Platelets (thrombocytes)
Thrombocytus
Also known as: platelet, thrombocyte, megakaryocyte
Platelets are small cell fragments without a nucleus, about 2–4 µm across, shed from megakaryocytes in the bone marrow. They stick to damaged vessel walls, clump together into a plug and provide the surface on which the clotting cascade runs.
Overview
Production. Megakaryocytes in the marrow are giant cells with many copies of their DNA (up to 64N). They push long processes (proplatelets) into the marrow sinusoids, which break up into thousands of platelets. Production is controlled mainly by thrombopoietin, made in the liver.
Numbers and lifespan. The normal count is 150–400 × 10⁹/L. Platelets survive about 7–10 days, and about a third of them are pooled in the spleen at any time.
Structure. Platelets contain an open canalicular system and a dense tubular system that stores Ca²⁺. They have two main kinds of granule. α-granules contain von Willebrand factor, fibrinogen, factor V, PDGF, platelet factor 4 and P-selectin. Dense (δ) granules contain ADP, ATP, Ca²⁺ and serotonin.
Surface receptors. GPIb–IX–V binds von Willebrand factor and allows adhesion. GPVI and integrin α2β1 bind collagen. GPIIb/IIIa (integrin αIIbβ3) binds fibrinogen and allows aggregation. P2Y12 responds to ADP, PAR-1 to thrombin, and the TP receptor to thromboxane A₂.
Thromboxane. Inside the platelet, cyclo-oxygenase-1 converts arachidonic acid into thromboxane A₂, which activates and recruits more platelets.
Function
- Form the primary haemostatic plug.
- Provide the phospholipid surface on which coagulation factors assemble (the tenase and prothrombinase complexes).
- Release vasoconstrictors, growth factors and inflammatory mediators.
- Retract the clot and promote wound repair.
- Physiology
When a vessel is injured, platelets act in sequence. Adhesion: they stick to exposed collagen through von Willebrand factor, which binds GPIb. Activation: they change shape, release their granules, make thromboxane A₂ and flip phosphatidylserine to their outer surface, where clotting factor complexes assemble. Aggregation: fibrinogen bridges activated GPIIb/IIIa receptors on neighbouring platelets. Clot retraction: contractile actomyosin pulls the clot tight. Finally, platelets release growth factors such as PDGF that help repair the vessel.
Clinical significance
Antiplatelet drugs
Aspirin irreversibly blocks COX-1. Because platelets cannot make new enzyme, the effect lasts for the life of the platelet, about 7–10 days. Clopidogrel, prasugrel and ticagrelor block the P2Y12 ADP receptor. GPIIb/IIIa inhibitors such as eptifibatide and tirofiban block aggregation directly. Dual antiplatelet therapy is standard after coronary stenting.
Thrombocytopenia
Thrombocytopenia is a platelet count below 150 × 10⁹/L. Spontaneous bleeding becomes likely below about 10–20 × 10⁹/L. Causes include immune thrombocytopenia (ITP), heparin-induced thrombocytopenia, thrombotic thrombocytopenic purpura, DIC, marrow failure and an enlarged, overactive spleen.
Heparin-induced thrombocytopenia (HIT) is caused by antibodies against PF4–heparin complexes. It typically appears 5–10 days after heparin is started and, paradoxically, causes thrombosis. Thrombotic thrombocytopenic purpura (TTP) is caused by deficiency of the enzyme ADAMTS13.
Inherited platelet disorders
Von Willebrand disease is the commonest inherited bleeding disorder, affecting up to about 1% of people. Bernard–Soulier syndrome is a lack of GPIb and features giant platelets. Glanzmann thrombasthenia is a lack of GPIIb/IIIa. Platelet-type bleeding affects skin and mucous membranes: petechiae, nosebleeds and heavy periods. Clotting-factor deficiencies cause bleeding into joints and muscles instead.
Compiled from standard anatomy and physiology references — see the Cardiovascular System sources. For education only; not medical advice.