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Giant platelet disorders, also known as macrothrombocytopenia, are rare disorders featuring abnormally large platelets, thrombocytopenia and a tendency to bleeding. Giant platelets cannot stick adequately to injured blood vessel walls, resulting in abnormal bleeding when injured.
An antiplatelet drug (antiaggregant), also known as a platelet agglutination inhibitor or platelet aggregation inhibitor, is a member of a class of pharmaceuticals that decrease platelet aggregation [1] and inhibit thrombus formation.
Glanzmann's thrombasthenia can be inherited in an autosomal recessive manner [3] [4] or acquired as an autoimmune disorder. [3] [5]The bleeding tendency in Glanzmann's thrombasthenia is variable, [3] some individuals having minimal bruising, while others have frequent, severe, potentially fatal hemorrhages.
The term thrombocyte (clot cell) came into use in the early 1900s and is sometimes used as a synonym for platelet; but not generally in the scientific literature, except as a root word for other terms related to platelets (e.g. thrombocytopenia meaning low platelets).
Thrombosis (from Ancient Greek θρόμβωσις (thrómbōsis) ' clotting ') is the formation of a blood clot inside a blood vessel, obstructing the flow of blood through the circulatory system.
Coagulation, also known as clotting, is the process by which blood changes from a liquid to a gel, forming a blood clot.It results in hemostasis, the cessation of blood loss from a damaged vessel, followed by repair.
Misfolded proteins can form protein aggregates or amyloid fibrils, get degraded, or refold back to its native structure.. In molecular biology, protein aggregation is a phenomenon in which intrinsically-disordered or mis-folded proteins aggregate (i.e., accumulate and clump together) either intra- or extracellularly.
The GPIb-IX-V complex is a profuse membrane receptor complex originating in megakaryocytes and exclusively functional on the surface of platelets. [1] It primarily functions to mediate the first critical step in platelet adhesion, by facilitating binding to von Willebrand factor (VWF) on damaged sub-endothelium under conditions of high fluid shear stress.