In organ transplantation, hyperacute rejection occurs within minutes to hours of transplantation. The mechanism responsible is:

• A CD8+ cytotoxic T-cell infiltration destroying tubular cells
• B NK cell-mediated antibody-dependent cellular cytotoxicity
• C Delayed-type hypersensitivity T-cell reaction causing chronic endothelial injury
• D Pre-formed recipient antibodies against donor HLA or ABO antigens causing complement activation, endothelial injury, and thrombotic occlusion of graft vasculature ✓

Explanation

Hyperacute rejection is mediated by pre-existing recipient antibodies (anti-HLA class I antibodies from prior sensitization by pregnancy, transfusion, or previous transplant; or ABO antibodies in ABO-incompatible transplants). These antibodies bind donor vascular endothelium immediately upon reperfusion, activating complement (C3a, C5a, MAC formation), causing endothelial cell death, platelet aggregation, and thrombotic occlusion of graft capillaries. Macroscopically, the graft turns blue-black within minutes. It is prevented by crossmatch testing and ABO compatibility. The graft is irreversibly damaged and must be removed.

Reference: Bailey & Love's Short Practice of Surgery, 27th ed.

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Written and medically reviewed by the StethoPrep medical team.