JAUNDICE

YELLOWISH DISCOLOURATION OF
SCLERA/TISSUE DUE TO INCREASED
LEVEL OF BILIRUBIN IN BODY.

Normal level of bilirubin in body-

<1MG/DL (0.3MG OF WHICH IS
CONJUGATED)
 D/D OF YELLOW SKIN
CAROTENODERMA
QUINACRINE/PHENOL POISONING
JAUNDICE
 PATHOPHYSIOLOGY OF JAUNDICE
INCREASED PRODUCTION OR DECREASED
EXCRETION OF BILIRUBIN
BILIRUBIN IS A BYPRODUCT OF METABOLISM OF
HEMOPROTEIN LIKE HAEMOGLOBIN,MYOGLOBIN
AND CYTOCHROMES
1g Hb - 34mg bilirubin
IT IS BEING PRODUCED IN
RETICULOENDOTHELIAL SYSTEM (LIVER AND
SPLEEN)
HAE HAEM
BILIVERDIN BILIRUBIN
OXYGENASE BILIVERDIN
M REDUCTASE
 THIS UNCONJUGATED BILIRUBIN IS BOUND TO
ALBUMIN AND TRANSPORTED TO LIVER
IN LIVER,BILIRUBIN IS BOUND TO
GLUCOURONIC ACID,MEDIATED BY ENZYME
UDPGT
THIS CONJUGATED BILIRUBIN IS WATER
SOLUBLE AND RELEASED INTO BILE VIA MDR-2
PROTEIN (RATE LIMITING STEP)
Bilirubin Metabolism
MEASUREMENT OF SERUM BILIRUBIN
VAN DEN BERGH REACTION
IT IMPLIES USAGE OF SULFANILLIC ACID AND
ALCOHOL IN CONSECUTIVE STEPS
URINARY BILIRUBIN IS DETECTED BY MEAN OF
DIPSTIC TEST-ICOTEST
APPROACH TO A PATIENT OF JAUNDICE
HISTORY
(TRAVEL,RESIDENCE,DIETARY,SEXUAL,BLOOD
TRANSFUSION OR ANY DRUG USAGE,ALCOHOL
CONSUMPTION)
PHYSICAL EXAMINATION (PALPATION OF
LIVER,SPLEEN,STIGMAS OF CHRONIC LIVER
DISEASE)
LAB INVESTIGATIONS(SGPT,SGOT,ALP,
P.T,S.PROTEIN,VIRAL MARKERS)
IMAGING (ULTRASOUND,MRCP,ERCP)
 ISOLATED HYPERBILIRUBINEMIA
CAN BE EITHER
1. CONJUGATED
HYPERBILIRUBINEMIA(>15%DIRECT BILIRUBIN)
OR
2. UNCONJUGATED
HYPERBILIRUBINEMIA(<15%DIRECT BILIRUBIN)
 UNCONJUGATED
HYPERBILIRUBINEMIA
1.CAUSED BY INCREASED PRODUCTION OF
BILIRUBIN (HEMOLYTIC ANAEMIA OR
INEFFECTIVE ERYTHROPOEISIS)
2.DECREASED UPTAKE OF UNCONJUGATED
BILIRUBIN BY HEPATOCYTES ( DRUGS LIKE
PROBENECID,RIFAMPICIN,RIBAVIRIN,BREAST
MILK JAUNDICE IN NEONATE).
3.DECREASED CONJUGATION OF BILIRUBIN IN
HEPATOCYTES(CRIGLER NAJJAR-I &II,GILBERT
SYNDROME)
 HEMOLYTIC JAUNDICE
SPHEROCYTOSIS,ELLIPTOCYTOSIS,G6PD
DEFFICIENCY,THALASSEMIA,HBS,AIHA,PNH
SERUM BILIRUBIN LEVEL RARELY INCREASE TO
MORE THAN 5MG/DL
HIGH ASSOSCIATION WITH GALL STONES
 CRIGLER NAJJAR SYNDROME
TYPE I: RARE DISEASE,CAUSED BY COMPLETE
ABSENCE OF ENZYME BILIRUBIN UDPGT.
S.BILIRUBIN>20 MG/DL
DEATH OCCUR IN INFANCY..
TYPE II:MORE COMMON,PARTIAL ABSENCE OF
ENZYME BILIRUBIN UDPGT.
S.BILIRUBIN-8 TO 25MG/DL
USUALLY SURVIVE UPTO ADULTHOOD
 GILBERT SYNDROME
COMMON CONDITION
MORE IN MALES
ALSO CAUSED BY DECREASED ACTIVITY OF
ENZYME BILIRUBIN UDPGT
S.BILIRUBIN RARELY EXCEED TO MORE THAN
6MG/DL
NO HEMOLYSIS
 ISOLATED CONJUGATED
HYPERBILIRUBINEMIA
DUBIN JOHNSON SYNDROME:MUTATION
IN MDR-2 PROTEIN
