DR NILESH KATE
MBBS,MD
ASSOCIATE PROF
DEPT. OF PHYSIOLOGY
JAUNDICE
OBJECTIVES.
 Definition
 Mechanism of production
 Types
 Characteristic features
 Physiological Jaundice
 Prevention
 Treatment .
Thursday, November 3, 2016
DEFINITION
 JAUNDICE is defined
as Yellowish
discoloration of skin,
sclera & mucous
membrane
Thursday, November 3, 2016
CAUSE
 Increase bilirubin concentration
( Hyperbilirubinemia) in the body fluids.
 Normal range of serum bilirubin – 2-3 mg/100ml.
 Jaundice when plasma bilirubin > 2-3 gm/dl.
Thursday, November 3, 2016
EXCEPTION
 All internal tissue & body fluids are yellow coloured
except BRAIN
 d/t – BLOOD BRAIN BARRIER which not allow
bilirubin to pass except in neonatal period.
Thursday, November 3, 2016
KERNICTERUS
 Deposition of excess
bilirubin to brain mainly
Basal Ganglia –
Kernicterus.
 C/f – 3 phases
 Decreased alertness,
Hypotonia, poor feeding,
 Hypertonia, Opisthotonus
 Hypotonia.
Thursday, November 3, 2016
BILIRUBIN & JAUNDICE
BILIRUBIN FORMATION.
Thursday, November 3, 2016
Tetra pyrrole straight chain with
Globin & Iron
BILIRUBIN & JAUNDICE
UPTAKE OF BILIRUBIN.
 After degradation of Hb
bilirubin is released into
circulation. Its free of Un-
conjugated Bilirubin.
 Its lipid soluble in plasma
& bound to albumin
 This binding prevents its
excretion by the kidneys.
Thursday, November 3, 2016
CONJUGATION OF BILIRUBIN
 This un-conjugated taken
up by liver, albumin
removed & enters hepatic
cells
 Conjugate with UDP-
Glucoronic acid to form
conjugated bilirubin
 Enzyme – UDP-
Glucoronyl transferase.
Thursday, November 3, 2016
EXCRETION OF BILIRUBIN
 Conjugated Bilirubin
from liver is excreted
into Bile Canaliculi
against conc gradient.
 Enters Intestine
Thursday, November 3, 2016
FORMATION & EXCRETION OF
UROBILINOGEN.
 In intestine Conjugated bilirubin is degraded by
intestinal bacteria
 β Glucoronidase convert Bilirubin to Urobilinogen
& Stercobilinogen.
 20% of Urobilinogen reabsorbed into portal system
to liver & escape into general circulation & re-
excreted into bile
 From General Circulation some filtered by kidney &
excreted in Urine.
Thursday, November 3, 2016
BILIRUBIN CIRCULATION IN
THE BODY
Thursday, November 3, 2016
MECHANISM OF PRODUCTION
 Excessive breakdown
( Hemolysis) of RBC so
called Hemolytic Jaundice
or Prehepatic Jaundice.
 Damage to liver cells –
Hepatic or Hepatocellular
Jaundice.
 Obstruction to bile duct –
Post hepatic or Cholestatic
Jaundice.
Thursday, November 3, 2016
TYPES
 Hemolytic Jaundice
( Pre-Hepatic)
 Hepatocellular
Jaundice (Hepatic
Jaundice)
 Cholestatic or
Obstructive
Jaundice.(Post-
Hepatic)
Thursday, November 3, 2016
HEMOLYTIC JAUNDICE ( PRE-
HEPATIC)
 Mechanism of production
 Types of serum bilirubin
accumulated.
 Van den Bergh test
 Urine bilirubin
 Urine urobilinogen.
 Faecal stercobilinogen.
 Faecal fat level.
 Specific blood tests
Thursday, November 3, 2016
MECHANISM OF PRODUCTION
 Excessive Breakdown
of RBC –
 Produces Un-
conjugated bilirubin
more than healthy
liver can conjugate &
excrete.
Thursday, November 3, 2016
TYPES OF SERUM BILIRUBIN
ACCUMULATED.
Unconjugated
Hyperbilirubinaemia.
