A patient undergoes heparin therapy and develops thrombocytopenia on day 8. Serotonin release assay (SRA) is positive. The pathogenesis of heparin-induced thrombocytopenia type II (HIT) involves:

• A IgG antibodies against heparin-PF4 complex activating platelets via FcγRIIA and causing thrombosis ✓
• B Heparin causing direct complement-mediated platelet destruction
• C Heparin directly inhibiting thrombopoiesis in the bone marrow
• D Immune complex deposition causing platelet sequestration in the spleen

Explanation

HIT type II is an immune-mediated drug reaction. Heparin complexes with platelet factor 4 (PF4, a chemokine released by activated platelets) to form a neoantigen. IgG antibodies (anti-heparin/PF4 antibodies) bind this complex → the Fc portion of IgG engages FcγRIIA receptors on platelets → platelet activation, aggregation, and platelet-rich thrombus formation. Platelet consumption causes thrombocytopenia while paradoxical thrombosis occurs (venous > arterial). This explains the 'white clot syndrome.' Platelet-activating antibodies are detected by SRA (gold standard) or PF4-heparin ELISA.

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

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Written and medically reviewed by the StethoPrep medical team.