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  1. Cirrhosis Biol E-163 TA session 1/8/06

  2. normal cirrhotic Cirrhosis • Fibrosis (accumulation of connective tissue) that progresses to cirrhosis • Replacement of liver tissue by regenerative nodules (areas of proliferating hepatocytes) surrounded by fibrous scar tissue, leading to progressive loss of liver function • Occurs as a consequence of chronic liver disease From: Current Diagnosis & Treatment in Gastroenterology - 2nd Ed. (2003)

  3. Common causes in developed countries Alcoholism Chronic Hepatitis C infection Asia and Africa Chronic Hepatitis B infection associated with diabetes, protein malnutrition, obesity, coronary artery disease, and treatment with corticosteroid medications From: Current Diagnosis & Treatment in Gastroenterology - 2nd Ed. (2003)

  4. hepatocellular hyperplasia regenerative nodules ** injury growth regulators arterial growth (angiogenesis) Pathophysiology • Variation from individual to individual in rate of progression from fibrosis to cirrhosis, even from the same underlying cause • Reason unknown Growth regulators = cytokines, epithelial growth factor, hepatocyte growth factor, transforming growth factor-a, tumor necrosis factor ** influenced by insulin, glucagon, and patterns of intrahepatic blood flow

  5. Symptoms & Complications Due to ↓ processing of bilirubin Portal blood flow through vessels here, likely to bleed Due to ↑ estradiol resulting from impaired estrogen metabolism Due to portal hypertension Accumulation of fluid in peritoneal cavity due to hepatic hypertention Umbilical vein opens, blood from portal-venous system gets shunted through here speckled mottling of the palm Other non-specific symptoms weakness, fatigue, anorexia, weight loss From: Current Diagnosis & Treatment in Gastroenterology - 2nd Ed. (2003)

  6. Main consequences of hepatic hypertension • Ascites = accumulation of fluid in intraperitoneal cavity • Formation of porto-systemic shunts = new blood vessels channel blood from intestines to heart instead of first passing through liver. • Ex: esophageal varices, caput medusae. • Esophageal varices are most dangerous because they often rupture. • Congestive splenomegaly = enlargement of the spleen • Hepatic encephalopathy = swelling of the brain caused by accumulation of toxic substances in the blood (esp. ammonia) due to porto-systemic shunts (blood bypasses cleaning by the liver) and decreased liver function • Signs can include impaired cognition, decreased level of consciousness, and coma

  7. Diagnosis • Displaying signs of portal hypertension • Liver function tests • If clinical data and lab tests suggest cirrhosis, confirm by liver biopsy

  8. Treatments • Eliminating injurious drugs, such as alcohol and hepatotoxic drugs • Reducing intake of drugs metabolized by the liver • Providing adequate nutrition • Therapy for patients with varices • Treatments to slow fibrosis • End stage disease requires liver transplant

  9. Primary Biliary Cirrhosis (PBC) • Autoimmune liver disease • Progressive destruction of intrahepatic bile ducts • Leads to cholestasis (blocked flow of bile), cirrhosis, liver failure • Most common chronic cholestatic liver disease in adults • More common in women than men • Clusters in families (genetic) • Specific cause is unknown

  10. PBC Pathophysiology • CD4 and CD8 T lymphocytes cause inflammation of the epithelial cells that line the small bile ducts in the liver • Bile ducts proliferate • Bile acids are retain and cause inflammation in the liver • Fibrosis occurs  cirrhosis

  11. PBC Symptoms • 30-50% asymptomatic • Abnormal liver function test (esp. elevated alkaline phosphatase) • Fatigue • Pruritus (itchy skin) • Complications of cirrhosis and portal hypertension

  12. PBC Diagnosis • Abnormal liver function tests (esp. elevated alkaline phosphatase) • Elevation of certain antibodies, particularly IgM and antimitochondrial antibodies • Liver biopsy to confirm diagnosis

  13. PBC Prognosis • Usually progresses to terminal stage over 15-20 years, though rate varies • Median life expectancy is ~ 10 years once symptoms develop

  14. PBC Treatment • Halting or reversing liver damage • Treating complications of chronic cholestasis and liver failure • Eventually will need a liver transplant • Eliminate use of alcohol and hepatotoxic drugs • Treatment with ursodeoxycholic acid (facilitates bile flow through liver) • decreases liver damage, prolongs survival, and delays need for liver transplant • Pruritus can be treated with cholestyramine (prevents bile reabsorption from the gut)