Thursday, November 3, 2016
VAN DEN BERGH TEST
 Reagent used – Diazo
reagent ( Mixture of
Sulphanilic acid,
Hydrochloric acid &
sodium Nitrite)
 Test – 2 types
 Direct
 Indirect.
Thursday, November 3, 2016
VAN DEN BERGH TEST
 Direct – when Diazo reagent added to serum
containing Conjugated Bilirubin Reddish Brown
colour developed in 30 sec.
 Indirect - when Diazo reagent added to serum
containing Un-Conjugated Bilirubin No colour
developed but when some alcohol added which
dissolves Unconjugated Bilirubin – reddish Brown
colour is obtained.
Thursday, November 3, 2016
VAN DEN BERGH TEST
 Indirect Positive
Reaction – Due to Un-
Conjugated Bilirubin.
Thursday, November 3, 2016
URINE BILIRUBIN
 Unconjugated
Bilirubin is insoluble in
water & transported n
plasma with albumin.
 Since albumin is not
Filtered it is not appear
in Urine.
Thursday, November 3, 2016
URINE UROBILINOGEN.
 Liver excrete lots of conjugated bilirubin in
intestine in bile & more Urobilinogen is formed
 So Urine Urobilinogen is increased.
Thursday, November 3, 2016
FAECAL STERCOBILINOGEN.
 Normal 25-250 mg/day.
 Same as more Urobilinogen & stercobilinogen
is formed
 Faeces is Dark Brown in colour.
Thursday, November 3, 2016
FAECAL FAT LEVEL.
 Normal
 5-6% of total intake /day
Thursday, November 3, 2016
SPECIFIC BLOOD TESTS
 Peripheral blood film – Haemolysis, Anaemia,
Reticylocytosis.
 Normal Plasma Albumin: Globulin ratio.
 Serum alkaline phosphatase Normal
 Liver function tests – Normal ( As liver is normal)
Thursday, November 3, 2016
HEPATOCELLULAR JAUNDICE
(HEPATIC JAUNDICE)
 Mechanism of production
 Types of serum bilirubin
accumulated.
 Van den Bergh test
 Urine bilirubin
 Urine urobilinogen.
 Faecal stercobilinogen.
 Faecal fat level.
 Specific blood tests
Thursday, November 3, 2016
MECHANISM OF PRODUCTION
 Inability of liver to conjugate & transport
bilirubin into bile duct due to Liver damage.
Thursday, November 3, 2016
TYPES OF SERUM BILIRUBIN
ACCUMULATED.
 Both conjugated & Unconjugated bilirubin
increased.
Thursday, November 3, 2016
VAN DEN BERGH TEST
 Biphasic Reaction as
both Conjugated & Un-
conjugated bilirubin
present.
Thursday, November 3, 2016
URINE BILIRUBIN
 Present
 As conjugated
bilirubin is water
soluble is dissolved,
filtered & appear in
urine
 Also called Choluric
Jaundice.
Thursday, November 3, 2016
URINE UROBILINOGEN.
 Decreases
 As damaged liver cells are producing & excreting
less of conjugated Bilirubin & thus less
Urobilinogen.
Thursday, November 3, 2016
FAECAL STERCOBILINOGEN.
 Less
 As less formation of Stercobilinogen
 So Faeces are Pale Coloured.
Thursday, November 3, 2016
FAECAL FAT LEVEL.
 Increased up to 40-50%.
 As less bile in intestine – less emulsification &
absorption of fat
 So bulky, pale, greasy & foul smelling faeces-
steatorrhoea.
Thursday, November 3, 2016
SPECIFIC BLOOD TESTS
 Peripheral blood film – Normal
 Albumin decreased, so albumin: globulin ratio
Decreased
 Serum alkaline phosphatase – Increased.
 Liver function test – impaired.
Thursday, November 3, 2016
CHOLESTATIC OR OBSTRUCTIVE
JAUNDICE.(POST-HEPATIC)
 Mechanism of production
 Types of serum bilirubin
accumulated.
 Van den Bergh test
 Urine bilirubin
 Urine urobilinogen.
 Faecal stercobilinogen.
 Faecal fat level.
 Specific blood tests
Thursday, November 3, 2016
MECHANISM OF PRODUCTION
 Obstruction to the
bile flow from
Hepatocytes to
duodenum.
Thursday, November 3, 2016
TYPES OF SERUM BILIRUBIN
ACCUMULATED.
