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how is Carbon Tetrachloride toxicity manifested?
in hepatocytes as the detachment of ribosomes from ER, fatty changes, necrosis
What is the purpose of the MFOS?
to make chemicals water soluble for excretion via the liver or kidenys, but may convert chemicals to a toxin
describe the pathogenesis of ischemic and hypoxic injury?
decreased O2 reducse oxidative phosphorylation and ATP production, so increased AMP stimulates phosphorylase and phosphofructokinase which increases anaerobic glygolysis (glycogen is depleted, lactic acid accumulates which drops pH, and clumping of nuclear chromatin is observed), ATP depletion reduces Na+ pump accounting for acute cellular swelling and dilation of ER (intracellular accumulation of Na+ and isosmotic gain of H20), detachment of ribosomes from RER and dissociation of polysomes into monosomes, and mitochondrial swelling, lesions are indicative of irreversible injury (amorphous densities in mitochondrial matrices, massive swelling of mitochondria, nuclear pyknosis, karyolysis or karyorrhexis, lysosomal rupture that occurs later)
what are observable characteristics of ischemic and hypoxic injury?
clumping of nuclear chromatin, cellular swelling and dilation of the ER, detachment of ribosomes from RER, dissociation of polysomes into monosomes, mitochondrial swelling and (when irreversible) amorphous densities in mitochondrail matrices, massive swelling of mitochondria, nuclear pkynosis, karyolysis, karyorrhexis, lysosoma rupture (occurs later)
What do the observable signs of clumping of nuclear chromatin, cellular swelling and dilation of the ER, detachment of ribosomes from RER, dissociation of polysomes into monosomes, mitochondrial swelling and (when irreversible) amorphous densities in mitochondrail matrices, massive swelling of mitochondria, nuclear pkynosis, karyolysis, karyorrhexis, lysosoma rupture (occurs later) indicate as a pathogenesis of cellular injury?
ischemic and hypoxic injury
what are the clinicopathological correlates of cell injury?
leakage of cystolic enzymes from cells into blood, which has specific mechanisms that influence timing and has a diagnostic application
what are the mechanisms of irreversible cell injur in ischemic and hypoxic injur?
inability to reverse mitochondrial dysfunction on erperfusion or reoxygenations (possibly due to excessive Ca++ influx), cell membrane damage with progress loss of phospholipids (activation of phospholipases by Ca++, decreased synthesis of phospholipids), reactive oxygen species, lipid breakdown products and loss of intracellular glycine and L-alanine
what is the morphology of cell swelling?
histologically appears as swollen cytoplasm, decreased staining density, clear cytoplasmic vacuoles
define necrosis in detail?
morphological changes following cell death in living tissue, largely resulting from degradative actio nof enzymes on lethally injured cells
what is the difference between cell death and necrosis?
necrosis results after cell death when tissues are not preserved
what is the difference between cell autolysis and necrosis?
autolysis is a series of morphological processes that occurs following cell death and is similar to necrosis, except the body's responses to necrosis (inflammation) doesn't occur
what are the morphological manifestations of necrosis determined by?
tissue, pathological process, etiologic agent, timer interval between cell death and tissue sampling
what are the types of morphological manifestations of necrosis?
coagulation necrosis, caseous necrosis, liquefaction necrosis
define coagulation necrosis?
gross and microscopic architecture of the necrotic tissue are still recognizable
define caseous necrosis?
a form of necrosis characterized by loss of recognizable tissue architecture and cellular detail
define liquefaction necrosis?
a form of necrosis in which dead tissue is converted to a liquefied mass
describe the morphology of coagulation necrosis?
gross consists of pale area (possibly red bordered) of dead tissue with decreased tensile strength and histological consists of a sharp zone of demarcation, cytoplasmic changes and nuclear changes
nuclear shrinkage, increased basophilia, DNA condenses into solid, darkly staining mass
structure of nucleus degenerates and becomes irregularly shaped and fragmented
basophilia of chromatin may fade due to DNAse activity, resulting in tiny fragments of debris in center of degenerating cell
nuclear shrinkage, increased basophilia, DNA condenses into solid, darkly staining mass is what pattern of nuclear change?
structure of nucleus degenerates and becomes irregularly shaped and fragmented is what pattern of nuclear change?
basophilia of chromatin may fade due to DNAse activity, resulting in tiny fragments of debris in center of degenerating cell is what pattern of nuclear change?
what is an infarction?
an infarct is a local area of coagulation necrosis due to ischemia, thrombosis of vessels is the most common cause
what are causes of Zenker's necrosis?
vitamin E & selenium deficiency, bacterial toxins (clostridium) and plant toxin (cassia)
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