Cellular Injury Adaptation

Cells respond to physiological stress and pathological stimuli through predictable adaptive mechanisms before progressing to irreversible injury and death. Hypertrophy is the increase in cell SIZE (not number) in response to increased workload — left ventricular hypertrophy from chronic hypertension is a classic example, where cardiac myocytes enlarge to generate more contractile force against elevated afterload. Hyperplasia is the increase in cell NUMBER through mitotic division, occurring only in cells capable of division — endometrial hyperplasia from excess estrogen and benign prostatic hyperplasia are clinical examples. Atrophy is the decrease in cell size from reduced workload, nutritional supply, or hormonal stimulation — muscle atrophy from disuse or denervation is common. Metaplasia is the reversible replacement of one differentiated cell type by another — Barrett esophagus (squamous to columnar epithelium from chronic GERD) is clinically significant because metaplasia can progress to dysplasia and carcinoma. When adaptive capacity is exceeded, cells progress through reversible injury (cellular swelling, fatty change) to irreversible injury (membrane disruption, mitochondrial dysfunction, nuclear changes: pyknosis, karyorrhexis, karyolysis) and cell death via necrosis or apoptosis.