Cellular Adaptations Dr. Peter Anderson, UAB Pathology.

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Presentation transcript:

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