1. Steatosis, or fatty liver, is common and usually benign but can progress to steatohepatitis if associated with conditions like obesity, diabetes, or alcohol use. 2. Alcohol is a leading cause of steatohepatitis and the most common type of liver disease in Western nations, due to the toxic byproducts produced when the liver metabolizes alcohol. 3. The pathology of alcohol-related liver disease ranges from reversible fatty liver to fibrosis, cirrhosis, and even liver cancer. Management involves cessation of alcohol and treatment of complications.

1. steatosis & steatohepatitis By Dr. Osman Bukhari

2. -Mild steatosis involving less than 10% of hepatocytes is common -Dtected icidentally & clinical manifestations are variable Causes: 1-Macrovesicular steatosis & st /hep\atitis: (Alcohol , obesity, D.M. , starvation , malabsorption , drugs.)

3. 2-Microvesicular steatosis: (fatty liver of pergnancy , Reyes syndr. ,drugs.) *Macrovesic.st. is generally bengin. *Microvesic. St. occurs in more serious conditions. *Steatosis usually occurs alone , in some pats. Macrovesic. St. is associated with hepatitis (steatohepatitis).

4. *Steatohepatitis is either alcoholic or non alcoholic (NASH). Clinic. Features &management: 1-Macrovesic. St: -Often asymtomatic & found incidentally. -Clinical features of the cause. -Tender hepatopmegally.

5. - Mild changes in LFT. -US :Bright liver. -Treatment is that of the cause. -Ursodeoxycholic acid improves liver LFT and histology in NASH .

6. 2- Microvesic. St.: -Associated with acute onset of fatigue & vomitting & progressing if severe to encephalopathy &coma. -Jaundice with fatty liver of pregnancy , alcohols .& drug induced steatosis. jaundice is absent in Reyes; -Acute hepatic failure : ICU.support & liver transplant. Prognosis: Excellent in most cases.

7. Alcohol Liver Disease -Alcohol is the most common preventable disease in the west. -Alcohol is exclusively metabolized in the liver. -Alcohol is metabolised to acetaldehyde by alcohol dehydrogenase (mitochondrial enzyme) & mixed function oxidase enzyme

8. ( smooth endoplasmic reticulin ) & then to acetate by acetaldehyde dehydrogenase which enters Krebs cycle with production of toxic metabolites (adducts) -Acohol is a powerful inducer of mixed function oxidases. Pathogenesis: -Depends on the amount & duration of consumption. Amount is less in females.

9. - Steady daily intake is more hazardadous. -Only 10-20% develop alcohol liver (?genetic) -fatty changes are due to increased production & impaired excretion of triacyl glycerolby the liver. -centrilobular necrosis & cirrhosis are attributed to toxic metabolites produced during alcohol metab. (adducts) & immune reaction.

10. Pathology : 1- Mitochondrial swelling & proliferation of endoplasmic reticulum. 2-Steatosis (reversible) 3-Mallroy hyaline bodies. 4-Siderosis

11. 5-Autoimmune hepatitis. 6-Central hyaline necrosis 7-Fbirosis & cirrhosis. 8-HCC. Clinical features: 1-Fatty liver : asymtomatic or non specific symptoms & hepatopmegally. 2-Hepatitis: severe illness with malnutrition ; jaundice, hepatopmegally , ascitis & encephalopathy.

12. 3-Cholestasis: abdomenal pain , jaundice & hepatopmegally. 4-Cirrrohsis. 5-HCC. Investigation: aimed at: 1-Establishing alcohol abuse. 2-Exclding other causes of liver disease. 3-Assessing severity of liver disease.

13. *Biological evidence of alcohol abuse include: 1-Peripheral macrocytosis in the absence of anaemia. 2-Increased plasma GTT. 3-Unexplained rib fracture. *LFT& investigations to exclude other causes liver disease including liver biopsy. *Imaging.

14. Management & Prognosis: 1- Stop alcohol intake (delirium tremens.) 2-Protien rich diet & Vit supplements. 3- Treat complication of liver cirrhosis. 4-Liver transplantation in advanced disease with hepatic failure. 5- Prognosis is good with fatty liver (reversible) & worst with hepatitis. 6-Cirrohsis may present with complication 7-HCC may complicate.