Cellular Adaptations Dr. Peter Anderson, UAB Pathology Cellular Adaptations Environmental Factors • • • • Increased or decreased stimulation Increased or decreased work Decreased blood flow Abnormal materials Response to Stress Response to Stress Normal Cells Hyperplasia Atrophy Metaplasia Hypertrophy Dysplasia Copyright © 2009 by Saunders, an imprint of Elsevier Inc. All rights reserved Atrophy • Shrinkage in the size of the cell by loss of structural components Atrophy • Shrinkage in the size of the cell by loss of structural components – Decreased work load – Loss of innervation – Diminished blood supply – Inadequate nutrition – Loss of endocrine stimulation Disuse Atrophy - Skeletal Muscle Disuse Atrophy - Skeletal Muscle Senile Atrophy Hypertrophy • Increased size of cells & the organ Hypertrophy • Increased size of cells & the organ • Physiologic – Hormonal stimulation e.g., uterus during pregnancy • Pathologic – Increased functional demand e.g., Left Ventricular Hypertrophy (LVH) - hypertension or valve stenosis Hypertrophy Hypertrophy Hypertrophy Normal Hypertrophy Postpartum Uterus HYPERTROPHY Hyperplasia • Increase in the number of cells in an organ or tissue Hyperplasia • Increase in the number of cells in an organ or tissue – Physiologic hyperplasia • hormonal induced – breast in pregnancy – Pathologic hyperplasia • viral induced – papillomaviruses • excessive hormonal stimulation - prostate Prostatic Hyperplasia Prostatic Hyperplasia Metaplasia • Reversible change in which one differentiated cell type is replaced by another cell type. Ciliated Columnar Epithelium Squamous epithelium Metaplasia Ciliated Columnar Epithelium Stem Cells Squamous epithelium Metaplasia Ciliated Columnar Epithelium Stem Cells Squamous Metaplasia Basement Membrane Squamous Metaplasia Squamous Metaplasia - Bronchus Kidney Stone Transitional Epithelium Squamous Metaplasia Squamous Metaplasia Metaplasia Summary • Reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type Cellular Adaptations Atrophy Hypertrophy Hyperplasia Metaplasia Cellular Accumulations Intracellular Accumulations Normal Cellular Constituents Abnormal or Exogenous • • • • • • • • Lipids Proteins Glycogen Carbohydrates Carbon Silica Asbestos Bacteria Fatty Change • Lipid in macrophages – foam cells - atherosclerosis • Lipid in parenchyma cells – alcoholic fatty liver Fatty Liver • Too much lipid going in • Not enough lipid going out Early Fatty Change - Liver Fatty Change - Liver Fatty Change - Liver – Oil Red O Stain Fatty Change Liver Normal Liver Fatty Change Liver Intracellular Proteins • Kidney Proximal Tubules – hyaline droplets • Plasma Cells – Russell bodies • Alcoholic Hyaline Intracellular Proteins Alcoholic Hyaline • Liver cells of alcoholics • Tangled skeins of cytokeratin intermediate filaments and other proteins • Eosinophilic cytoplasmic inclusions • Called Mallory Alcoholic hyaline Alcoholic Hyalin Pigments • Exogenous pigments – Carbon (anthracosis) – Tattooing – Natural substances • b carotiene – Poisons • lead (pica) Anthracosis Pigments • Endogenous Pigments – Lipofuscin – Melanin – Hemosiderin Melanin - Malignant Melanoma Iron Overload • Hemosiderosis – Iron overload in phagocytic cells – No tissue damage • Hemochromatosis – Iron overload in parenchymal cells – Tissue damage Iron - Hemochromatosis Iron - Hemochromatosis Hemochromatosis - Liver and Pancreas Metastatic Calcification • Deposition of calcium in normal tissues due to hypercalcemia • Interstitial tissues of blood vessels, kidneys, lungs, and gastric mucosa Metastatic Calcification Metastatic Calcification Dystrophic Calcification • Deposition of calcium salts in necrotic tissues • Intracellular, extracellular, or both • Heterotopic bone may form with time Dystrophic Calcification Dystrophic Calcification The End Cellular Adaptations & Cellular Accumulations