Urine urobilinogen and others

[acciddropping]

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Hey guys...
Can you help me with this and see if my thinking is correct? I am trying to understand a table from FA and half makes sense but the other half does not....Thanks in advance!!

Here is how I think. Please correct me if I am wrong.
1) Hepatocellular jaundice ==> the reason it's both direct and indirect billirubin (Br) is because it can either be an uptake problem, conjugation problem or exit problem from the hepatocyte. The reason it can increase urine Br is based on the assumption that the conjugation has occured (that excluded Crig.Naj and Gilbert syndromes) (am I correct?).. BUT, i don't understand WHY urine uroBr is low in this case (is it based on the assumption that some pathology such as Gilbert did not get conjugated??)

2) Obstructive jaundice ==> obstruction post liver and before MRP2 (correct?), therefore, always direct billirubin (BR) is increased. The reason it has increased urine BR is because direct BR is water soluble and it can pee out. The reason it has low urine uroBR is because of the obstruction (correct?) ==> so I should also expect pale poop??? (correct?) because you are not getting uroBR in the gut (so no stercoBr)..

3) Hemolytic jaundice ==> lots of heme should get you lots of unconjugated Br. Conjugation requires the enzyme UDPGT. WHY is Urine Br absent here??? I would think that UDPGT can conjugate the Br. WHY is urine UroBr increased here????

 

[Oblique]

Hey guys...
Can you help me with this and see if my thinking is correct? I am trying to understand a table from FA and half makes sense but the other half does not....Thanks in advance!!
View attachment 180783

Here is how I think. Please correct me if I am wrong.
1) Hepatocellular jaundice ==> the reason it's both direct and indirect billirubin (Br) is because it can either be an uptake problem, conjugation problem or exit problem from the hepatocyte. The reason it can increase urine Br is based on the assumption that the conjugation has occured (that excluded Crig.Naj and Gilbert syndromes) (am I correct?).. BUT, i don't understand WHY urine uroBr is low in this case (is it based on the assumption that some pathology such as Gilbert did not get conjugated??)

2) Obstructive jaundice ==> obstruction post liver and before MRP2 (correct?), therefore, always direct billirubin (BR) is increased. The reason it has increased urine BR is because direct BR is water soluble and it can pee out. The reason it has low urine uroBR is because of the obstruction (correct?) ==> so I should also expect pale poop??? (correct?) because you are not getting uroBR in the gut (so no stercoBr)..

3) Hemolytic jaundice ==> lots of heme should get you lots of unconjugated Br. Conjugation requires the enzyme UDPGT. WHY is Urine Br absent here??? I would think that UDPGT can conjugate the Br. WHY is urine UroBr increased here????

1) Hepatocellular jaundice is problem @ the liver (hepatitis) -> leakiness @ hepatocellular system & sinuses -> both direct & indirect Br leak out. With decreased amount of direct Br going into the GI, less uroBr made, thus less uroBr @ urine.

2) You are correct. Pale stool & dark color urine is caused by the obstruction.

3) Hemolytic jaundice -> increase indirect Br but the hepatocellular system is intact.
Why is urine Br absent?: There may be an increased in indirect Br in the blood, but once the liver conjugate the Br, direct Br goes straight into the GI (there is no reason why they would leak into the blood and get excreted into urine).
WHY is urine UroBr increased here????: UDPGT is saturated in hemolytic jaundice because there is a lot of indirect Br being poured in. If you are making a lot of direct Br -> a lot will go to GI -> a lot of UroBr will be made @ GI -> alot more UroBr will be reabsorbed -> increased in UroBr @ urine.

Hope that helps. If it still doesn't make sense, try taking a look @ Goljan RR.

 

[CherryRedDracul]

Old version of FA? In FA 2014, they divided hyperbilirubinemia into 3 categories (unconjugated, conjugated, mixed) and then listed the diseases that fall under them; I feel that the updated table is far clearer than the old one you posted. Goljan RR also does the same thing and it's worth checking out.

