Heparin-induced thrombocytopenia type II (HIT-II) is a prothrombotic disorder. The pathophysiological mechanism is:

• A IgG antibodies form against heparin–platelet factor 4 (PF4) complexes, activating platelets via FcgammaRIIA, causing thrombin generation and thrombocytopenia with paradoxical thrombosis ✓
• B Heparin directly suppresses megakaryocyte platelet production in bone marrow
• C Heparin activates complement, leading to MAC-mediated platelet lysis
• D Heparin inhibits thrombopoietin receptor signalling, reducing platelet count

Explanation

HIT-II is an immune-mediated reaction in which heparin binds to platelet factor 4 (PF4 released from activated platelets), forming an antigenic complex. IgG antibodies generated against this complex bind to PF4-heparin on platelet surfaces and cross-link FcgammaRIIA receptors, causing platelet activation, aggregation, and massive thrombin generation—leading to paradoxical thrombosis (arterial and venous) despite thrombocytopenia. Management requires immediate cessation of all heparin and substitution with a non-heparin anticoagulant (e.g., argatroban, fondaparinux, or danaparoid).

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.