Caused by deposition of bile pigments in the sclera, skin and mucous membranes Associated with elevated levels of bilirubin in the blood Clinically bilirubin levels are detectable at 2 to 2.5img/ dL or above Where is bilirubin first clinically observed ? The sclera per Tintinalli , but a little board review is actually underthe tongue JAUNDICE
Skin may take on a greenish tint due to longstanding jaundice The bilirubin has actually been metabolized to biliverdin As a side note: B-carotene and hemachromatosis may cause yellow-orange discoloration of the skin, but will spare the sclera JAUNDICE
Bilirubin is made in the reticulendothelial system Once broken down, it is released into plasma and bound to albumin Hepatocytes conjugate the bilirubin Conjugated bilirubin is then excreted into the small intestines as urobilinogen Reabsorbed in the portal circulation Secreted as bile into the intestines with very small urinary excretion The life of Bilirubin
If bilirubin levels exceed liver conjugation capabilities indirect levels will rise Examples: hemoglobinopathies , hemolytic anemias , transfusion rxns , inborn errors in metabolism If extrahepatic excretion is altered, conjugated bilirubin levels rise Examples: intra, extrahepatic obstruction, congenital defects, inflammation, masses Pathology
Family history of mild and recurrent jaundice should prompt thoughts of Gilbert, Rotor, Crigler-Najjar , or Dubin Johnson Syndrome Hepatic causes: sudden onset in previously healthy patients should prompt thoughts of viral hepatitis(blood transfusions, STD's, IV drug abuse, travel to foreign countries , tattoos RUQ abdominal pain, hepatomegaly, absent pruritis Clinical Atributes
Hepatocellular damage may result from Tylenol, halothane, methyldopa, INH, phenytoin, amanita poisoning, carbon tetrachloride, phosphorus may cause massive hepatic necrosis Alcoholic cirrhosis- ascites, weakness, peripheral muscle wasting, spider angiomata , pruritis Clinical Cont
RUQ pain, vomiting, fever and acute onest of jaundice: think ascending cholangitis Most commonly form choledocholitasis Colecistitis alone will not cause jaundice Painless jaundice in eldery should promt thoughts of malignancy Beware!
СВС РТ аРТТ Alkaline Phosphatase AST ALT LABS UA for bilirubin and Urobilinogen Bilirubin total Bilirubin direct Any other appropriate labs forthe case
Unconjugated hyperbilirubinemia Tightly bound to albumin and will not appear in the urine Should have normal liver labs, CBC and smear may show anemia and hemolysis Gilbert's is most common cause Increased bili may be seen with fever, exertion, fasting, surgery, and heavy alcohol use Evaluation of Labs
Conjugated bilirubinemia Water soluble and is seen in urine at low levels Urobilinogen will be absent in urine with cholestasis Abnormal liver labs Elevated alk phos and gamma- glutamyl transpeptidase ( GGTP) suggest intra/ extrahepatic obstruction Evaluation of Labs
Jaundice alone is not criteria for admission If liver failure present or suspected extrabiliary compression then admit Surgery consult if appropriate GOOD LUCK FRIENDS! I'LL MISS YOU!! Dispo