Liver Question

[UCSBMed1]

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Hey guys just going over some liver stuff, and I have a question.

How is that, a person with a hemolytic anemia, which would elevate their unconjugated bilirubin, can have an elevated Urinary urobilinogen?

Because they are not able to conjugate this massive amount of unconjugated bilirubin, the conjugated variety will not be present in the urine. How is that, urobilinogen is, when bilirubin requires to first be conjugated and excreted by the liver before intestinal bacteria have access to it in order to convert it to urobilinogen?

I've looked everywhere for the answer, and its driving me crazy. Can anyone help me out?

 

[HiddenTruth]

Hey guys just going over some liver stuff, and I have a question.

How is that, a person with a hemolytic anemia, which would elevate their unconjugated bilirubin, can have an elevated Urinary urobilinogen?

Because they are not able to conjugate this massive amount of unconjugated bilirubin, the conjugated variety will not be present in the urine. How is that, urobilinogen is, when bilirubin requires to first be conjugated and excreted by the liver before intestinal bacteria have access to it in order to convert it to urobilinogen?

I've looked everywhere for the answer, and its driving me crazy. Can anyone help me out?

Ok, first off, most of the credit to this knowledge goes to ramoray cuz he explained it to me raelly well. You might want to look up one of my posts on this subject, and read our discussion. But, bascailly what's happening in the sitatuon you are describing is oversaturation of the liver with bilirubin. So, normally, say a liver takes up 5mg (arbitrary, but takes up much less than its capacity), and is able to conjugate 100mg of BR. So, in severe cases of hemolytic anemia, you have basically saturated the liver's capacity to conjugate any more BR, and therefore you get an increase in UCB-->jaundice. So, the point is that there is more BR uptake in the liver-->incresaed urinary urobillinogen. So, what i am getting at is that in many cases you can have mild-moderate hemolytic anemia and will not see jaundice because the liver's capactiy to conjugate is much greater than what it normally takes up. But, in this case you can still have elevated urinary urobillinogen. Remember, that urinary urobillin is comming from conj BR from the liver--bile duct-->duodenum, etc. Where as if there is straight up BR in urine, then it's an obstructive type of problem, and there is backup. So, basically there is a balance between liver's enzymatic ability to conjugate and capacity of uptake..so in diseased states, the livers capacity to uptake of UCB mite be diminished. But, the key point I think is that the livery takes up only a fraction of what it can. And...so in severe hemolytic anemia..its like you've filled the barrel up (normally it was only 1/4 full), and now everything is just flowing out. So urinary urobillinogen is elevated (because more is getting to the gut, so more is being reabs to kindey, because remember, normally 10% or so is taken up into kidney) and your UCB in blood is elev (jaundice). Alrite, sorry for the drawn out explanation. And, hopefully i cleared this up--I rememver I had some trouble with this, and it's hard to find it straight up in books.

 

[Flintstone]

Hello! Thank you for writing this up. I also am very confused in this matter.

I understand that when the "liver barrel" is filled, then no more conjugation can be done and the bilirubin stays uncongugated. In a normal situation, the conjugated bilirubin, when passed down to the gut (via bile), are reduced by bacteria to become urobilinogen. Part of this urobilinogen pool is oxidized to become urobilin to make the color of our stool and urine; and the rest is recycled to the liver. So, what I don't understand is, in hemolytic disease, there are a lot of unconjugated bilirubin, how do they turn into urobilinogen and excrete in urine? The unconjugated form is not soluble, I suppose? Is it right that there are other metabolic pathways to change the unconjugated bilirubin into urobilinogen?

I guess I am confused in how the gut stuff gets to the urine. Such as in obstructive problem, conjugated bilirubin build up, and how does this contribute to the increase in urine bilirubin? I understand why it is going to decrease the urine urobilinogen (as it cannot pass through the gut and hence not oxidized by bacteria to urobilinogen).

Any help is appreciated.

Thanks very much in advance.

