3. BY DR WAQAR MBBS, MRCP ASSISTANT PROFESSOR INTERNAL MEDICINE
JAUNDICE BY
DR WAQAR
MBBS, MRCP
ASSISTANT PROFESSOR
INTERNAL MEDICINE

4. DEFINITION
Yellow discoloration of the skin, sclera & mucus membranes due to bilirubin deposition, is called jaundice

5. Normal Bilirubin Metabolism
Bilirubin is formed by the breakdown of RBCs
& hemoglobin in the spleen
* It is an excretory product

6. Bili. Metabolism (contd)

7. Contd.
Old RBCs destroyed in the spleen Hb. is released changed to bilirubin ( this is indirect or unconjugated bili.) carried in the blood by albumin reaches the liver joined with glucuronic acid to form direct or conjugated bili. Excreted in the bile changed to urobilinogen & then stercobilin in the intestine excreted in the stool ( sterco. gives color to the stools. If no stercobilin, then stools will be pale). Some urobilin is absorbed & excreted in urine

8. TYPES OF BILIRUBIN INDIRECT ( Also called unconjugated)
*Not soluble in water
*Does not come in urine
DIRECT ( Also called conjugated)
* Indirect bili. + glucuronic acid =
direct or conjugated bili.
*Water soluble
*Can come in urine
TOTAL BILIRUBIN ( SUM OF ABOVE)

9. Normal Values Total serum bilirubin: 0.2 to 1.2 mg/100ml
Direct: 0.1 to 0.3 mg%
Remaining is indirect
If total bili. more than 3mg% jaundice

10. Types of Jaundice PREHEPATIC JAUNDICE HEPATIC JAUNDICE
POSTHEPATIC JAUNDICE
* In pre-hepatic jaundice, indirect bilirubin is
high in the blood.
* In hepatic & post-hepatic jaundice,“mainly”
direct bili. is high .

11. LAB COMPARISON PREHEPATIC HEPATIC & POST-HEP.
Blood : a) Indirect bili a) Mainly direct
b) ALT, AST & b) High enzymes
Alk.Phos “norm.”
2) Urine : a) No bilirubin a) Bili. present l

12. Causes of Pre-Hepatic Jaundice
HEMOLYSIS CONGENITAL
HYPERBILIRUBINEMIA
Hereditary sphero-
-cytosis
2) Autoimmune hemo ) Gilbert’s Syndrome
anemia
3) Megaloblastic anemia ) Criggler-Najjar syndr.
4) Transfusion reaction
5) Neonatal jaundice (intramedullary hemolysis)

13. NEONATAL JAUNDICE ( a kind of prehepatic jaundice)
Occurs in 50% of newborns
Due to destruction of fetal RBCs
Rx : Phototherapy ( blue light ) or phenobarbital.
If not treated, or if severe, can cause brain damage ( kernicterus) due to deposition of indirect bilirubin in the brain.

14. Who can answer this?
WHY DOES BRAIN DAMAGE “NOT” OCCUR IN ADULTS WITH HEMOLYTIC ANEMIAS?

15. LABS IN HEMOLYTIC JAUNDICE
Blood:
* High bilirubin ( indirect & total)
* Blood picture of hemolysis ( low Hb., low
haptoglobin, high LDH)
2) Stool:
* stool color is normal ( not pale)
3) Urine:
* No bili. ( indirect bili is insoluble)
4) Liver enzymes normal in blood (AST,ALT etc)

16. GILBERT’S SYNDROME * A genetic disorder of the liver Normally :
indirect bili. ( coming to the liver) + glucoronic acid direct bili.
The enzyme causing this reaction is absent in
Gilbert’s syndrome indirect bilirubin
accumulates in the blood jaundice

17. Gilbert’s ( contd)
* Benign condition * Usually asymptomatic * Patient may complain of fluctuating jaundice ( comes & goes), specially after stress, fasting. * Usually, no treatment needed, just reassure

18. Hepatic Jaundice CAUSES All kinds of hepatitis: * Viral: A,B,C etc
* Drugs: Panadol,Halothane, INH
* Autoimmune hepatitis
* Alcohol
2) Cirrhosis (any type)
3) Liver mass eg. hepatoma, metastases,lymphoma
4) Pregnancy: In pregnancy, there is poor flow of
bile in the intrahepatic ducts (intrahepatic stasis)
5) CHF: Causes backpressure & passive liver
congestion intrahepatic stasis

19. Labs in Hepatic causes of Jaundice
Blood: * High bili ( mainly direct but indirect
also)
* High liver enzymes ( ALT, AST,
Alkaline phosphatase)
( In hepatitis, ALT & AST are much higher than
Alk. Phosph)
2) Urine:
* Bilirubin present (which type?)

