Causes of jaundice vary from non-serious phototherapy for neonatal jaundice pdf potentially fatal. Conjugated bilirubin can be confirmed by finding bilirubin in the urine. Treatment of jaundice is typically determined by the underlying cause.
Medical management may involve treating infectious causes and stopping medication that could be contributing. Urine is dark in colour. Slight increases in serum bilirubin are best detected by examining the sclerae, which have a particular affinity for bilirubin due to their high elastin content. Depending on the level of exposure, the effects range from clinically unnoticeable to severe brain damage and even death. Newborns are especially vulnerable to hyperbilirubinemia-induced neurological damage and therefore must be carefully monitored for alterations in their serum bilirubin levels. When a pathological process interferes with the normal functioning of the metabolism and excretion of bilirubin just described, jaundice may be the result. Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects.
Intrinsic defects in RB cells B. The pathology is located within the liver caused due to disease of parenchymal cells of liver. The pathology is located after the conjugation of bilirubin in the liver caused due to obstruction of biliary passage. The increased breakdown of red blood cells leads to an increase in the amount of unconjugated bilirubin present in the blood and deposition of this unconjugated bilirubin into various tissues can lead to a jaundiced appearance.
In jaundice secondary to hemolysis, the increased production of bilirubin leads to the increased production of urine-urobilinogen. The blood contains an abnormally raised amount of conjugated bilirubin and bile salts which are excreted in the urine. Laboratory findings depend on the cause of jaundice. Kernicterus is a condition not associated with increased conjugated bilirubin. Plasma protein show characteristic changes. Plasma albumin level is low but plasma globulins are raised due to an increased formation of antibodies.
Bilirubin transport across the hepatocyte may be impaired at any point between the uptake of unconjugated bilirubin into the cell and transport of conjugated bilirubin into biliary canaliculi. Hence in hepatocellular jaundice, concentration of both unconjugated and conjugated bilirubin rises in the blood. However, excretion is the rate-limiting step, and usually impaired to the greatest extent. As a result, conjugated hyperbilirubinaemia predominates. The unconjugated 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 unconjugated type, and this conjugated bilirubin which did not go to intestine to become urobilinogen gives the urine the dark color. In complete obstruction of the bile duct, no urobilinogen is found in the urine, since bilirubin has no access to the intestine and it is in the intestine that bilirubin gets converted to urobilinogen by microorganisms, with the urobilinogen later being partially reabsorbed from the intestine into the general circulation, and then excreted into the urine. However, although pale stools and dark urine are a feature of biliary obstruction, they can occur in many intra-hepatic illnesses and are therefore not a reliable clinical feature to distinguish obstruction from hepatic causes of jaundice. Patients also can present with elevated serum cholesterol, and often complain of severe itching or “pruritus” because of the direct and indirect effects of pruritogens in bile such as bile salts.
No single test can differentiate between various classifications of jaundice. A combination of liver function tests is essential to arrive at a diagnosis. Serum bilirubin normally drops to a low level without any intervention required. This condition has been rising in recent years due to less time spent outdoors. Bilirubin count is lowered through bowel movements and urination, so frequent and effective feedings are especially important. Jaundice itself is not a disease, but rather a sign of one of many possible underlying pathological processes that occur at some point along the normal physiological pathway of the metabolism of bilirubin in blood.
When red blood cells have completed their life span of approximately 120 days, or when they are damaged, their membranes become fragile and prone to rupture. Two reactions then take place with the heme molecule. The next step is the reduction of biliverdin to a yellow color tetrapyrol pigment called bilirubin by cytosolic enzyme biliverdin reductase. This bilirubin is “unconjugated,” “free” or “indirect” bilirubin.
Approximately 4 mg of bilirubin per kg of blood is produced each day. The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described. The reaction is catalyzed by the enzyme UDP-glucuronyl transferase. From here urobilinogen can take two pathways. Stercobilin and urobilin are the products responsible for the coloration of feces and urine, respectively. It is unclear how common it is among adults. Most patients presenting with jaundice will have various predictable patterns of liver panel abnormalities, though significant variation does exist.