Study Set Content:
Human and animal data inadequate
Agent is not classifiable as to carcinogenicity to humans
Human and animal data negative
Agent is probably not carcinogenic to humans
Amiodarone, CCl4, ethanol, fialuridine, tamoxifen, valproic acid
Fatty liver
Acetaminophen, allyl alcohol, Cu, dimethylformamide, ethanol
Hepatocyte death
Diclofenac, ethanol, halothane, tienilic acid
Immune-mediated response
Chlorpromazine, cyclosporin A, 1,1- dichloroethylene, estrogens, Mn, phalloidin
Canalicular cholestasis
Alpha-naphthylisothiocyanate, amoxicillin, methylene dianiline, sporidesmin
Bile duct damage
Anabolic steroids, cyclophosphamide, microcystin, pyrrolizidine alkaloids
Sinusoidal disorders
CCl4, ethanol, thioacetamide, vitamin A, vinyl chloride
Fibrosis and cirrhosis
Aflatoxin, androgens, arsenic, thorium dioxide, vinyl chloride
Tumors
CELL DEATH • Based on morphology, liver cells can die by two different modes,
necrosis or apoptosis
• It is characterized by cell swelling, leakage, nuclear disintegration (karyolysis), and an influx of inflammatory cells.
Necrosis
characterized by cell shrinkage, nuclear fragmentation, formation of apoptotic bodies, and a lack of inflammation
Apoptosis
Hepatocyte death can occur in a
focal, zonal, or panacinar (widespread) pattern
is characterized by the randomly distributed death of single hepatocytes or small clusters of hepatocytes.
Focal cell death
is death to hepatocytes in certain functional regions.
Zonal necrosis
is massive death of hepatocytes with only a few or no remaining survivors.
Panacinar necrosis
MECHANISMS OF TOXICANT-INDUCED INJURY TO LIVER CELLS
It includes include
lipid peroxidation, binding to cell macromolecules, mitochondrial damage, disruption of the cytoskeleton, and massive calcium influx.
haracterized by the elevated serum levels of bile salts and bilirubin • defined physiologically as a decrease in the volume of bile formed or an impaired secretion of specific solutes into bile.
CANALICULAR CHOLESTASIS
when biliary excretion of the yellowish bilirubin pigment is impaired, this pigment accumulates in the skin and eyes, producing(), and spills into urine, which becomes bright yellow or dark brow
jaundice
