Hepatobiliary Disorders

HEPATOBILIARY DISORDERS

LIVER CIRRHOSIS Irreversible chronic inflammatory disease characterized by massive degeneration and destruction of hepatocytes. Types 1. Laennec’s cirrhosis - the most common - Caused by the toxic effect of alcohol - Occurs primarily in middle-aged men 2. Postnecrotic cirrhosis - Results from severe liver disease 3. Post - acute viral or chemical hepatitis 4. Primary biliary cirrhosis - inflammation and intrahepatic bile duct destruction. 5. Secondary biliary cirrhosis - chronic partial or complete common bile duct obstruction due to gall stones, pancreatitis or tumor. 6. Cardiac cirrhosis - results from right-sided CHF. PATHOPHYSIOLOGY Laennec’s Cirrhosis Alcohol causes changes --- fatty infiltration of the hepatocytes --- liver cell necrosis and scarring --- as it progresses, inflammation decreases but fibrosis increases --- liver distortion --- structural (biliary channel) and vascular changes. Scar tissue formation and irregular hepatocyte regeneration --compression of portal vein --- obstruction --- portal hypertension Decreased Vitamin ADEK absorption ➔ bleeding tendencies ➔ poor calcium transport ➔ poor skin turgor ➔ visual disturbances Depletion of glycogen --- hypoglycemia Decreased albumin --- decreased COP --- anasarca Increased HP --- ascites Decreased bilirubin metabolism --- hyperbilirubinemia --- jaundice MANIFESTATIONS POSTNECROTIC - SAME AS LAENNEC’S CIRRHOSIS Biliary cirrhosis Chronic obstruction --- increased pressure in the hepatic bile duct --accumulation of bile --- areas of necrosis --- edema, fibrosis and hepatocellular destruction --- scar tissue destruction --- hepatomegaly Hyperbilirubenemia Jaundice Pruritus clay-colored stools RUQ pain. CARDIAC CIRRHOSIS Enlarged liver --- congested venous blood flow --- failure of the heart to pump blood to different areas of the body. Congestion causes anoxia to the liver --- necrosis and fibrosis HEPATORENAL SYNDROME

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A major complication of cirrhosis characterized by renal failure in an anatomically normal kidneys --- progressive oliguria and azotemia. Nursing Interventions 1. Assess for signs of bleeding 2. Monitor V/S and laboratory results (platelets, creatininine) 3. Monitor I/O. 4. Monitor daily weight and abdominal girth to detect ascites. 5. Administer the following as ordered to combat symptoms: a. Vitamin K b. Stool softeners c. Diuretics 6. Assess for changes in cardiac output, decreased renal function and electrolyte imbalances. 7. Assess for impaired skin integrity related to edema, ascites and pruritus. 8. Use preventive measures to keep skin intact. 9. Assess the patient for signs of impaired breathing related to congestion or infection. 10. Relieve breathing difficulty. 11. Observe for signs of encephalopathy (lethargy, confusion, personality changes, motor changes, depression, irritability). 12. Teach ways to decrease bleeding tendencies. Patient teaching: 1. Nutritional needs 2. Avoidance of alcohol 3. Drug interactions related to decreased liver function. 4. Enough rest 5. Signs and symptoms needing medical intervention. 6. Provide counseling for the patient and family.

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