In certain illnesses of the human body, the skin, the whites of the eye and mucous membranes appear increasingly yellow. This can occur acutely or could even be present from the early days of life. The condition is known as 'icterus' or in other words 'jaundice'.
A) What causes 'jaundice'?
The element in the blood that causes the yellowish discoloration is 'bilirubin'. Usually the amount of Bilirubin in the circulation should be elevated to three times its normal amount for it to precipitate as jaundice.
B) How does bilirubin gets metabolized?
Bilirubins are produced as a byproduct in the breakdown process of red blood cells which usually has a life span of 120 days. Following the breaking up of the cells in the spleen, it gives rise to bilirubin. Usually the bilirubins are shunted to the liver by binding on to albumins in the circulation and will be combined with glucuronide to form the conjugated form of the bilirubin in the liver. The conjugated bilirubin would then be able to pass through the liver channels and enter the gut through absorption by bile and excreted via faeces. Even though this is the usual mechanism in metabolism, sometimes the processes are disrupted.
The disruption of the conjugation process of bilirubin results in the accumulation of the un-conjugated portion in the circulation. The result will be its ability to concentrate in the extra cellular fluid and show up in the mucous membranes.
C) What are the different types of 'Jaundice'?
This could occur in 3 different places, thus named, pre-hepatic, hepatic and post-hepatic.
Pre-hepatic
Causes of increased red cell breakage will give rise to pre-hepatic causes of jaundice. Malaria, congenital spherocytosis and sickle cell disease are conditions giving rise to increased cell breakdown.
Hepatic
The scenario occurs when the liver is unable to do its job in binding the bilrubins adequately with the glucuronides. Any kind of liver cell damage can give rise to this kind of jaundice and alcoholic liver disease and hepatitis is probably the most common of the examples in the community. Hepatotoxicity due to various drugs or substances can give rise to hepatic jaundice.
Neonatal jaundice is also a form of hepatic jaundice where immature liver cells are unable to still function as normal and gives rise to harmless jaundice condition. This usually fades away after few days of birth and usually does not require treatment.
Post-hepatic
The scenario can occur when the hepatic outflow has been blocked and normal bilirubin drainage does not take place. This condition is sometimes called 'obstructive type of jaundice' and can be caused by Gall stones and even cancers. Out of which, cancers of the head of the pancreas, ductal carcinomas and pancreatic psudocysts can also give rise to this condition.
D) What are the investigations available in cases of 'Jaundice'?
Once identified, the clinicians will probe the patients from their history, examination findings and investigations to assess the cause, unless it is obvious, the extent of the damage and available options to further manage the patient. Liver enzyme levels, serum bilirubin levels, serum amylase levels, clotting profile, full blood count would be useful investigations. Apart from these, ultra sound examination of the abdomen, CT and MRI will also be useful.
E) What are the treatment options available for 'jaundice'?
Treatment will be based on its patho-physiology and extent of liver damage, if any. In jaundice appearing in the neonates adequate feeding with close monitoring of the blood bilirubin levels would be sufficient. The danger in neonates is the potential for the bilirubin to cross the barriers to the brain and damage the brain cells, in a condition called 'Kernicterus'. The damage would be irreversible and lifelong. Sometimes the high bilirubin levels in neonates would require a procedure called 'exchange transfusion' where baby's blood is replaced by mother's blood.
In adults, the treatment would be aimed at relieving the underlying problem. The jaundice itself would not be causing any problems for the patient.
A) What causes 'jaundice'?
The element in the blood that causes the yellowish discoloration is 'bilirubin'. Usually the amount of Bilirubin in the circulation should be elevated to three times its normal amount for it to precipitate as jaundice.
B) How does bilirubin gets metabolized?
Bilirubins are produced as a byproduct in the breakdown process of red blood cells which usually has a life span of 120 days. Following the breaking up of the cells in the spleen, it gives rise to bilirubin. Usually the bilirubins are shunted to the liver by binding on to albumins in the circulation and will be combined with glucuronide to form the conjugated form of the bilirubin in the liver. The conjugated bilirubin would then be able to pass through the liver channels and enter the gut through absorption by bile and excreted via faeces. Even though this is the usual mechanism in metabolism, sometimes the processes are disrupted.
The disruption of the conjugation process of bilirubin results in the accumulation of the un-conjugated portion in the circulation. The result will be its ability to concentrate in the extra cellular fluid and show up in the mucous membranes.
C) What are the different types of 'Jaundice'?
This could occur in 3 different places, thus named, pre-hepatic, hepatic and post-hepatic.
Pre-hepatic
Causes of increased red cell breakage will give rise to pre-hepatic causes of jaundice. Malaria, congenital spherocytosis and sickle cell disease are conditions giving rise to increased cell breakdown.
Hepatic
The scenario occurs when the liver is unable to do its job in binding the bilrubins adequately with the glucuronides. Any kind of liver cell damage can give rise to this kind of jaundice and alcoholic liver disease and hepatitis is probably the most common of the examples in the community. Hepatotoxicity due to various drugs or substances can give rise to hepatic jaundice.
Neonatal jaundice is also a form of hepatic jaundice where immature liver cells are unable to still function as normal and gives rise to harmless jaundice condition. This usually fades away after few days of birth and usually does not require treatment.
Post-hepatic
The scenario can occur when the hepatic outflow has been blocked and normal bilirubin drainage does not take place. This condition is sometimes called 'obstructive type of jaundice' and can be caused by Gall stones and even cancers. Out of which, cancers of the head of the pancreas, ductal carcinomas and pancreatic psudocysts can also give rise to this condition.
D) What are the investigations available in cases of 'Jaundice'?
Once identified, the clinicians will probe the patients from their history, examination findings and investigations to assess the cause, unless it is obvious, the extent of the damage and available options to further manage the patient. Liver enzyme levels, serum bilirubin levels, serum amylase levels, clotting profile, full blood count would be useful investigations. Apart from these, ultra sound examination of the abdomen, CT and MRI will also be useful.
E) What are the treatment options available for 'jaundice'?
Treatment will be based on its patho-physiology and extent of liver damage, if any. In jaundice appearing in the neonates adequate feeding with close monitoring of the blood bilirubin levels would be sufficient. The danger in neonates is the potential for the bilirubin to cross the barriers to the brain and damage the brain cells, in a condition called 'Kernicterus'. The damage would be irreversible and lifelong. Sometimes the high bilirubin levels in neonates would require a procedure called 'exchange transfusion' where baby's blood is replaced by mother's blood.
In adults, the treatment would be aimed at relieving the underlying problem. The jaundice itself would not be causing any problems for the patient.
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