S3M1 path

Chemical, O2 deprivation, Infectious agent, Genetic, Aging, Physical agent, Nutritional Imbalance, Immunological

"Causes Of Injury Give A Physician Necessay Information"

• - increase in cell size (not number)
• - mechanical stress==> physiological hypertrophy
• - GF's and agonist==> pathological hypertrophy

• - cardiac myocytes, skeletal muscle and nerves
• - permanent tissue cannot make new cells

1- cellular swelling= blebbing, mtch swelling, ER dilation, nuclear alterations. hydropic change.

2- fatty change= lipid vacuoles in the cytoplasm (hepatocytes and myocardial cells)

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)

• - 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)

- 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

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

apoptotic cells showing peripheral chromatin condensation, the most characteristic feature of apoptosis

• - 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

• - Cell shrinkage
• - PM stays intact, phosphotidylserine flips to outer leaflet
• - no inflammation
• - caspase mediated
• - DNA ladder pattern (multiples of oligonucleosomes)

• 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)

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

cholesterolosis of the gallbladded

• - 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)