 

[UCSBMed1]

Ok, first off, most of the credit to this knowledge goes to ramoray cuz he explained it to me raelly well. You might want to look up one of my posts on this subject, and read our discussion. But, bascailly what's happening in the sitatuon you are describing is oversaturation of the liver with bilirubin. So, normally, say a liver takes up 5mg (arbitrary, but takes up much less than its capacity), and is able to conjugate 100mg of BR. So, in severe cases of hemolytic anemia, you have basically saturated the liver's capacity to conjugate any more BR, and therefore you get an increase in UCB-->jaundice. So, the point is that there is more BR uptake in the liver-->incresaed urinary urobillinogen. So, what i am getting at is that in many cases you can have mild-moderate hemolytic anemia and will not see jaundice because the liver's capactiy to conjugate is much greater than what it normally takes up. But, in this case you can still have elevated urinary urobillinogen. Remember, that urinary urobillin is comming from conj BR from the liver--bile duct-->duodenum, etc. Where as if there is straight up BR in urine, then it's an obstructive type of problem, and there is backup. So, basically there is a balance between liver's enzymatic ability to conjugate and capacity of uptake..so in diseased states, the livers capacity to uptake of UCB mite be diminished. But, the key point I think is that the livery takes up only a fraction of what it can. And...so in severe hemolytic anemia..its like you've filled the barrel up (normally it was only 1/4 full), and now everything is just flowing out. So urinary urobillinogen is elevated (because more is getting to the gut, so more is being reabs to kindey, because remember, normally 10% or so is taken up into kidney) and your UCB in blood is elev (jaundice). Alrite, sorry for the drawn out explanation. And, hopefully i cleared this up--I rememver I had some trouble with this, and it's hard to find it straight up in books.

You know logically, that is kinda what I was thinking, but that doesn't explain why urine bilirubin is absent. If the liver was still able to conjugate some (but not all) of this massive amount of UCB, there would be CBili in the urine--but there isn't. That is where I get confused. If you aren't conjugating any bilirubin (signified by the lack of of it in the urine) how the h*ll are you getting urobilinogen in the urine, when UCB must first be converted to CBili before it can be excreted by the intestines, and then reabsorbed as urobilinogen?

 

[UCSBMed1]

Hello! Thank you for writing this up. I also am very confused in this matter.

I understand that when the "liver barrel" is filled, then no more conjugation can be done and the bilirubin stays uncongugated. In a normal situation, the conjugated bilirubin, when passed down to the gut (via bile), are reduced by bacteria to become urobilinogen. Part of this urobilinogen pool is oxidized to become urobilin to make the color of our stool and urine; and the rest is recycled to the liver. So, what I don't understand is, in hemolytic disease, there are a lot of unconjugated bilirubin, how do they turn into urobilinogen and excrete in urine? The unconjugated form is not soluble, I suppose? Is it right that there are other metabolic pathways to change the unconjugated bilirubin into urobilinogen?

I guess I am confused in how the gut stuff gets to the urine. Such as in obstructive problem, conjugated bilirubin build up, and how does this contribute to the increase in urine bilirubin? I understand why it is going to decrease the urine urobilinogen (as it cannot pass through the gut and hence not oxidized by bacteria to urobilinogen).

Any help is appreciated.

Thanks very much in advance.

Well your first question is the same one I have, but the second question I can answer.

Remember that urine bilirubin is just conjugated bilirubin. Therefore, in an obstructive disease, you have no problem conjugating bilirubin, but can't excrete it into the bile and therefore duodenum. Thus, this CB is able to be filtered by the kidneys and excreted.

Now if someone can answer how UCB-->urobilinogen, I would be very happy!

 

[Flintstone]

Why did I have so much trouble with Urine bilirubin = Congujaged bilirubin!

I got it now. 🙂 Thank you! Will post if I know the answer to the first Q.

 

[fuegorama]

Now if someone can answer how UCB-->urobilinogen, I would be very happy!

Giving this a stab.
Urobilinogen starts its short life as a bilirubin glucuronide in bile just like everybody else. IT IS CONJUGATED.

However, the glucuronides destined to be urobilinogen are deconjugated by B-glucuronidase in the gut and "degraded to urobilinogen". (quote from Robbins 6th p.848)
The urobilinogen along with the pigment residues that are not absorbed are excreted.

Please let me know if this is how you see this. i have been struggling with the jaundice paths for a while.

 

[Flintstone]

Urobilinogen starts its short life as a bilirubin glucuronide in bile just like everybody else. IT IS CONJUGATED.......
However, the glucuronides destined to be urobilinogen are deconjugated by B-glucuronidase in the gut and "degraded to urobilinogen". (quote from Robbins 6th p.848)
The urobilinogen along with the pigment residues that are not absorbed are excreted.

