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Platelets are the smallest blood cells, typically around 2 μm in diameter and anucleated, with an average lifespan of 7 to 10 days in humans.[1][2] Platelets first gained recognition as having a role in hemostasis more than 100 years ago by the Italian pathologist Giulio Bizzozero, and significant progress was made in elucidating their role in hemostasis and thrombosis during the 20th century using light microscopy techniques.[3] More recently, advanced techniques such as electron microscopy and immunofluorescence have allowed far more detailed analysis of platelet ultrastructure and function.

Because of platelets’ essential role in hemostasis, platelet pathology correlates with excessive bleeding. Patients with thrombocytopenia or reduced platelet function tend to present with petechiae and mucocutaneous bleeding. Following small endothelial lesions, primary hemostasis is often ineffective, and so bleeding, such as epistaxis, gingival bleeding, and purpura occur. Patients with coagulation disorders such as Haemophilia, on the other hand, tend not to experience excessive bleeding from small cuts but struggle to control larger bleeds where fibrin reinforcement of the primary clot is required.[1] Platelet abnormalities are categorized into quantitative disorders (thrombocytopenia or thrombocytosis) and qualitative disorders (thrombasthenias). Thrombocytopenia is common and usually acquired. Common causes include hypersplenism, drugs (e.g., heparin-induced thrombocytopenia), infections, pregnancy, and immune thrombocytopenia. Hereditary thrombocytopenias are rare but merit consideration, especially if giant platelets are visible on the blood film.[1] Thrombocytosis is also common, with 88 to 97% of cases attributed as reactive in origin and the remainder being clonal disorders and spurious results.[14] A wide variety of thrombasthenias have been identified, with some examples provided above. Platelets are also involved in the pathophysiology of atherosclerosis. They play an obvious role in thrombus formation on the surface of a ruptured plaque in response to the exposure of subendothelial structures. Platelets also appear to be involved in the recruitment of leukocytes to plaques during their formation through cytokine release and receptor-ligand interactions.[15]