Pathophysiology

• Platelets participate in blood coagulation mechanisms and maintain the integrity of vascular endothelial structures. They are an essential component of primary hematuria.
• Primary immune-mediated thrombocytopenia involves the evolution of a close of B-lymphocytes that begin to produce immunoglobulin against various glycoprotein complexes expressed on the exterior surface membrane of platelet populations.
• Binding of immunoglobulin to the surface membrane of platelets promotes, cytolysis, agglutination, complement activation and accelerated removal of platelets from the systemic circulation by the mononuclear phagocytic system residing primarily within the spleen and liver. More antibody = further destruction and removal    →   faster onset of signs.
• Antibodies also affect megakaryocytes in bone marrow   →   reduced platelet production.
• In primary IMT, the binding avidity of immunoglobulin is directed specifically against certain cell membrane associated antigens, but in secondary IMT, immune complexes non-specifically bind to the exterior surface of platelets.
• Secondary immune-mediated thrombocytopenia has been found to be induced by a wide spectrum of pharmaceutical agents, several infectious pathogens and neoplasia.
• In most cases the etiological cause cannot be determined (suspected primary thrombocytopenia).
• Drugs associated with secondary thrombocytopenia include digoxin, erythromycin, heparin, penicillin, quinidine, sulfas and thiazides.
• Infectious agents associated with secondary thrombocytopenia include equine infectious anemia andAnaplasma phagocytophilum.
• Neoplasia.