Thanks you for your input 🙂 I think you are right; and this is how I understand it also. Do you know, in the situation of overwhelming hemolysis (hemolytic jaundice), how do those bilirubin (unconjugated and riding on albumin, I suppose) become urine urobilinogen? The urine urobilinogen is found to increase and the urine bilirubin absent (acholuria) in these patients. These unconjugated bilirubin are insoluable and they can't get to the gut via the conjugate-deconjugate process either.....😕

 

[Ramoray]

ha good job hidden, that was a solid epxlanation it looks like you did indeed learn that topic well. I know everything you have posted ordiscussed or anyone else, and then i read i have really learned alot! anyway here is the thread me and hidden were talking about should help out ill cut a copy one section but search for the whole thread if you want to see the whole discussion on the topic
........
Ya bilirubin **** is confusing i hear ya. I will try to give you an answer for all 3 in one explanation instead of answering each one individually but let me know if i didnt cover something you needed as i am not the most clear explaner of things but ill give it a shot.

So lets start out with intravascular hemolysis--> lysis of RBC in serum leads in release of hemoglobin--> the hemoglobin binds to haptoglobin and makes a complex--> this hem-hap complex is taken up by Mphages where hemoglobin is broken down and the heme group gets converted to bilirubin and released back into teh blood as Unconjugated BR--> the unconj BR binds to albumin.

Now following lysis of rbcs, depending on how much lysis occurs, there is only so much haptoglobin, therefore once its gone the excess hemoglobin cannot bind to hapto, therefore no hem-hap complexes can be made and therefore Mphages cannot take up just plain hemoglobin unless it is in the form of a hem-hap complex which it can recognize. Therefore this hemoglobin free in the serum, and unbounded to haptoglobin is excreted in the urine.

Therefore we can point out a few things
1. lets say just for sake of clarity that 75% of all the hemoglobin released in the lysis was able to bind to haptoglobin and 25% was not due to lack of haptoglobin, therefore 75 percent of the hemoglobin was in essence broken down in Mphages and Unconj. Bilirubin was ultimatly produced and is now in the serum bound. 25% of hemoglobin however was lost in the urine and therefore none of it was ever broken down, and thus none of that 25 percent got converted to bilirubin.
2. The above explains the classic signs of intravasc Hemolysis- Hemoglobinuria, Hemoglobinemia, Jaundice(will explain in a min)

Now lets talk extravascular-lets say for whatever diseased the damaged RBC goes through Spleen and is taken up by the splenic Mphages and hemoglobin from cell is broken down to hemoglobin and released as unconj. Bilirubin, which binds to albumin. Now here is a big DIFF- notice in extravascular,100% of the hemoglobin from the damaged RBC was taken up by the Mphages and thus 100 percent of the hemoglobin of the RBCs was converted to bilirubin.

So the classic findings of extravasc hemolysis is Jaundice with NO hemoglobinuria or hemoglobinemia(because all hemoglobin was taken up by splenic Mphages.

So at this point,regardless of which path, intra or extra you have unconjugated bilirubin bount to albumin in the plasma. From there, none can go into kidney or urine, so all of it ends up at the liver, where it is removed from albumin, taken up by hepatocyte, conjugated, secreted intil bile--> within the gut, the conjugated bilirubin within the bile, is mostly deconjugated by bacteria and converted to urobilinogen.-->70% of uro is excreted in feces, 20% is put into enterohepatic circulation back to liver for reconjugation and excretion, and 10% is absorbed into system circulation, where the urobil is excreted in the urine. So you can see in this relationship and in general, the more Bilirubin the liver takes up-the more it conjugates and excretes into bil-->the more of it gets turned into urobilinogen-> the more urobil there is, the more goes out each path- which means the 10 percent that is absorbed systemically is increased with more total bilirubin excretion.

Now back to all the unconjugated bilirubin we have from our intra and extravasc hemolysis-so lets say we have 2 pools
1. Extravascular pool- Since 100% of the hemoglobin was converted to unconj bilir lets say we have 100 Unconj. Bilirubin bound to albumin
2. Intravascular pool produced only 75% of its hemoglobin to bilirubin so lets say we have 75 bilirubin bound to albumin.