21. Post Hepatic Jaundice
Here, there is obstruction to the flow of bile outside the liver & bile does not reach the intestine.
CAUSES
Common bile duct stone
Strictures of the CBD
Cholangiocarcinoma (cancer of gall bladder)
Ca head of pancreas
Pancreatitis
Primary Sclerosing Cholangitis

22. LABS IN POSTHEPATIC JAUNDICE
1) BLOOD : * Bilirubin ( mainly direct) *AST, ALT ( but not like hepatic jaundice) * ALK PHOS & GGT: (very high)

23. REMEMBER Alkaline Phosphatase & GGT will be very high
whenever there is obstruction or stasis to the
flow of bile eg:
Bile duct obstruction (eg stone)
Primary biliary cirrhosis (intrahepatic stasis)
Mass lesions in the liver (Ca., liver abscesses)
Pregnancy

24. Post hepatic jaundice labs (contd)
2) Stool: * Pale stools ( no bili. Coming to the intestine, so no urobilin and stercobilin formed. * Steatorrhea ( excess fat in the stools) 3) Urine: * Bilirubin present ( which type? )

25. APPROACH TO A JAUNDICED PATIENT
Keeping in mind all the major causes of jaundice, take a detailed history.
Ask the duration:
* Short duration in acute hepatitis, long in
cirrhosis, CBD obstruction.
2) Persistent or fluctuating:
* Gilbert’s syndrome: Fluctuating
* All other conditions “usually” persistent
3) Any abdominal pain?
* Hepatitis RHC discomfort
* CBD stone severe colicky pain in upper abd.
* Ca pancreas continuous pain in mid abd.

26. Approach (contd)
4) Any wt. loss? * Significant wt loss in Ca. pancreas, hepatoma 5) Nausea/vomiting? * Hepatitis, Ca., CBD stone 6) Stool color: * Pale in post hepatic jaundice(all causes), * Primary biliary cirrhosis * Somewhat pale in hepatitis 7) Family history of jaundice/ anemia * eg hereditary spherocytosis

27. Approach (contd)
8) Drug history: ( even over the counter drugs) * Drug induced hepatitis (panadol, INH) 9) Any pruritus? ( HIKKA) * PBC, & post hepatic obstructions (Ca, CBD stone etc) 10) H/O iv drugs, blood transfusion, multiple unknown sexual partners, H/O nonsterile syringe use high risk of Hep B & C,

28. Approach (contd)
11) Travel history (v. important) * Hep A ( food & water borne) 12) Any recent surgery? * Hepatitis due to anesthetic agents 13) Alcohol & other addictions * Alcoholic hepatitis & cirrhosis 14) Any recent flu like illness? * Ebstein Barr virus & many other viruses can cause mild jaundice.

29. Approach (contd)
15) On Exam., look for * Signs of chronic liver disease( cirrhosis) * Mass in the abdomen ( Ca pancreas) * Anemia ( hemolytic anemias) * Hepatomegaly( hepatitis & many other diseases) * Scratch marks ( pruritus) * Cachexia /wt loss (cirrhosis,Ca.).

30. Approach (contd) INVESTIGATIONS TO ORDER IN JAUNDICE CBC
LFTs ( bili, liver enzymes)
Serum albumin
Urine
Stool not done routinely
U/S abdomen
Once the diagnosis is narrowed, do specific
tests for the suspected disease.

31. Investigations (contd)
CBC:
* Anemia in case of hemolysis & chronic liver
diseases ( cirrhosis)
* Low platelets ( in cirrhosis)
2) LFTs (most important) :
*High indirect bili Hemolysis, Gilbert’s
* High mainly direct Hepatic & post-hepatic
causes
* AST & ALT very Hepatitis
* Alk Phos very high PBC, Liver mass, all post
hepatic causes

32. Investigations (contd)
3) Serum albumin: low in cirrhosis 4) U/S abdomen : * Will show hepatic & post hepatic lesions

33. THANK YOU
BUT WAIT,
WE HAVE ANOTHER
LECTURE