 Conjugated Hyperbilirubinaemia due to
impaired flow of bile.
Thursday, November 3, 2016
VAN DEN BERGH TEST
 Direct Positive
reaction.
 As only conjugated
bilirubin present.
Thursday, November 3, 2016
URINE BILIRUBIN
 Present.
 As conjugated
bilirubin filtered in
urine.
Thursday, November 3, 2016
URINE UROBILINOGEN.
 Markedly decreased or absent.
 As due to obstruction conjugated bilirubin is not
released in intestine
 No Urobilinogen is formed.
Thursday, November 3, 2016
FAECAL STERCOBILINOGEN.
 Absent – when obstruction is complete.
 Stools are clay coloured.
Thursday, November 3, 2016
FAECAL FAT LEVEL.
 Increased.
Thursday, November 3, 2016
SPECIFIC BLOOD TESTS
 Peripheral blood film – normal.
 Plasma albumin, globulin & ratio – Normal
 Serum Alkaline phosphatase – markedly
increased.
 Liver function tests - normal
Thursday, November 3, 2016
Thursday, November 3, 2016
PHYSIOLOGICAL JAUNDICE
 NEONATAL JAUNDICE.
 Mechanism of
production
 Appears 2-5 days after
birth & disappears in 2
weeks.
 Excessive destruction of
RBC & hepatic Immaturity
in first 7-10 days.
Thursday, November 3, 2016
SIGNS & SYMPTOMS
Thursday, November 3, 2016
Thursday, November 3, 2016
PREVENTION
 By giving Hepatic Microsomal enzyme inducers
(Phenobarbital) to pregnant mother or
newborn-
 Increases activity of Glucoronyl Transferase.
Thursday, November 3, 2016
TREATMENT .
 PHOTOTHERAPY
 Exposure of skin to
white light – PHOTO-
ISOMERIZATION of
Bilirubin to water
soluble Lumirubin
which is excreted in
Bile without
conjugation
Thursday, November 3, 2016
TREATMENT OF PATHOLOGICAL
JAUNDICE IN ADULT
Thursday, November 3, 2016
Thank
You

JAUNDICE

  • 1.
    DR NILESH KATE MBBS,MD ASSOCIATEPROF DEPT. OF PHYSIOLOGY JAUNDICE
  • 2.
    OBJECTIVES.  Definition  Mechanismof production  Types  Characteristic features  Physiological Jaundice  Prevention  Treatment . Thursday, November 3, 2016
  • 3.
    DEFINITION  JAUNDICE isdefined as Yellowish discoloration of skin, sclera & mucous membrane Thursday, November 3, 2016
  • 4.
    CAUSE  Increase bilirubinconcentration ( Hyperbilirubinemia) in the body fluids.  Normal range of serum bilirubin – 2-3 mg/100ml.  Jaundice when plasma bilirubin > 2-3 gm/dl. Thursday, November 3, 2016
  • 5.
    EXCEPTION  All internaltissue & body fluids are yellow coloured except BRAIN  d/t – BLOOD BRAIN BARRIER which not allow bilirubin to pass except in neonatal period. Thursday, November 3, 2016
  • 6.
    KERNICTERUS  Deposition ofexcess bilirubin to brain mainly Basal Ganglia – Kernicterus.  C/f – 3 phases  Decreased alertness, Hypotonia, poor feeding,  Hypertonia, Opisthotonus  Hypotonia. Thursday, November 3, 2016
  • 7.
    BILIRUBIN & JAUNDICE BILIRUBINFORMATION. Thursday, November 3, 2016 Tetra pyrrole straight chain with Globin & Iron
  • 8.
    BILIRUBIN & JAUNDICE UPTAKEOF BILIRUBIN.  After degradation of Hb bilirubin is released into circulation. Its free of Un- conjugated Bilirubin.  Its lipid soluble in plasma & bound to albumin  This binding prevents its excretion by the kidneys. Thursday, November 3, 2016
  • 9.
    CONJUGATION OF BILIRUBIN This un-conjugated taken up by liver, albumin removed & enters hepatic cells  Conjugate with UDP- Glucoronic acid to form conjugated bilirubin  Enzyme – UDP- Glucoronyl transferase. Thursday, November 3, 2016
  • 10.
