concept. Build, build. Okay. Let us talk about
here obviously. Distal convoluted tubule,
the problem has nothing to do with your sodium-
potassium-2 chloride, does it? No. Gitelman
will be dealing with your sodium and chloride
channel. Now what is interesting about this?
Take a look at the name. Hypomagnesemia. Correct
Losing magnesium. Hypokalemia, losing potassium
correct. However, this is the big thing.
It is hypocalciuria. Now understand that Gitelman
syndrome is much more common than Bartter
granted, but know both for any of your exams.
So here in Bartter syndrome, there was hypercalciuria
and in Gitelman, it will be hypocalciuria.
In Bartter syndrome, there is an issue with
concentration of your urine and Gitelman not
so much, but both will have issues with diluting.
So these are things that you want to keep
in mind when distinguishing one from the other.
Continue. Autosomal recessive, there is the
actual gene, SLC12A3, gene product of NCCT. In
other words think about the sodium chloride
channel. Thiazide sensitive. T think thiazide
at least be able to identify that. You end
up having this pretty much the same issue
except for one big thing. Hypokalemia present
in both Bartter and Gitelman, metabolic alkalosis
both in Bartter, in Gitelman, hypomagnesemia
both. Hypocalciuria. Whereas in Bartter get
hypercalciuria resulting in secondary hypoparathyroidism.
Normal blood pressure. It contracts the lateral
two findings meaning the calcium and the blood
pressure to Bartter and exactly the
point that we made. Now Gitelman usually diagnosed
until late childhood or adulthood whereas
in Bartter childhood we did antenatal. Remember
the prostaglandin levels, They're quite high in Bartter
more so hence the indomethacin an COX inhibitor.
In Gitelman, it is not so much concentrating
ability whereas ability to properly dilute.
Hence the ADH will be suppressed, but that
is pretty much in both.
Cramps of the arms and legs due to hypokalemia,
muscle weakness. What happens to resting membrane
potential? One more time it becomes more negative.
You are further away from the threshold. So,
therefore, more difficult to trigger an action
potential. Welcome to fatigue. Maybe perhaps
tetany, polyuria, nocturia that is pretty
big in Gitelman. Approximately 80 percent
of your patients could have nocturia. That
is amazing. Now why in Gitelman more so than
Bartter? I couldn’t exactly answer that
for you, but look for this clinically because
we know it occurs. Chondrocalcinosis due to
interesting concept, unexpected hypertension
may present later. Keep that in mind. However,
you have enough information now to distinguish
between Gitelman and Bartter. Please don't
miss these questions. It is all here. Go back
and review. I would say if you have never
heard of these before that you keep going
over them a few times. If you have reviewed
and now you should be able to add in little
bit more information where you truly able
to understand these conditions. Here once
again for the most part potassium sparing
ACE inhibitor sometimes with Gitelman, you
will have increased prostaglandin. I can’t
say for sure that you wouldn’t with Gitelman.
I would not be doing justice. Clinically speaking
both Gitelman and Bartter have shown an increase
in prostaglandin, but more so in the Bartter
that we talked about. Sites of drug action, we
talked about the
thiazide. This would be up in your distal
convoluted tubule and this would be more about
your Gitelman. Remember the name of the gene
there with NCCT, sodium chloride and thiazide
sensitive type of area. With thiazides, it
works in the distal convoluted tubule.
If both patient populations mean to say you have
your African and elderly who have hypertension
often times being the main stay of therapy
and important, Thiazides behave like PTH.
So if your patient does have hypercalciuria,
what kind of diuretic would you want to avoid? Loop.
Because loop would make the hypocalciuria
worse. Thiazide would be used to perhaps remove
the calcium from the urine. Please highlight
in your mind. Calcium renal stone formers.
The drug attaches chloride and by doing so
is able to then reabsorb the calcium.
Now there is a lot more mechanics to it beyond
the scope of your exams at this point, but
clinically speaking if you are thrown any
question about thiazides or Gitelman on the
distal convoluted tubule, you shouldn't miss
them if you are comfortable with it, welocme
it. Thiazide, hyponatremia due to loss of your
sodium. Electrolyte abnormality includes your
hypokalemia, metabolic alkalosis. Now hypercalcemia
is an uncommon complication. Keep that in
mind clinically, please. So even though you
know thiazides remove calcium from the urine
and so, therefore, those patients that you
worried about hypercalciuria genetically or
maybe due to let us say calcium stones or
what not, you are not going to have so much
calcium that results in hypercalcemia. I can
tell you that comfortably. Uncommon. More likely
if the patient has primary hyperparathyroidism
for obvious reasons if the patient is already
in a state of primary hyperparathyroidism
that we talked about and use thiazide. Of
course, you might be exacerbating issue that
is something that you do want to keep in mind.