cellular adaptations dr. peter anderson, uab pathology

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Cellular Adaptations Dr. Peter Anderson, UAB Pathology

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Cellular Adaptations

Dr. Peter Anderson, UAB Pathology

Cellular AdaptationsEnvironmental Factors

• Increased or decreased stimulation• Increased or decreased work• Decreased blood flow • Abnormal materials

Response to Stress

Normal Cells

Atrophy

Hypertrophy

Hyperplasia

Metaplasia

Dysplasia

Response to Stress

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 UterusHYPERTROPHY

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

Stem CellsBasement Membrane

Ciliated Columnar Epithelium

Squamous Metaplasia

Squamous MetaplasiaSquamous 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

AtrophyHypertrophyHyperplasiaMetaplasia

CellularAccumulations

Intracellular Accumulations

• Lipids• Proteins• Glycogen• Carbohydrates

• Carbon• Silica• Asbestos• Bacteria

Normal CellularConstituents

Abnormal or Exogenous

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

• Liver cells of alcoholics• Tangled skeins of cytokeratin intermediate

filaments and other proteins• Eosinophilic cytoplasmic inclusions• Called Mallory Alcoholic hyaline

Intracellular ProteinsAlcoholic 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