PA2.8 | Cell Injury Morphology — Practical — Summary & Reflection

REFLECT

Look back at the opening scenario: a pale, firm, wedge-shaped slice of kidney with no clinical history.

Using the checklist above, write down (in your notebook or in the space provided):
1. What type of necrosis do you expect, and why?
2. What H&E features will you look for at each power step?
3. What are the two most likely aetiologies?
4. Which special stain (if any) would you order?

Compare your answer with the pattern-recognition steps in the 'Coagulative Necrosis' section. Did you get all four points? If you missed the special-stain step, note that a clinical history (hypertension, atherosclerosis) usually guides whether further stains are needed.

KEY TAKEAWAYS

Reversible injury produces hydropic swelling (pale watery cytoplasm, intact nucleus) or fatty change (clear vacuoles on H&E, confirm with Oil Red O on frozen sections).

Coagulative necrosis — ghost outlines preserved, eosinophilic, karyolysis, no infiltrate acutely. Gross: pale infarct. Organ: kidney, heart, spleen.

Liquefactive necrosis — architecture destroyed, cystic cavity, neutrophils (abscess) or macrophages (brain). Gross: pus or cystic space.

Caseous necrosis — amorphous granular eosinophilic debris + epithelioid granuloma + Langhans giant cells. Pathognomonic of TB. Confirm with ZN stain.

Fat necrosis — basophilic Ca²⁺ deposits (unique), ghost adipocytes, foam cells. In pancreatic fat or breast.

Apoptosis — isolated eosinophilic bodies (Councilman), no inflammation, membrane-bound.

Systematic approach: low → medium → high power; architecture → staining → nuclear change → infiltrate → name → infer cause → state confirming stain.

This checklist is your practical examination answer template.