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now tubular secretion
overall we've talked about this in
previous discussions and lectures in
which
we discussed physiologic components such
as perimenopausal acid and creatinine
we'll quickly walk through clinical
correlation of some of our important
tubular secretion first and foremost you
tell me what's happening
you're secreting the substance into
where good
into the urine these include bile salts
and uric acid
now substances that are being secreted
and on this picture giving an overview
as to those substances that are secreted
and such but let's just keep things
relatively simple in terms of process
first and foremost
you're going from where close your eyes
peritubular capillary
most likely pct you're passing across
the
endothelial cell you're entering the
interstitium step one
next what are you going to hit the
basolateral membrane
of whom the epithelial cell right
basolateral membrane
and here you have your organic
transporters these organic transporters
will then help
a substance be secreted into the urine
next are transported out of the cell
into the tuberolumin
aluminum membrane transporters where am
i when i say luminal apical
facing the urine what is the entire
objective of this
of this discussion how do i get a
substance
from the blood stop there through
interstitium through my cell
in to the urine into the urine secretion
you need organic transporters now the
sites of drug
action include the following number one
mannetal with mannitol works
primarily on the pct in which in its
abundance
may then bring about diuresis in general
the classification of drugs that we're
dealing here
are your diuretics when would you think
about
giving mannitol maybe if your patient
had increased
intracranial pressure huh and manitoba
would try to help
to decrease that pressure by removing
some of that fluid
carbonic anhydrase inhibitor when would
we when did we last talk about this
high altitude what kind of ph imbalance
good respiratory alkalosis because of
hyperventilation
and high altitude acutely a couple days
later
the kidney should kick in and get rid of
the bicarb
what if it doesn't maybe perhaps you'd
think about giving acetazolamide a
carbonic anhydrase inhibitor
loop diuretic number three where are you
thick ascending limb number one symport
for reabsorption
sodium potassium two chloride you knock
it out you have massive diuresis
and you're specifically focusing upon
potassium as that's important
now thiazide as being a drug inhibits
your sodium chloride synport what's also
interesting about thiazide
is that it is pth receptor sensitive
in other words it behaves like pth think
of it as such
where it's responsible for interesting
interesting feature huh
reabsorption and calcium no other
diuretic will do that
no other diuretic will do that except
for thiazide
reabsorb calcium now to the point where
it causes hypercalcemia
uh depends usually not but understand
that it has
it has a mechanism of reabsorbing
calcium no other diuretic will do that
potassium sparing diuretic now there are
two classes here
the one that your focus should be at
this point from pathology
is the fact that you are antagonizing
the aldosterone
so it's an aldosterone antagonistic
drug in which if you antagonize the
aldosterone
what are you doing you are now sparing
your potassium
it's not being secreted it'll be held
back in your plasma
hence a potassium spheric diuretic the
second class let it be
tramterine or amiloride those will work
on the sodium channel
those are not aldosterone receptor
antagonists
now the secretion in diuretics important
here now this will go back to
our topic of secretion and you needed
organic transporters
those were a list of previously
diuretics let's put everything together
most diuretics gain access by how
tuber lumen to act okay so far so good
most are highly protein bound and does
not freely filter through the glomerulus
that must be understood when you're
protein-bound remember you're not going
to filter through so therefore
transporters into the tuberolumin via
aha organic ion transporters
the one big one that i had mentioned
already was the loop
the way that it reaches what's this what
is its target the sodium potassium two
chloride
how does it get there through your
organic ion transporter
now what's my clinical correlate now if
you have renal failure pay attention
please
if there's renal failure then guess what
now you'll have competition
i mean to say that normally speaking in
a renal failure you can't get rid of the
substances that you need to
right because your gfr drops how can you
then confirm this because your plasma
creatinine is then going to
increase your creatinine clearance is
going to decrease
listen to what i just said that make
should make sense
don't just breeze through that little
fact that i put out there
next with renal failure the organic ions
are going to then accumulate and they
compete
compete with the diuretic remember a lot
of times you want to use a diuretic in a
patient
in renal failure to remove that fluid
but
with renal failure you might actually
have to increase the dosage
okay increase a dosage of your loop
diuretic
so that you can out compete
your organic substances that are then
competing for that transporter
large dose of diuretic must be given to
overcome the competition
that is being provided by the renal
failure
substances keep that in mind extremely
important
once again dose adjustment
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you