Heparin-induced thrombocytopenia (HIT) type II is paradoxically prothrombotic despite thrombocytopenia. The mechanism involves:

• A Direct heparin-mediated platelet membrane disruption causing platelet lysis
• B Heparin blocking GPIIb/IIIa preventing platelet aggregation while thrombin generation continues
• C IgG antibodies against PF4-heparin complexes binding platelet FcγRIIA receptors, causing platelet activation, aggregation, and procoagulant microparticle release ✓
• D Antithrombin-heparin complex directly activating coagulation cascade

Explanation

HIT type II is an immune-mediated reaction where heparin binds to platelet factor 4 (PF4) released from activated platelets, forming PF4-heparin complexes. These complexes are immunogenic and elicit IgG antibodies. The IgG-PF4-heparin immune complexes bind platelet Fcγ receptor IIA (FcγRIIA/CD32), causing massive platelet activation, aggregation, release of procoagulant microparticles, and clearance (thrombocytopenia). The procoagulant state and monocyte/endothelial activation paradoxically cause venous and arterial thrombosis despite low platelet counts.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.