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Causes of Macronodular (nodule > 3mm) cirrhosis
  1. Cryptogenetic (Most common cause is non–alcoholic fatty liver disease) 
  2. Chronic viral Hepatitis (Post necrotic)
  3. Wilson disease
  4. Alpha-1 antitrypsin deficiency
  5. Drug induced
  6. Alcoholic Liver disease (late stage)
Causes of Micronodular (<3mm) cirrhosis
  1. Alcoholic Liver disease (early stage)
  2. Primary Biliary Cirrhosis
  3. Large bile duct obstruction
  4. Hemochromatosis
  5. Indian childhood cirrhosis
  6. Budd Chiari
  7. Cirrhosis following jejunoilleal bypass
Types of cirrhosis
Alcoholic Cirrhosis (Ref. Hari. 18th ed., Pg - 2589)
It is also known as Laënnec’s cirrhosis. It is characterized by diffuse fine scarring, uniform loss of liver cells and small regenerative nodules.

Clinical syndromes of alcoholic liver disease
  1. Fatty liver
    1. Asymptomatic abnormal liver biochemistry
    2. Large liver (Increase liver span)
  2. Alcoholic hepatitis
    1. Jaundice
    2. Malnutrition
    3. Hepatomegaly
    4. Feature of portal hypertension (e.g. ascites, encephalopathy)
  3. Cirrhosis
    1. Large, normal or small liver
    2. Ascites/varices/encephalopathy
    3. Hepatocellular carcinoma
Stigmata of chronic liver disease. More commonly seen in alcoholic cirrhosis
  1. Signs of liver cell failure,Q
  2. Parotid and lacrimal, Gland enlargement,Q 
  3. Clubbing,Q
  4. Gynecomastia,Q
  5. Testicular atrophyQ
  6. Dupuytren’s contracture are seen.Q
​​Pathological features of alcoholic liver disease
  1. Alcoholic hepatitis
    1. Lipogranuloma
    2. Neutrophil infiltration
    3. Mallory’s hyaline
  2. Macrovesicular cirrhosis
    1. Fibrosis and cirrhosis
    2. Central hyaline sclerosis
    3. Pericellular fibrosis
Causes of Mallory’s hyaline
  1. Primary Biliary Cirrhosis
  2. Indian Childhood Cirrhosis
  3. Alcoholic liver disease

Laboratory features:
  1. Anemia - due to GIT
    1. Blood loss,
    2. Nutritional deficiency (Folate, vit. B12)Q
    3. HypersplenismQ,
    4. A direct suppressive effect of alcohol on bone marrow.
    5. Hemolytic anemia due to effect of hypercholesterolemia on RBC membrane (Acanthocytosis)Q.
    6. A unique form of hemolytic anemia (with spur cell & acanthocyte) called Zieve’s syndrome can occur is patient of severe alcoholic hepatitis.
  2. ↑ Tg
  3. AST/ALT ratio > 2 is highly suggestive of alcoholic liver disease. ALP is increase but level are < 3 times of normal
  4. Serum Albumin is decreased while serum globulin are increased.
  5. Increased ammonia levels in hepatic encephalopathy are seen.
  6. Hypokalemia due to hyper aldosteronism
  7. AST, ALT raised but not more then 400IU/L
  8. Increase gamma GT
    (Note: In toxic liver disease & viral hepatitis AST , ALT level are > 400 IU/L
  9. ↑ PT
  10. ↑ Bilirubin)
Causes of AST >ALT
  1. Alcoholic hepatitis
  2. Fatty liver in Pregnancy

Extra Edge


In Alcoholic liver diseases

  1. Increase TG
  2. Increase Cholesterol,
  3. Increase TLC,
  4. Macrocytosis
  1. In alcoholic liver disease there is iron over load state i.e. increase serum ferritin and increase serum iron.
  2. In men, 40–80 g/d of ethanol produces fatty liver; 160 g/d for 10–20 years causes hepatitis or cirrhosis. Only 15% of alcoholics develop alcoholic liver disease.
  3. Women exhibit increased susceptibility to alcoholic liver disease
  4. HCV infection concurrent with alcoholic liver disease is associated with younger age for severity,
  5. Cytochrome P4502E1 is implicated in the development of this disease in alcoholics.


Treatment (Ref. Hari. 18th ed., Pg - 2593)
  1. Pentoxifylline In Alcoholic Hepatitis: ‘In severe alcoholic hepatitis, oral pentoxifylline reduces, Mortality, particularly from hepatorenal failure.
  2. Glucocorticoids is helpful in pts with severe alcoholic hepatitis. But no role in established cirrhosis.

Recent Advances:


Treatment with glucocorticoid is restricted to patients with a discriminant function (DF) value of >32.


