okay so welcome to another MedCram
lecture we’re going to talk about acute renal failure and for that I’m going to
sort of bring up our chem-7 again we talked about this before you remember
you’ll see this a lot its standard we have sodium you’ve got potassium you’ve
got chloride you’ve got the bicarb and we’re going to talk about the B UN the
creatinine okay so that’s this third column B UN should be referred to as the
B I never call it the bun it stands for the blood urea nitrogen okay blood urea
nitrogen and the CR is simply creatinine okay
so blood urea nitrogen and creatinine so these things have to do with acute renal
failure but let’s get into a little bit about what they are and where they came
from and as you know of when you’re talking about energy you remember
something from biochemistry called the Krebs cycle Krebs cycle okay and it goes
around and around and you remember what went into it first there’s this thing
called acetyl co a okay and it was basically two carbons went into a steel
Kuwait and what came out of Krebs cycle ATP you know you had these reducing
agents nadh fadh2 they went into a electron transport chain down the
electron transport chain and you got ATP okay so basically you need to have two
carbon units to get into this Krebs cycle well let’s talk about what are the
three different types of energy sources in the body there’s three types we know
that there’s carbs okay and carbs are usually six carbon chains and six carbon
chains get broken down into two times three carbon chains and then remember
one of these carbons comes off in the form of co2 during glycolysis and then
you’ve got a two carbon chain and boom you’re ready to enter Krebs cycle
the other one is fats or lipids okay you remember that it had the carboxyl
to end on it and you had a bunch of these carbons that went off it was 16
carbons in its palmitate co way and then remember beta oxidation it chops these
things up in – guess what – carbon units you’re able to enter into Krebs cycle
well the last energy group is you guessed it proteins proteins if you
recall is a collection or a string of amino acids which have the backbone of n
C C then you have another n c c well you would have protease is that are chopping
up these proteins they’re chopping them up into these NCC units these are amino
acids how do you get these NCC s to C C’s well you basically chop off this n
group and then boom you’ve got CCS going in and you can make ATP the problem is
is that there’s these ends that are left behind so what are these ends these ends
are something called ammonia or nh3 okay so we’ve got to get rid of these NH 3
groups well these NH 3 groups ammonia is what it’s known as okay ammonia is toxic
to the body it’s toxic to the brain if you have too much of it it can cause
hepatic encephalopathy so the body’s got to do something about it somehow to get
rid of it and that’s where we talk about the BU n ok so clear the screen here
we’ve got nh3 which is ammonia and nh3 goes to the liver okay here’s my picture
of the liver so it goes into the liver and what comes out is something that
looks like this C double bond o 1 to the NH 3 or NH 2 on one side and an NH 2 on
the other this is your Rhea okay you are e a it goes into the blood then
you get blood urea nitrogen so the nitrogen is now compounded this is not
as toxic so this is really nice to have because you can
excrete this through the kidney so again ammonia goes to the liver and then gets
made into your reer through something called the urea cycle which we won’t get
into and then you get this bu n now bu n blood urea nitrogen goes to the kidney
okay here’s my little picture of the kidney and it goes out and that’s how
you get rid of B went so we know how that happens now let’s talk a little bit
about bu and remember a first point is is it’s made in the liver okay and there
are a couple of things that have absolutely nothing to do with the
kidneys that could increase the amount of bu n that you measure in the blood
first of all let’s talk about burns so burns is a catabolic state what do you
what do you think is going to happen when you have a burn burns are going to
cause you to have more protein breakdown as we already know more protein
breakdown is going to give you more ammonia all right what about steroids
again steroids induces a catabolic state accountable ik state is going to give
you more breakdown of proteins that’s going to give you more ammonia liver is
going to make more urea what about certain antibiotics tetracycline okay so
here is tetra cycling burns can do it and steroids catabolic state okay all of these things can do it let’s
think about something else let’s say you’ve got liver problems now in liver
problems or liver failure or cirrhosis you can get esophageal varices
esophageal varices is basically situation where blood is trying to get
back to the heart through the liver the livers dysfunctional and because of that
the blood has to find an alternative route back to the heart and one of those
ways is through the esophagus so these tiny veins which are normally built only
to take so much blood become engorged and so these veins can burst and high
mortality high mortality associated with this so you’ve got bleeding
what is believing bleeding into bed into the digestive tract well when that
happens you’ve got these red blood cells okay red blood cells are full of globin
globin is a protein you digest down all this protein guess what you’re going to
get you’re going to get ammonia well you already have liver failure so you’re not
making this urea and so what’s going to skyrocket your ammonia level is going to
skyrocket that’s why we see in patients with liver failure who have bleeding
esophageal bleeding they get hepatic encephalopathy and in fact that’s how
you can tell they’re having a patek encephalopathy now let’s say that they
have a GI bleeding and it’s not due to liver failure if their livers working
just fine you won’t see a buildup of ammonia but in fact the liver will take
