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Hyperplasia
Increase number of cells
- Physiological
- hormone induced - breast
- compensatory - regen liver
- Pathology
- endometrial hyperplasia from unopposed estrogen
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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
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Atrophy
Dec cell size
Physiologic: dev, post pg
Pathologic: disuse, loss of inn, dec bl supply, inadequate nutrition, loss of endocrine stim, pressure
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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
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Mechanisms of Cellular Injury
- ATP depletion
- Mito damage
- Loss of Ca homeostasis
- Oxidative stress and free radical injury
- Defects in memb perm
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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)
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Necrosis
- Coagulative (kidney)
- Liquefactive (brain, zits)
- Caseous (TB, granulomatous)
- Fat (acute pancreatitis)
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Reperfusion Injury
- Oxygen free radical generation (further damge to memb)
- Cytokine adn adhesion molecule production (recruit inflam cells)
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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)
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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
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Intrinsic apoptotic proteins
- Pro: Bim Bid Bad
- Anti: Bcl-2, Bcl-x, Mcl-1
- Death: Bak Bax
- Act Caspase 9
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Extrinsic apoptotic proteins
Death R: TNFR, Fas (Fas-L on T cells)
Act Caspase 8
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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
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Intracellular Accumulations
- Lipids
- Proteins
- Hyaline change
- Glycogen
- Pigments
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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)
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Protein accumulation
- Peabsorption droplets in renal tubular cells in proteinuria
- Russell bodies (plasma cells)
- Protein misfolding (alpha1antitypsin, huntington, alzheimer, parkinson)
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Hyaline change
Nonspec histo desc term - smooth, glassy, pink
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Glycogen accumulation
- Diabetes - renal tubular cells, hepatocytes, islet cells
- glycogen storage disease
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Pigment accumulation
- (usually stuck in Mphage)
- Anthracosis
- Tattoo
- Lipofuscin
- Melanin
- Homogentisic acid
- Hemosiderosis
- Hemochromatosis
- Bilirubin
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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
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Metastatis calcification
- Deposition of calcium salts in normal tissue in the setting of hypercalcemia
- Ex: hyperparathyroidism, bone destruction, vit D disorders, chronic renal failure
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