Now for example sake, lets say the maximum a healthy liver can take in, conjugate and excrete is 100- therefore the liver will take up 100 unconj bilirubins and excrete it therefore neither path will be a problem and you will have no jaundice from either since all the bilirubin was successfully excreted.
But to illustrate how jaundice occurs, lets say the liver had a capacity of 75, therefore the amount in the intravasc path would be fine and no jaundice would occur from the intravasc path but the extra path has 25 bilirubins too many for the liver to handle, therefore those 25 unconjugated bilirubins are stuck in the serum of the body, circulating around to various tissues--> lets say the icterus of the eye. The bilirubin in tissues now causes jaundice since it has no way to be excreted.

Now lets say the liver capacity in someone with liver disease is 50- in this case both paths would be too much to handle and intra and extra would produce jaundice. Basically if a healthy liver is functioning properly, neither intra or extra will cause jaunidice in a mild/moderate hemolytic episode, however if one were MORE LIKELY to cause jaundice, it would the extrav. path for reasons illustrated above. So basically it is a balance of liver function and bilirubin produced and the answer to your first question is both types CAN cause jaunice, but normally niether do, but if one were to happen its going to be extrav, that is why texts/review books tend to list jaunidice under extravasc.

Now as far as urine is concerned
Intravascu- Hemoglobinuria and Urobilinogen will be in teh urine. The urobilinogen is directly related to amt of bilirubin produced and processed by liver. If intravas episode released 50 bilirubins that are fully processed by liver it might give 2 into urine. If intra released 100 bilirubins and liver was healthy and able to process all 100 then maybe 4 would be released as urobil into urine.

Extravasc. No hemoglobinuria is present as discussed way up top, and justlike intra, there is Urobilinogen in urine, based on amount of bilirubin produced in teh episode, justl ike explained for intrav.

Now both of those are assuming a liver is healthy and processed the bilirubin. If you get into diseased where the liver conjugates bilirubin but cant excrete it, then you can have a back up of conjugated bilirubin into system blood and urine excretion of conjugated bilirubin out urine but the ONLY way conjugated gets into urine is if the liver takes up unconj bilirubin, conjugates it and then has a problme excreting it- it will "back up" into systemic circ.> But under your 2 examples the only things youl see in urine is urobil( in both tyeps) and hemoglobin( in intra). gee that was long sorry about that, i geuss it isnt the most concise explanation, hope it was good for something!

 

[HiddenTruth]

You know logically, that is kinda what I was thinking, but that doesn't explain why urine bilirubin is absent. If the liver was still able to conjugate some (but not all) of this massive amount of UCB, there would be CBili in the urine--but there isn't. That is where I get confused. If you aren't conjugating any bilirubin (signified by the lack of of it in the urine) how the h*ll are you getting urobilinogen in the urine, when UCB must first be converted to CBili before it can be excreted by the intestines, and then reabsorbed as urobilinogen?

ok this is the way i understand this. In a nonobstructive situation, like the hemolytic anemia, the reason you don't get increase in conjugated BR, and likewise, urinary conj BR, is because the liver cannot UPTAKE anymore UCB. UCB is insoluble, rite, so that UCB gets deposited in various tissues, giveing you jaundice. So, the point is, that liver can take up UCB up to an extent, and beyond that it won't take up any to even give you conjugated BR. So, I don't think you will have some conj, some unconj in a nonobstructive picture (unless we're talking about cirrhosis or viral hepatitis, in that case u get both, but that is a difft. scenario)....in straight up severe hemolytic anemia--you pushed and pushed all this UCB into the liver, which got conjugated, and went to the gut, and thus, you got increased urobillinogen both in the gut and likeise, reabs to kidney-->increased urinary urobillinogen. So, after you maxed out the liver's ability to UPTAKE, it's not going to take up anymore UCB...remember, the problem here is UPTAKE, not enzymatic ability to conjugate. So, there is no conj BR in the urine, because there is no backflow (no onstruction or damage in liver)...you've just oversaturated it's ability to UPTAKE any more UCB. So, liver allows UCB to come in---then once saturated, barrel closes, no more UCB can enter, and so whatever doesn't enter, obviously doesn't get conjugated (not that there is overflow or back flow of CONJ BR-- sorry, my bad on the earlier post when i chose the wrong symantics), and that will give u jaundice and acholuria (sp?) becuase of the increased UCB. I think this is what you are asking....if not, sorry for just reitterating what i said previously. Does this make sense?

