Jaundice - Dr Rohit Bhaskar

JAUNDICE
©2021 Dr Rohit Bhaskar PT https://www.pt-pedia.com

OBJECTIVES.
■ Definition
■ Mechanism of production
■ Types
■ Characteristic features
■ Physiological Jaundice
■ Prevention
■ Treatment .

DEFINITION
■ JAUNDICE is defined
as Yellowish
discoloration of skin,
sclera & mucous
membrane

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.

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.

KERNICTERUS
■ Deposition of excess
bilirubin to brain mainly
Basal Ganglia –
Kernicterus.
■ C/f – 3 phases
■ Decreased alertness,
Hypotonia, poor feeding,
■ Hypertonia, Opisthotonus
■ Hypotonia.

BILIRUBIN & JAUNDICE
BILIRUBIN FORMATION.
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.

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.

EXCRETION OF BILIRUBIN
■ Conjugated Bilirubin
from liver is excreted
into Bile Canaliculi
against conc gradient.
■ Enters Intestine

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.

BILIRUBIN CIRCULATION IN
THE BODY

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.

TYPES
■ Hemolytic Jaundice ( Pre-Hepatic)
■ Hepatocellular Jaundice (Hepatic Jaundice)
■ Cholestatic or Obstructive Jaundice.(Post-
Hepatic)

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

■ Excessive Breakdown
of RBC –
■ Produces Un-
more than healthy
liver can conjugate &
excrete.

TYPES OF SERUM BILIRUBIN
ACCUMULATED.
■ Unconjugated
Hyperbilirubinaemia.

VAN DEN BERGH TEST
■ Reagent used – Diazo
reagent ( Mixture of
Sulphanilic acid,
Hydrochloric acid &
sodium Nitrite)
■ Test – 2 types
■ Direct
■ Indirect.

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.

VAN DEN BERGH TEST
■ Indirect Positive
Reaction – Due to Un-
Conjugated Bilirubin.

URINE BILIRUBIN
■ Unconjugated Bilirubin
is insoluble in water &
transported n plasma
with albumin.
■ Since albumin is not
Filtered it is not appear
in Urine.

URINE UROBILINOGEN.
■ Liver excrete lots of conjugated bilirubin in
intestine in bile & more Urobilinogen is formed
■ So Urine Urobilinogen is increased.

FAECAL STERCOBILINOGEN.
■ Normal 25-250 mg/day.
■ Same as more Urobilinogen & stercobilinogen is
formed
■ Faeces is Dark Brown in colour.

FAECAL FAT LEVEL.
■ Normal
■ 5-6% of total intake /day

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)

HEPATOCELLULAR JAUNDICE
(HEPATIC JAUNDICE)
■
■
■
■
■
■
■
■
accumulated.
Van den Bergh test
urobilinogen.
Faecal fat level.

■ Inability of liver to conjugate & transport
bilirubin into bile duct due to Liver damage.

ACCUMULATED.
■ Both conjugated & Unconjugated bilirubin
increased.

VAN DEN BERGH TEST
■ Biphasic Reaction as
both Conjugated & Un-
present.

URINE BILIRUBIN
■ Present
■ As conjugated
bilirubin is water
soluble is dissolved,
filtered & appear in
urine
■ Also called Choluric
Jaundice.

URINE UROBILINOGEN.
■ Decreases
■ As damaged liver cells are producing & excreting
less of conjugated Bilirubin & thus less Urobilinogen.

■ Less
■ As less formation of Stercobilinogen
■ So Faeces are Pale Coloured.

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.

■ Peripheral blood film – Normal
■ Albumin decreased, so albumin: globulin ratio
Decreased
■ Serum alkaline phosphatase – Increased.
■ Liver function test – impaired.

CHOLESTATIC OR OBSTRUCTIVE
JAUNDICE.(POST-HEPATIC)
■
■
■
■
■
■
■
■
accumulated.
Van den Bergh test
urobilinogen.
Faecal fat level.

■ Obstruction to the
bile flow from
Hepatocytes to
duodenum.

ACCUMULATED.
■ Conjugated Hyperbilirubinaemia due to
impaired flow of bile.

VAN DEN BERGH TEST
■ Direct Positive
reaction.
■ As only conjugated
bilirubin present.

URINE BILIRUBIN
■ Present.
■ As conjugated
bilirubin filtered in
urine.

URINE UROBILINOGEN.
■ Markedly decreased or absent.
■ As due to obstruction conjugated bilirubin is not
released in intestine
■ No Urobilinogen is formed.

■ Absent – when obstruction is complete.
■ Stools are clay coloured.

FAECAL FAT LEVEL.
■ Increased.

■ Peripheral blood film – normal.
■ Plasma albumin, globulin & ratio – Normal
■ Serum Alkaline phosphatase – markedly
increased.
■ Liver function tests - normal

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.

SIGNS & SYMPTOMS

PREVENTION
■ By giving Hepatic Microsomal enzyme inducers
(Phenobarbital) to pregnant mother or
newborn-
■ Increases activity of Glucoronyl Transferase.

TREATMENT .
■ PHOTOTHERAPY
■ Exposure of skin to
white light – PHOTO-
ISOMERIZATION of
Bilirubin to water
soluble Lumirubin
which is excreted in
Bile without
conjugation

TREATMENT OF PATHOLOGICAL
JAUNDICE IN ADULT

Jaundice - Dr Rohit Bhaskar

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