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JAUNDICEJAUNDICE
ByBy
RajasriRajasri
ManimaranManimaran
Group 2Group 2
What is jaundice?What is jaundice?
O It is yellowish
discoloration of
Skin, mucous
membranes,
sclera.. Due to
excess plasma
bilirubin.
Signs and symptomsSigns and symptoms
O Skin and sclerae - yellow
O Stool - light colour, clay coloured
O Dark urine
O Pain in abdomen
O Itching
O Trouble with sleeping
O Fatigue, swelling
O Ascites
O Mental confusion, coma
O Bleeding
O The differential diagnosis for yellowing
of the skin is limited. In addition to
jaundice, it includes Carotenoderma.
O In carotenoderma the pigment is
concentrated on the palms, soles,
forehead, and nasolabial folds.
Carotenoderma can be distinguished
from jaundice by the sparing of the
sclerae.
Carotenoderma vs jaundiceCarotenoderma vs jaundice
Is it disease?Is it disease?
O Is not a disease but rather a sign that
can occur in many different diseases.
O Normal plasma bilirubin range 5-17 m
mol/l
O Clinically obvious   50 mmol/l (2.5mg/dl)
Normal bilurubin production andNormal bilurubin production and
metabolismmetabolism
Types of jaundiceTypes of jaundice
category definition
Pre-hepatic/ hemolytic The pathology is occurring prior to
the liver.
Hepatic/ hepatocellular The pathology is located within the
liver.
Post-Hepatic/ cholestatic
The pathology is located after the
conjugation of bilirubin in the liver.
Prehepatic jaundicePrehepatic jaundice
O Pre-hepatic jaundice is caused by
anything which causes an increased rate
of hemolysis.
O In jaundice secondary to hemolysis, the
increased production of bilirubin, leads
to the increased production of urine-
urobilinogen. Bilirubin is not usually
found in the urine because unconjugated
bilirubin is not water-soluble.
Hepatocellular jaundiceHepatocellular jaundice
O  Cell necrosis reduces the liver's ability
to metabolize and excrete bilirubin
leading to a buildup of unconjugated
bilirubin in the blood.
O Other causes include primary biliary
cirrhosis leading to an increase in
plasma conjugated bilirubin because
there is impairment of excretion of
conjugated bilirubin into the bile.
Posthepatic jaundicePosthepatic jaundice
O  is caused by an interruption to the
drainage of bile in the biliary system
O In complete obstruction of the bile
duct, no urobilinogen is found in the
urine, since bilirubin has no access to
the intestine and it is in the intestine
that bilirubin gets converted to
urobilinogen to be later released into
the general circulation.
Differential diagnosisDifferential diagnosis
Neonatal jaundiceNeonatal jaundice
O Yellowish staining of the skin and whites of
the newborn's eyes (sclerae) by pigment of
bile (bilirubin)
O Breakdown of red blood cells (which release
bilirubin into the blood) and immaturity of
the newborn's liver (which cannot
effectively metabolize bilirubin and prepare
it for excretion into urine)
O Normal neonatal jaundice appears between
the 2nd and 5th days of life and clears with
time
O Kernicterus – brain damage - lifelong
disability.
Bili light and sunbathBili light and sunbath
DiagnosisDiagnosis
O History
O Physical examination
O Blood tests - laboratory
O Ultrasonography
O CT
O MRI
O Liver biopsy
O ERCP (Endoscopic retrograde
cholangiopancreatography)
O Endoscopic ultrasound
Physical examination
Biliary tract dilation due to obstruction
Gall stone
TreatmentTreatment
O Treatment requires a precise diagnosis of the
specific cause and should be directed to the specific
problem.
O Complications of jaundice include sepsis
especially cholangitis, biliary
cirrhosis, pancreatitis , coagulopathy, renal and liver
failure.
O Cholangitis, especially the suppurative type (Charcot’s
triad or Reynolds' pentad), is usually secondary
to choledocholithiasis. It may also complicate
procedures like ERCP.
