The primary function of a platelet is in hemostasis, the cessation of bleeding from an injured vessel.
Platelets are cell fragments that break off from larger cells, called megakaryocytes, that reside within the bone marrow. Megakaryocytes synthesize platelets in response to a protein (thrombopoietin) made by the liver when the number of circulating platelets falls.
Once in the circulation, platelets survive for eight to ten days before they are filtered out by the spleen and liver, whereupon they are replaced by new platelets arising from the bone marrow.
A normal platelet count ranges from 140,000 to 440,000 per microliter. Pregnancy, inflammation, or menstrual phase can influence this number to a certain extent.
Platelets contain storage granules that hold clotting factors and other proteins, calcium, serotonin, ADP or ATP, and growth mediators. When activated, platelets release the contents of these granules in order to initiate clotting and, eventually, healing.
Platelet Activation and Clotting
- In the normal state, blood vessels are lined by endothelial cells which produce nitrous oxide, prostacyclins, and mediating enzymes that prevent platelets from sticking together, or aggregating.
- When a blood vessel is injured, endothelial cells stop producing mediators, so platelets immediately become more “sticky.”
- Injury to a vessel wall exposes collagen and von Willebrand’s factor (VWF), both of which stimulate platelets to change shape, adhere to the vessel wall, and begin releasing the contents of their granules.
- Release of granular contents initiates a series of reactions that attracts and activates other platelets and triggers the plasma-based coagulation cascade.
- Activated platelets assemble receptors on their surfaces that attract fibrinogen, which is then converted by a plasma protein called thrombin to fibrin.
- Fibrin strands form a meshwork which traps still more platelets and generates a plug, or clot.
Disorders of Platelets
1. Decreased numbers of platelets (thrombocytopenia)
- Loss of megakaryocytes in bone marrow: leukemia; aplastic anemia; myelosuppressive drugs (e.g., chemotherapy)
- Diminished platelet production: HIV; alcohol-induced bone marrow damage; megaloblastic anemias; myelodysplasia
- Platelet sequestration: cirrhosis with splenomegaly (or other causes of enlarged spleen); Gaucher’s disease
- Increased or accelerated platelet consumption or destruction: HIV; HELLP syndrome; transfusion; drug-induced (quinine, sulfa, sulfonylureas, gold salts, etc.); autoimmune conditions; idiopathic thrombocytopenic purpura; lymphomas; acute respiratory distress syndrome; disseminated intravascular coagulation (e.g., sepsis, massive burns); hemolytic-uremic syndrome
2. Increased numbers of platelets (thrombocytosis)
- Overproduction of platelets: essential thrombocythemia (abnormal proliferation of platelets arising from a blood-producing stem cell); chronic inflammatory diseases (rheumatoid arthritis, sarcoidosis, inflammatory bowel disease, etc.); acute infection; tumors; polycythemia vera; certain leukemias; iron deficiency; abnormal proliferation of bone marrow (myeloproliferative syndromes)
- Decreased removal of platelets: splenectomy
3. Abnormal platelet function
- Decreased function: drug induced (aspirin or other non-steroidal anti-inflammatories); kidney failure; multiple myeloma; cirrhosis; lupus; hereditary (von Willebrand disease; defects in storage granule release, Glanzmann’s disease, Bernard-Soulier syndrome, etc.)
Platelets are integral to the coagulation and healing processes. Abnormalities in platelet count or platelet function can be secondary to a variety of disorders or drugs.
(From The Merck Manual, 18th Edition 2006:1064-73;1099-1101 and Wagner D, et al. Platelets in inflammation and thrombosis. Thromb Vasc Biol 2003;23:2131-2137)
Stephen Allen Christensen - Dr. Steve Christensen's writing has appeared in magazines, professional journals, poetry anthologies, and children's books since 1976.
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