JAUNDICE

51
DR NILESH KATE MBBS,MD ASSOCIATE PROF DEPT. OF PHYSIOLOGY JAUNDICE

Transcript of JAUNDICE

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DR NILESH KATE

MBBS,MD ASSOCIATE PROF

DEPT. OF PHYSIOLOGY

JAUNDICE

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

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DEFINITION JAUNDICE is defined

as Yellowish discoloration of skin, sclera & mucous membrane

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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.

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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.

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KERNICTERUS Deposition of excess

bilirubin to brain mainly Basal Ganglia – Kernicterus.

C/f – 3 phases Decreased alertness,

Hypotonia, poor feeding, Hypertonia, Opisthotonus Hypotonia.

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BILIRUBIN & JAUNDICEBILIRUBIN FORMATION.

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Tetra pyrrole straight chain with Globin & Iron

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BILIRUBIN & JAUNDICEUPTAKE 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.

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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.

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EXCRETION OF BILIRUBIN Conjugated Bilirubin

from liver is excreted into Bile Canaliculi against conc gradient.

Enters Intestine

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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.

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BILIRUBIN CIRCULATION IN THE BODY

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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.

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TYPES Hemolytic Jaundice

( Pre-Hepatic) Hepatocellular

Jaundice (Hepatic Jaundice)

Cholestatic or Obstructive Jaundice.(Post-Hepatic)

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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

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MECHANISM OF PRODUCTION Excessive Breakdown

of RBC – Produces Un-

conjugated bilirubin more than healthy liver can conjugate & excrete.

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TYPES OF SERUM BILIRUBIN ACCUMULATED.

Unconjugated Hyperbilirubinaemia.

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VAN DEN BERGH TEST Reagent used – Diazo

reagent ( Mixture of Sulphanilic acid, Hydrochloric acid & sodium Nitrite)

Test – 2 types Direct Indirect.

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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.

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VAN DEN BERGH TEST

Indirect Positive

Reaction – Due to Un-

Conjugated Bilirubin.

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URINE BILIRUBIN Unconjugated

Bilirubin is insoluble in water & transported n plasma with albumin.

Since albumin is not Filtered it is not appear in Urine.

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URINE UROBILINOGEN.

Liver excrete lots of conjugated bilirubin in

intestine in bile & more Urobilinogen is formed

So Urine Urobilinogen is increased.

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FAECAL STERCOBILINOGEN.

Normal 25-250 mg/day.

Same as more Urobilinogen & stercobilinogen

is formed

Faeces is Dark Brown in colour.

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FAECAL FAT LEVEL.

Normal

5-6% of total intake /day

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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)

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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

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MECHANISM OF PRODUCTION

Inability of liver to conjugate & transport

bilirubin into bile duct due to Liver damage.

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TYPES OF SERUM BILIRUBIN ACCUMULATED.

Both conjugated & Unconjugated bilirubin

increased.

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VAN DEN BERGH TEST

Biphasic Reaction as

both Conjugated & Un-

conjugated bilirubin

present.

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URINE BILIRUBIN Present As conjugated

bilirubin is water soluble is dissolved, filtered & appear in urine

Also called Choluric Jaundice.

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URINE UROBILINOGEN.

Decreases

As damaged liver cells are producing & excreting

less of conjugated Bilirubin & thus less

Urobilinogen.

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FAECAL STERCOBILINOGEN.

Less

As less formation of Stercobilinogen

So Faeces are Pale Coloured.

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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.

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SPECIFIC BLOOD TESTS

Peripheral blood film – Normal

Albumin decreased, so albumin: globulin ratio Decreased

Serum alkaline phosphatase – Increased.

Liver function test – impaired.

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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

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MECHANISM OF PRODUCTION Obstruction to the

bile flow from Hepatocytes to duodenum.

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TYPES OF SERUM BILIRUBIN ACCUMULATED.

Conjugated Hyperbilirubinaemia due to

impaired flow of bile.

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VAN DEN BERGH TEST

Direct Positive

reaction.

As only conjugated

bilirubin present.

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URINE BILIRUBIN

Present.

As conjugated

bilirubin filtered in

urine.

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URINE UROBILINOGEN.

Markedly decreased or absent.

As due to obstruction conjugated bilirubin is not

released in intestine

No Urobilinogen is formed.

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FAECAL STERCOBILINOGEN.

Absent – when obstruction is complete.

Stools are clay coloured.

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FAECAL FAT LEVEL. Increased.

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SPECIFIC BLOOD TESTS

Peripheral blood film – normal.

Plasma albumin, globulin & ratio – Normal

Serum Alkaline phosphatase – markedly increased.

Liver function tests - normal

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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.

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SIGNS & SYMPTOMS

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PREVENTION

By giving Hepatic Microsomal enzyme inducers

(Phenobarbital) to pregnant mother or

newborn-

Increases activity of Glucoronyl Transferase.

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TREATMENT . PHOTOTHERAPY Exposure of skin to

white light – PHOTO-ISOMERIZATION of Bilirubin to water soluble Lumirubin which is excreted in Bile without conjugation

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TREATMENT OF PATHOLOGICAL JAUNDICE IN ADULT

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Thank You