    EXCRETION OF BILIRUBIN Conjugated Bilirubin from liver is excreted into Bile Canaliculi against conc gradient.  Enters Intestine Thursday, November 3, 2016
  • 11.
    FORMATION & EXCRETIONOF UROBILINOGEN.  In intestine Conjugated bilirubin is degraded by intestinal bacteria  β Glucoronidase convert Bilirubin to Urobilinogen & Stercobilinogen.  20% of Urobilinogen reabsorbed into portal system to liver & escape into general circulation & re- excreted into bile  From General Circulation some filtered by kidney & excreted in Urine. Thursday, November 3, 2016
  • 12.
    BILIRUBIN CIRCULATION IN THEBODY Thursday, November 3, 2016
  • 13.
    MECHANISM OF PRODUCTION Excessive breakdown ( Hemolysis) of RBC so called Hemolytic Jaundice or Prehepatic Jaundice.  Damage to liver cells – Hepatic or Hepatocellular Jaundice.  Obstruction to bile duct – Post hepatic or Cholestatic Jaundice. Thursday, November 3, 2016
  • 14.
    TYPES  Hemolytic Jaundice (Pre-Hepatic)  Hepatocellular Jaundice (Hepatic Jaundice)  Cholestatic or Obstructive Jaundice.(Post- Hepatic) Thursday, November 3, 2016
  • 15.
    HEMOLYTIC JAUNDICE (PRE- HEPATIC)  Mechanism of production  Types of serum bilirubin accumulated.  Van den Bergh test  Urine bilirubin  Urine urobilinogen.  Faecal stercobilinogen.  Faecal fat level.  Specific blood tests Thursday, November 3, 2016
  • 16.
    MECHANISM OF PRODUCTION Excessive Breakdown of RBC –  Produces Un- conjugated bilirubin more than healthy liver can conjugate & excrete. Thursday, November 3, 2016
  • 17.
    TYPES OF SERUMBILIRUBIN ACCUMULATED. Unconjugated Hyperbilirubinaemia. Thursday, November 3, 2016
  • 18.
    VAN DEN BERGHTEST  Reagent used – Diazo reagent ( Mixture of Sulphanilic acid, Hydrochloric acid & sodium Nitrite)  Test – 2 types  Direct  Indirect. Thursday, November 3, 2016
  • 19.
    VAN DEN BERGHTEST  Direct – when Diazo reagent added to serum containing Conjugated Bilirubin Reddish Brown colour developed in 30 sec.  Indirect - when Diazo reagent added to serum containing Un-Conjugated Bilirubin No colour developed but when some alcohol added which dissolves Unconjugated Bilirubin – reddish Brown colour is obtained. Thursday, November 3, 2016
  • 20.
    VAN DEN BERGHTEST  Indirect Positive Reaction – Due to Un- Conjugated Bilirubin. Thursday, November 3, 2016
  • 21.
    URINE BILIRUBIN  Unconjugated Bilirubinis insoluble in water & transported n plasma with albumin.  Since albumin is not Filtered it is not appear in Urine. Thursday, November 3, 2016
  • 22.
    URINE UROBILINOGEN.  Liverexcrete lots of conjugated bilirubin in intestine in bile & more Urobilinogen is formed  So Urine Urobilinogen is increased. Thursday, November 3, 2016
  • 23.
    FAECAL STERCOBILINOGEN.  Normal25-250 mg/day.  Same as more Urobilinogen & stercobilinogen is formed  Faeces is Dark Brown in colour. Thursday, November 3, 2016
  • 24.
    FAECAL FAT LEVEL. Normal  5-6% of total intake /day Thursday, November 3, 2016
  • 25.
    SPECIFIC BLOOD TESTS Peripheral blood film – Haemolysis, Anaemia, Reticylocytosis.  Normal Plasma Albumin: Globulin ratio.  Serum alkaline phosphatase Normal  Liver function tests – Normal ( As liver is normal) Thursday, November 3, 2016
  • 26.
    HEPATOCELLULAR JAUNDICE (HEPATIC JAUNDICE) Mechanism of production  Types of serum bilirubin accumulated.  Van den Bergh test  Urine bilirubin  Urine urobilinogen.  Faecal stercobilinogen.  Faecal fat level.  Specific blood tests Thursday, November 3, 2016
  • 27.
