Jaundice.

The normal total bilirubin concentration is

in the rangeof 0.2 to 1.0mg/dl. Bilirubin is
a natural yellow substance that form when
old red bloodcells break down in our
bodies. Bilirubin is like a helpful waste
product that needs to be removed.Our
liver does this job of clearingit out of body
 Definition:
Jaundace is a clinical condition characterised by yellow color of
the sclera and skin.

• It is caused by the deposition of of bilirubin

due to elevated level in the serum.The term
hyperbilirubinemia is used .
• Classification of jauandice.
• 1)Hemolytic jaudance.
• This condition is associated with increased
hemolysis of RBC ,incomplet blood
transfusion, malaria, sickle cell anemia.
 This results in the overprduction of bilirubin beyond
the ability of the liver to congugate and excrete it.

• It should be noted that liver have a large

capacity to congugate about3.0 g of bilirubin per
day against the normal bilirubin production of
0.3 g/day.
• In hemolytic jaudance,more bilirubin is excreted
intoo the bile leading to the increased formation
of urobilinogen and stercobilinogennn.
• Elevation in the serum unconjugated bilirubin.
• Increased excretion of urobilinogen in urine.
 Darkbrown color of feeces due to high content of
stercobilinogen.

• Hepatic(hepatocellular) jaundace.
• This type of jaudance is caused by
dysfunction of the liver due to damage to the
liver parenchyma.
• Cause is viral infection ,poisons, and
toxins( chloroform, carbon tetrachlorides,
phosphorus, cirrosis of liver and heat falure
etc . Viral hepatitis is more comon.
 Hepatic jaundace is characterised by
increased level of conjugated and uncongugated bilirubin in
the serum .

• Dark color urine due to excessive excretion of

bilirubin and urobilinogen.
• Increased level of alanine transaminase(a
• SGPT)
• Aspartate transaminase(SGOT) is increased in
circulation due to liver damage.
• The patient pass pale,claycolored stools due to
stercobilinogen.
• Loss of apetite (anorexia).
 Obstructive jaundace .

• This is due to an obstruction in the bile duct

• That prevents the passage of bile in to intestine.
• This obstruction is caused by gall stones,
tumours etc.
• Due to the blockage in bile ductthe
congugated bilirubin from the liver enters the
circulation.
 Obstructive jaundace is due to
increased concentration of conjugated
• Bilirubin in serum.
• Serum alkaline phosphatase is elevated as it is
realeased from cell of damaged duct.
• Dark colored urine due to elevated excretion of
of bilirubin and clay colored feces due to
absence of stercobilinogen.
• Fecess contain excess fat indicating
impairement in fat digestion and absorption in
the absence of bile(bile salts)
 The patients experience nausia and git pain.

• Jaundice due to genetic defects .

• Certain hereditary defects that cause jaundice .
• NEONATAL-PHYSIOLOGIC JAUNDICE .
• It is caused by increased hemolysis with
immature hepatic system for the
uptake,conjugation and secretion of bilirubin.
• The activity of the enzyme UDP-glucuronyl-
transferase is low in the newborn.
 The net effect is that in some infants the serum
unconjugated bilirubin is

• Elevated(may go25mg/dl.)which can cross the

blood brain barrier.
• This causes hyperbilirubinemic toxic
encephlopathy orKernicterus that causes
mental retardation.
• TREATMENT.drug phenobarbital is used for
neonatal jaundice.
• It induces bilirubin metabolizing enzyme in
liver.
 PHOTOTHERAPY.
• Bilirubin can absorb blue light(420 -470nm)
maximally. This process is
calledphotoisomerization , the toxic
unconjugated bilirubin gets converted in to
nontoxic isomer namely lumirubin.Lumerubin
can be easily excreted by the kiney.
 CRIGLER-NAJJAR SYNDROME TYPE 1.
• This is also known as congenital non-
hemolytic jaundace.
• It is rare disorder and is defect in the hepatic
enzymeUDP-
GLUCUROTRANSFERASE.Generally child will
die within 2 years of life.
CRIGLER-NAJJAR SYNDROME TYPE 11.
• This is rare hereditary disorderand is due to
less severe defect in the bilirubin conjugation .
• It is seen that hepaticUDP-
GLUCURONYTRANSFERASE that catalyse the
additionof second glucuronyl is defective.This
is less dangerous type .