Heparin-induced thrombocytopenia type II (HIT-II) is a prothrombotic complication of heparin therapy. The pathogenesis involves:

• A IgG antibodies against heparin-PF4 complex that bind and activate FcgammaRIIA receptors on platelets, causing platelet aggregation, thrombocytopenia, and paradoxical thrombosis ✓
• B Direct bone marrow suppression by heparin inhibiting megakaryocyte maturation
• C Complement-mediated destruction of platelets through deposition of C3b on platelet surfaces
• D IgM antibodies directed against heparin forming immune complexes that are cleared along with platelets by the spleen

Explanation

HIT-II is an immune-mediated disorder in which IgG antibodies form against a complex of heparin and platelet factor 4 (PF4), a platelet protein released on activation. These antibodies bind the heparin-PF4 complex on the platelet surface, and their Fc regions cross-link platelet FcgammaRIIA receptors, causing platelet activation, aggregation, and thrombocytopenia. Simultaneously, platelet activation generates microparticles that amplify thrombin generation, creating a paradoxical hypercoagulable state—explaining why thrombosis (both arterial and venous) occurs despite thrombocytopenia. Management requires immediate heparin cessation and substitution with a non-heparin anticoagulant (argatroban or fondaparinux).

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.