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Next, all these are things that we have talked
about over and over again. Here is everything
officially for you in words. Aldosterone,
reabsorption of sodium, excretion of potassium,
sodium diffuses into the cell, the primary
site here where potassium is to get rid of
it for aldosterone. Sodium-potassium pump.
Know its activity with aldosterone. It reabsorbs
the sodium. It gets rid of the potassium.
Ultimately if you have too much aldosterone,
it may result in hydrogen getting rid of and
may result in getting rid of your potassium
hypokalemia. The bicarb is reabsorbed into
the ECF causing metabolic alkalosis. So remember
whenever there is issues with hydrogen, you
are getting rid of it as soon as you think
about hydrogen and bicarb, you are thinking
about that formula and for the most part,
there even though it is not pictured, I assume
that you know at this juncture with hydrogen
and bicarb, they are going to be all part
of the carbonic anhydrase formula, aren't
they? And what kind of direction are they
always moving in with bicarb and hydrogen?
In opposite direction. So wherever were hydrogen
is going, let it be into the lumen or into
the blood, bicarb will be moving in the opposite
direction. Here hydrogen will be moving into
the urine with the help of aldosterone and
then your bicarb will be coming out into the
blood all contributing to your metabolic alkalosis.
Now, a couple of important potassium-sparing
drugs, that you want to keep in mind especially
for example let me give you a clinical situation.
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If you have a patient who has hypokalemia
secondary to loop diuretics, correct. And so
therefore, you might want to think about giving
that patient a potassium sparing drug. With
amiloride and triamterene, little bit different,
isn't it? Because these are not drugs that
work on the aldosterone receptor. These are
drugs that work on the luminal. Highlight that in
your head. Membrane sodium channel. Inhibits
sodium reabsorption and thus inhibits potassium
excretion. Isn't that the point of these drugs
is to spare the excretion of potassium, isn't
it? The effect of increased distal delivery
of sodium, pay attention, loop or thiazide,
the increased delivery of sodium because you
are blocking the sodium channels of different
types. Loop where are you? The case in England.
Thiazide, where are you? DCT while the diuretics
acting proximal to this channel, augmented
sodium reabsorption and potassium excretion,
may produce hypokalemia if potassium supplements
are not taken. So often times when this is
going to be increased delivery of sodium,
please understand that sodium is going to try to
be reabsorbed and potassium potentially could
be lost. Hypokalemia may produce metabolic
alkalosis. So you can think of this as being
a natural form of aldosterone and this is
a problem when you give such diuretics that
end up increasing delivery of sodium. So,
effective increase distal delivery of sodium
from loop and thiazide diuretics acting proximal
to this channel. What channel? Proximal to
collecting duct and if you increase the delivery
of sodium to it and whatever the cause maybe
keep this in mind that it behaves like a natural
aldosterone. It will do everything in it is power
to reabsorb the sodium, gets rid of potassium
and gets rid of hydrogen. Do not forget that,
please. That is an important point
clinically.