O Treatment should include correction of coagulopathy,
fluid/electrolyte anomaly, antibiotics and biliary
drainage with ERCP where available or trans-hepatic
drainage or surgery.
Jaundice

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Jaundice

  • 2. What is jaundice?What is jaundice? O It is yellowish discoloration of Skin, mucous membranes, sclera.. Due to excess plasma bilirubin.
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  • 4. Signs and symptomsSigns and symptoms O Skin and sclerae - yellow O Stool - light colour, clay coloured O Dark urine O Pain in abdomen O Itching O Trouble with sleeping O Fatigue, swelling O Ascites O Mental confusion, coma O Bleeding
  • 5. O The differential diagnosis for yellowing of the skin is limited. In addition to jaundice, it includes Carotenoderma. O In carotenoderma the pigment is concentrated on the palms, soles, forehead, and nasolabial folds. Carotenoderma can be distinguished from jaundice by the sparing of the sclerae.
  • 7. Is it disease?Is it disease? O Is not a disease but rather a sign that can occur in many different diseases. O Normal plasma bilirubin range 5-17 m mol/l O Clinically obvious   50 mmol/l (2.5mg/dl)
  • 8. Normal bilurubin production andNormal bilurubin production and metabolismmetabolism
  • 9. Types of jaundiceTypes of jaundice category definition Pre-hepatic/ hemolytic The pathology is occurring prior to the liver. Hepatic/ hepatocellular The pathology is located within the liver. Post-Hepatic/ cholestatic The pathology is located after the conjugation of bilirubin in the liver.
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  • 11. Prehepatic jaundicePrehepatic jaundice O Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis. O In jaundice secondary to hemolysis, the increased production of bilirubin, leads to the increased production of urine- urobilinogen. Bilirubin is not usually found in the urine because unconjugated bilirubin is not water-soluble.
  • 12. Hepatocellular jaundiceHepatocellular jaundice O  Cell necrosis reduces the liver's ability to metabolize and excrete bilirubin leading to a buildup of unconjugated bilirubin in the blood. O Other causes include primary biliary cirrhosis leading to an increase in plasma conjugated bilirubin because there is impairment of excretion of conjugated bilirubin into the bile.
  • 13. Posthepatic jaundicePosthepatic jaundice O  is caused by an interruption to the drainage of bile in the biliary system O In complete obstruction of the bile duct, no urobilinogen is found in the urine, since bilirubin has no access to the intestine and it is in the intestine that bilirubin gets converted to urobilinogen to be later released into the general circulation.
  • 14.
  • 16. Neonatal jaundiceNeonatal jaundice O Yellowish staining of the skin and whites of the newborn's eyes (sclerae) by pigment of bile (bilirubin) O Breakdown of red blood cells (which release bilirubin into the blood) and immaturity of the newborn's liver (which cannot effectively metabolize bilirubin and prepare it for excretion into urine) O Normal neonatal jaundice appears between the 2nd and 5th days of life and clears with time O Kernicterus – brain damage - lifelong disability.
  • 17. Bili light and sunbathBili light and sunbath
  • 18. DiagnosisDiagnosis O History O Physical examination O Blood tests - laboratory O Ultrasonography O CT O MRI O Liver biopsy O ERCP (Endoscopic retrograde cholangiopancreatography) O Endoscopic ultrasound
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  • 25. Biliary tract dilation due to obstruction
  • 27. TreatmentTreatment O Treatment requires a precise diagnosis of the specific cause and should be directed to the specific problem. O Complications of jaundice include sepsis especially cholangitis, biliary cirrhosis, pancreatitis , coagulopathy, renal and liver failure. O Cholangitis, especially the suppurative type (Charcot’s triad or Reynolds' pentad), is usually secondary to choledocholithiasis. It may also complicate procedures like ERCP. O Treatment should include correction of coagulopathy, fluid/electrolyte anomaly, antibiotics and biliary drainage with ERCP where available or trans-hepatic drainage or surgery.