Cirrhosis

Liver cirrhosis aetiology, pathogenesis, clinical features, treatment

1. CIRRHOSIS

2. INTRODUCTION Hepatic cirrhosis is a common disease characterised by diffuse hepatic fibrosis and nodule formation. Occurs at any age and has significant morbidity and is an important cause of premature death. Most common cause-chronic viral hepatitis and prolonged excessive alcohol consumption. Most common cause of portal hypertension and its associated complications

3. ALCOHOLIC CIRRHOSIS Excessive chronic alcohol use can cause several types of chronic liver disease including alcoholic fatty liver,alcoholic hepatitis,alcoholic cirrhosis. Contributes to liver damage in patients with other liver disease such as hepatitis C hemochromatosis and fatty liver disease related to obesity. It can produce fibrosis in the absence of accompanying inflammation and necrosis.

4. Fibrosis can be cenrilobular , pericellular , periportal . When fibrosis reaches certain degree there is disruption of normal liver architecture and replacement of liver cells by regenerative nodules. Nodules – micronodules -<3mm diameter macronodules - >3mm diameter

5. Pathogenesis

6. Clinical symptoms: Non specific sympoms : right upper quadrant abdominal pain, fever, nausea, vomiting, diarrhea , anorexia and malaise. Specific symptoms : ascites , edema , upper gastrointestinal hemorrhage . Many present incidentally at the time of autopsy or elective surgery. Others : jaundice or encephalopathy.

7. On physical examination liver and spleen may be enlarged with liver edge being firm and nodular. Other frequent findings include scleral icterus , palmar erythema , spider angiomas , parotid gland enlargement, digital clubbing, muscle wasting. Men – decreased body hair, and gynecomastia as well as testicular atrophy. Women-advanced alcoholic cirrhosis menstural irregularities ,some woman may be amenorrheic this changes are often reversible following cessation of alcohol.

8. Lab tests normal in early cases , abnormal in advanced stages. Anemic -chronic GI blood loss, nutritional deficiency, hyper splenism related to portal hypertension, direct suppressive effect of alcohol on bone marrow. Zieve’s syndrome-haemolytic anemia with spur cells and acanthocytes . Platelets reduced early in the disease reflective of portal hypertension. Total serum bilirubin normal or elevated.

9. Direct bilirubin mildly elevated, progresses as disease worseness. Prothrombin time prolonged, not respond to IV vit -K. Serum sodium levels normal unless patient have ascites and depressed largely due to ingestion of excess of free water. ALT,AST elevated in patients who continue to drink,with AST levels higher than ALT,2:1ratio. Liver biopsy can be helpful to confirm diagnosis but when patients present with alcoholic cirrhosis and are still drinking liver biopsy is withheld until abstinence for atleast 6months to determine non-reversible disease.

10. TREATMENT Abstinence is the corner stone of therapy. Good nutrition and long term medical supervision to maintain underlying complications. Complications requires specific management. Glucocorticoids in the absence of infections. DF- discriminant function value – serum total bilurubin + differnce in patient’s prothrombin time compared to control (in seconds) Х 4.6

11. Treatment is restricted to patient’s with DF value more than 32, with use of gluco corticoids improved survival at 28 days. Oral pentoxifylline - decrease production of TNF α and other proinflammatory cytokinins , easy to adminster with few side effects. Recent studies used parenterally adminstered inhibitors of TNF α such as infliximab or etanercept . Anabolic steroids, propylthiouracil , antioxidants,colchicine,penicillamine used but no clear cut benefits. Medications that reduce craving for alcohol such as acamprosate calcium have been favourable. They can take other medicines in the presence of cirrhosis

12. Acetaminophen is discouraged in patients with liver disease, however if no more than 2grams per day are consumed, there generally are no problems.