximab, eptifibatide, and tirofiban.

Drugs which stimulate production of platelets and thus increase platelet count are Oprelvekin, Romiplostim, Eltrombopag.

Clinical use[edit]



Platelet transfusion is most frequently used to correct unusually low platelet counts, either to prevent spontaneous bleeding (typically at counts below (10–15)×109/L) or in anticipation of medical procedures that will necessarily involve some bleeding. For example, in patients undergoing surgery, a level below 50×109/L is associated with abnormal surgical bleeding, and regional anaesthetic procedures such as epidurals are avoided for levels below 80×109/L.[39] Platelets may also be transfused when the platelet count is normal but the platelets are dysfunctional, such as when an individual is taking aspirin or clopidogrel.[40] Finally, platelets may be transfused as part of a massive transfusion protocol, in which the three major blood components (red blood cells, plasma, and platelets) are transfused to address severe hemorrhage. Platelet transfusion is contraindicated in thrombotic thrombocytopenic purpura (TTP), as it fuels the coagulopathy.


Platelet concentrate.

Platelets are either isolated from collected units of whole blood and pooled to make a therapeutic dose, or collected by platelet apheresis: blood is taken from the donor, passed through a device which removes the platelets, and the remainder is returned to the donor in a closed loop. The industry standard is for platelets to be tested for bacteria before transfusion to avoid septic reactions, which can be fatal. Recently the AABB Industry Standards for Blood Banks and Transfusion Services ( has allowed for use of pathogen reduction technology as an alternative to bacterial screenings in platelets.[41]

Pooled whole-blood platelets, sometimes called “random” platelets, are separated by one of two methods.[42] In the US, a unit of whole blood is placed into a large centrifuge in what is referred to as a “soft spin.” At these settings, the platelets remain suspended in the plasma. The platelet-rich plasma (PRP) is removed from the red cells, then centrifuged at a faster setting to harvest the platelets from the plasma. In other regions of the world, the unit of whole blood is centrifuged using settings that cause the platelets to become suspended in the “buffy coat” layer, which includes the platelets and the white blood cells. The “buffy coat” is isolated in a sterile bag, suspended in a small amount of red blood cells and plasma, then centrifuged again to separate the platelets and plasma from the red and white blood cells. Regardless of the initial method of preparation, multiple donations may be combined into one container using a sterile connection device to manufacture a single product with the desired therapeutic dose.

Apheresis platelets are collected using a mechanical device that 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. Pathogen reduction of platelets using for example, riboflavin and UV light treatments can also be carried out to reduce the infectious load of pathogens contained in donated blood products, thereby reducing the risk of transmission of transfusion transmitted diseases.[43][44] In addition, apheresis platelets tend to contain fewer contaminating red blood cells because the collection method is more efficient than “soft spin” centrifugation at isolating the desired blood component.


Platelets collected by either method have a very short shelf life, typically five days. This results in frequent problems with short supply, as testing the donations often requires up to a full day. Since there are no effective preservative solutions for platelets, they lose potency quickly and are best when fresh.

Platelets are stored under constant agitation at 20–24 °C (68–75.2 °F). Storage at room temperature provides an environment where any bacteria that are introduced to the blood component during the collection process may proliferate and subsequently cause bacteremia in the patient. Regulations are in place in the United States that require products to be tested for the presence of bacterial contamination before transfusion.[45]

Delivery to Recipients[edit]

Platelets do not need to belong to the same A-B-O blood group as the recipient or be cross-matched to ensure immune compatibility between donor and recipient unless they contain a significant amount of red blood cells (RBCs). The presence of RBCs imparts a reddish-orange color to the product, and is usually associated with whole-blood platelets. An effort is sometimes made to issue type specific platelets, but this is not critical as it is with RBCs.

Prior to issuing platelets to the recipient, they may be irradiated to prevent transfusion-associated graft versus host disease or they may be washed to remove the plasma if indicated.

The change in the recipient's platelet count after transfusion is termed the "increment" and is calculated by subtracting the pre-transfusion platelet count from the post-transfusion platelet count. Many factors affect the increment including the recipient's body size, the number of platelets transfused, and clinical features that may cause premature destruction of the transfused platelets. When recipients fail to demonstrate an adequate post-transfusion increment, this is termed platelet transfusion refractoriness.

Platelets, either apheresis-derived or random-donor, 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. Such volume-reduced platelets are normally transfused only 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.[46] Volume reduced platelets have a shelf life of only four hours.[47]

Wound therapy[edit]

Platelets release platelet-derived growth factor (PDGF), a potent chemotactic agent; and TGF beta, which stimulates the deposition of extracellular matrix; fibroblast growth factor, insulin-like growth factor 1, platelet-derived epidermal growth factor, and vascular endothelial growth factor. Local application of these factors in increased concentrations through Platelet-rich plasma (PRP) is used as an adjunct in wound healing.[48]


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External links[edit]

Michelson, Alan D. (2013). Platelets (3rd ed.). Academic. ISBN 0-12-387837-3.  - 1400 pages, 60,000 references. Excerpts free online.