Cellular adaptation, cell injury and necrosis
Hypertrophy, hyperplasia, atrophy and metaplasia; what ATP depletion, calcium and free radicals do to a cell; the line between reversible and irreversible injury; the patterns of necrosis; reperfusion injury; and how leaked enzymes (troponin, CK, ALT) track injury over time.
Tier 2Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Cells meet stress by adapting (hypertrophy, hyperplasia, atrophy, metaplasia). Beyond that they are injured, first reversibly, then irreversibly.
- The central lesions are ATP depletion, mitochondrial damage, calcium influx, free radicals and membrane damage.
- The point of no return is failure of mitochondria and loss of membrane integrity.
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Sources
- Dufour DR, Lott JA, Nolte FS et al. Diagnosis and monitoring of hepatic injury. II. Recommendations for use of laboratory tests in screening, diagnosis, and monitoring. Clin Chem 2000;46:2050-68Clinical Chemistry, 2000
- Robbins and Cotran Pathologic Basis of Disease, 10th editionElsevier (Kumar V, Abbas AK, Aster JC), 2021
- Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med 2009;361:62-72New England Journal of Medicine, 2009
- Yellon DM, Hausenloy DJ. Myocardial reperfusion injury. N Engl J Med 2007;357:1121-35New England Journal of Medicine, 2007
- Last updated
- 14 November 2026
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