Heparin-induced thrombocytopenia type II (HIT-II) is a prothrombotic disorder, NOT primarily a haemorrhagic complication. The pathogenesis is:

• A IgG antibodies form against heparin-PF4 complexes; the Fc portion of these antibodies binds FcgammaRIIA receptors on platelets, causing massive platelet activation, granule release, and a hypercoagulable state ✓
• B Heparin directly binds and activates platelet FcgammaRIIA receptors, triggering platelet aggregation and thrombocytopenia
• C Heparin causes complement-mediated destruction of platelets bearing heparin-PF4 complexes via the classical pathway
• D Heparin displaces PF4 from endothelial surfaces, exposing tissue factor and activating the extrinsic coagulation cascade

Explanation

In HIT type II, heparin forms antigenic complexes with platelet factor 4 (PF4) released from platelet alpha-granules. These complexes are recognised by IgG antibodies. The IgG-heparin-PF4 immune complexes bind to FcgammaRIIA (low-affinity IgG Fc receptor) on platelet surfaces, causing massive platelet activation, platelet microparticle formation, thrombin generation, and thrombocytopenia (from consumption/clearance). The paradox is that this leads to thrombosis (venous > arterial), not bleeding. Management requires immediate cessation of heparin and substitution with a non-heparin anticoagulant (argatroban or fondaparinux/danaparoid).

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

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Written and medically reviewed by the StethoPrep medical team.