Heparin-induced thrombocytopenia type II (HIT) is a prothrombotic paradox. The pathogenesis involves IgG antibodies against platelet factor 4–heparin complexes. These IgG antibodies cause thrombocytopenia and thrombosis by which mechanism?

• A IgG binds to platelet GPIIb/IIIa directly, blocking fibrinogen binding and causing bleeding
• B IgG activates complement C5b-9 causing direct platelet lysis and thrombocytopenia
• C IgG/PF4-heparin complexes bind FcγRIIA on platelets, activating them and causing platelet aggregation and thrombosis ✓
• D IgG cross-reacts with endothelial heparan sulfate, activating the extrinsic coagulation pathway

Explanation

In HIT type II, IgG antibodies against PF4-heparin complexes bind via their Fc regions to FcγRIIA (CD32a) on platelets, crosslinking and activating platelets to release more PF4 and form procoagulant microparticles — creating a paradoxical thrombotic state (venous > arterial thrombosis) despite thrombocytopenia. Treatment involves cessation of heparin and use of direct thrombin inhibitors (argatroban, bivalirudin).

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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