Pathology · Cell Injury, Death and Adaptations (Apoptosis, Necrosis, Free Radicals)

A 28-year-old man presents with low-grade fever, night sweats, and weight loss. A cervical lymph node biopsy shows granulomas with central areas of amorphous, granular, eosinophilic debris completely lacking cellular outlines, surrounded by epithelioid histiocytes and multinucleate giant cells. This pattern of cell death results primarily from:

  • A Coagulative necrosis modified by a lipid-rich bacterial wall and delayed hypersensitivity
  • B Enzymatic digestion by neutrophilic lysosomal hydrolases
  • C Release of activated pancreatic lipases into the tissue
  • D Immune complex deposition with fibrinoid vascular injury
Correct answer: A. Coagulative necrosis modified by a lipid-rich bacterial wall and delayed hypersensitivity

Explanation

Caseous necrosis is characteristic of tuberculosis. It combines coagulative architecture loss with granular cheesy debris, attributed to the waxy lipid-rich capsule of Mycobacterium tuberculosis and the intense type IV hypersensitivity response that restricts drainage, so neither coagulative nor liquefactive patterns dominate. Neutrophilic enzymes produce liquefactive necrosis in abscesses, lipases produce fat necrosis in pancreatitis, and immune complexes produce fibrinoid necrosis in vasculitis.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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