Jaundice are three Hemolytic, Hepatic and Obstructive Jaundice.
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Language: en
Added: Mar 27, 2014
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M.Prasad Naidu
MSc 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
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%
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