I replied to someone on here regarding jaundice. Perhaps it may be of help.

http://forums.studentdoctor.net/threads/question-about-bilirubun.1068075/

With that said ...

Indirect hyperbilirubinemia: hemolytic anemia would present with increased urine uroBr. Physiologic neonatal jaundice can actually vary (immature UDPGT). Crigler-Najjar and Gilbert would present with none or low, respectively.

Direct hyperbilirubinemia: it's a problem with excretion (obstruction, biliary tract disease, Dubin-Johnson or Rotor which are transport protein defects), so conjugated Br doesn't get squeezed into the intestine. Naturally, less processing into uroBr will occur.

Mixed hyperbilirubinemia: this is in hepatitis and cirrhosis. In FA 2014, it says that urine uroBr could be normal, or it can be increased because the liver cannot re-excrete the reabsorbed uroBr back into the intestines; it shunts it to the kidneys instead. However, it can also be decreased depending on how distorted the liver architecture is. In other words, urine urobilinogen can vary significantly.

All in all, urine urobilinogen isn't a fantastic way to tease out the underlying pathology. Not sure what the exam writers think of that.

 

[acciddropping]

Old version of FA? In FA 2014, they divided hyperbilirubinemia into 3 categories (unconjugated, conjugated, mixed) and then listed the diseases that fall under them; I feel that the updated table is far clearer than the old one you posted. Goljan RR also does the same thing and it's worth checking out.

I replied to someone on here regarding jaundice. Perhaps it may be of help.

http://forums.studentdoctor.net/threads/question-about-bilirubun.1068075/

With that said ...

Indirect hyperbilirubinemia: hemolytic anemia would present with increased urine uroBr. Physiologic neonatal jaundice can actually vary (immature UDPGT). Crigler-Najjar and Gilbert would present with none or low, respectively.

Direct hyperbilirubinemia: it's a problem with excretion (obstruction, biliary tract disease, Dubin-Johnson or Rotor which are transport protein defects), so conjugated Br doesn't get squeezed into the intestine. Naturally, less processing into uroBr will occur.

Mixed hyperbilirubinemia: this is in hepatitis and cirrhosis. In FA 2014, it says that urine uroBr could be normal, or it can be increased because the liver cannot re-excrete the reabsorbed uroBr back into the intestines; it shunts it to the kidneys instead. However, it can also be decreased depending on how distorted the liver architecture is. In other words, urine urobilinogen can vary significantly.

All in all, urine urobilinogen isn't a fantastic way to tease out the underlying pathology. Not sure what the exam writers think of that.

Yes, it's from FA2013.

 

[chronicidal]

I have the impression that urine urobilinogen is low yield and not used clinically. Just know it increases with hemolytic anemia.

Also the table in FA 2014 is erroneous insofar as causes of indirect hyperbilirubinemia other than hemolysis would not cause increased urobilinogen. Check out the not-yet-accepted errata spreadsheet on the FA website.

 

[CherryRedDracul]

I have the impression that urine urobilinogen is low yield and not used clinically. Just know it increases with hemolytic anemia.

Also the table in FA 2014 is erroneous insofar as causes of indirect hyperbilirubinemia other than hemolysis would not cause increased urobilinogen. Check out the not-yet-accepted errata spreadsheet on the FA website.

You're absolutely correct on both counts. Urine urobilinogen is not very clinically relevant because it can be so variable and there are better things to look at. Insider info tells me that the FA guys are looking into removing the urine urobilinogen portion of the table altogether.

 

[DermViser]

You're absolutely correct on both counts. Urine urobilinogen is not very clinically relevant because it can be so variable and there are better things to look at. Insider info tells me that the FA guys are looking into removing the urine urobilinogen portion of the table altogether.

It may not be used clinically (as are many other tests learned in basic sciences not used in real life), however, the point is more to test your knowledge of basic science mechanisms.