A patient develops immune thrombocytopenic purpura (ITP). The primary mechanism of platelet destruction involves antiplatelet IgG antibodies binding to GPIIb/IIIa. These opsonized platelets are primarily destroyed in which location and by which mechanism?

• A Bone marrow — FcγRIII on megakaryocytes inhibits thrombopoiesis
• B Liver — complement-mediated lysis after C3b opsonization
• C Peripheral blood — NK cell-mediated ADCC targeting GPIIb/IIIa-coated platelets
• D Spleen — FcγRI/III on splenic macrophages mediate Fc-receptor-dependent phagocytosis ✓

Explanation

In ITP, anti-GPIIb/IIIa (and anti-GPIb/IX) IgG antibodies opsonize platelets, which are then recognized by FcγRI (CD64) and FcγRIII (CD16) on splenic macrophages leading to Fc-receptor-mediated phagocytosis — this is the primary destruction mechanism. The spleen is also the site of autoantibody production by pathogenic plasma cells. This explains why splenectomy leads to remission in ~66% of ITP patients. Additionally, the anti-platelet antibodies cross-react with megakaryocytes, impairing thrombopoiesis directly.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.