A simple presentation of jaundice by first year medical students in Uganda

1. JAUNDICE
BY
TOOLIT GIVENS
AYIKORU HILDA DIANA
WABULE ARLENA

2. DEFINITION
 Is the yellowish discoloration of the skin, sclera of the eyes and mucosa
due deposition of bilirubin.
 Imbalance between production and clearance of bilirubin.
 Sclera has a high affinity due to elastin content-3mg/dl

3. CAUSES
 Excessive hemolysis
 Acute inflammation of the liver (hepatitis) due to: -
viruses (hepatitis A ,B, C ) ,CMV, EBV), alcohol, drugs
e.g. overdose of paracetamol ,anti-TB, halothane
 Glucuronyl transferase deficiency (Gilbert’s syndrome
and Crigler-Najjar syndrome
 Obstruction of the bile duct
 Cholestasis

4. Rare causes
 Crigler-Najjar syndrome –impairment of specific
enzymes responsible for processing bilirubin
 Dubin-Johnson syndrome- form of chronic jaundice that
prevents conjugated bilirubin from being secreted from
the cells of the liver.
 Pseadujaundice- harmless form of jaundice. Causes
yellowing of the skin due to eating large quantities of
carrots, pumpkin, melon

5. Bilirubin Levels
 Adults and older children- 0.3-0.6mg/dL.
 Greater than 1.2mgdL is when it becomes visible as
jaundice.
 Around 97% of infants borne after 9months of pregnancy
have levels lower than 13mg/dL. If greater than this,
they are referred for further investigation.
 NB: ranges vary between laboratories.

6. Signs and Symptoms
 A yellow tinge to the skin and whites of the eye.
 Pale stool
 Dark urine
 Itchiness

7. Bilirubin Metabolism

8. Enterohepatic Urobilinogen

9. Bilirubin metabolism
Haem (e.g from Hb,myoglobin and
cytochromes)
Biliverdin
Haem OxygenaseIron,carbondioxide
Biliverdin reductase
Bilirubin
Conjugated bilirubin
Glucoronyl transferase

10. Types of Jaundice
 Hemolytic Jaundice
 Hepatocellular Jaundice (Intrahepatic)
 Obstructive Jaundice(extrahepatic)

11. Hemolytic Jaundice
 Caused by excessive lysis of RBCs beyond the liver’s
capacity to conjugate it. Therefore the body cannot
excrete all the released bilirubin.
 Is the pre hepatic cause of jaundice.
 It is seen in transfusion reactions, RBC lysis associated
with faulty Hb (eg sickle cell anaemia and thalassemia)
and autoimmune destruction of RBCs.

12. Hemolytic jaundice
 Much of the bilirubin is still unconjugated therefore
urine and stool color are still normal.
 Unconjugated bilirubin levels are elevated because the
liver’s ability to conjugate bilirubin can not keep up
with the magnitude of RBC destruction.

13. Intrahepatic
jaundice(hepatocellular)
 Obstruction in canaliculi decreases the passage of the
passage of conjugated bilirubin into the bile duct
resulting into increased amount of conjugated bilirubin
entering into the bloodstream.
 Here, the urine is dark and frothy and stool may be pale
or nearly normal in color.

14. Intrahepatic (Hepatocellular)
Jaundice
 This occurs in within the liver.
 Decreased hepatic uptake, conjugation, or excretion of
bilirubin due to dysfunction of hepatocytes or
obstruction of the bile canaliculi.
 Liver dysfunction can occur if the hepatocytes are
infected by viruses (e.g. hepatitis ) or if the cells of the
liver are damaged by cancer of cirrhosis.

15. Hepatocellular jaundice
 Can also be caused by drugs(e.g. steroids,
paracetamol,halothane, anti biotics), alcohol,
 Intrahepatic jaundice can also be caused by obstruction
of the bile canaliculi by tumors(cancer) and stones or it
may result from widespread inflammation.

16. Extrahepatic obstructive
jaundice
 In obstructive jaundice, caused either by obstruction of the
bile ducts (which most often occurs when a gallstone or
cancer blocks the common bile duct) or by damage to the
hepatic cells (which occurs in hepatitis).
 The rate of bilirubin formation is normal, but the bilirubin
formed cannot pass from the blood into the intestines.
 The free bilirubin still enters the liver cells and becomes
conjugated in the usual way.
 This conjugated bilirubin is then returned to the blood,
probably by rupture of the congested bile canaliculi and
direct emptying of the bile into the lymph leaving the liver.
 Thus, most of the bilirubin in the plasma becomes the
conjugated type rather than the free type.

17. Obstructive/post hepatic jaundice

18. Jaundice in Newborns
 Around 60% of newborns experience jaundice and this
increases to 80% of premature infants born before 37
weeks of pregnancy.
 Signs will show within 72 hours of birth.

19. Jaundice in Newborns
 Infants with high bilirubin levels will require treatment with either a
blood transfusion or phototherapy.
 In these cases, treatment is vital as jaundice in newborns can lead to
kernicterus, a very rare type of permanent brain damage.

20. Causes of Jaundice in
Newborns
 Frequent breakdown of redblood cells in infants leading
to production of more bilirubin.
 The liver of infants are less developed and therefore
less effective in filtering bilirubin from the body.
 Symptoms will usually resolve without treatment with in
two weeks.

21. Differences between conjugated
conjugated and unconjugaated bilirubin
CONJUGATED UNCONJUGATED
Soluble Insoluble
Can be secreted by the kidneys Bound to albumin and cannot be
secreted.

22. Complications
 Intense itching can cause raw scratching of the skin
leading to insomnia and suicidal thoughts.
 Uncontrolled bleeding because blockage leads to the
shortage of vitamins needed for clotting.
 Kernicterus (common in newborns)

23. Prevention
Maintain health of liver by
-eating a balanced diet
-regular exercise
-not consuming more than the recommended
amounts of alcohol.