PA2.4-5 | Cell Death — Necrosis, Apoptosis, Gangrene & Calcification — Summary & Reflection

KEY TAKEAWAYS

Core take-aways from this module:

1. Necrosis = passive, unregulated death with membrane rupture and inflammation. Nuclear sequence: pyknosis → karyorrhexis → karyolysis.

2. Six necrosis types — tie each to its organ and mechanism:
• Coagulative (solid organ infarcts) • Liquefactive (brain, abscess) • Caseous (TB) • Fat (pancreatitis) • Fibrinoid (immune vasculitis) • Gangrenous (large-scale)

1. Gangrene — Dry (arterial, coagulative), Wet (arterial + venous + infection, liquefactive), Gas (Clostridium, crepitus, emergency).

1. Apoptosis = regulated, energy-dependent, single-cell, no inflammation. Intrinsic pathway: p53 → BAX/BAK > BCL-2 → cytochrome c → apoptosome → caspase-9. Extrinsic: FasL–Fas → FADD → caspase-8. Both → caspases-3/7 → DNA laddering, blebbing, apoptotic bodies.

1. Necrosis vs apoptosis pivot: inflammation (necrosis = yes; apoptosis = no); cell size (necrosis = swollen; apoptosis = shrunken); single vs group cells.

6. Calcification:
• Dystrophic = dead/damaged tissue, normal serum Ca (TB, atherosclerosis, psammoma bodies)
• Metastatic = normal tissue, elevated serum Ca (hyperparathyroidism, malignancy → lungs/kidney/gastric mucosa)

REFLECT

Return to the hook scenario:
• The pale, firm myocardium in the MI patient — what type of necrosis is it, and what would you see under the microscope at 48 hours?
• The chalky-white deposit in the TB lymph node — is this dystrophic or metastatic? What would the serum calcium show?
• If the same patient with TB also develops hypercalcaemia (from granuloma-driven vitamin D activation), which additional calcification type could supervene, and where in the body would you look for it?

Write a 5-line clinico-pathological note for each patient as if presenting to your pathology demonstrator. This exercise prepares you for the spotter-with-clinical-correlation format used in MBBS Part II practicals.