 

[HiddenTruth]

If you aren't conjugating any bilirubin (signified by the lack of of it in the urine) how the h*ll are you getting urobilinogen in the urine, when UCB must first be converted to CBili before it can be excreted by the intestines, and then reabsorbed as urobilinogen?

ok , let me see...i don't really get what you're asking..but i'll try. You are conjugating BR, a crap load of it, but ONLY until you reach the liver's maximum capacity to uptake it. Beyond that, you're not going to take up any UCB. So, all that excess UCB that u were able to take up is gonna show up as increased urinary urobillinogen. (Remember, normally barrel [liver] only 1/4full of BR, now u took up 3/4 more--so that 3/4 that u were able to take up is going to be increased in every location from the liver onwards. But, anything after that 3/4, you're not even going to let it enter in the liver).
alrite, im gonna stop, and let u answer to see if this is what you're asking.

 

[Ramoray]

hidden isnt this topic a bitch to explain as far as trying to express what you are trying to explain to someone, like when you understand it it finally clicks but its hard to explain i find, atleast concisely! hopefully your great explanations helped these folks it is a confusing topic in general i alwasy found. That along with hematology i find a bitch

 

[UCSBMed1]

ok , let me see...i don't really get what you're asking..but i'll try. You are conjugating BR, a crap load of it, but ONLY until you reach the liver's maximum capacity to uptake it. Beyond that, you're not going to take up any UCB. So, all that excess UCB that u were able to take up is gonna show up as increased urinary urobillinogen. (Remember, normally barrel [liver] only 1/4full of BR, now u took up 3/4 more--so that 3/4 that u were able to take up is going to be increased in every location from the liver onwards. But, anything after that 3/4, you're not even going to let it enter in the liver).
alrite, im gonna stop, and let u answer to see if this is what you're asking.

Your explanation doesn't make sense based on the fact that NO CB shows up in the urin with a hemolytic disease, so how can you be still be conjugating it? Sure, I understand that the liver may have reached its max, etc., but if that's the case, why isn't ANY CB showing up in the urine, and only urobilinogen is, when the latter is a byproduct of CB???

 

[Ramoray]

i wish i had a pen and could draw a picture. well i guess ill stick with the barell example. so lets try somenumbers
1. Hemolytic anemia gives you 80 bilirubins, the liver capacity is 100. The 80 are all processed and excreted giving you the 10 percent reabsorption of urobilingoen so you get urobilinogen in urine and no CB since it is all being processed just fine
2. hem anemia increases and gives you 110 bilirubins, more than the liver capacity, so the liver will process 100 since that is its capacity and process and excrete the 100 bilirubins, like usual reabsorbing 10 percent into system giving you urobilinogen in urine, but this time it is more than in number one since 10 percent of 110 is mroe than 10 percent of 90. Now the 10 that were not able to be processed you can think of they are just waiting in line for a coaster. They werent able to get a seat on this time round but they are next in line to get on the next roller coaster, so you have unconj. bilirubins sitting in the blood that are unable to be processed. These can cause jaundice because they are just sitting around in the blood. When the liver again regains its capacity after some time, these boys hop on the roller coaster, andget processed by liver-- they are conjugated like normal, and excreted, giving your urobilinogen in urine like usual.
You see no matter how much poors in, assuming there is no block in the liver excretion path causing a "dammiing" of CB, it all will eventually be excreceted, it just has to wait its turn, and at no time is there CB being put into the blood because the bilirubin that gets conjugated is excreted properly since there is no problem with the pathway of conjugatino and excretion. The only problem is that there is a wait time for the bilirubin to become processed.
So in the urine of a liver that reached its max, you will have a steading of the urobilinogen. if capacity is 100 of liver, 10 percent of that is 10, so the max urobilinogen youll see in the urine is 10, and at this point youll konw you reached your livers max.

Now there are a ton of assumptions and fakeness, and it doesnt actually steady off completely and you really coudlnt use this to tell if the liver is at capacity but its all to illustrate the general point that the processing is fine, it is just overwhelmed and takes longer so nothing goes awry its just being overworked

 

[Ramoray]

did this get posted my internet is being dumb

 

[UCSBMed1]

did this get posted my internet is being dumb

Hey bro your explanation made sense, thanks. But my remaining problem is this. Conjugated bilirubin appears in the urine when the conjugation pathway is normal and no hemolysis exists. But when hemolysis occurs, it magically does not, and its byproduct (urobilinogen) continues to appear.

