1. Cellular Adaptations
Dr. Peter Anderson, UAB Pathology

2. Cellular Adaptations Environmental Factors
Increased or decreased stimulation
Increased or decreased work
Decreased blood flow
Abnormal materials

3. Response to Stress

4. Response to Stress Hyperplasia Normal Cells Atrophy Metaplasia
Hypertrophy
Dysplasia
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5. Atrophy
Shrinkage in the size of the cell by loss of structural components

6. 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

7. Disuse Atrophy - Skeletal Muscle

8. Disuse Atrophy - Skeletal Muscle

9. Senile Atrophy

10. Hypertrophy
Increased size of cells & the organ

11. 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

12. Hypertrophy

13. Hypertrophy

14. Hypertrophy
Hypertrophy
Normal

15. Postpartum Uterus
HYPERTROPHY

16. Hyperplasia
Increase in the number of cells in an organ or tissue

17. 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

18. Prostatic Hyperplasia

19. Prostatic Hyperplasia

20. Metaplasia
Reversible change in which one differentiated cell type is replaced by another cell type.
Ciliated Columnar
Epithelium
Squamous epithelium

21. Metaplasia
Ciliated Columnar
Epithelium
Squamous epithelium
Stem Cells

22. Metaplasia Squamous Metaplasia Ciliated Columnar Epithelium Stem Cells
Basement
Membrane

23. Squamous Metaplasia - Bronchus

24. Kidney Stone

25. Transitional Epithelium

26. Squamous Metaplasia

27. Squamous Metaplasia

28. Metaplasia Summary
Reversible change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type

29. Cellular Adaptations
Atrophy
Hypertrophy
Hyperplasia
Metaplasia

30. Cellular
Accumulations

31. Intracellular Accumulations
Abnormal or
Exogenous
Normal Cellular
Constituents
Carbon
Silica
Asbestos
Bacteria
Lipids
Proteins
Glycogen
Carbohydrates

32. Fatty Change Lipid in macrophages Lipid in parenchyma cells
foam cells - atherosclerosis
Lipid in parenchyma cells
alcoholic fatty liver

33. Fatty Liver
Too much lipid going in
Not enough lipid going out

34. Early Fatty Change - Liver

35. Fatty Change - Liver

36. Fatty Change - Liver – Oil Red O Stain

37. Fatty Change Liver

38. Normal Liver

39. Fatty Change Liver

40. Intracellular Proteins
Kidney Proximal Tubules
hyaline droplets
Plasma Cells
Russell bodies
Alcoholic Hyaline

41. Alcoholic Hyaline Intracellular Proteins Liver cells of alcoholics
Tangled skeins of cytokeratin intermediate filaments and other proteins
Eosinophilic cytoplasmic inclusions
Called Mallory Alcoholic hyaline

42. Alcoholic Hyalin

43. Pigments Exogenous pigments Carbon (anthracosis) Tattooing
Natural substances
b carotiene
Poisons
lead (pica)

44. Anthracosis

45. Pigments
Endogenous Pigments
Lipofuscin
Melanin
Hemosiderin

46. Melanin - Malignant Melanoma

47. Iron Overload Hemosiderosis Hemochromatosis
Iron overload in phagocytic cells
No tissue damage
Hemochromatosis
Iron overload in parenchymal cells
Tissue damage

48. Iron - Hemochromatosis

49. Iron - Hemochromatosis

50. Hemochromatosis - Liver and Pancreas

51. Metastatic Calcification
Deposition of calcium in normal tissues due to hypercalcemia
Interstitial tissues of blood vessels, kidneys, lungs, and gastric mucosa

52. Metastatic Calcification

53. Metastatic Calcification

54. Dystrophic Calcification
Deposition of calcium salts in necrotic tissues
Intracellular, extracellular, or both
Heterotopic bone may form with time

55. Dystrophic Calcification

56. Dystrophic Calcification

57. Cellular Accumulations
The End
Cellular Adaptations
&
Cellular Accumulations