Back To CoursePathophysiology Textbook
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There's plenty of stuff around you that is dangerous to you and can kill you. Parasites can kill you, drugs can do the same, and frankly, just by aging, you begin to slowly wither away and break down.
The same exact things can cause the same exact problems to cells in your body called red blood cells. They're the guys that help to transport oxygen all over your body. Just like a deceased person decays and breaks down with time, so too does a red blood cell and its components. The stuff a decaying red blood cell releases is very important in monitoring not only red blood cell health but many other organ systems, as we'll soon find out.
Normally, even in a healthy person, red blood cells eventually reach the end of their life. They live far less than a human, about 120 days in total. But the cool thing is that in that short space of time, they can travel upwards of a total of 300 miles within our body.
Once red blood cells reach their end, either naturally or due to disease, they either burst open in the bloodstream or are removed from circulation by the spleen, an organ that's a retirement and a funeral home all in one for red blood cells. Of course, the spleen only retires the really old, sick, and decrepit red blood cells and lets the healthy ones pass through.
Once a red blood cell dies, its hemoglobin, which is a protein in red blood cells that actually carries the oxygen, is broken down into parts like an old car would be broken down into different parts. One part of hemoglobin is known as 'heme,' and it is this part that's broken down into bilirubin.
More specifically, this bilirubin is known as indirect bilirubin or unconjugated bilirubin; they're synonymous terms. Again, indirect bilirubin is a yellow pigment formed from the destruction of red blood cells. It is released into circulation, but because it's water-insoluble, it must be bound to a blood protein called albumin. Basically, albumin has to hold unconjugated bilirubin's hand because the latter is scared of water. But because albumin cannot be excreted by healthy kidneys, the unconjugated bilirubin cannot be excreted either and therefore must go elsewhere to be ridden of.
That's why unconjugated bilirubin flows into the liver via the bloodstream, where a compound known as glucuronic acid is tacked on (or conjugated to) the unconjugated bilirubin, resulting in the formation of conjugated bilirubin or direct bilirubin, which then becomes the water-soluble form of bilirubin. Again, the terms 'conjugated bilirubin' and 'direct bilirubin' are synonymous.
This water-soluble conjugated bilirubin is then put into a fluid called bile that is formed in the liver, stored in the gallbladder, and secreted into the intestines to be excreted out of the body.
Once in the intestines, some of the conjugated bilirubin is converted by gut bacteria into a compound called urobilinogen. Most of this substance is converted into another compound called stercobilin, which gives feces its yellow-brown color.
The remaining urobilinogen is absorbed back into circulation, some of which goes back into bile and some of which goes into the urine, where it's converted to urobilin, which is partially responsible for urine's yellow color.
There's a reason I explained all of that. It will help you understand why there may be increases in conjugated or unconjugated bilirubin and what that may mean clinically.
If hyperbilirubinemia, abnormally increased levels of bilirubin in the blood, is noted in blood work, it will concurrently cause a person's skin and the whites of their eyes to turn, obviously, a yellow color. We term this coloration 'jaundice.' Jaundice is classified into three categories: prehepatic, hepatic, and posthepatic.
'Prehepatic' implies that the increase in bilirubin is occurring as a result of something occurring 'pre,' or before, the bilirubin even gets to the liver. This is commonly associated with hemolytic anemia, where red blood cells are destroyed en masse for any number of reasons and thereby overwhelm the liver's ability to conjugate the crazy amounts of indirect bilirubin being released into the bloodstream.
Another reason for prehepatic hyperbilirubinemia is as a result of improper delivery of blood to the liver, as per congestive heart failure. Here the liver is simply not receiving an adequate supply of indirect bilirubin for conversion into direct bilirubin.
In either case, the levels of unconjugated bilirubin will usually be higher than the levels of conjugated bilirubin in prehepatic hyperbilirubinemia.
Now, if the liver itself is sick, the cause of the hyperbilirubinemia can be skewed toward the conjugated or unconjugated side, depending on the problem. If the liver cannot take up or convert indirect bilirubin, then levels of unconjugated bilirubin will rise. If, however, the liver cells cannot excrete already-conjugated bilirubin, then the levels of conjugated bilirubin will be higher in hepatic causes of hyperbilirubinemia.
Finally, if the cause of the hyperbilirubinemia is posthepatic, then our problem isn't with the liver. The problem lies somewhere in the biliary tree. If something like a stone is blocking the outflow of bile from the gallbladder, then our levels of conjugated bilirubin will be much higher than unconjugated bilirubin.
In the cases where there is biliary tree obstruction, the conjugated bilirubin is regurgitated back into the bloodstream since it can't go into the intestines. This is what causes conjugated hyperbilirubinemia. Because the conjugated bilirubin is water-soluble, it will be excreted into the urine, unlike unconjugated bilirubin, resulting in bilirubinuria, which is conjugated bilirubin in the urine. This excess pigment causes the urine to become darker than usual (tea-colored). You can boil it down to the fact that bilirubin is like food coloring, and because there's more of it in the urine, the urine will gain more color.
On the flip side, because the conjugated bilirubin isn't reaching the intestines as it should, it cannot be used to give feces its yellow-brown pigment, causing the feces to become paler or clay-colored instead, since our supply of food coloring is diminished. More technically, this is termed acholic stool.
Now you know why I forced you to learn all that stuff in the beginning!
This lesson covered indirect bilirubin and unconjugated bilirubin. Both of them are a yellow pigment formed from the destruction of red blood cells.
When indirect bilirubin is conjugated in the liver, it is called conjugated bilirubin, or direct bilirubin, which then becomes the water-soluble form of bilirubin.
If hyperbilirubinemia, abnormally increased levels of bilirubin in the blood, is noted on blood work, it may be a result of prehepatic, hepatic, and posthepatic causes.
If conjugated bilirubin is inappropriately thrown back into circulation, then bilirubinuria, conjugated bilirubin in the urine, will cause the urine to turn a dark color.
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Back To CoursePathophysiology Textbook
20 chapters | 274 lessons