You are on page 1of 3

JAUNDICE = icterus = yellow / greenish pigmentation of the skin that caused by hyperbilirubinemia ( total plasma bilirubin conc.

above 2.5 to 3 mg/dl) = can result from: 1) excessive hemolysis of RBC or 2) obstructive disorders of the bile ducts/ liver cells 3) also by metabolic defects that impair the uptake/ conjugation of unconjugated bilirubin in liver * gilbert dzs :cause an elevation of unconjugated bilirubin in the plasma but no other symptoms of liver dzs caused by an inherited def of glucoranyl transfrease enzyme ( required for the hepatic uptake of unconjugated bilirubin)

= jaundice in newborns is caused by impaired bilirubin uptake & conjugation PATHOPHYSIOLOGY 1) obstructive jaundice  can result from extrahepatic/ intrahepatic obstruction  extrahepatic obstruction jaundice  dvlp if the common bile duct is occluded by a gallstone, tumor, or compression from edema of pancreatitis  bcoz the bile duct is obstructed  bilirubin is conjugated by the hepatocytes, but cannot flow into the duodenum (conjugated bilirubin is soluble in water & is then soluble in aqueous bile)  it accumulates in the liver & enter the bloodstream  HYPERBILIRUBINEMIA  bcoz conjugated bilirubin is water soluble , it appears in the urine  stools  may be light colored/ clay colored bcoz they lack bile pigments  lack urobilinogen bcoz bile is not available for conversion to urobilinogen  intrahepatic obstructive jaundice  involves disturbances in hepatocyte fx & obstruction of bile canaliculi  the uptake, conjugation & excretion of bilirubin are affected with elevated levels of both conjugated & unconjugated bilirubin  hepatocellular damage increases plasma conc. of unconjugated bilirubin  obstruction of bile canaliculi (major disorder)  diminishes flow of conjugated bilirubin into the common bile duct with elevation in the plasma  in mild cases  some of the bile canaliculi opes  amount of bilirubin in intestinal tract may be only slightly decreased  stool may appear normal/ light colored

anorexia. malaie & fatigue . Bilirubin  indicate liver injury / extrahepatic obstruction  history & physical exam identify the underlying disorder  treatment : correcting the cause .2) excessive hemolysis (breakdown) of RBC / absorbtion of hematoma  cause hemolytic jaundice (prehepatic jaundice)  an increased amount of unconjugated bilirubin is formed tru metabolism of heme component of destroyed RBC  extra amount of unconjugated bilirum exceeds the conjugation ability of the liver  cause blood levels of unconjugated bilirubin to rise  unconjugated bilirubinemia  the major cause of hemolytic jaundice  bcoz unconj bilirubin is not water soluble  not excreted in urine  reserve conjugation ability of the liver usually prevents long-term unconjugated hyperbilirubinemia greater than 4 to 5 mg/dl  cause severe hemolytic crisis like sickle cell dzs  if unconjugated hyperbilirubinemia exceeds 5 mg /dl  both hemolytic & liver disorders r indicated CLINICAL MANIFESTATION  vary & r related to underlying pathology  conj. resulting from viral / bact inflammation of liver  manifestation of liver injury from any cause commonly : . Hyperbilirubinemia  cause urine to darken to darken several days b4 the onset of jaundice  complete obstruction of bile flow from the liver to duodenum  light-colored stools  partial obstruction  stools r normal in colour & bilirubin is present in the urine  fever. chills & pain often accompany jaundice.yellow discoloration may first occur in the sclera of eye & then progress to skin  pruritus commonly accompanies jaundice with an elevation of serum alkaline phosphatase & bilirubin accumulation in skin EVALUATION & TREATMENT  lab evaluation of serum  whether elevated plasma bilirubin is conj / unconj/ both  unconjugated bilirubinemia  results from hemolysis / hereditary disorders of bilirubin metabolism  elevated in conj.