Steatosis & Steatohepatitis

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Steatosis & Steatohepatitis

  1. 1. steatosis & steatohepatitis By Dr. Osman Bukhari
  2. 2. <ul><li>-Mild steatosis involving less than 10% of hepatocytes is common </li></ul><ul><li>-Dtected icidentally & clinical manifestations are variable </li></ul><ul><li>Causes: </li></ul><ul><li>1-Macrovesicular steatosis & st /hepatitis: </li></ul><ul><li>(Alcohol , obesity, D.M. , starvation , </li></ul><ul><li>malabsorption , drugs.) </li></ul>
  3. 3. <ul><li>2-Microvesicular steatosis: (fatty liver of </li></ul><ul><li>pergnancy , Reyes syndr. ,drugs.) </li></ul><ul><li>*Macrovesic.st. is generally bengin. </li></ul><ul><li>*Microvesic. St. occurs in more serious </li></ul><ul><li>conditions. </li></ul><ul><li>*Steatosis usually occurs alone , in some </li></ul><ul><li>pats. Macrovesic. St. is associated with </li></ul><ul><li>hepatitis (steatohepatitis). </li></ul>
  4. 4. <ul><li>*Steatohepatitis is either alcoholic or </li></ul><ul><li>non alcoholic (NASH). </li></ul><ul><li>Clinic. Features &management: </li></ul><ul><li>1-Macrovesic. St: </li></ul><ul><li>-Often asymtomatic & found incidentally. </li></ul><ul><li>-Clinical features of the cause. </li></ul><ul><li>-Tender hepatopmegally. </li></ul>
  5. 5. <ul><li>- Mild changes in LFT. </li></ul><ul><li>-US :Bright liver. </li></ul><ul><li>-Treatment is that of the cause. </li></ul><ul><li>-Ursodeoxycholic acid improves liver LFT </li></ul><ul><li>and histology in NASH . </li></ul>
  6. 6. <ul><li>2- Microvesic. St.: </li></ul><ul><li>-Associated with acute onset of fatigue & </li></ul><ul><li>vomitting & progressing if severe to </li></ul><ul><li>encephalopathy &coma. </li></ul><ul><li>-Jaundice with fatty liver of pregnancy , </li></ul><ul><li>alcohols .& drug induced steatosis. </li></ul><ul><li>jaundice is absent in Reyes; </li></ul><ul><li>-Acute hepatic failure : ICU.support & </li></ul><ul><li>liver transplant. </li></ul><ul><li>Prognosis: Excellent in most cases. </li></ul>
  7. 7. <ul><li>Alcohol Liver Disease </li></ul><ul><li>-Alcohol is the most common preventable disease in the west. </li></ul><ul><li>-Alcohol is exclusively metabolized in </li></ul><ul><li>the liver. </li></ul><ul><li>-Alcohol is metabolised to acetaldehyde </li></ul><ul><li>by alcohol dehydrogenase (mitochondrial </li></ul><ul><li>enzyme) & mixed function oxidase enzyme </li></ul>
  8. 8. <ul><li>( smooth endoplasmic reticulin ) & then to </li></ul><ul><li>acetate by acetaldehyde dehydrogenase which </li></ul><ul><li>enters Krebs cycle with production of toxic </li></ul><ul><li>metabolites (adducts) </li></ul><ul><li>-Acohol is a powerful inducer of mixed </li></ul><ul><li>function oxidases. </li></ul><ul><li>Pathogenesis: </li></ul><ul><li>-Depends on the amount & duration of </li></ul><ul><li>consumption. Amount is less in females. </li></ul>
  9. 9. <ul><li>- Steady daily intake is more hazardadous. </li></ul><ul><li>-Only 10-20% develop alcohol liver (?genetic) </li></ul><ul><li>-fatty changes are due to increased production </li></ul><ul><li>& impaired excretion of triacyl glycerolby </li></ul><ul><li>the liver. </li></ul><ul><li>-centrilobular necrosis & cirrhosis are attributed to toxic metabolites produced </li></ul><ul><li>during alcohol metab. (adducts) & immune </li></ul><ul><li>reaction. </li></ul>
  10. 10. <ul><li>Pathology : </li></ul><ul><li>1- Mitochondrial swelling & proliferation of </li></ul><ul><li>endoplasmic reticulum. </li></ul><ul><li>2-Steatosis (reversible) </li></ul><ul><li>3-Mallroy hyaline bodies. </li></ul><ul><li>4-Siderosis </li></ul>
  11. 11. <ul><li>5-Autoimmune hepatitis. </li></ul><ul><li>6-Central hyaline necrosis </li></ul><ul><li>7-Fbirosis & cirrhosis. </li></ul><ul><li>8-HCC. </li></ul><ul><li>Clinical features: </li></ul><ul><li>1-Fatty liver : asymtomatic or non specific </li></ul><ul><li>symptoms & hepatopmegally. </li></ul><ul><li>2-Hepatitis: severe illness with malnutrition ; </li></ul><ul><li>jaundice, hepatopmegally , ascitis & encephalopathy. </li></ul>
  12. 12. <ul><li>3-Cholestasis: abdomenal pain , jaundice & </li></ul><ul><li>hepatopmegally. </li></ul><ul><li>4-Cirrrohsis. </li></ul><ul><li>5-HCC. </li></ul><ul><li>Investigation: aimed at: </li></ul><ul><li>1-Establishing alcohol abuse. </li></ul><ul><li>2-Exclding other causes of liver disease. </li></ul><ul><li>3-Assessing severity of liver disease. </li></ul>
  13. 13. <ul><li>*Biological evidence of alcohol abuse include: </li></ul><ul><li>1-Peripheral macrocytosis in the absence of </li></ul><ul><li>anaemia. </li></ul><ul><li>2-Increased plasma GTT. </li></ul><ul><li>3-Unexplained rib fracture. </li></ul><ul><li>*LFT& investigations to exclude other causes </li></ul><ul><li>liver disease including liver biopsy. </li></ul><ul><li>*Imaging. </li></ul>
  14. 14. <ul><li>Management & Prognosis: </li></ul><ul><li>1- Stop alcohol intake (delirium tremens.) </li></ul><ul><li>2-Protien rich diet & Vit supplements. </li></ul><ul><li>3- Treat complication of liver cirrhosis. </li></ul><ul><li>4-Liver transplantation in advanced disease </li></ul><ul><li>with hepatic failure. </li></ul><ul><li>5- Prognosis is good with fatty liver (reversible) & worst with hepatitis. </li></ul><ul><li>6-Cirrohsis may present with complication </li></ul><ul><li>7-HCC may complicate. </li></ul>

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