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ADAPTATION, INJURY and DEATH of CELLS

ADAPTATION, INJURY and DEATH of CELLS. Learning Objectives. 1. List examples of hypertrophy, hyperplasia, atrophy, hypoplasia, metaplasia and dysplasia 2. List examples of reversible and irreversible cell injury 3. Diagram abscess, granuloma, renal infarction and fat necrosis

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ADAPTATION, INJURY and DEATH of CELLS

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  1. ADAPTATION, INJURY and DEATH of CELLS

  2. Learning Objectives 1. List examples of hypertrophy, hyperplasia, atrophy, hypoplasia, metaplasia and dysplasia 2. List examples of reversible and irreversible cell injury 3. Diagram abscess, granuloma, renal infarction and fat necrosis 4. List consequences of ATP loss 5. List consequences Ca++ increase and release

  3. Pathology: the Study of Disease Etiology or cause: infection, genetic etc. and often mutifactoral Pathogenesis: progression of the disease (Molecular and Morphologic Changes) Clinical Manifestations: signs and symptoms

  4. Cellular Adaptations Hypertrophy Hyperplasia Atrophy Metaplasia Dysplasia

  5. HYPERTROPHY Increase in cell size with subsequent increase in organ size

  6. Causes of Hypertrophy Increased functional demand Hormonal stimulation

  7. Hypertrophy of Uterus During Pregnancy

  8. Hypertrophy of Uterus During Pregnancy No new cells; Cells just bigger

  9. Hypertrophy can be physiologic or pathologic

  10. Cardiac Muscle Hypertrophy and Infarction

  11. Results from increased production of cellular proteins

  12. HYPERPLASIA Increase in the number of cells in an organ which may then increase organ size. Physiologic or Pathologic

  13. PHYSIOLOGIC HYPERPLASIA Hormonal hyperplasia- female breast at puberty and in pregnancy Compensatory hyperplasia- liver regeneration after partial resection

  14. Female Breast Tissue after Puberty

  15. Lactating breast during pregnancy

  16. Causes of Pathologic Hyperplasia Excess hormone- endometrial hyperplasia due to estrogens

  17. Hyperplasia is NOT a neoplastic process, but it may be fertlie soil for malignancy “Atypical Hyperplasia” in the endometrium carries an increased risk for development of endometrial adenocarcinoma

  18. Endometrial Hyperplasia

  19. Normal Proliferative Endometrium

  20. Endometrial Hyperplasia

  21. Benign Prostatic Hypertrophy

  22. ATROPHY Decrease in the size of a cell or organ by loss of cell substance (both size and number)

  23. Physiologic Atrophy • Normal development • Notochord • Thyroglossal duct • Uterus following childbirth

  24. Causes of Pathologic Atrophy Decreased workload Loss of innervation Decreased blood supply Inadequate nutrition Loss of endocrine stimulation Pressure

  25. * * **Central skeletal muscle bundle is atrophic

  26. Atrophic Brain Normal Brain

  27. Atrophy results from both… Decreased protein synthesis Increased protein degradation

  28. Protein degradation is important in atrophy Lysosomes with hydrolytic enzymes The ubiquitin-proteasome pathway

  29. HYPOPLASIA Incomplete development of an organ so that it fails to reach adult size

  30. Examples of Hypoplasia Hypoplastic Left Ventricle Hypoplastic Kidney

  31. METAPLASIA A reversible change in which one ADULT cell type is replaced by another ADULT cell type

  32. Metaplasia • Caused by: • Chronic irritation (cigarette smoke; calculi in ducts) • Vitamin A deficiency • Cervix- squamous epithelium of the endocervix replaces columnar (dysplasia and squamous CA may develop) • Barrett esophagus- gastric reflux results in columnar epithelium replacing squamous epithelium in the esophagus (dysplasia and adenocarcinoma may occur)

  33. Squamous cells replace columnar cells

  34. Esophagus: glandular epithelium (R) is metaplastic

  35. Hyperplasia and Metaplasia are not premalignant changes, however they are “fertile fields” for Dysplasia which is a premalignant change

  36. DYSPLASIA Atypical proliferative changes due to chronic irritation or inflammation; Premalignant change

  37. DYSPLASIA IN THE CERVIX Mild dysplasia Moderate dysplasia Marked dysplasia

  38. CELL INJURY PRINCIPLES The cellular response to injurious stimuli depends on the type of injury, its duration and its severity. The consequences of cell injury depend on the type, state, and adaptability of the injured cell Cell injury results from different biochemical mechanisms acting on several essential cellular components

  39. 1. The cellular response to injurious stimuli depends on the type of injury, its duration and its severity.

  40. Cellular Changes Secondary to Injury REVERSIBLE • Cellular swelling • Cell membrane blebs • Detached ribosomes • Chromatin clumping IRREVERSIBLE • Lysosomes rupture • Dense bodies in mitochondria • Cell membrane rupture • Karyolysis, karyorrhexis, pyknosis

  41. Myocardial Infarction Markers Cardiac specific enzymes and proteins appear in serum within 2 hours post infarction Morphologic (light microscopic) changes in 4-12 hours

  42. Normal Myocardium Coagulation Necrosis at 24-48 hours post MI

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