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Cellular adaptation, reversible injury, accumulations and pathological calcification

A cell exposed to stress adapts — by hypertrophy, hyperplasia, atrophy or metaplasia — and when the stress exceeds its capacity it is injured: first reversible injury with swelling and fat, then irreversible injury; along the way various substances accumulate in the cell, and dead tissue or serum with high calcium calcifies.

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Why it matters in the exam

The bank tests examples of each adaptation and the distinction between types of calcification. Hypertrophy is an increase in cell size (heart muscle in hypertension, uterus in pregnancy); hyperplasia is an increase in cell number (endometrium under oestrogen, prostate); atrophy is shrinkage, through the ubiquitin–proteasome system and autophagy — a protein tagged with a ubiquitin chain is sent to the proteasome for degradation. Metaplasia is replacement of one mature cell type by another: squamous epithelium in the bronchi of smokers, and columnar epithelium with goblet cells in the oesophagus in Barrett oesophagus.

Reversible injury appears as cell swelling (hydropic change) with clear vacuoles from dilated endoplasmic reticulum, as fatty change, membrane blebs and mitochondrial swelling. Accumulation of misfolded proteins in the endoplasmic reticulum activates the unfolded protein response, and when it fails — apoptosis. Examples of accumulations: fat in the liver; glycogen in renal tubular cells and hepatocyte nuclei in diabetes; Mallory-Denk bodies — eosinophilic aggregates of intermediate filaments (keratin) in hepatocytes in alcoholic liver disease; lipofuscin — a brown "wear-and-tear" pigment in ageing cells; and haemosiderin from blood breakdown.

Dystrophic calcification occurs in damaged or dead tissue when blood calcium is normal — in atherosclerotic plaque, damaged valves and the centre of necrotic tumours; psammoma bodies are laminated calcifications in papillary tumours (thyroid, ovary, meningioma). Metastatic calcification occurs in normal tissue when blood calcium or phosphate is high — in the lungs, kidneys, stomach and vessel walls. Caloric restriction is one of the factors shown to extend lifespan in experiments, through reduced growth-factor signalling and activation of sirtuins.

Key points

• Hypertrophy enlarges cells; hyperplasia increases their number.
• Metaplasia: Barrett and smokers' bronchi.
• Reversible injury: swelling with dilated reticulum, fat.
• Accumulations: fat, glycogen in diabetes, Mallory-Denk, lipofuscin.
• Dystrophic in dead tissue; metastatic with high calcium.

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Sources

• Robbins and Cotran Pathologic Basis of Disease, 10th edition (2021) — The cell as a unit of health and disease; cellular responses to stress
• Rubin's Pathology: Mechanisms of Human Disease, 8th edition (2020) — Cell adaptation, cell injury and cell death
• Kumar V et al. Robbins Basic Pathology, 11th edition (2023) — Intracellular accumulations and pathologic calcification

Sources are given for further reading; the text is written afresh and not copied from them.

Reviewed by the Examqo AI Professor · 2026-11-06. The text may contain errors; when in doubt, check the source.