Coupon Accepted Successfully!



Fulminant Hepatitis

  1. Chronic autoimmune hepatitis:
  1. Female predisposition
  2. Elevated IgG levels
  3. Absence of serologic markers
  4. High titres of anti-nuclear; antismooth muscle and antimitochondrial antibodies; positive LE test
  5. Plasma cell infiltrate in periportal inflammation
  1. Chronic active hepatitis:
  1. Piecemeal necrosis
  2. Bridging necrosis (Hallmark)
  3. Portal inflammatory infiltrate spilling out of portal tracts
  4. Progressive fibrosis leading to cirrhosis
  5. Rosette formation and regenerative pseudotubules

A. Progression from onset to hepatic encephalopathy / death

B. Within 2-3 weeks- fulminant hepatitis

C. Within 3 months - subfulminant failure

  1. CausesQ
    1. Viral infections: HAV, HBV, HCV, HDV, HEV
    2. Drugs and chemicals: Acetaminophen" INH, a- methyl DOPA, Amanita phalloides Q
    3. Ischemic hepatitic necrosis
    4. Obstruction of hepatic vein
    5. Massive malignant infiltration of liver
    6. Wilson' disease, stroke, fatty liver pregnancy
  2. Morphology:
    1. Liver Shrunk - 500-700 gm's red, limp organ covered by wrinkled capsule.
    2. Necrotic areas: Muddy red, mushy appearance Q
    3. Collapsed Reticulum
    4. Prognosis: 25-90% mortality in absence of liver transplant
Autoimmune Hepatitis
Histologically similar to chronic hepatitis
  1. Features
    1. Female predominance (78%)
    2. Absence of viral serologic markers
    3. Elevated serum IgG and gamma globulin levels (>1.5 times)
    4. High serum titre of auto antibodies (in 80% of cases) antinuclear, anti smooth muscles, and/or anti liver/kidney   microsomes antibodies(anti LKMI)
    5. Negative antimitochondrial antibodies
    6. Untreated severe disease leads to death in 40% patients and cirrhosis develops in atleast 40% of survivors.
    7. Rx - Immuno suppressive therapy,
    8. Frequency of HLAB8 HLA DR W3
    9. Other Auto immune disease present 60% patients like R.A, thyroiditis, Sjögren’s, UC
      2 subgroups:
      1. Type I - Most common has ANA and / or SMA serum marker
      2. Type II - Younger patients, anti liver/kidney micro some antibodies. 
  2. Drug Injury
    1. Direct injury
    2. Conversion of xenobiotic to an active toxin
    3. Through immune mechanism
  3. Drug reactions
    1. → Predictable / Intrinsic
    → e.g., tetracycline, Acetaminophen, anti neoplastic agents, CCI4
    Amanita phalloides­
    2. → Unpredictable /Idiosyncratic
    e.g., Chlorpromazine, sulfonamides, methyldopa, allopurinol Q
Neonatal Hepatitis/ Cholestasis
  1. 1 in 2500 births
  2. Clinical data and Liver biopsy are crucial in D/D of neonatal hepatitis and biliary atresia Neonatal hepatitis - Prolonged, conjugated hyper bilirubinemia Q
  3. H/P
    1. Lobular disarray with focal liver necrosis
    2. Panlobular giant cell formation of hepatocytes
    3. Hepatocellular & canalicular cholestasis
    4. Mononuclear infiltration (periportal) with Kupffer cell hyperplasia)
    5. Extramedullary hematopiesis
  4. Neonatal cholestasis
    - Causes Q
    1. Extrahepatic biliary Atresia (20%)
    2. Idiopathic Neonatal hepatitis (50%)
    3. Neonatal infectious CMV, Bacterial, Sepsis, UTI etc.
    4. Toxic - Drugs
    5. Metabolic diseases ­
      1. a1AT Deficiency (15%)                                              
      2. Tyrosinemia
      3. Niemann - Pick disease                                                
      4. Galactosemia                                
      5. Cystic fibrosis
  5. Miscellaneous
Reye's syndrome:
  1. Characterized by fatty vacuolization in liver and renal tubules along with neural degeneration and encephalopathy.
  2. Microvesicular fatty liver and mitochondrial injury.
  3. Age group affected < 15 year. Caused by influenza virus type B, aspirin toxicity; aflatoxin and varicella virus.
  4. Elevated serum levels of ammonia and aminotransferases but jaundice is absent.
  5. There is cerebral edema also and hypoglycemia.
  6. Patient may present with vomiting and metabolic acidosis.
  7. Prothrombin time is raised.
  8. Stain used for its diagnosis 'oil red O'
  9. It is suspected as in born error of coenzyme A dehydrogenase.
  1. Three characteristics ­-
  1. Bridging fibrous septae
  2. Parenchymal Nodules
  • < 3mm - Micronodular
  • 3 mm - Macronodular
  1. Disruption of architecture => Abnormal vascular interconnection
  2. Diffuse
  3. Irreversible
Regression in fibrosis is seen inQ
  1. Schistosomiasis                                            
  2. Hemochromatosis (rare case)
Causes -
  1. Alcoholic liver disease-60-70%                
  2. Viral Hepatitis 10%
  3. Biliary Cirrhosis 5-10%                                               
  4. Primary Hemochromatosis 5%
  5. Wilson Disease Rare                                   
  6. α1 AT def (Rare)
  7. Cryptogenic cirrhosis 10-15%                  
  8. Drug Induced α methyl dopa
  1. Type I & III (interstitial collagen – Portal Tract and around CVs (Central vein)
Type IV- in space of Disse (along side hepatocytes)
Cirrhosis - Type I and III and collagen in lobules
- Loss of (n) fenestrations in sinusoidal endothelial cells due to deposition of collagen in the space of Disse
  1. Source of collagen:
Perisinusoidal hepatic stellate cells/Ito cells
Transformed into 'myofibroblast like cells
  1. Cause of death:
    1. Progressive Liver failure                            
    2. Portal hypertension                  
    3. ​Hepato cellular carcinoma

Test Your Skills Now!
Take a Quiz now
Reviewer Name