JAUNDICE

M.Prasad Naidu
MSc Medical Biochemistry,
Ph.D.Research Scholar


JAUNDICE
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.
PATHOPHYSIOLOGY
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)
WHAT IS BILIRUBIN?
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.
WHAT CAUSES BILIRUBIN?
Overproduction by reticuloendothelial system
Failure of hepatocyte uptake
Failure to conjugate or excrete
Obstruction of biliary excretion into intestine
UNCONJUGATED VS. CONJUGATED
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
CLINICAL FEATURES
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)
CLINICAL FEATURES
Gradually develops symptoms = hepatic/bile
duct obstruction (consider ETOH liver
dz/cirrhosis)
Develops acutely with abd pain = acute
cholangitis 2 to choledocholithiasis
CLINICAL FEATURES
Painless jaundice in older person with
epigastric mass & weight loss = biliary
obstruction from malignancy
Hepatomegaly with pedal edema, JVD, and
gallop = CHF
LABORATORY TESTS
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
DISPOSITION
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
CHOLECYSTITIS AND BILIARY COLIC
Tintanalli Chapter 85
Pages 561-566
BILIARY TRACT EMERGENCIES RELATED TO
GALLSTONES
1) Biliary Colic
2) Cholecystitis
3) Gallstone pancreatitis
4) Ascending cholangitis

GALLSTONES
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
GALLSTONES
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%
GALLSTONE RISK FACTORS
Familial
Asian descent
Chronic biliary tract infections
Parasitic infections (ascaris lumbricoides)
Chronic liver dz (ETOH)
Chronic intravasular dz (Sickle Cell, Hereditary
Scherocytosis)
Hepatitis A, B, C, E
HIV
Herpesvirus
PATHOPHYSIOLOGY
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
PATHOPHYSIOLOGY
Release of bile stimulated by cholecystokinin
secreted from small int. mucosal cells when
fats & AA enter duodenum
PATHOPHYSIOLOGY
Symptomatic cholelithiasis = stone migration
from GB into biliary tract with eventual
obstruction obstruction of hollow viscus
pain, nausea & vomiting acute
cholecystitis
PATHOGENS INVOLVED IN ACUTE
CHOLECYSTITIS
E. coli/Klebsiella-70%
Enterococci-15%
Bacteroides-10%
Clostridium-10%
Group D Strep
Staphylococcal species
CLINICAL FEATURES
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