By Dr.Hepa

1. jaundice

2. Jaundice
• define as the yellow discoloration of the
skin, sclerae and mucous membranes due to
an increased bilirubin concentration in the
body fluids.
• It is usually detectable clinically when
the plasma bilirubin exceeds 50 μmol/l (∼3
mg/dl)
• Normal bilirubin (0.3–1.2 mg/dL ) 5–21
μmol/
• sclerae,have a particular affinity for
bilirubin due to high elastin content

3. • Overview of Haeme Degradation
• After 120 days RBCs are taken up and
degraded by the RES, (liver and spleen)
• 85% of heme comes from mature RBCs.
• 15% is from turnover of immature RBCs
, cytochromes from extraerythroid tissues

4. • Bilirubin metabolism
• Between (250-300 mg) of bilirubin is
produced from the catabolism of haem
every day.
• Bilirubin in the blood is almost all
unconjugated and it is not water-soluble, it
bound to albumin and does not pass into the
urine.

6. • Conjugated bilirubin is metabolised by
colonic bacteria to form stercobilinogen,
which may be further oxidised to
stercobilin.
• A small amount of stercobilinogen (4
mg/day) is absorbed from the bowel and
excreted in the urine, is known as
urobilinogen or, with further oxidisation to
urobilin

8. posthepaticic
hepatic
Pre-hepatic
Defective transport
of bilirubin by the
biliary duct system
Defective
uptake
Increased quantity
of bilirubin.
e
Defective
conjugation
Decreased transport to
the liver.
e
Defective excretion
of bilirubin by liver
cells.

9. Causes of hemolytic jaundice
Hemolytic anaemia
Hepatic jaundice
• Hepatitis
• Cirrhosis
• Drugs & Toxins
• Genetic condition (Gilbert’s etc)
• Liver tumour (primary or secondary)
• Obstructive jaundice
• Obstruction in the lumen (gallstone)
• Obstruction in the wall (atresia, stricture, Chronic
cholangitis, tumour of bile duct)
• External compression (pancreatitis, tumour, pancreatic
cysts

10. • Causes of Hyperbilirubinemia
• I. Indirect hyperbilirubinemia
• A. Hemolytic disorders
• 1. Inherited:
• Spherocytosis, elliptocytosis, G6PD and pyruvate kinase
deficiencies
• Sickle cell anemia
• 2. Acquired: auto immune hemolysis
• B. Ineffective erythropoiesis
• B12, folate,, and severe iron deficiencies
• C. Drugs: rifampicin,probenecid, ribavirin
• D. Inherited conditions
• a. Crigler-Najjar types I and II
• b. Gilbert’s syndrome

11. • 2.Direct hyperbilirubinemia
• A. Inherited conditions
• Dubin-Johnson syndrome
• Rotor’s syndrome
• B. Acquired: obstruction to biliary system

12. • Haemolytic jaundice
• It results from ↑ destruction of RBC or their precursors
in the marrow, causing ↑ bilirubin production.
• It is usually mild because a healthy liver can excrete a
bilirubin load six times greater than normal before
unconjugated bilirubin accumulates in the plasma.
• ↑ excretion stercobilinogen leads to normal-coloured or
dark stools. (↑ stercobilin)
• ↑ urobilinogen excretion causes the dark urine colour
because urobilin is formed. (↑ urobilin)
• Pallor due to anaemia, and splenomegaly due to
excessive reticulo-endothelial activity are usually present.
• The plasma bilirubin is usually less than 100 μmol/l (∼6
mg/dl) and the Liver functions are otherwise normal.

13. • Hepatocellular jaundice
• Hepatocellular jaundice results from an inability of the
liver to transport bilirubin into the bile, occurring as a
result of parenchymal liver disease.
• Bilirubin transport across the hepatocytes may be
impaired at any point between uptake of unconjugated
bilirubin into the cells and transport of conjugated bilirubin
into the canaliculi.
• In addition, swelling of cells and oedema resulting from
the disease itself may cause obstruction of the biliary
canaliculi.
• The concentrations of both unconjugated and conjugated
bilirubin in the blood increase.
• The severity of jaundice, the other clinical features, the
investigation and treatment vary with the underlying
disease.

14. • Obstructive jaundice
• Cholestasis may be due to failure of the
hepatocytes to generate bile flow, to
obstruction of bile flow in the bile ducts in
the portal tracts, or to obstruction of bile
flow in the extrahepatic bile ducts between
the porta hepatis and the papilla of Vater.

15. • Causes :
• Intrahepatic
• Primary biliary cirrhosis
• Primary sclerosing cholangitis
• Alcohol & Drugs
• Autoimmune hepatitis
• Cystic fibrosis
• Post-operative
• Hodgkin lymphoma

16. • Extrahepatic
• A. Malignant
Cholangiocarcinoma, CA Pancreatic,
Gallbladder cancer, Malignant involvement of
the porta hepatis lymph nodes
• B. Benign
• 1. Choledocholithiasis
• 2. Primary sclerosing cholangitis
• 3. Chronic pancreatitis
• 4. AIDS cholangiopathy

17. • Approach to patient with jaundice
• History
• Fever? abdominal pain ?anorexia?---
infection.
• Recent use of drug?---hepatic toxicity or
hemolysis
• Injection drug user, blood transfusion,
unsafe sex-----viral hepatitis.
• Chronic alcoholic-----alcoholic liver
disease
• Chang incolour of stool & urine.
• Clay colour stool in obstructive jaundice

18. • Physical exam.
• General
Pallor, evidence of bleeding tendency, scrash
marks, sign of chronic liver disease,LN
enlargment.
• systemic
Ascites, splenomegaly, Palpable
gallbladder+Jaundice------ most likely cancer
(courvoisier”s law).

19. • Investigation
• CBC, blood film---??
• LFT - ↑ ALT, AST---inflammation of liver.
• ↑ Alkaline phosphotase& GGT---- obstruction
of bileduct.
• Low albumin -----chronic liver disease.
• Viral marker (hepatitis B,C,D).
• Ultrasound: gallstone or stone in CBD, tumour
in liver or pancrease …etc.
• MRCP ---MRI of billiary system
• ERCP.-diagnostic
• therapeutic: remove stone ,relive obstruction.

20. Conditions mimic jaundice
Carotenoderma is the yellow color of the
skin by the presence of carotene;
healthy individuals who ingest excessive
amounts of vegetables and fruits contain
carotene In carotenoderma the pigment is
concentrated on the palms, soles, forehead,
and nasolabial folds, but sparing of the
sclerae.
drug.. Quinacrine can cause discoloration
of the sclerae

21. Function test Pre-hepatic jaundice Hepatic jaundice Post-hepatic jaundice
Total bilirubin Normal / increased increase
Conjugated bilirubin Normal Increased Increased
Unconjugated bilirubin Normal / increased Increased Normal
Urobilinogen Normal / increased Decreased Decreased / negative
Urine color Normal
Dark (urobilinogen + conjugated
bilirubin)
Dark (conjugated bilirubin)
Stool color Normal Normal/pale Pale
Alkaline phosphatase levels
Normal
Increased
Alanine transferase and aspartate
transferase levels
Increased
Conjugated bilirubin in urine Not present Present
Splenomegaly Present Present Absent