liver and gallbladder

• liver failure: liver has large reserve: destruction of hepatocytes to level that liver is unable to carry out normal physiological function
• liver failure

  • causes: cirrhosis, chronic active hepatitis, liver cancer
• cirrhosis: chronic, progressive nodular scarring of liver -> structural and functional changes

  • types (related to the cause of the cirrhosis)
• Cirrhosis

  • types
  • Laennec's Cirrhosis: alcohol related or drug induced
  • Alcohol transformed to acetaldehyde
  • inhibits removal of proteins and alters metabolism of vitamins and minerals
  • leads to accumulation of fat in liver (fatty liver)
  • drugs: toxic effect
• Cirrhosis

  • types
  • biliary cirrhosis: autoimmune destruction or obstruction of biliary ducts
  • retention of bile: gallbladder involvement and gallstones seen
• cirrhosis

  • pathophysiology
  • fatty infiltration and stimuli lead to inflammation and scarring (poor nutrition leads to more severe damage)
  • altered membrane transport of hepatocytes and transformation of fat storing cells
  • obstructed flow of bile and blood
  • increased pressure -> development of portal hypertension
  • pressure on abdominal and esophageal vessels
  • increased stasis of blood in splenic vein
  • increased break down of WBCs, RBCs, and platelets
  • decreased production of albumin
  • decreased metabolism of aldosterone
  • inability to break down ammonia
  • decreased synthesis of clotting factors
• Hepatitis: inflammation of liver tissue with necrosis of hepatocytes; most commonly viral (hepatoviruses)

  • types: A, B, C, D, E, or autoimmune
  • etiology: blood and body fluids (C, D, E) or contaminated food and water ( A, B)
• hepatitis

  • pathophysiology
  • virally induced inflammation
  • activation of immune response promotes diffuse cellular injury and necrosis of hepatocytes
  • interruption of normal liver function followed by regeneration of liver cells
  • antigen markers in serum: i.e. Hepatitis B serum antigen = HBsAg
  • prodromal (preicteric) phase: about two weeks after initial exposure
  • flu like symptoms
  • highly transmissible
  • Icteric phase (up to six weeks)
  • symptomatic phase of illness (jaundice or other liver manifestations)
  • recovery (posticteric) phase (signs and symptoms are resolving)
• hepatitis

  • fulminant (chronic) hepatitis (seen with type B or C and is severe in liver necrosis)
• Congenital Disorders

  • biliary atresia: congenital closure or absence of extrahepatic bile ducts
  • retention of bile -> inflammation
  • destruction of bile ducts
  • leads to cirrhosis (80% fatal by 3 years without a transplant)
• liver cancer: primary or metastatic (came from other place)

  • associated with: chronic cirrhosis, toxic exposure, alcohol use
  • hepatocellular carcinoma: nodular, massive and diffuse
  • metastasizes to heart, lung, brain, kidney and spleen through hepatic and portal vein
• manifestations of liver disease (there are several)

  • Jaundice (icterus): yellowish hue
  • disturbed flow and accumulation of bile or bilirubin -> stains skin, sclera, and tissues
  • serum bilirubin 3-4 times normal before symptoms
  • pruritis (itching)
  • specific types
  • pre-hepatic: excessive RBC destruction
  • intrahepatic (liver unable to remove bilirubin from the blood)
  • post hepatic
  • neonatal jaundice: immature liver -> deficiency of enzyme needed for conjugation of bilirubin
  • phototherapy causes isomerization of bilirubin to excretable form
• Manifestations of liver disease

  • Ascites: accumulation of fluid in the peritoneal cavity
  • pathophysiology
  • increased portal venous pressure
  • increased capillary pressure disrupts osmotic forces
  • decreasing plasma protein levels: albumin
  • reduction in plasma colloid osmotic pressure
  • decreases reabsorption and promotes fluid shift into peritoneal cavity
  • hypoalbuminemia results
• Manifestations of liver disease

  • Ascites "water belly"
  • compensation through activation of RAAS
  • increased aldosterone secretion -> retention of sodium and water
  • increased secretion of antidiuretic hormone in response to low central volume
• Manifestations of liver disease

  • Ascites
  • clotting disturbances
  • depletion of clotting factors and malabsorption of vitamin K leads to bleeding tendencies
  • esophageal varicies
  • resistance in the portal vein
  • alternative channels sought
  • esophageal veins bulge
  • esophageal irritation
  • gastric acids, vomiting, alcohol etc.
  • rupture
• Manifestations of liver disease

  • Ascites
  • neurologic changes: hepatic encephalopathy
  • accumulation of ammonia
  • agitation, disorientation, confusion
  • asterixis
  • fetor hepaticus: acetone breath
  • progression to coma
  • hepatomegaly
  • RUQ tenderness
  • damaged hepatocytes release liver enzymes into blood
  • alkaline phosphatase, aspartate aminotransferase (AST), alanine aminotransferase (ALT)
  • dark urine, light colored stools
• Gall bladder disease

  • cholecystitis: inflammation usually due to gallstones in a duct
  • inflammation can lead to necrosis
  • leads to prevention of outflow of bile
  • cholelithiasis: gallstones
  • cholesterol sludge
  • precipitates with calcium to form crystals
  • stasis of bile promotes growth of crystals -> cholesterol stones formed
  • obstruction
  • hepatic duct, cystic duct, common bile duct
  • perforation a risk (large stone or increased number of stones)
  • clinical manifestations
  • pain (distended gallbladder) RUQ, nausea, vomiting
  • intolerance to fatty foods
  • gall bladder cancer