Platelets are small anucleate blood cells that are produced in the bone marrow from the cytoplasm of megakaryocytes. Circulating platelets are essential for primary hemostasis and also involved in pathological thrombosis. For the platelet hemostatic functions, platelet surface membrane glycoproteins are crucial to form platelet-subendothelial matrix and platelet-platelet interactions. At the site of blood vessel injury, platelets are captured by platelet GPIb-IX-V interaction with von Willebrand factor which bound to exposed collagen followed by direct platelet-collagen interaction by GPIa-IIa (integrin α2β1) and GPVI. Platelet fibrinogen receptor GPIIb-IIIa (integrin αIIbβ3) is the most abundant glycoprotein on platelet surface, and its affinity for fibrinogen is tightly regulated by inside-out signaling. The platelet-platelet interaction mediated by activated GPIIb-IIIa is necessary for platelet accumulation on the layer of adhered platelets at the injured vessel. Both quantitative and qualitative abnormalities in these platelet glycoproteins can be a cause of platelet dysfunctions and bleeding disorders. In addition, platelet glycoproteins are also important in the pathogenesis of idiopathic thrombocytopenic purpura (ITP). In the majority of patients with ITP, antiplatelet autoantibodies in plasma are directed against platelet glycoproteins especially GPIIb-IIIa and GPIb-IX-V.