I realize that sure normal processing will be backed up by increased amounts of UCB due to hemolysis, but why does it no longer appear when the system is backed up, when it appeared when the system was working fine as in the normal state?

Or stated another way, why is not necessary for conjugation to occur in order for urobilinogen to be formed?

 

[Ramoray]

It doesnt normally appear other than mildly from some that escapes the liver and goes into the blood as a normal function there is always going to be a certain normal value for CB which also will occur with hemolysis. The only time you get a rise pathologically is if the liver has a problem excreting the CB into the caniculi, or if there is a posthepatic block in the ducts causing a back up. Those types of disease.. intraheptatic and posthep obstruction types are the only time you see a real amt of CB. So yes there is the same small amt of CB in the urine as normal in hemolysis but it is nothing other than the normal amount that escapes for whatever reason, it doesnt magically disapear.

 

[Ramoray]

It doesnt normally appear other than mildly from some that escapes the liver and goes into the blood as a normal function there is always going to be a certain normal value for CB which also will occur with hemolysis. The only time you get a rise pathologically is if the liver has a problem excreting the CB into the caniculi, or if there is a posthepatic block in the ducts causing a back up. Those types of disease.. intraheptatic and posthep obstruction types are the only time you see a real amt of CB. So yes there is the same small amt of CB in the urine as normal in hemolysis but it is nothing other than the normal amount that escapes for whatever reason, it doesnt magically disapear.

sorry to add. Conjugation is required for Urobil to be formed. Dont take this the wrong way but i dont think you understand the physiological path of everything cause i can tell from what your asking your missing a couple steps that would tie all this together. If you have a robbins there is like one page that givefs a nice explanation of the normal path of everything. Then come back and read the explanations people have been giving and it will all click once you see how everything flows from the minute RBC is broken down until you poop out the remainsand all the steps in between. Its hard to explain the path when the phys base isnt there.

 

[UCSBMed1]

sorry to add. Conjugation is required for Urobil to be formed. Dont take this the wrong way but i dont think you understand the physiological path of everything cause i can tell from what your asking your missing a couple steps that would tie all this together. If you have a robbins there is like one page that givefs a nice explanation of the normal path of everything. Then come back and read the explanations people have been giving and it will all click once you see how everything flows from the minute RBC is broken down until you poop out the remainsand all the steps in between. Its hard to explain the path when the phys base isnt there.

No I understand the pathway, thanks. 🙄 I read the Robbins section...

I guess I figured it out. FA kinda confused me into thinking that CB NORMALLY appears in the urine, when in fact it doesn't. I understand the pathway now.

 

[Ramoray]

No I understand the pathway, thanks. 🙄 I read the Robbins section...

I guess I figured it out. FA kinda confused me into thinking that CB NORMALLY appears in the urine, when in fact it doesn't. I understand the pathway now.

why take such offense your the one who needed 13 explanations and thought CB was a normal part of urine ...your right you must have had a firm grasp on the subject i apologize 🙄

 

[UCSBMed1]

why take such offense your the one who needed 13 explanations and thought CB was a normal part of urine ...your right you must have had a firm grasp on the subject i apologize 🙄

Why should I not take offense? You tried to explain something and then started saying that, "oh you need to read Robbins to figure it out..."

DOn't you think I would have read Robbins already? If you didn't want to explain you shouldn't have, man. No one made you. Thanks for the effort, but if your 3 page long, convoluted explanations made sense, then I wouldn't have had to ask the same question over and over again.

 

[UCSBMed1]

One last question for anyone willing to help me out.

What is the mechanism behind acholuria? Why, when hemolysis occurs, does CB not appear in the urine? Is it because bilirubin that is lysed intravascularly is bound to haptoglobin and excreted without having a chance to be conjugated? If thats the case, what explains the mechanism behind extravascular hemolysis?

 

[Ramoray]

One last question for anyone willing to help me out.

What is the mechanism behind acholuria? Why, when hemolysis occurs, does CB not appear in the urine? Is it because bilirubin that is lysed intravascularly is bound to haptoglobin and excreted without having a chance to be conjugated? If thats the case, what explains the mechanism behind extravascular hemolysis?

