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How to pronounce urobilinogen in English?

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Jaundice, which doesn’t have the most intuitive name, comes from the french jaunice, meaning
yellowing.
It’s also sometimes referred to as icterus though, the origin of which is even less intuitive,
coming from the thought that jaundice could once be cured by looking at a yellow bird,
the more you know!
Anyways, as you’ve probably gathered, jaundice involves someone taking on yellow pigments,
specifically in the skin and eyes.
The yellowing pigment is caused by a compound called bilirubin, a component of bile and
the main cause of bruises being yellow, and after its metabolism, the yellow-ness of urine
and brown-ness of feces.
So since bilirubin’s our main culprit of yellow-ness, it’s super important to know
where it comes from.
As red blood cells near the end of their lifespan—which is about 120 days—they’re eaten up or
phagocytosed by macrophages in the reticuloendothelial system, aka the macrophage system, where the
spleen plays the largest part, but it’s also made of parts of the lymph nodes.
K so first the macrophage eats up the blood cell, and hemoglobin is broken up into heme
and globin, the globin is further broken into amino acids.
The heme on the other hand is split into iron and protoporphyrin, protoporphyrin is then
converted into unconjugated bilirubin, or UCB.
Unconjugated bilirubin is the form of bilirubin that’s lipid-soluble, meaning it’s not
water-soluble, sometimes it’s also known as indirect bilirubin.
Albumin in the blood then binds to UCB and gives it a lift over to the liver where it’s
taken up by hepatocytes, where it’s conjugated by an enzyme called uridine glucuronyl transferase
(UGT), making it now water soluble.
At this point the conjugated bilirubin is secreted out the bile canaliculi where it
drains into the bile ducts and sent to the gallbladder for storage as bile.
Now when you eat a donut or something, your gallbladder secretes the bile and CB, it moves
through the common bile duct to the duodenum of the small intestine and is converted to
urobilinogen, or UBG, by intestinal microbes in the gut.
Now some of that urobilinogen is reduced to stercobilin which is excreted and responsible
for the brown color of feces.
Some of that UBG is actually recycled, though, and it gets reabsorbed into the blood and
spontaneously oxidizes into urobilin, most of which is sent to the liver to the liver
and some of which goes to the kidneys.
It’s then excreted and is responsible for the yellow-ness of urine!
And there you have it, bilirubin metabolism in a nutshell.
Now if some point in this process is disrupted, for example if your liver cells are damaged
and can’t conjugate bilirubin anymore, or if they die and release their bilirubin, you
can end up with increased bilirubin in the blood, which can be conjugated or unconjugated,
or both!
This is what accounts for the yellow color in the skin and eyes.
Usually it takes about 2.5 mg/dL or greater of serum bilirubin to give the skin that Simpsons-esque
yellow skin tone.
The earliest sign of jaundice and increased bilirubin in the blood is by looking at the
sclera of the eyes.
Scleral tissue is high in elastin, which has a particular fondness for bilirubin and binds
it with a high affinity, giving the scleral tissue a yellow color often before the skin.
Now as you might imagine after looking at this process, there’re quite a few potential
pitfalls along the way that can lead to jaundice, and they’re lumped together depending on
whether they have more UCB in the blood, more CB in the blood, or more of both in the blood.
Two types of disorders that have increased UCB and similar presentation of jaundice are
extravascular hemolytic anemias, where red blood cells are broken down earlier than they
normally would, and ineffective hematopoesis, where your blood cells don’t form quite
right in your bone marrow, causing macrophages to break them down.
In both cases, the red blood cells are broken down, causing high levels of UCB.
Since your hepatocytes can only work so hard converting UCB to CB, they can get overwhelmed.
As an imaginary example, say that this liver cell can conjugate 10 molecules of UCB a minute,
max, but normally they only see 5, so that’s easy.
If all the sudden your body starts breaking down more blood cells and the UCB molecules
on this cell’s docket jumps to 15/min, this liver cell can’t keep up, and that excess
of 5 molecules of UCB stays in the blood, that’s the first issue.
In addition, as the liver cells max out, now there’s all this CB that goes to the bile,
which increases the risk for pigmented bilirubin gallstones.
Not only that, once all that CB is sent to the duodenum, it’s converted to urobilinogen.
Remember some of that urobilinogen is recycled back into the blood, oxidized to urobilin,and
excreted in the urine, giving it a much darker color.
The UCB is not excreted because it’s not water soluble!
