steatosis & steatohepatitis
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steatosis & steatosis & steatohepatitissteatohepatitis
By Dr. Osman BukhariBy Dr. Osman Bukhari
-Mild steatosis involving less than 10% of -Mild steatosis involving less than 10% of hepatocytes is common hepatocytes is common
-Dtected icidentally & clinical manifestations -Dtected icidentally & clinical manifestations are variableare variable
Causes:Causes:
1-Macrovesicular steatosis & st /hep\atitis:1-Macrovesicular steatosis & st /hep\atitis: (Alcohol , obesity, D.M. , starvation ,(Alcohol , obesity, D.M. , starvation , malabsorption , drugs.)malabsorption , drugs.)
2-Microvesicular steatosis:2-Microvesicular steatosis: (fatty liver of (fatty liver of
pergnancy , Reyes syndr. ,drugs.)pergnancy , Reyes syndr. ,drugs.)
*Macrovesic.st. is generally bengin.*Macrovesic.st. is generally bengin.
*Microvesic. St. occurs in more serious*Microvesic. St. occurs in more serious
conditions.conditions.
*Steatosis usually occurs alone , in some*Steatosis usually occurs alone , in some
pats. Macrovesic. St. is associated with pats. Macrovesic. St. is associated with
hepatitis (steatohepatitis).hepatitis (steatohepatitis).
*Steatohepatitis is either alcoholic or *Steatohepatitis is either alcoholic or non alcoholic (NASH).non alcoholic (NASH).
Clinic. Features &management:Clinic. Features &management: 1-Macrovesic. St:1-Macrovesic. St: -Often asymtomatic & found incidentally.-Often asymtomatic & found incidentally. -Clinical features of the cause.-Clinical features of the cause. -Tender hepatopmegally.-Tender hepatopmegally.
--Mild changes in LFT.Mild changes in LFT. -US :Bright liver.-US :Bright liver. -Treatment is that of the cause.-Treatment is that of the cause. -Ursodeoxycholic acid improves liver LFT-Ursodeoxycholic acid improves liver LFT and histology in NASHand histology in NASH..
2-2-Microvesic. St.:Microvesic. St.: -Associated with acute onset of fatigue &-Associated with acute onset of fatigue &vomitting & progressing if severe to vomitting & progressing if severe to encephalopathy &coma.encephalopathy &coma. -Jaundice with fatty liver of pregnancy , -Jaundice with fatty liver of pregnancy , alcohols .& drug induced steatosis. alcohols .& drug induced steatosis. jaundice is absent in Reyes;jaundice is absent in Reyes; -Acute hepatic failure : ICU.support &-Acute hepatic failure : ICU.support & liver transplant.liver transplant.
Prognosis: Prognosis: Excellent in most cases.Excellent in most cases.
Alcohol Liver DiseaseAlcohol Liver Disease -Alcohol is the most common preventable -Alcohol is the most common preventable
disease in the west. disease in the west. -Alcohol is exclusively metabolized in-Alcohol is exclusively metabolized in the liver.the liver. -Alcohol is metabolised to acetaldehyde-Alcohol is metabolised to acetaldehyde by alcohol dehydrogenase (mitochondrialby alcohol dehydrogenase (mitochondrial enzyme) & mixed function oxidase enzymeenzyme) & mixed function oxidase enzyme
((smooth endoplasmic reticulin ) & then tosmooth endoplasmic reticulin ) & then to
acetate by acetaldehyde dehydrogenase whichacetate by acetaldehyde dehydrogenase which
enters Krebs cycle with production of toxicenters Krebs cycle with production of toxic
metabolites (adducts)metabolites (adducts)
-Acohol is a powerful inducer of mixed-Acohol is a powerful inducer of mixed
function oxidases.function oxidases.
Pathogenesis:Pathogenesis: -Depends on the amount & duration of -Depends on the amount & duration of
consumption. Amount is less in females.consumption. Amount is less in females.
--Steady daily intake is more hazardadous.Steady daily intake is more hazardadous.
-Only 10-20% develop alcohol liver (?genetic)-Only 10-20% develop alcohol liver (?genetic)
-fatty changes are due to increased production-fatty changes are due to increased production
& impaired excretion of triacyl glycerolby & impaired excretion of triacyl glycerolby
the liver.the liver.
-centrilobular necrosis & cirrhosis are -centrilobular necrosis & cirrhosis are attributed to toxic metabolites produced attributed to toxic metabolites produced
during alcohol metab. (adducts) & immune during alcohol metab. (adducts) & immune
reaction.reaction.
PathologyPathology::
1-1-Mitochondrial swelling & proliferation ofMitochondrial swelling & proliferation of
endoplasmic reticulum.endoplasmic reticulum.
2-Steatosis (reversible)2-Steatosis (reversible)
3-Mallroy hyaline bodies.3-Mallroy hyaline bodies.
4-Siderosis4-Siderosis
5-Autoimmune hepatitis.5-Autoimmune hepatitis.
6-Central hyaline necrosis6-Central hyaline necrosis
7-Fbirosis & cirrhosis.7-Fbirosis & cirrhosis.
8-HCC.8-HCC.
Clinical features:Clinical features:
1-Fatty liver1-Fatty liver: : asymtomatic or non specific asymtomatic or non specific
symptoms & hepatopmegally.symptoms & hepatopmegally.
2-Hepatitis: severe illness with malnutrition ;2-Hepatitis: severe illness with malnutrition ;
jaundice, hepatopmegally , ascitis & encephalopathy.jaundice, hepatopmegally , ascitis & encephalopathy.
3-Cholestasis: abdomenal pain , jaundice &3-Cholestasis: abdomenal pain , jaundice & hepatopmegally. hepatopmegally. 4-Cirrrohsis.4-Cirrrohsis. 5-HCC.5-HCC.
Investigation:Investigation: aimed at: aimed at:
1-Establishing alcohol abuse.1-Establishing alcohol abuse. 2-Exclding other causes of liver disease.2-Exclding other causes of liver disease. 3-Assessing severity of liver disease.3-Assessing severity of liver disease.
*Biological evidence of alcohol abuse include:*Biological evidence of alcohol abuse include:
1-Peripheral macrocytosis in the absence of1-Peripheral macrocytosis in the absence of
anaemia.anaemia.
2-Increased plasma GTT.2-Increased plasma GTT.
3-Unexplained rib fracture.3-Unexplained rib fracture.
*LFT& investigations to exclude other causes*LFT& investigations to exclude other causes
liver disease including liver biopsy.liver disease including liver biopsy.
*Imaging.*Imaging.
Management & Prognosis:Management & Prognosis: 1- 1- Stop alcohol intake (delirium tremens.)Stop alcohol intake (delirium tremens.) 2-Protien rich diet & Vit supplements.2-Protien rich diet & Vit supplements. 3- Treat complication of liver cirrhosis.3- Treat complication of liver cirrhosis. 4-Liver transplantation in advanced disease4-Liver transplantation in advanced disease with hepatic failure.with hepatic failure. 5- Prognosis is good with fatty liver (reversible) & 5- Prognosis is good with fatty liver (reversible) &
worst with hepatitis.worst with hepatitis. 6-Cirrohsis may present with complication6-Cirrohsis may present with complication 7-HCC may complicate.7-HCC may complicate.