Dude another question taht shows you dont understand whats going on with bilirubin processing. just go read a physio book and when you can handle that come back and we can talk about the path. your questions show that you dont even have a clue, or are even in the same timezone of what goes on with bili processing. get it through your head, despite how bad you want CB to be in the urine.. its NOT. go learn about CB and how it gets into urine and stop asking the same question over and over and then bitching out the people who answer you.. *******

 

[UCSBMed1]

Dude another question taht shows you dont understand whats going on with bilirubin processing. just go read a physio book and when you can handle that come back and we can talk about the path. your questions show that you dont even have a clue, or are even in the same timezone of what goes on with bili processing. get it through your head, despite how bad you want CB to be in the urine.. its NOT. go learn about CB and how it gets into urine and stop asking the same question over and over and then bitching out the people who answer you.. *******

LOL. I'm the *******? First off, you were the one getting indignant with me. Go learn how to speak English you illiterate prick before you try to bad mouth me. Your posts are long, incoherent, and lack paragraphs.

Did I hurt your feeling because you couldn't help? Well you did help me figure out what I was missing, but don't trying to flame me because you got pissy when your little explanation didn't make sense. If anyone can read that bull*hit of an explanation and understand it, its beyond me...

Go look at first aid, look at Robbins. It says that CB is in the urine when hepatocellular or Obstructive mechanisms are behind jaundice. Now if you don't want to help me figure out why it is absent in hemolysis, leave the thread, bro, no one's making you read it. I hope you're not going into academics, because your students would sure hate a guy as impatient and pompous as you. 👎

 

[HiddenTruth]

LOL. I'm the *******? First off, you were the one getting indignant with me. Go learn how to speak English you illiterate prick before you try to bad mouth me. Your posts are long, incoherent, and lack paragraphs.

Did I hurt your feeling because you couldn't help? Well you did help me figure out what I was missing, but don't trying to flame me because you got pissy when your little explanation didn't make sense. If anyone can read that bull*hit of an explanation and understand it, its beyond me...

Go look at first aid, look at Robbins. It says that CB is in the urine when hepatocellular or Obstructive mechanisms are behind jaundice. Now if you don't want to help me figure out why it is absent in hemolysis, leave the thread, bro, no one's making you read it. I hope you're not going into academics, because your students would sure hate a guy as impatient and pompous as you. 👎

Dude, UCSB, chill out man. Ramoray was really trying to help, but I do agree with him, you are lacking some concepts, which is why you are repeteadly asking the same questions. And, I completely understood everything he was referring to.

Now, to get back to what you are saying. CB is in the urine normally to a minor extent, and will be in hemolytic anemia to the same extent. You have to understand the physiology behind this. The ONLY way conj BR is going to be elevated in the URINE beyond it's normal level, is going to be as a result of some obstruction at the hepatic level or post hepatic (panc ca of the tail) level, when there is "backflow". Also, in cases of viral hepatitis and ETOhic hepatitis, you can get it as well because of injury to hepatocytes, etc.

Seriously, I highly reccomend you read his post on the EV and IV hemolysis again, if you didn't understand it. It all makes sense. The acholuria is referring to the lack of UCB in the urine in cases of hemolytic anemias, because UCB is insoluble and there is no way it's gonna get into the urine (that is why u get jaundice, because it gets deposited in tissues). Alrite, I really don't know what else to explain. Everything has been covered in quite some detail.

 

[fuegorama]

Wow everybody it's an honest-to-gawd....


Nerd Fight!

 

[Ramoray]

sorry ucsb i honestly was just trying to help and didnt mean anything other than i think all these explanations or the ones in other sources would make a little more sense if you reviewed the physio of it all briefly, regardless of if you know it, we all forget some steps ina process that causes us to see certain things clearly, especially something as finicky as all these levels going up, down, stay same, why etc. I apologize didnt mean any harm and im sorry my explanation didnt help. I hope you find your info. Uptodate has a good chunk on it if you type in hemolysis. good luck!

 

[UCSBMed1]

sorry ucsb i honestly was just trying to help and didnt mean anything other than i think all these explanations or the ones in other sources would make a little more sense if you reviewed the physio of it all briefly, regardless of if you know it, we all forget some steps ina process that causes us to see certain things clearly, especially something as finicky as all these levels going up, down, stay same, why etc. I apologize didnt mean any harm and im sorry my explanation didnt help. I hope you find your info. Uptodate has a good chunk on it if you type in hemolysis. good luck!

Well thanks for the apology. 😀

I do appreciate you trying to help me, I honestly do. The boards are on Saturday for me, and I guess I'm just getting nervous. Good luck to you on the wards! 🙂