Steatosis & Steatohepatitis
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Steatosis & Steatohepatitis

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    Steatosis & Steatohepatitis Steatosis & Steatohepatitis Presentation Transcript

    • steatosis & steatohepatitis By Dr. Osman Bukhari
      • -Mild steatosis involving less than 10% of hepatocytes is common
      • -Dtected icidentally & clinical manifestations are variable
      • Causes:
      • 1-Macrovesicular steatosis & st /hepatitis:
      • (Alcohol , obesity, D.M. , starvation ,
      • malabsorption , drugs.)
      • 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).
      • *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.
      • - Mild changes in LFT.
      • -US :Bright liver.
      • -Treatment is that of the cause.
      • -Ursodeoxycholic acid improves liver LFT
      • and histology in NASH .
      • 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.
      • 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
      • ( 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.
      • - 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.
      • Pathology :
      • 1- Mitochondrial swelling & proliferation of
      • endoplasmic reticulum.
      • 2-Steatosis (reversible)
      • 3-Mallroy hyaline bodies.
      • 4-Siderosis
      • 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.
      • 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.
      • *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.
      • 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.
    •