DF = 4.6 [PT (T)-PT (C)] + T.Bil

In patients for whom this value is >32, there is improved survival with the use of glucocorticoids.


Exclusion criteria include active gastrointestinal bleeding, renal failure, or pancreatitis.


Lille score is used to identify patient unresponsive therapy. PNQ (Ref. Hari. 18th ed., Pg - 2591)

Lille score
  1. Early identification of patients with severe (discriminant function > or = 32) alcoholic hepatitis (AH) not responding to corticosteroids is crucial.
  2. Specific prognostic model (Lille model) is used to identify candidates early on for alternative therapies.
  3. Baseline data and a change at day 7 were tested.
  4. The model combining six reproducible variables
    1. Age,
    2. Renal insufficiency,
    3. Albumin,
    4. PT
    5. Bilirubin
    6. Evolution of bilirubin at day, all these are highly predictive of death at 6 months.
  5. Acamprosate is indicated for the maintenance of abstinence from alcohol in patients with alchohol dependence who are abstinent at treatment initiation.
2. Post Necrotic Cirrhosis
Also known as coarsely nodular, multinodular and post hepatitic cirrhosis.

Pathologically, post hepatitic liver is typically shrunken in size, distorted in shape and composed of nodules of liver cells separated by dense and broad bands of fibrosis.

Causes – Post hepatitic cirrhosis is seen in:
  1. Viral hepatitis – HBV, HCV
  2. Drugs and toxins – alcohol, amiodarone, arsenicals.
  3. Autoimmune hepatitis
  4. Non-alcoholic steato hepatitis
Clinical features – They are those of initial disease process. Later features of portal hypertension occur.
Treatment – Management of complications of portal hypertension.

Extra Edge Alcoholic hepatitis: NASH, Wilson, PBC all have hepatomegaly but in post necrotic cirrhosis liver is shrunken.!!!

3. Biliary Cirrhosis: (Ref. Hari. 18th ed., Pg - 2595)

Biliary cirrhosis results from injury to or prolonged obstruction of either intrahepatic or extrahepatic biliary system. It is of two types – Primary biliary cirrhosis and secondary biliary cirrhosis.
  1. Primary biliary cirrhosis
    It is characterized by chronic inflammation and fibrous obliteration of intrahepatic bile ductules.
    Pathogenesis – Autoimmune diseases, may be associated with like CREST syndrome, sicca syndrome, auto immune thyroiditis, type I DM and IgA deficiency. QRTA (Renal tubular acidosis)
Clinical Features – women aged 30-60 years. 
  1. The earliest symptom is pruritus. 
  2. Jaundice and gradual darkening of the exposed areas of the skin occur later, steatorrhea with malabsorption of lipid soluble vitamins occur. 
  3. Xanthelasma, Xanthomas
Laboratory features:
  1. Increased levels of serum alkaline phosphatase. Q (2 to 5 fold)
  2. Serum 5’ – nucleotidase and γ – glutamyl transpeptidase levels increased.
  3. ALT and AST are minimally increased.
  4. Serum bilirubin is usually normal or slightly raised.
  5. Anti mitochondrial antibodies Q (IgG) are seen in 90% cases. 
  6. Hyper lipidemia Q is seen.
  7. Abnormal lipoprotein y occur is RBC (it occur in many forum of chronic cholestasis)
  1. Ursodiol (Ursodeoxycholic acid) 
  2. Pruritus is treated with
    1. Antihistamines
    2. Narcotic receptor antagonists (naltrexone) 
    3. Rifampin
    4. Cholestyramine
    5. Plasmapheresis has been used rarely in patients with severe intractable pruritus. (Ref. Hari. 18th ed., Pg- 2596)
  3. Vitamin A, K, D supplements.
  4. Hepatic transplantation (but reoccur in PBC and autoimmune hepatitis)
  5. Colchicine, methotrexate and cyclosporine to slow the progression.
  1. Secondary biliary cirrhosis - It is the result of long standing obstruction of the larger extrahepatic ducts. The causes of obstruction are:
    1. Postoperative strictures.
    2. Gall stones
    3. Chronic pancreatitis
    4. Primary sclerosing cholangitis
    5. Congenital biliary atresia
    6. Cystic fibrosis
    7. Choledochal cyst
Clinical features –
  1. Jaundice and pruritus are most common symptoms. 
  2. Fever and right upper quadrant Q pain is typical.
  3. Treatment – Relief of obstruction results in improvement in both symptoms and survival, even in patients with established cirrhosis.
4. Cardiac Cirrhosis
  1. It results from prolonged severe right sided congestive heart failure.Q 
  2. There is characteristic alternate red (congested) and pale (fibrotic) area known as nutmeg liver.
  3. Bleeding from esophageal varices is rare.Q
    1. Treatment consists of underlying cardiac disease.

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