Platelets are tiny, disc-shaped components found in blood. Their primary function involves preventing excessive bleeding by initiating blood clot formation following an injury to a blood vessel. This protective mechanism ensures the circulatory system remains sealed and functional.
What Are Platelets
Platelets, also known as thrombocytes, are small, anucleated cell fragments, meaning they lack a nucleus. They originate from very large cells called megakaryocytes, found primarily in the bone marrow. Megakaryocytes extend pseudopods that break off to form platelets. A healthy human typically has between 150,000 to 400,000 platelets per microliter of blood. They have an average lifespan of about 7 to 10 days before being removed from circulation, mainly in the spleen and liver.
How Platelets Stop Bleeding
When a blood vessel sustains an injury, exposing the subendothelial matrix, platelets quickly respond to prevent blood loss. The first step is platelet adhesion, where platelets stick to the injured vessel wall. This is facilitated by molecules like von Willebrand factor (vWF), which acts as a bridge between exposed collagen in the vessel wall and specific receptors on the platelet surface, such as the GPIb receptor.
Following adhesion, platelets undergo activation, changing their shape and releasing signaling molecules from their internal granules. Alpha granules contain compounds like P-selectin, GPIIb/IIIa, GPIb, vWF, and various clotting factors. Dense granules store substances such as calcium, potassium, serotonin, ATP, and ADP, all of which contribute to further platelet activation and aggregation.
These released molecules, particularly ADP and thrombin, promote platelet aggregation, causing more platelets to clump together at the injury site. This forms a temporary platelet plug, the initial step in stopping bleeding, known as primary hemostasis. Concurrently, the exposed tissue factor in the subendothelial matrix activates the coagulation cascade, a series of reactions involving various clotting factors. This cascade culminates in the production of fibrin, a protein that forms a mesh-like network around the platelet plug, stabilizing it and forming a more robust and lasting blood clot.
When Platelets Don’t Function Properly
Problems can arise when platelet numbers are outside their normal range or when their function is impaired. A low platelet count, known as thrombocytopenia, can increase the risk of bleeding, manifesting as external bleeding or internal hemorrhages. Immune thrombocytopenia (ITP), for instance, is an autoimmune condition where antibodies target and destroy platelets, leading to a reduced platelet count and increased bleeding risk.
Conversely, an abnormally high platelet count, termed thrombocytosis, can elevate the risk of blood clot formation. If the cause of high platelet count is unknown, it’s called thrombocythemia. Platelet dysfunction, where platelets are present in normal numbers but do not work effectively, can also lead to excessive bleeding. An example is von Willebrand Disease, where platelets cannot properly adhere to vessel walls or clump together, impairing clot formation.