Hepatocellular jaundice and urine urobilinogen - First Aid and Goljan disagree

[strongboy2005]

So, according to First Aid 2010 (page 326, "Jaundice"), hepatocellular jaundice leads to a normal or decreased urine urobilinogen. The logic seems to be that the decreased-to-normal excretion of conjugated bilirubin into the gut leads to a decreased-to-normal reabsorption of urobilinogen from the gut leading to a decreased-to-normal urinary excretion of urobilinogen. Makes sense.

However, Goljan Rapid Review Pathology (3rd ed, 2010, box 18-1, page 360-361), disagrees saying, "(in hepatocellular jaundice) there is generalized liver dysfunction involving uptake and conjugation of unconjugated bilirubin, secretion of conjugated bilirubin into bile ducts, and recycling of unconjugated bilirubin... Urine urobilinogen is increased (++) because urine urobilinogen is redirected from the liver to the kidneys." He basically says the liver is unable (due to the hepatocellular disease) to take up and recycle its normal quantity of urobilinogen, so more ends up in the urine.

Which explanation is right? Is urine urobilinogen increased, normal, or decreased in hepatocellular jaundice???

Thanks for your help.

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[Encephalectomy]

So, according to First Aid 2010 (page 326, "Jaundice"), hepatocellular jaundice leads to a normal or decreased urine urobilinogen. The logic seems to be that the decreased-to-normal excretion of conjugated bilirubin into the gut leads to a decreased-to-normal reabsorption of urobilinogen from the gut leading to a decreased-to-normal urinary excretion of urobilinogen. Makes sense.

However, Goljan Rapid Review Pathology (3rd ed, 2010, box 18-1, page 360-361), disagrees saying, "(in hepatocellular jaundice) there is generalized liver dysfunction involving uptake and conjugation of unconjugated bilirubin, secretion of conjugated bilirubin into bile ducts, and recycling of unconjugated bilirubin... Urine urobilinogen is increased (++) because urine urobilinogen is redirected from the liver to the kidneys." He basically says the liver is unable (due to the hepatocellular disease) to take up and recycle its normal quantity of urobilinogen, so more ends up in the urine.

Which explanation is right? Is urine urobilinogen increased, normal, or decreased in hepatocellular jaundice???

Thanks for your help.

I'm pretty sure that first aid is correct here. There should be elevated bilirubin in the urine, but not urobilinogen. Urobilinogen isn't made in the liver anyways, it is made as the bilirubin gets broken down in the gut, so there is no way that hepatocellular jaundice, which should decrease the amount of bilirubin that gets into the gut would increase urobilinogen.

 

[fahimaz7]

I'm pretty sure that first aid is correct here. There should be elevated bilirubin in the urine, but not urobilinogen. Urobilinogen isn't made in the liver anyways, it is made as the bilirubin gets broken down in the gut, so there is no way that hepatocellular jaundice, which should decrease the amount of bilirubin that gets into the gut would increase urobilinogen.

I'm with you on this one. Could always open up Robbins as well.

 

[Fuzuli]

Goljan is correct here. Urine urobilinogen is the portion of urobilinogen which arrives to liver by portal circulation, but escapes excretion. Normally this is a small percentage of total urobilinogen arriving to liver. In case of hepatitis, there would be a decrease in excretion of urobilinogen into bile ductules, like you've written. If there's a decrease in excretion of urobilinogen, more will escape into systemic circulation > more will be filtered in kidneys > more urobilinogen in urine.

 

[strongboy2005]

Goljan is correct here. Urine urobilinogen is the portion of urobilinogen which arrives to liver by portal circulation, but escapes excretion. Normally this is a small percentage of total urobilinogen arriving to liver. In case of hepatitis, there would be a decrease in excretion of urobilinogen into bile ductules, like you've written. If there's a decrease in excretion of urobilinogen, more will escape into systemic circulation > more will be filtered in kidneys > more urobilinogen in urine.

But if there is less conjugated bilirubin in the gut, then I would also expect the total production of urobilinogen to drop.

I took a brief look in Robbins and it didn't say one way or another.

 

[Fuzuli]

But if there is less conjugated bilirubin in the gut, then I would also expect the total production of urobilinogen to drop.

I took a brief look in Robbins and it didn't say one way or another.

That's true, but even when there's a less amount of urobilinogen returning to liver, much of it will escape to systemic circulation due to the transport defect seen in hepatocytes (keep in mind that urobilinogen is water soluble, like conjugated bilirubin).

This is illustrated well in Goljan. In acute hepatitis (C in the diagram), there's hyperbilirubinemia with both conjugated and unconjugated bilirubin increased, which the latter is indicated as [UCB++]. But because of the hepatocyte dysfunction, a less amount of conjugated bilirubin (compared to the unconjugated bilirubin) will reach the bowels, which is indicated as [CB+]. In comparison, in extravascular hemolysis (B in the diagram) the amount of UCB reaching the liver and the amount of CB reaching the intestine is the same [UCB++, CB++].

Let's go back to (C). Even though there's less amount CB reaching the bowel and therefore less UBG reaching back to the liver [UBG+ in the liver, indicated by the thin line at top], most of the UBG will not go back to the intestines. Since UBG is water soluble, it will pass into serum. This is indicated as a thicker line below the thin line. Ultimately, UBG and CB will pass into urine, which is indicated as [UBG+++, CB++].

