Heparin-induced thrombocytopenia type II (HIT) is characterised by thrombocytopenia plus paradoxical thrombosis. The immunological mechanism is:

• A IgG antibodies form against the heparin-PF4 complex; these antibodies bind and activate platelet FcγRIIa receptors causing platelet activation, aggregation, and thrombosis; platelet destruction lowers count ✓
• B Heparin directly destroys platelets via complement activation
• C Heparin inhibits von Willebrand factor causing platelet clearance from circulation
• D Anti-platelet IgM antibodies induced by heparin cross-react with thrombin

Explanation

In HIT type II, heparin binds platelet factor 4 (PF4) forming an immunogenic complex. The immune system generates IgG antibodies against this complex within 5–14 days of heparin exposure. These IgG-heparin-PF4 complexes bind platelet FcγRIIa receptors, triggering massive platelet activation and aggregation — paradoxically causing thrombosis (HITT) despite thrombocytopenia from platelet consumption. Management requires immediate cessation of all heparin (including flushes) and substitution with a non-heparin anticoagulant (argatroban, fondaparinux, or a DOAC).

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.