M.Prasad NaiduMSc Medical Biochemistry,Ph.D.Research Scholar

Clinical marker of defect in metabolism &/or excretion of bilirubin.

ER task to initiate lab eval or imaging studies to identify cause and determine admission or outpt therapy.

Yellow discoloration of sclera, skin, mucous membranes due to deposition of bile pigment

Clinically detected with serum bilirubin 2-2.5mcg/dL or (2 times nl)

The breakdown product of Hgb from injured RBCs and other heme containing proteins.

Produced by reticuloendothelial system Released to plasma bound to albumin Hepatocytes conjugate it and extrete

through bile channels into small intest.

Overproduction by reticuloendothelial system

Failure of hepatocyte uptake Failure to conjugate or excrete Obstruction of biliary excretion into

intestine

Unconjugated production

exceeds ability of liver to conjugate

Ex. Hemolytic anemias, hemoglobinopathies, in-born errors of metab., transfusion rxn.

Conjugated Can produce but not

excrete Metabolic defect Intra- or extrahepatic

obstruction

Careful history and PE Family history (Gilbert, Rotor, Crigler-

Najjar, Dubin-Johnson, Sickle Cell)

Healthy young person with fever, malaise, myalgias = viral hepatitis (try to locate source)

Gradually develops symptoms = hepatic/bile duct obstruction (consider ETOH liver dz/cirrhosis)

Develops acutely with abd pain = acute cholangitis 2° to choledocholithiasis

Painless jaundice in older person with epigastric mass & weight loss = biliary obstruction from malignancy

Hepatomegaly with pedal edema, JVD, and gallop = CHF

Serum bilirubin level (total and direct)

Liver aminotransferase levels

Alk. Phos U/A for bilirubin and

urobilogen

CBC PT Other labs pertinent

to history Coombs test Hgb electrophoresis Viral hepatitis panel U/S Gallbladder

Hemodynamically stable, new-onset jaundice, no evidence of liver failure or acute biliary obstruction discharge with follow up

If one of above violated admission with surgery consult

Tintanalli Chapter 85Pages 561-566

1) Biliary Colic 2) Cholecystitis 3) Gallstone pancreatitis 4) Ascending cholangitis

Most gallstones are asymptomatic Usually seen in obese females 20-40

yoa and pregnancy (Remember fat, fertile, flatulent, female, forty)

Associated with upper abdominal pain

Uncommon in children (seen with hemolytic d/o, idiopathic, cystic fibrosis, obesity, ileal resection, long term use of TPN)

Elderly 14-27% symptomatic gallstone dz. More likely biliary sepsis/gangrenous GB perioperative morbidity Mortality rate 19%

FamilialAsian descentChronic biliary tract infectionsParasitic infections (ascaris lumbricoides)Chronic liver dz (ETOH)Chronic intravasular dz (Sickle Cell,

Hereditary Scherocytosis)Hepatitis A, B, C, EHIVHerpesvirus

Bile Manufactured & secreted from hepatocytes

GB storage in canaliculi, ductiles, & bile ducts bile ducts enlarge form R and L hepatic ducts form common hepatic duct joins cystic duct from GB to form CBD Ampulla of Vater duodenum

Release of bile stimulated by cholecystokinin secreted from small int. mucosal cells when fats & AA enter duodenum

Symptomatic cholelithiasis = stone migration from GB into biliary tract with eventual obstruction obstruction of hollow viscus pain, nausea & vomiting acute cholecystitis

E. coli/Klebsiella-70% Enterococci-15% Bacteroides-10% Clostridium-10% Group D Strep Staphylococcal species

Overlap of s/s of PUD, gastritis, GERD, nonspecific dyspepsia

RUQ pain Upper abd/epigastric pain Radiation to L upper back Pain persisant lasting 2-6h

THANKING U