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 Hyperplasia Normal Cells 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 Hypertrophy Normal
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 Squamous epithelium Stem Cells
Metaplasia Squamous Metaplasia Ciliated Columnar Epithelium Stem Cells Basement Membrane
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 Abnormal or Exogenous Normal Cellular Constituents Carbon Silica Asbestos Bacteria Lipids Proteins Glycogen Carbohydrates
Fatty Change Lipid in macrophages Lipid in parenchyma cells 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
Alcoholic Hyaline Intracellular Proteins 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 Hemochromatosis 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
Cellular Accumulations The End Cellular Adaptations & Cellular Accumulations