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Bilirubin metabolism.docx

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University of Calgary
NURS 203

Bilirubin metabolism: Most of the bilirubin in our blood is unconjugated and derived from the RBC’s when they are old, phagocytosed and destroyed. Unconj bilirubin is the end product, goes to the bloodstream and binds with albumin, goes to the liver and is taken up. Majority of bilirubin is from breakdown of RBC’s (99%), which is all unconj. None of this is in the urine b/c it is lipid soluble. So, it gets taken up by the liver and is conjugated. Any time the cytochrome p450 conjugates bilirubin, or metabolizes any drug, it renders it water soluble. So, we have a lipid soluble unconjugated bilirubin is converted to conjugated bilirubin (direct bilirubin), which is water soluble. One of the purposes of the liver is to render lipid soluble drugs water soluble, so you can pee them out. So, we conjugate it and have water soluble bilirubin. Once bilirubin is taken up by the liver, it is never close to a vessel. So, there is no way it can get into a vascular channel (once it is taken up by the liver). So, if direct conjugated bilirubin is in our urine, this is b/c something happened (either in the liver or bile duct) to have caused it to get there b/c it shouldn’t have access to our blood stream. So, it is taken up in the liver, conjugated, and pumped into the bile ductules; which go into the triad, goes up the common bile duct, some is stored in the GB and goes into the small intestine through the common bile duct. Therefore, bile contains conjugated bilirubin. Its also contains bile salts, cholesterol and estrogen, but has conjugated bilirubin that we will get rid of. So, this conjugated bilirubin takes a long trip down to the colon and the bacterial have been waiting for the conjugated bilirubin and will break it down back into unconjugated bilirubin. Then, it continues to break it down. The bacteria breaks it down to stercobilinogen (what it used to be called). Stercobilinogen oxidizes to stercobilin produces the color of stool. This term is no longer used. Now, it is called urobilinogen (which makes the color of the pigment). It is easier to understand the concept. So, the unconjugated bilinogen is broken down to urobilinogen. All porphyrins are colorless when they are in an ‘-ogen’ compound; however, when you oxidize them, they have color. So, urobilinogen, when it becomes oxidized in the stool becomes urobilin, which is the color of stool. A small portion of urobilinogen is reabsorbed out of the colon. Most of it goes back to the liver. A little of it goes to the kidney and ends up in the urine, where it get oxidized into urobilin. This is the cause of the color of urine. So, the same pigment that colors stool is responsible for coloring urine. We were taught that stercobilinogen is in the stool and urobilinogen is in the urine; however, sterco = uro, so the same compound is responsible for color change in feces and urine. They are not diff pigments, they are the same. So, if you have obstructed bile flow (in the liver or CBD), what should the color of the stool be? Light colored – b/c the urobilinogen would not have access to the stool to color it. Also, would not have urobilinogen in the urine. This leads to jaundice. Jaundice To calculate jaundice, they take the total bilirubin and find out the percentage of bilirubin that is conjugated (direct bilirubin). Example: total is 10, conj = 5, therefore conj bilirubin = 50%. So, they subdivide jaundice into 3 types – conjugated bilirubin less than 20% (therefore most of it is unconjugated), btwn 20-50% (therefore some is conj and unconj), and greater than 50% (most of it is conjugated bilirubin). Its also means that you have obstruction. If it is under 20%, this primary unconjugated hyperbilirubinemia. So what can increase unconj bilirubin? Hemolytic anemias, spherocytosis, SCDz, ABO hemolytic dz of the newborn, Rh hemolytic dz of the newborn, physiologic jaundice of the newborn (b/c they cannot conjugate it). So, there is increased unconjugated bilirubin b/c breaking down more RBC’s, have problems with conjugating enzymes – either too immature or they are missing enzymes (Craigler Najjar syndrome). So, we are either making too much b/c we are breaking down too many RBC’s or we have a problem with conjugating enzymes – which is little babies with physiologic jaundice dz of the newborn, or rare dz’s where we are deficient in the enzyme (Craigler Najjar). The dz’s btwn 20- 50% are hepatitis. Hepatitis = inflammation of the liver (not just some of it, all of it). So, b/c it’s a sick liver, it doesn’t want to take up the unconjugated bilirubin. Unconj liver builds up behind the liver. Inflammation in the liver will maybe destroy the architecture in the liver and break open bile ducts that have conj bilirubin in them. Now, b/c you have disrupted the architecture, there is a possibility of water soluble bilirubin to get into the blood stream (b/c there is necrosis of liver cells and bile ducts – so you will get conjugated bilirubin in there, too) - leading to 20-50%. This includes all the hepatitis (including alcoholic). If it is greater than 50%, this is a NO BRAINER – it is clearly an obstruction of bile. We have intrahepatic obstruction (intrahepatic cholestasis), meaning that you are blocking bile flow in the liver (triad is blocked). Also have extrahepatic cholestasis (outside of the liver). There is only one thing outside the liver that can lead to this – CBD (common bile duct). Therefor
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