Hyperbilrubinemias??

[NRAI2001]

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Anyone know of a good way to remember them? I seem to learn them and then repeatedly forget them..

What causes and pathogenisis behind:

conjugated hyperbili.

unconjugated hyperbilli

urine bilirubinemia

..etc

 

[Sol Rosenberg]

Anyone know of a good way to remember them? I seem to learn them and then repeatedly forget them..

What causes and pathogenisis behind:

conjugated hyperbili.

unconjugated hyperbilli

urine bilirubinemia

..etc

Just make sure you understand the pathway of bilirubin excretion, and you'll get these.

REMEMBER: The liver conjugates bilirubin. Unconjugated bilirubin goes in, conjugated bilirubin goes out. Therefore, you can get an unconjugated hyperbilirubinemia if things "back up," BEFORE conjugation either because there is too much production of unconjugated bilirubin (e.g. hemolysis,) because there is a shortage of the conjugating enzymes coupled with a physiologic increase in production of unconjugated bilirubin (Gilbert's) or because there is little to no conjugating enzyme (Crigler-Najar.)

If things "back up" after conjugation either from anatomic (choledocholithiasis, etc) or functional (Dubin-Johnson, Rotor's) obstruction, you will get a conjugated hyperbilirubinemia.

Bilirubin in the urine means conjugated hyperbilirubinemia. The kidney has a very small capacity to excrete conjugated bilirubin (most is excreted in the stool as urobilin, which is conjugated bilirubin that has been modified by gut bacteria.)

If you have all that down cold, most of the pathology is pretty straightforward.

 

[NRAI2001]

Just make sure you understand the pathway of bilirubin excretion, and you'll get these.

REMEMBER: The liver conjugates bilirubin. Unconjugated bilirubin goes in, conjugated bilirubin goes out. Therefore, you can get an unconjugated hyperbilirubinemia if things "back up," BEFORE conjugation either because there is too much production of unconjugated bilirubin (e.g. hemolysis,) because there is a shortage of the conjugating enzymes coupled with a physiologic increase in production of unconjugated bilirubin (Gilbert's) or because there is little to no conjugating enzyme (Crigler-Najar.)

If things "back up" after conjugation either from anatomic (choledocholithiasis, etc) or functional (Dubin-Johnson, Rotor's) obstruction, you will get a conjugated hyperbilirubinemia.

Bilirubin in the urine means conjugated hyperbilirubinemia. The kidney has a very small capacity to excrete conjugated bilirubin (most is excreted in the stool as urobilin, which is conjugated bilirubin that has been modified by gut bacteria.)

If you have all that down cold, most of the pathology is pretty straightforward.

Thanks👍

I guess I m partly confused on what type of bilirubins can be seen in the urine? Is it always urobilin (conjugated form)? Can there be an increase in unconjugated bilirubin in the urine?

Do both conjugated and unconjugated bilirubins cause the physical symptoms of jaundice (ie yellow sclera?)

 

[FutureDoc4]

Thanks👍

I guess I m partly confused on what type of bilirubins can be seen in the urine? Is it always urobilin (conjugated form)? Can there be an increase in unconjugated bilirubin in the urine?

Do both conjugated and unconjugated bilirubins cause the physical symptoms of jaundice (ie yellow sclera?)

You NEVER see unconjugated bilirubin in the urine. Why?

Unconjugated bilirubin is EXTREMELY insoluble... this is the whole point of the glucuronidation system (to make bilirubin soluble). Hence, when its in the blood it is strictly bound to albumin (which drops it off at the liver). So, you will never see unconjugated bilirubin in the urine.

You will see only 1 of 2 things in the urine:

urobilin and conjugated bilirubin (that's it).

