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