Path Cell Adaptations

  1. Hyperplasia
    Increase number of cells

    • Physiological
    • hormone induced - breast
    • compensatory - regen liver

    • Pathology
    • endometrial hyperplasia from unopposed estrogen
  2. Hypertrophy
    Increased SIZE cells/organ

    Ex. uterus, cardiac/skel m

    May be accomanied by gene exp changes: ANP in ventricle, embyonic contractile proteins, inc R
  3. Atrophy
    Dec cell size

    Physiologic: dev, post pg

    Pathologic: disuse, loss of inn, dec bl supply, inadequate nutrition, loss of endocrine stim, pressure
  4. Metaplasia
    Reversible change replacing one adult cell with another

    Cell response to adverse conditions

    • Columnar to squamous - smoker's resp tracts, cervical transformation zone
    • Squamous to columnar - Barrett's esophagus
    • Connective tissue - myositis ossificans
  5. Mechanisms of Cellular Injury
    • ATP depletion
    • Mito damage
    • Loss of Ca homeostasis
    • Oxidative stress and free radical injury
    • Defects in memb perm
  6. Reversible injury
    • Cellular swelling (hydropic change)
    • Fatty change
    • Ultrastructure (PM blebs, loss of microvilli, mito swelling, ER swell, loss of ribosome, nuclear changes)
    • Molecular (Inact Na-K ATPase, deplete glycogen stores, decrease pH)
  7. Necrosis
    • Coagulative (kidney)
    • Liquefactive (brain, zits)
    • Caseous (TB, granulomatous)
    • Fat (acute pancreatitis)
  8. Reperfusion Injury
    • Oxygen free radical generation (further damge to memb)
    • Cytokine adn adhesion molecule production (recruit inflam cells)
  9. Free Radical Damage and Repair
    • Peroxidation of lipids
    • Cross-linking/oxidation of aa residues
    • Creating TT ss breaks

    • Anti-oxidants (Vit A/E)
    • Sequestration of metals (transferrin, ceruloplasmin)
    • Enzyme degradation (catalase, glutathione, superoxide dismutase)
  10. Apoptosis
    • Programmed cell death
    • Dev, maintain homeostasis, defense against immune rxns, aging
    • Cell shrinkage, chromatin condenses, cytoplasmic blebs and apoptotic bodies
    • Protein cleavage (caspases), protein cross-linking, DNA ladder, phagocytic recognition
  11. Intrinsic apoptotic proteins
    • Pro: Bim Bid Bad
    • Anti: Bcl-2, Bcl-x, Mcl-1
    • Death: Bak Bax
    • Act Caspase 9
  12. Extrinsic apoptotic proteins
    Death R: TNFR, Fas (Fas-L on T cells)

    Act Caspase 8
  13. Subcellular responses to cell injury
    • Lysosome catabolism (lipofuscin, tattoos, chloroquine)
    • Hypertrophy of smER
    • Mito changes (alcoholic liver disease, nutritional deficiencies, mito myopathies, oncocytomas)
    • Cytoskeletal changes
  14. Intracellular Accumulations
    • Lipids
    • Proteins
    • Hyaline change
    • Glycogen
    • Pigments
  15. Lipid accumulations
    • Steatosis in liver (toxins, obesity, diabetes, viral infection, alcohol abuse)
    • Athlerosclerotic plaques
    • Xanthomas (cholesterol in soft tissues)
    • Cholesterolosis (foamy Mph in gallbladder lamina propria)
  16. Protein accumulation
    • Peabsorption droplets in renal tubular cells in proteinuria
    • Russell bodies (plasma cells)
    • Protein misfolding (alpha1antitypsin, huntington, alzheimer, parkinson)
  17. Hyaline change
    Nonspec histo desc term - smooth, glassy, pink
  18. Glycogen accumulation
    • Diabetes - renal tubular cells, hepatocytes, islet cells
    • glycogen storage disease
  19. Pigment accumulation
    • (usually stuck in Mphage)
    • Anthracosis
    • Tattoo
    • Lipofuscin
    • Melanin
    • Homogentisic acid
    • Hemosiderosis
    • Hemochromatosis
    • Bilirubin
  20. Dystrophic calcification
    • Deposition of Ca salts in nonviable or dying tissues despite normal serum ca levels
    • Ex: necrosis, atheroma, heart valves
    • Lamellated psammoma bodies in papillary cancer
  21. Metastatis calcification
    • Deposition of calcium salts in normal tissue in the setting of hypercalcemia
    • Ex: hyperparathyroidism, bone destruction, vit D disorders, chronic renal failure
Card Set
Path Cell Adaptations
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