A 30-year-old woman develops thrombocytopenia 5 days after starting unfractionated heparin for DVT prophylaxis. Platelet count drops from 220 × 10⁹/L to 55 × 10⁹/L. A new iliac vein thrombus is detected. Serotonin release assay is positive. The pathophysiology involves:

• A Direct heparin-mediated platelet destruction by complement
• B Heparin-induced IgM antibodies causing platelet agglutination
• C Heparin blocking thrombopoietin receptor and reducing platelet production
• D IgG antibodies against heparin-PF4 complexes activating FcγRIIa on platelets, causing thrombosis and thrombocytopenia ✓

Explanation

Heparin-induced thrombocytopenia type II (HIT) is an immune-mediated prothrombotic disorder. Heparin binds platelet factor 4 (PF4), forming heparin-PF4 complexes that elicit IgG antibodies (4–14 days after exposure). These IgG–PF4–heparin immune complexes bind FcγRIIa on platelets, causing platelet activation, aggregation, and release of procoagulant microparticles — paradoxically leading to thrombosis (arterial and venous) despite thrombocytopenia. The 4Ts score and serotonin release assay confirm diagnosis. Heparin must be stopped immediately and replaced with a non-heparin anticoagulant (argatroban, bivalirudin).

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.