S3M1 path

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sweetlu
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S3M1 path
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2012-06-08 18:48:19
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S3M1 path
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  1. 8 causes of cellular injury
    Chemical, O2 deprivation, Infectious agent, Genetic, Aging, Physical agent, Nutritional Imbalance, Immunological

    "Causes Of Injury Give A Physician Necessay Information"
  2. hypertrophy
    • - increase in cell size (not number)
    • - mechanical stress==> physiological hypertrophy
    • - GF's and agonist==> pathological hypertrophy
  3. These tissues can NOT undergo hyperplasia and why
    • - cardiac myocytes, skeletal muscle and nerves
    • - permanent tissue cannot make new cells
  4. LM manifestations on REVERSIBLE cell injury
    1- cellular swelling= blebbing, mtch swelling, ER dilation, nuclear alterations. hydropic change.

    2- fatty change= lipid vacuoles in the cytoplasm (hepatocytes and myocardial cells)
  5. reversible ischemia showing surface blebs, increased eosinophilia of cytoplasm and swelling
    • - reversible fatty liver (often seen with EtOH use)
    • - hypoxic, toxic or metabolic injury
    • - lipid vacuoles (Sudan IV or Oil-Red-O stain confirms vacuoles are fat and not water)
  6. Necrotic cell morphological alterations
    • - eosinophilia and glassy appearance
    • - vacuolated cytoplasm
    • - myelin figures
    • - protein denaturation by lysosomes
    • - loose membrane integrity
    • - inflammation
    • myocardial necrosis caused by myocardial ischemia
    • - cardiac specific ez (TrI, CK-MB, etc) in blood as early as 2 hours post
    • - necrosis 4-12 hours later
    • - n0 infiltration within 12-24 hours
    • - brisk interstitial infiltrate of n0 (not infection)
  7. nuclear changes in necrosis
    - karyolysis- chromatin basophila fades, loss of DNA

    - pyknosis- nuclear shrinkage, chromatin condensation, increased basophila (also seen in apoptosis)

    -karyorrhexis- fragmentation of pyknotic nucleus
    • Coagulative necrosis (I=infarct, N=normal)
    • - architecture preserved
    • - anuleate cells
    • - Leukocyte lysosomal digestion of dead tissue
    • - caused by ischemic infarct in all organs but the brain
    • - localized area is called an infarct
    • Liquefactive necrosis
    • - results from hypoxic death within the CNS
    • - digestion of dead cells by n0
    • - transformation of tissue into a liquid viscous mass
    • - seen in focal bacterial or, occasional, fungal infections
    • - necrotic material is frequently creamy yellow (pus)
    • Gangrenous necrosis (coag+liq)
    • - not a specific pattern of cell death (resemble mummified tissue)
    • - often seen in diabetics
    • - ischemia with superimposed bacterial infection
    • - coag nec + liq nec = wet gangrene
  8. liquefactive necrosis of the brain
    • - caseous (cheese-like) necrosis of the lung
    • - seen often in foci of TB infection
    • Caseous (cheese-like) necrosis
    • - seen most often in TB
    • - fragmented and lysed cells & amorphous granular debris
    • - enclosed within a distinctive inflammatory border
    • - granuloma- a focus of inflammation
    • Fat necrosis (pancreatitis)
    • - white spots are calcification of adipose tissue
    • - not a specific pattern of necrosis
    • - focal areas of fat destruction
    • - results from release of activated pancreatic lipases
    • - FA + Ca= fat saponification (chalky-white areas)
    • - seen in pancrease and peitoneal cavity
    • -shawdowy outlines of necrotic fat cells with basophilic Ca deposits
    • fat necrosis of pancreas
    • - production of soaps by enzymatic reaction on adipose tissue appear as soft, chalky white areas
    • -fat necrosis
    • - remaining steatocytes on left are not necrotic
    • - necrotic fat cells on the right have vague cellular outline, lost their peripheral nuclei and cytoplasm has become pink and amorphous
    • Traumatic fat necrosis of breast showing microcalcifications
    • - dystophic calcifications is a marker of cell death
    • - microcalcifications are easliy confused with cancer
    • Fibrinoid necrosis
    • - seen in IR involving blood vessels
    • - immune complex deposition in walls of arteries
    • - fibrin leaks out of cells and combines with IC deposition
    • - bright pink and amorphous appearance in H&E stain
    • - **n0 infiltration can also be seen**
    • - apoptotic epidermal cell in an immune reaction
    • - cell becomes very pink and highly eosinophilic
    • - cell shrinks and chromatin condenses
    • - blebs and apoptotic bodies form
    • - CELL MEMBRANE STAYS INTACT
  9. apoptotic cells showing peripheral chromatin condensation, the most characteristic feature of apoptosis
  10. caspases
    • - presence of cleaved, active caspases is a marker of apoptosis
    • - initiatiors: caspase-8(death-r) and -9(mtch)
    • - executioners: caspase-3 and -6 ==> trigger degradation
  11. idicators of apoptosis
    • - Cell shrinkage
    • - PM stays intact, phosphotidylserine flips to outer leaflet
    • - no inflammation
    • - caspase mediated
    • - DNA ladder pattern (multiples of oligonucleosomes)
  12. Intracellular lipid accumulations
    • EtOH= inc synthesis and dec breakdown of lipids
    • CCl4 & protein malnutrition= dec syn of apoproteins
    • Hypoxia= inhibit FA oxidation
    • Starvation= inc FA mobilization from peripheral stores
    • IC lipid accumulation
    • - Sudan IV or Oil Red-O Stain is used to differentiate from indistinct vacuoles which could be H2O or polysaccharides
    • - polysaccharide(glycogen) stain is PAS + diatase
    • - liver steatosis
    • - lobules are indistinct though and would require staining with Oil Red-O or Sudan IV to prove accumulations are fat (would stain red)
  13. high power detail of fatty change in liver
    • Xanthoma
    • - seen in hyperlipidemic states
    • - clusters of foamy cells are found in the subepithelial connective tissue
    • Cholesterolosis of lamina propria of the gallbladder
    • focal accumulations of cholesterol-laden m0
  14. cholesterolosis of the gallbladded
  15. Amyloid accumulation
    • - abnormal protein where it does not belong
    • - amorphous, fibillar, crystalinne in appearance on EM
    • - Congo Red stain will stain proteins pink
    • Intracellular protein accumulation in the kidney
    • - seen in renal disease associated with proteinuria
    • - appear as pink hyaline droplets within cytoplasm
    • - reversible if proteinuria diminished
    • Accumulation of normal proteins in excessive amounts
    • - russel bodies= distended ER (homogenous eosinophilic inclusions)
    • - plasma cells secreting Ig
    • Alpha-1-antitrypsin deficiency (emphysema)
    • - A-1-A is a protease inhibitor
    • - slow and partially folded proteins accumulate in the ER of the liver causing liver damage as well as leaving lungs suceptible to n0(elastase) induced damage
    • Accumulation of neurofilaments
    • - neurofibrillary tangle in brain of AD patient
    • - tangle contains neurofilament and other proteins
    • Alcoholic liver disease
    • - alcoholic accumulations of keratin
    • - alcoholic hyaline (eosinophilic cytoplasmic inclusions in hepatocytes)

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