that ammonia and guess what you’re going to have it increase in you’re gonna have
an increase in ABI um so you can have an increase in your bu n if you have GI
bleeding and your liver is working what are some things that could cause your bu
n to be decrease so all of these things cause your bu n to go up okay what are
some things that could cause your bu n to go down well the obvious thing is
this your liver is not working because if your liver is not working you’re not
going to make bu n and so liver failure I see this all the time patients come in
with liver failure and I’ll look on the chem-7 and their bu n is pretty low
sometimes it’s really even undetectable okay so we’ve talked about bu and let’s
review that again it’s the size in the liver things that
increase it that have nothing to do the kidney would be fever catabolic state GI
bleeding tetracyclines all sorts of things things that decrease it would be
liver failure because it can’t make the B UN okay with all those things in mind
let’s talk about what we’re talking about today which is kidney failure so
I’m going to draw a nephron here’s my little stylized nephron okay this is
number the kidney works kind of like you should clean out your closet you take
everything out of the closet everything and then you put back just the stuff
that you want to keep and everything else gets thrown away so here’s the
nephron and here is the blood supply so you have the afferent arteriole going in
and the efferent this is a bunch of capillaries and what you have is you’ve
got flow of fluid into Bowman’s capsule or the glomerulus and things go down and
basically everything that you want to keep gets reabsorbed and what get what
is left gets dumped out into the toilet okay but remember stuff that you want to
keep gets reabsorbed and most of the stuff that gets reabsorbed gets
reabsorbed right here at something we call the proximal convoluted tubule
probably 70% of the stuff that gets reabsorbed gets reabsorbed here at the
proximal convoluted tubule so how much so about 70% of stuff here in the
proximal combo to it gets reabsorbed and so really there’s two things that you’ve
got to be aware of that effect the serum concentration of things in the serum so
if things here are being reabsorbed back into the serum and those two things are
is the GFR the glomerular filtration rate so in other words how much what is
the rate at which stuff is being filtered into Bowman’s capsule if you’ve
got acute renal failure this is going to be reduced and therefore if less for
instance if less bu n is being filtered into Bowman’s capsule you’re going to
have an increase in your bu n outside that goes for just about anything that’s
being filtered the less filtration rate the greater that accumulation is going
to be in the serum because it’s just not being filtered but there’s an extra
added thing here with bu in and that is is that once it gets filtered if this
GFR or this glomerular filtration rate is low it’s going to go along here some
more slowly and if it goes along here more slowly it’s more likely to be a
reabsorbed because bu n is specifically reabsorbed here at the proximal
convoluted tubule so there are in fact two reasons why the BU n would go up in
a low GFR situation number one it’s because it’s not being filtered at the
same rate and the stuff that is being filtered is more likely to be reabsorbed
that’s going to become very important later on now this is a contra
distinction to something called creatinine we’ll talk about creatinine
cratan basically comes from muscle but specifically creatinine is also filtered
here at Bowman’s capsule but it is not reabsorbed it just keeps going through
and right on out in fact there are areas here where creatinine is actually
actively secreted okay so what does that mean that means that if there is a low
glomerular filtration rate that’s a reason why cracking is going to go up
but it’s not going to have the other reason to go up because it’s not being
actively reabsorbed in fact it’s being secreted and so creatinine only goes up
for one reason in a low GFR State that’s the major difference here between
creatinine and the vun let’s talk a little bit about
creatinine what is creatinine okay creatinine again and the chem seven is
this area down here and where does it come from it comes from muscles so
muscle breakdown is going to give you creatinine it’s just a natural byproduct
so the more muscle you have the higher your correcting is going to be normally
and the less muscle you have the less your Kratt name is going to be and
typically you need to see a reduction in your GFR by at least 50 percent before
you see an increase in your creatine so what are some non renal things that
could increase creatinine things that have absolutely nothing to do with the
GFR well as we talked about remember there are areas here in the nephron
specifically where creatinine is secreted if you could take a inhibitor
of that and block it you would block the secretion of cranny that would increase
your serum concentration of creatinine and there are a couple of drugs that do
that one of them is called cimetidine tagamet it’s an h2 blocker and the other
one is an antibiotic called trimethoprim okay so you’ll see an increase in
creating for that what about decreased cracking what could cause a decrease in
creatinine we talked about profound muscle wasting so low muscles so if you
don’t have any muscles that would cause you’re creating to go down and that
would be a reason for your cretin to be low okay so to review remember bu and is
synthesized in the liver it is both reabsorbed it is filtered and
reabsorbed the creatinine is filtered and secreted it is not reabsorbed so if
there is a slow down infiltration the B UN is going to be increased
because of lack of filtration and also because reabsorption the cratan is only
going to be increased because of lack of filtration therefore you’re going to see
a larger B un increase than you would creatinine in a low-flow state all right
that that does it for part 1 join me for part 2