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Jaundice is caused by abnormalities in bilirubin metabolism and excretion.
Abnormalities in the metabolism or excretion of bile result in development of jaundice.
Clinical jaundice is evident when levels are above 50 µmol/l (2.5 mg/dl)manifesting as a yellow discoloration of the sclerae and skin.

Jaundice is biochemically divided into conjugated and unconjugated types.
Jaundice can be caused by impaired bilirubin metabolism at several levels. It can be divided into two
main biochemical types.

In unconjugated hyperbilirubinaemia there is excessive unconjugated bilirubin in the blood.
Disorders causing this pattern of disease are mainly excessive generation of bilirubin
or abnormal hepatocyte metabolism.

Many disorders cause the pattern of jaundice known as conjugated hyperbilirubinaemia,
in which there is excessive conjugated bilirubin in the blood. The most common cause
is obstruction of bile secretion.
Jaundice is caused by abnormalities in bilirubin metabolism and excretion
Abnormalities in the metabolism or excretion of bile result in development of jaundice.
Biochemical jaundice can be defined as an increase in the plasma bilirubin level above
the normal level of about 18-24 µmol/l (1.2 mg/dl).

Different laboratories may have different reference ranges.
Jaundice is biochemically divided into conjugated and unconjugated types
Disease which causes generalized damage to hepatocytes results in
a predominant conjugated hyperbilirubinaemia, as the main rate-limiting step in bilirubin
metabolism is excretion by the canaliculi rather than conjugation. Levels often exceed100 µmol/l.
Many of the population have impaired conjugation of bilirubin
Excessive generation of bilirubin is the most important cause of unconjugated hyperbilirubinaemia
Increased bilirubin generation results from excessive destruction of red cells, the main
causes of which are: haemolytic anaemia breakdown of large haematomas;
and abnormal formation of red cells (dyserythropoiesis), which is seen in megaloblastic and
sideroblastic anaemias.

The amount of bilirubin generated exceeds the capacity of the liver to conjugate and
excrete it. Bilirubin circulating in the blood is unconjugated, circulates complexed
to albumen, and does not appear in the urine.
The amount of conjugated bilirubin excreted into the intestine is increased because of
the increased load; some is resorbed as urobilinogen, and this is excreted in increased amounts in the urine.

Reduced uptake of bilirubin by hepatocytes can also cause unconjugated hyperbilirubinaemia.
This may be seen in generalized hepatocellular damage but is a less significant contributor
to jaundice than failure of excretion of conjugated bilirubin. Drugs such as rifampicin interfere
with bilirubin uptake.

Decreased transport of conjugated bilirubin causes conjugated hyperbilirubinaemia and is
mainly caused by biliary obstruction
Abnormal secretion or excretion of conjugated bilirubin results in accumulation of conjugated
bilirubin in the blood. The key clinical features, the combination of which is also known as
cholestatic or obstructive jaundice, are:
• Jaundice.
• Bile is absent from the stools, which are pale as a result.
• Fat absorption is disturbed (development of steatorrhoea) and, as a consequence, there is impaired  absorption of vitamin K.
• Itching develops (pruritus) from accumulated bile salts.
• The urine contains bilirubin (dark urine),as conjugated bili-rubin is soluble in water and can be excreted.
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