Heparin-induced thrombocytopenia type II (HIT type II) is caused by antibodies against platelet factor 4 (PF4)-heparin complex. The resulting thrombocytopenia and paradoxical thrombosis occur because:

• A Heparin directly activates complement via the classic pathway, consuming platelets in inflammatory complexes
• B Anti-PF4-heparin IgG binds FcγRIIA receptors on platelets, causing massive platelet activation, aggregation and thrombin generation ✓
• C Anti-PF4 antibodies bind platelet GPIIb/IIIa receptors, competitively displacing fibrinogen and causing platelet destruction by spleen
• D Heparin-PF4 complexes deposit in bone marrow sinusoids, inhibiting megakaryocyte thrombopoietin responsiveness

Explanation

In HIT type II, heparin binds PF4 (released from platelet α-granules) forming immunogenic PF4-heparin complexes; IgG antibodies form against this complex. These IgG-PF4-heparin immune complexes bind and crosslink FcγRIIA receptors on platelet surfaces, causing massive platelet activation, degranulation and aggregation — generating large amounts of thrombin and thrombus. Paradoxical thrombocytopenia occurs due to platelet consumption. Alternative anticoagulation (argatroban, fondaparinux, bivalirudin) must be started immediately.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.