Urobilin means that there was no blockage getting to the intestines:

Conjugated bilirubin--convereted to urobilinogen---urobilin (this process by bacterial flora) (which gives stool its color)

Small percentage of urobilin is reabsorbed into the blood it goes to ways to the liver (most) and to the kidney (urine) (responsible for the color of urine)

Conjugated bilirubin is NEVER a normal finding in the urine because conjugated bilirubin should never have any direct contact with blood during its metabolism

Hope that clears things up.


A point I often find confusing (hopefully someone else can chime in), is when you have cholesthiasis (conjugated hyperbilirubinemia), you have light color stools due to lack of urobilin.

But, is it the conjugated bilirubin that then enters the blood into the urine (because of the back up), that gives urine its DARK color ?

 

[NTF]

View hyperbillirubinemias on whether the problem is prehepatic, hepatic and posthepatic.

👍👍 That makes much more sense to me. Thanks!

 

[NRAI2001]

Don't memorize this topic, just use logic. When you rotate in hospitals you'll be able to clinical differenciate each instantly in a jiff because it's something you see everyday.

View hyperbillirubinemias on whether the problem is prehepatic, hepatic and posthepatic.

Prehepatic: Anything that causes your blood to blow up. Huge spleen, sickle cell disease, incompatible blood transfusion, physiologic jaundice of babies, etc.. Liver works fine, just that because red blood cells have blown up, a normal functioning liver can't process (conjugation) billirubin fast enough so some non conjugated billirubin is present in most tissues. High billirubin in tissues is pretty much harmless to anyone that isn't a newborn baby (babies can get kernicterus).

Hepatic: Any problem in the liver. Acute hepatitis, cirrhosis, etc.. Non conjugated billirubin levels aren't increased initially, but the liver works slower and can't process it so non conjugated billis increases in the blood. Gilbert syndrome isn't considered to be a disease, the person is genetically only able to process billis at a slower rate than people without the trait. I have a few friends that have Gilbert syndrome and they have jaundice during periods of stress (poor diet, no sleep) or after drinking alcohol.

Post hepatic: Liver can process and conjugate billis correctly, but there's a problem that billis can't be transported to the intestines. Most common cause: gallbladder stones. Any problem with the gallbladder and it's ducts (inflammation, cancer) will cause this. An unusual cause is Mirizzi syndrome where the obstruction is higher up in the liver ducts. I saw one of these cases as an intern. Clinically the jaundice has acolia and coluria.

Medicine is logical, don't kill yourself memorizing everything!!! 😎

What about increased levels of urobilin? I think that comes into the pre-hepatic category? = increased breakdown leads to increased secretion into the gut and increased reabsorption of urobilin...

When they say bilirubin gives your urine its color, are they refering to urobilin? or any bilirubin (ie conjugated bilirubin)?

Where do primary billiary cirrhosis and primary sclerosising cholangitis fit in?

 

[Sol Rosenberg]

What about increased levels of urobilin? I think that comes into the pre-hepatic category? = increased breakdown leads to increased secretion into the gut and increased reabsorption of urobilin...

When they say bilirubin gives your urine its color, are they refering to urobilin? or any bilirubin (ie conjugated bilirubin)?

Where do primary billiary cirrhosis and primary sclerosising cholangitis fit in?

I disagree with the previous poster's way of looking at things and prefer my own, because things like PBC and PSC are both hepatic and post-hepatic. But, do whatever works for you.

Although urobilin in the urine is normal, increased urobilin (I presume that you mean in the urine) is a sign of an unconjugated hyperbilirubinemia. Basically, if unconjugated bilirubin builds up because of hemolysis the liver will work as hard as it can to get rid of it through the normal pathway: Unconjugated bilirubin -> Conjugated bilirubin (but not in serum) -> urobilin

The only thing you DO have to memorize is what all of the disorders do. PSC and PBC are cholestatic (obstructive intra and extra hepatic) disorders and, like I said in a previous post result in a conjugated hyperbilirubinemia = no/reduced urobilin production = conjugated bilirubin in the urine. Also (memorization) PBC is associated with anti-mitochondrial antibodies and PSC is associated with ulcerative colitis.