Aetiology of cirrhosis
• Alcoholic cirrhosis
• Post-necrotic cirrhosis or post-viral cirrhosis
• Hepatitis B • Hepatitis C • Delta hepatitis (hepatitis D) + hepatitis B Chronic autoimmune hepatitis
• Drug-induced cirrhosis
• Methotrexate • Methyldopa, isoniazid • Sulphonamides
• Biliary cirrhosis
• Primary • Secondary
• Non-alcoholic fatty liver disease (NAFLD) • Cardiac cirrhosis • Haemochromatosis
• Wilson's disease • alpha 1 -antitrypsin deficiency • Glycogen storage diseases
• Galactosaemia • Intestinal bypass surgery • Hepatic outflow tract obstruction
• Veno-occlusive disease • Cryptogenic (Idiopathic) cirrhosis
Pathology and Pathogenesis
• Cirrhotic changes affect the whole liver, but not necessarily every lobule.
• Widespread necrosis of liver cells.
• Extensive fibrosis that distorts the hepatic architecture.
• Regenerative, nodular hyperplasia of the remaining surviving liver cells leads to regenerating nodules.
• Destruction and distortion of hepatic vasculature by fibrosis lead to obstruction of blood flow, which eventually leads to portal hypertension and its sequelae.
• Ascites and hepatic encephalopathy result from both hepatocellular insufficiency and portal hypertension.
• Hepatocellular damage leads to jaundice, oedema, coagulopathy and a variety of metabolic abnormalities.
• Alcoholic cirrhosis:
• Safe limits of alcohol are 200 g and 140 g of alcohol per week in males and females, respectively.
• 10 g of alcohol equals 30 mL of whisky, 100 mL of wine and 250 mL of beer.
• Occurrence of cirrhosis six times when alcohol intake is double the safety limit.
• Ingestion of 180 g of alcohol/day for 25 years increases the risk of developing cirrhosis 25 times.
• Hepatitis C infection is an important contributor for progression to cirrhosis.
• Low-grade fever. • Weakness, fatigue and weight loss. • Anorexia, nausea, vomiting and upper abdominal discomfort. • Abdominal distension due to ascites and gas. • Loss of libido. • Menstrual irregularities like amenorrhoea and irregular menses. • Haemorrhagic tendencies like easy bruising, purpura, epistaxis, menorrhagia and gastrointestinal bleeding. • Haemorrhagic tendencies are due to underproduction of coagulation factors by the liver and thrombocytopenia resulting from hypersplenism. • Symptoms of hepatic insufficiency • Symptoms of portal hypertension and its sequelae
Signs of hepatocellular failure
• Jaundice • Palmar erythema • Parotid enlargement • Dupuytren's contracture
• Diminished body hair • Clubbing • Spider naevi • White nails • Flapping tremors
• Gynaecomastia • Testicular atrophy • Ascites
Features dominant in alcoholic cirrhosis
• Parotid enlargement • Gynaecomastia • Spider naevi • Dupuytren's contractures (related to alcoholism) • Liver enlarged, normal or small in size
• End stage of cirrhosis is characterised by:
• Chronic jaundice.
• Progressive, refractory ascites. Worsening of signs of portal hypertension.
• Progressive renal dysfunction.
• Most of them die in hepatic encephalopathy.
• Complete blood picture • Liver function tests
•Prothrombin time • Hepatitis B and C markers • Blood ammonia estimation
• Respiratory alkalosis • Metabolic abnormalities • Ultrasonographic examination
• Fibroscan to determine amount of fibrosis • Liver biopsy confirms the diagnosis of cirrhosis
• Relevant investigations related to the specific aetiologies of cirrhosis in individual patients
• Ascitic fluid examination, barium swallow for demonstration of varices, upper gastrointestinal scopy for delineation of varices
• Treatment of underlying causes
• Removal of causative agents like drugs, alcohol, etc.
• High-protein diet-minimum 1 g/kg/day.
• 2000--3000 kcal/day.
• Diets enriched in branched-chain amino acids, in patients predisposed to hepatic encephalopathy.
• Multivitamin supplementation daily.
• Vaccination against hepatitis A and B viruses, influenza virus, and pneumococcus.
• Specific treatment of complications-e.g. variceal bleeding, hepatic encephalopathy and ascites
TREATMENT AT DR. SOHAN LAL CLINIC
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