ROTOR SYNDROME:CAUSED BY DEFECTIVE
STORAGE OF BILIRUBIN IN HEPATOCYTES
BOTH ARE BENIGN CONDITIONS,REQUIRE NO
TREATMENT
HYPERBILIRUBINEMIA WITH ALTERED
L.F.TS
HEPATOCELLULLAR PATTERN: ELEVATED ALT/AST
OUT OF PROPORTION TO ALKALINE PHOSPATASE
CHOLESTATIC PATTERN: ELEVATED ALKALINE
PHOSPATASE OUT OF PROPORTION TO AMINO
TRANSFERASE
 HEPATOCELLULAR JAUNDICE
1. VIRAL HEPATITIS
(HAV,HEV,HBV,HCV,..EBV,CMV)
2. ALCOHOLIC LIVER DISEASE
3. DRUG INDUCED(H,R,Z,
HALOTHANE,PHENYTOIN,VALPORATE,NSAID,
PIS,NRTIS)
4. WILSONS DISEASE
5. AUTOIMMUNE HEPATITIS
 CHOLESTATIC JAUNDICE
INTRAHEPATIC CHOLESTASIS:(VIRAL
HEPATITIS,ALCOHOLIC HEPATITIS,DRUG
TOXICITY,PRIMARY BILLIARY CIRRHOSIS,PRIMARY
SCLEROSING CHOLANGITIS,VANISHING BILE DUCT
SYNDROME, T.P.N, PARANEOPLASTIC SYNDROME, GVH
RXN)
EXTRAHEPATIC CHOLESTASIS:
(CHOLEDOCHOLITHIASIS,STRICTURE,PERIAMPULLARY
TUMOUR,CHRONIC PANCREATITIS)
 L.F.TS AND ITS IMPLICATION IN
DIAGNOSIS OF JAUNDICE
S.BILIRUBIN AND ITS FRACTIONS (DELTA BILIRUBIN)
LIVER ENZYMES: 1 A.L.T
2 A.S.T
3 ALP
4 GGT
5 NUCLEOTIDASE5
S.PROTEIN
CLOTTING FACTOR
PROTHROMBIN TIME
 1.SERUM BILIRUBIN
HAS 2 COMPONENTS-DIRECT AND INDIRECT
>3MG/DL-RESPONSIBLE FOR YELLOW SCLERA
USED TO DIFFERENTIATE B/W
HEPATOCELLULAR AND CHOLESTATIC
JAUNDICE
DELTA BILIRUBIN-CONJUGATED BILIRUBIN BOUND TO
ALBUMIN
 LIVER ENZYMES
A.L.T: SPECIFIC TO LIVER,VALUE INCREASED
SIGNIFICANTLY IN HEPATOCELLULAR JAUNDICE.
A.S.T:FOUND IN LIVER,CARDIAC MUSCLE,SKELTAL
MUSCLE,KIDNEY, BRAIN,RBCS &WBCS
AST/ALT>3:1- INDICATOR OF ALCOHOLIC LIVER DISEASE
ALP,GGT,5NUCLEOTIDASE-MARKERS OF CHOLESTASIS
 S.PROTEIN
DECREASED ALBUMIN IS INDICATOR OF
CHRONIC LIVER DISEASE
ELEVATED GLOBULIN IS ALSO SEEN
 COAGULATION FACTORS
ALL CLOTTING FACTOR ARE SYNTHESISED IN
LIVER(EXCEPT FACTOR VIII)
FACTOR V IS MOST SPECIFIC TO LIVER INJURY
 PROTHROMBIN TIME
INCREASED IN CASE OF HEPATOCELLULAR AS
WELL AS CHOLESTATIC JAUNDICE.
IF CORRECTED BY GIVING VITAMIN K-
INDICATES CHOLESTATIC COMPONENT
ALTERED EVEN IN ACUTE LIVER INJURY
 Investigations
Pre-hepatic Hepatic Post-hepatic

Urine No Bilirubin ? Bilirubin Bilirubin

Urobilinogen Urobilinogen Urobilinogen
Faeces Dark Pale Pale
Blood FBC - Reticulocyte Bilirubin Bilirubin (>15%
count mixed conjugated conjugated)
Coombs test & unconjugated ALP, GT
Bilirubin (<15% ALP, GT PT correctable
conjugated) AST, ALT with Vit K
ALP Normal PT not
PT Normal correctable with
Vit K
 Management
Symptom relief
Pain, itch
Fluid resuscitation
Correction of coagulopathy
Treat secondary complications
Sepsis, bleeding, anaemia
Treat underlying cause
Medical or surgical
THANK YOU