In the previous two cases, too much UCB was created, but you can also have hepatocytes
that just can’t work hard enough and keep up.
Physiologic jaundice of newborn is one of these cases; newborn livers having a lower
amount of UGT in the liver to convert UCB, and after birth, UCB levels can be high due
to the natural process of macrophages destroying fetal red blood cells.
Typically this is normal, but can cause complications if UCB rises a LOT; since it’s fat soluble,
it can collect in the basal ganglia of the brain, which is called kernicterus, and cause
damage to the brain or death.
Treatment of this condition is usually phototherapy, which uses light to induce structural and
configurational changes in the bilirubin molecule, basically it absorbs the energy from the light
and changes shape.
These new shapes are more soluble, and can be excreted in the urine.
This can be a super effective and non-invasive way to get excess UCB out of the blood.
Another potential case where not enough UCB can be conjugated is through hereditary defects.
One case is called Gilbert’s syndrome, where their UGT enzyme activity is low and has a
hard time cranking up when needed, so maybe this liver cell can only pump through a max
of 6 molecules/minute.
Unfortunately, if something comes along that increases hemolysis, like infection, stress,
or starvation, the unconjugated bilirubin load will increase which can easily overwhelm
these hepatocytes, cause buildup of unconjugated bilirubin in the blood and lead to jaundice.
Another genetic example is called Crigler Najjar syndrome, where gilbert’s syndrome
was a low amount of UGT, Crigler Najjar is where there’s pretty much no UGT and therefore
no ability to conjugate UCB, this will lead to SUPER high levels of UCB, and likely UCB
deposits in the brain and kernicterus; Crigler Najjar syndrome is usually fatal.
The previous couple examples focused on high levels of unconjugated bilirubin in the blood,
but there are also examples of jaundice with high levels of conjugated bilirubin in the
blood.
Dubin-Johnson syndrome is an autosomal recessive disorder where there’s a deficiency in the
protein that helps move CB from the liver cell to the bile ducts, called MRP2, so CB
builds up in the hepatocyte.
It’s thought that when the MRP2 transporter is defected, another transporter, MRP3 is
upregulated, though this transporter moves it into the interstitial space and blood flow,
as opposed to the bile canaliculus, so in this case you’ll have increased CB in the
blood, which also gets excreted into the urine, giving it a darker color, this leakage also
causes the liver itself to get super dark.
Another high-CB category of jaundice is called obstructive jaundice, and this is basically
where something blocks the flow of bile, these blockages could be anything from gallstones,
pancreatic carcinomas and cholangiocarcinomas, to parasites like the liver fluke.
Remember that bile’s made up of conjugated bilirubin and this blockage basically causes
pressure to rise in the bile duct, which literally causes bile to leak through the tight junctions
between hepatocytes, but that’s not the only thing that leaks out though; bile salts,
bile acids, and cholesterol all can can get into the blood.
If they deposit in the skin, it could lead to itchiness or pruritus, but also lead to
things like hypercholesterolemia and xanthomas.
The excess CB is excreted in the urine, leading again to dark urine.
Also, since you’re losing bile, you won’t be able to absorb fat as well, which (1) causes
you to excrete a ton of fat, a condition called steatorrhea, and (2) causes you to not be
able to absorb as many fat-soluble vitamins as you need.
Finally, viral hepatitis leads to both conjugated and unconjugated bilirubin in the blood.
When hepatocytes get infected and start to die off, they both lose the ability to conjugate
bilirubin, leading to excess UCB in the blood, AND since they also line the bile ducts, when
they die they let bile leak out into the blood, causing an increase in blood CB as well.
Again, since CB is up, patients will have more CB excreted and darker urine.
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Jaundice, which doesn’t have the most intuitive name, comes from the french jaunice, meaning

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urobilinogen::noun | Spocien Dictionary

urobilinogen

noun

a chromogen formed in the intestine from the breakdown of bilirubin; yields urobilins on oxidation; some is excreted in the feces and some is resorbed and excreted in bile or urine

Type	Words
Synonyms	stercobilinogen
Type of	chromogen

Examples of urobilinogen

urobilinogen

Urobilinogen leaves the body in faeces, in a pigment called stercobilin.

From the en.wikipedia.org

Intestines metabolise bilirubin into urobilinogen.

From the en.wikipedia.org

How to pronounce urobilinogen in English?

urobilinogen::noun | Spocien Dictionary

abandonment

Related words

Examples of urobilinogen

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