Think of it as a one way valve: All the UBG from the bowel can enter into the liver, but almost none of it can go back. Therefore, UBG in the liver will continue to increase, which means that UBG in the urine will increase.

 

[turkeyjerky]

Agree w/ above--Goljan's right here. I spent a fair amount of time looking into this last year when I was studying for step 1. The FA explanation makes sense at first--and screws a lot of people up, but Goljan's is correct.

 

[Encephalectomy]

I'm sold, thanks for the help guys!

 

[hrandani]

I used to be a very patient and understanding person, but whenever I see two books contradict each other about a basic point like this I just want to throw everything out my third story window and live under a bridge.

I don't know why. Maybe it's just one of those things where you think about why you wanted to go to medical school, to really learn about how stuff works. Instead you just end up memorizing a bunch of disconnected stuff someone else doesn't bother to explain fully. There's just never enough time to work it out on your own either.

Like when you read in a pharm book that the mechanism isn't known for sure, but then on your exam they list all 4 possible theories as answers and then ask you which one is correct. I don't know, I wasn't in the lab man!

 

[OveractiveBrain]

I used to be a very patient and understanding person, but whenever I see two books contradict each other about a basic point like this I just want to throw everything out my third story window and live under a bridge.

I don't know why. Maybe it's just one of those things where you think about why you wanted to go to medical school, to really learn about how stuff works. Instead you just end up memorizing a bunch of disconnected stuff someone else doesn't bother to explain fully. There's just never enough time to work it out on your own either.

Like when you read in a pharm book that the mechanism isn't known for sure, but then on your exam they list all 4 possible theories as answers and then ask you which one is correct. I don't know, I wasn't in the lab man!

The effort youre putting in now will pay you back in spades later. I looked at this post to see if I could offer insight. Unfortunately, its been too long for me to actually recall urobilinogen pathways. There was no question as to the theory, only the memroization of the detail (up or down). While in some ways its frustrating for you to study now, knowing that you will never use the specific details now, realize how useful it will be later.

The very fact that this argument is happening is NOT because two review books disagree. It is because the learner has taken the time to develop an understanding of the material, and is trying to rationalize the concept. Water-solubility, hepatocellular versus hemolytic vs obstructive jaundice, conjugated vs unconjugated bilirubin ALL ACTUALLY MATTER. This one minutia of urobilinogen (which is never considered in real life) has prompted a mastery of what actually matters. It forced you to study something useful in order to get the useless thing (the thing that will probably get you more points).

Look at a second benefit. This attending says one thing, this says another. What was the response in this thread? Look it up yourself. That is exactly what you SHOULD so. Look at the evidence (in this case, look at Robbins) and try to rationalize which was correct. In this instance it was two review books. In real life it will be two papers, two attendings, or two colleagues. The life skill of looking up the information and rationalizing through the concepts you already know will make you a better physician down the road.

Finally, it has prompted a discussion in open forum for everyone struggling with the same concept to read, contribute to, and learn from. While stuck in the library cramming for a test, stressed out harder than you ever thought possible, seeing nothing but the dismal end of your medical career (don't worry, you WILL pass) most learners in their second year fail to see just how awesome this process is. You suffer, but you become better doctors, a stronger community, and better people for it.

Take heart. The mass of details you are learning (and will promptly forget on diarrhea day, i mean test day) are reinforcing fundamental concepts that will make understanding diagnosis and treatment of disease infinitely easier in your third year and in your residency. It is not the details but rather the forced understanding of the fundamentals by those details that makes Step studying worth while.

That, and the 242 you need for your Ortho residency, since you this thread is about such minutia where the concept has clearly already been mastered.

 

[kstreet]

In hepatic jaundice, the urinary urobilinogen may be low when the amount of bilirubin released into the gut is significantly reduced. It may, however, be elevated if damage to the liver cell results in deficient uptake of the circulating urobilinogen.

 

[dangit]

so on the actual exam, what is the right answer? elevated urine urobilinogen or normal/decreased? or does it not matter?

 

[hrandani]

Awesome post OveractiveBrain.

 

[unsung]

so on the actual exam, what is the right answer? elevated urine urobilinogen or normal/decreased? or does it not matter?

Haha. FA has SO many errors (just spent an annoying bit of time look over the posted "known" errata & annotating into my book)...

Thing about Goljan is, he actually dives into the pathoPHYS... FA merely lists some lab findings & a bunch of facts, so it's not hard to imagine FA getting it wrong. That diagram in Goljan showing obstructive vs hemolytic, UCB/CB levels etc seems to make sense to me... I'm trusting Goljan on this.

 

[mrmandrake]

Thanks for all the answers here guys. Took me thirty minutes just to understand what was going on. It seems pretty simple now but I was pretty confused.

I think some guys here explained it pretty well but the main concept I had to understand that was not clear in the image in Goljan 3rd edition was that urobilinogen is reabsorbed into the blood and makes it back to the liver. At that point, it can be excreted as bile back into the intestines. This is the mechanism that is messed up with viral hepatitis and so urobilinogen has to go into the urine and so it is increased in the urine. I struggled to understand that one point and I hope that helps someone else reading this.