    MECHANISM OF PRODUCTION Inability of liver to conjugate & transport bilirubin into bile duct due to Liver damage. Thursday, November 3, 2016
  • 28.
    TYPES OF SERUMBILIRUBIN ACCUMULATED.  Both conjugated & Unconjugated bilirubin increased. Thursday, November 3, 2016
  • 29.
    VAN DEN BERGHTEST  Biphasic Reaction as both Conjugated & Un- conjugated bilirubin present. Thursday, November 3, 2016
  • 30.
    URINE BILIRUBIN  Present As conjugated bilirubin is water soluble is dissolved, filtered & appear in urine  Also called Choluric Jaundice. Thursday, November 3, 2016
  • 31.
    URINE UROBILINOGEN.  Decreases As damaged liver cells are producing & excreting less of conjugated Bilirubin & thus less Urobilinogen. Thursday, November 3, 2016
  • 32.
    FAECAL STERCOBILINOGEN.  Less As less formation of Stercobilinogen  So Faeces are Pale Coloured. Thursday, November 3, 2016
  • 33.
    FAECAL FAT LEVEL. Increased up to 40-50%.  As less bile in intestine – less emulsification & absorption of fat  So bulky, pale, greasy & foul smelling faeces- steatorrhoea. Thursday, November 3, 2016
  • 34.
    SPECIFIC BLOOD TESTS Peripheral blood film – Normal  Albumin decreased, so albumin: globulin ratio Decreased  Serum alkaline phosphatase – Increased.  Liver function test – impaired. Thursday, November 3, 2016
  • 35.
    CHOLESTATIC OR OBSTRUCTIVE JAUNDICE.(POST-HEPATIC) Mechanism of production  Types of serum bilirubin accumulated.  Van den Bergh test  Urine bilirubin  Urine urobilinogen.  Faecal stercobilinogen.  Faecal fat level.  Specific blood tests Thursday, November 3, 2016
  • 36.
    MECHANISM OF PRODUCTION Obstruction to the bile flow from Hepatocytes to duodenum. Thursday, November 3, 2016
  • 37.
    TYPES OF SERUMBILIRUBIN ACCUMULATED.  Conjugated Hyperbilirubinaemia due to impaired flow of bile. Thursday, November 3, 2016
  • 38.
    VAN DEN BERGHTEST  Direct Positive reaction.  As only conjugated bilirubin present. Thursday, November 3, 2016
  • 39.
    URINE BILIRUBIN  Present. As conjugated bilirubin filtered in urine. Thursday, November 3, 2016
  • 40.
    URINE UROBILINOGEN.  Markedlydecreased or absent.  As due to obstruction conjugated bilirubin is not released in intestine  No Urobilinogen is formed. Thursday, November 3, 2016
  • 41.
    FAECAL STERCOBILINOGEN.  Absent– when obstruction is complete.  Stools are clay coloured. Thursday, November 3, 2016
  • 42.
    FAECAL FAT LEVEL. Increased. Thursday, November 3, 2016
  • 43.
    SPECIFIC BLOOD TESTS Peripheral blood film – normal.  Plasma albumin, globulin & ratio – Normal  Serum Alkaline phosphatase – markedly increased.  Liver function tests - normal Thursday, November 3, 2016
  • 44.
  • 45.
    PHYSIOLOGICAL JAUNDICE  NEONATALJAUNDICE.  Mechanism of production  Appears 2-5 days after birth & disappears in 2 weeks.  Excessive destruction of RBC & hepatic Immaturity in first 7-10 days. Thursday, November 3, 2016
  • 46.
  • 47.
  • 48.
    PREVENTION  By givingHepatic Microsomal enzyme inducers (Phenobarbital) to pregnant mother or newborn-  Increases activity of Glucoronyl Transferase. Thursday, November 3, 2016
  • 49.
    TREATMENT .  PHOTOTHERAPY Exposure of skin to white light – PHOTO- ISOMERIZATION of Bilirubin to water soluble Lumirubin which is excreted in Bile without conjugation Thursday, November 3, 2016
  • 50.
    TREATMENT OF PATHOLOGICAL JAUNDICEIN ADULT Thursday, November 3, 2016
  • 51.