1. The Liver

2.  Carbohydrate storage and metabolism.  Storage of vitamin A and D.  Biosynthesis of glycogen, albumin, globulin, steroids, blood-clotting factors and angiotensinogen.  Biotransformation and excretion of xenobiotics.  Fat metabolism.  Metabolism of hormones.

3.  Synthesis of bile acids/salts that aid in digestion of fats.  Formation of urea from amino acids.  Transport & storage of lipids, metals such as iron, copper, Zinc, and cadmium.  Phagocytosis of micro-organism and other foreign bodies.  Degradation of hemoglobin (bilirubin) and root of elimination for bile pigments & hemoglobin metabolites.

6. 1. portal triad 2. lobule 3. central vein 4. bile canaliculi 5.common bile duct 6. hepatic portal vein 7. hepatic artery 8. hepatocyte plate (with hepatocytes) 9.sinusoids

8.  Periportal: High respiratory enzyme activity & glutathione contents. Take up more bile acid & secrete more bile constituents. Detoxification of ammonia to urea.  Midzonal region: High regenerative activity  Centrilobular: High concentration of P450 enzyme & low concentration of glutathione. MID ZONAL Periportal Centrilobular

9.  Biotransformation  Detoxification  Bioactivation

10.  Ethanol  Vinyl chloride  Acetaminophen  Arsenic  Carbon tetrachloride

11.  Kupffer cell  Lipocytes (Ito cell)  Endothelial cell  Pit cell  Oval cell or stem cells Hepatocytes are characterized by their abundant Endoplasmic reticulum, mitochondria and secretory organelles. Hepatic Sinusoid Source of liver regeneration NK

14. Xylene Steatosis, fibrosis, necrosis. Toluene Styrene AcrylonitrileNecrosis. Carbon disulfide Necrosis. IsopropanolNecrosis. Dimethylformamide Necrosis, steatosis. Trichloroethane Liver tumors, biliary tract tumour. Methylene chloride Liver tumors, biliary tract tumour. White spirit Steatosis, fibrosis, necrosis.

16.  Necrosis  Steatosis (lipidosis or fatty liver)  Cholestasis  Cirrhosis (fibrosis)  Vascular injury  Neoplasm

17.  Hepatocytes death can be focal, zonal (Centrilobular, midzonal,periportal) or massive (Panlobular).  Cell life span is about 6 months.  Hepatocytes die by either necrosis or apoptosis.  ALT (Aalanine aminotrasferase)  AST (Aspartate aminotrasferase)  Irreversible cell injury leads to cellular death.

21.  It is characterized by increase in hepatic lipid content to greater than 5% of liver weight.  Liver enlarges due to accumulation of lipid and triglycerides.  The lipid appear as vacuoles in hepatic cytoplasm, often displacing the nucleus of the cell.  Factors (obesity, alcoholisms, protein deficient diet).

22. Carbon tetrachloride (lipidosis) Interfering with fatty acid oxidation. Inhibition of Mitochondrial function Lipoprotein synthesis

23.  Accumulation with in the bile canliculi of bile pigments and other products that restrict the normal flow of bile.  Liver retains bile salts and bilirubin which can lead to jaundice.  Cholestasis that is toxicant induced can be reversible or chronic.  Canalicular cholestasis include the presence of bile within the hepatocytes and canalicular spaces.

26.  Bile salts are strong surfactants, their accumulation with in hepatocytes can produce cell membrane injury.  Toxicants that can produce canalicular cholestasis:  Anabolic steroids, cyclosporin, phallodin, 1,1dichloroethylene, chlorpromazine, organic arsenicals, erythromycin, oral contraceptive