of impaired fat digestion in the absence of intestinal bile. AST, ALT, and GGT
levels generally rise only moderately, but bilirubin and alkaline phosphatase
levels are elevated.- Hereditary Hyperbilirubinemia
Results from several inherited disorders can also produce jaundice. Gilbert‘s
syndrome is a familial disorder characterized by an increased level of
unconjugated bilirubin that causes jaundice. Other conditions that are probably caused by inborn errors of biliary
metabolism include Dubin–Johnson syndrome (chronic idiopathic jaundice,
with pigment in the liver) and Rotor‘s syndrome (chronic familial conjugated
hyperbilirubinemia without pigment in the liver.II. PORTAL HYPERTENSION
Obstructed blood flow through the damaged liver results in increased blood
pressure (portal hypertension) throughout the portal venous system. It is commonly associated with hepatic cirrhosis, but can also occur with
noncirrhotic liver disease. Portal hypertnesion leads to :- Splenomegaly (enlarged spleen )
- Ascites
- Varices.
III. ASCITES - Pathophysiology
Caused by portal hypertension and the resulting increase in capillary pressure
and obstruction of venous blood flow through the damaged liver. The failure of the liver to metabolize aldosterone increases sodium and water
retention by the kidney. Sodium and water retention, increased intravascular
fluid volume, and decreased synthesis of albumin by the damaged liver all
contribute to fluid moving from the vascular system into the peritoneal space Loss of fluid into the peritoneal space causes further sodium and water retention
by the kidney in an effort to maintain the vascular fluid volume, and the process
becomes self-perpetuating. As a result of liver damage, large amounts of albumin-rich fluid, 15 L or more,
may accumulate in the peritoneal cavity as ascites.