So for the most part I don't typically teach endocrine
anymore. I think mine is on demand
correct? If I'm not mistaken mine is on
demand. But this was something that I
wanted to add in as a for a long time is I've been wanting to
compare the difference between Cushing's, Addison's, and Khan
syndrome. Cushing's being
hypercortisolism, Addison's being adrenal insufficiency.
Remember the ADI and Addison's and adrenal insufficiency, and
then Kahn's syndrome, which is primary hyperaldosteronism.
So again, all of these are kind of working in the adrenals.
That's where the confusion comes in.
Briefly we'll go over Cushing's, then briefly we'll go over
Addison's and then I'm going to dive into Kahn's because that is
something that I don't really cover anywhere else.
So that way everyone here is able to see exactly the
difference between Kahn's, Addison's and Cushing's disease.
So just kind of a recap on Cushing's and the recap on
Cushing's is that it is hypercortisolism.
Now we think about cortisol and we think about the adrenals.
Remember it's the the peripheral portion of the adrenal.
So the cortex, not the medulla. I call the medulla not the
medulla, right. So it's not the middle portion
of it or the medulla, it's the cortex.
And remember the deeper you get, the sweeter get.
So it goes salt, sugar and then sex hormones.
So the salt is that aldosterone, that sugar is that cortisol.
And then are sex, androgens, testosterone and estrogen right
in the bottom there before we hit the medulla.
So in Cushing's, we can have a tumor in the adrenals in that
middle portion of the cortex. That's where that cortisol
producing area is. So now we've got excess cortisol
being made because we have some sort of a growth hyperplasia
tumor which is causing cortisol to be elevated.
We know that when cortisol is elevated, a big fib, appetite,
blood pressure increase, insulin resistance increase,
gluconatogenesis increase and then fib, the fibroblast
decrease, immune system decrease and our bone density decrease.
So again a big fib. But that's not the only place
that can happen with increase cortisol.
As far as tumor goes, we can have it in the pituitary.
Just as a recap. You have it in the pituitary
where we're producing too much ACTH, ACTH, adrenocorticotropin
hormone is going to increase cortisol production.
So tumor in the brain, so secondary in the brain in the
pituitary, too much ACTH, in turn too much cortisol, that's
secondary primaries in the adrenals.
And then our third one is exogenous where again, think
about long term and we talked about this in respiratory
chronic bronchitis where we're taking steroids over and over
and over again for a long duration.
And we're kind of like, wait, it's not going to hurt our body
with a big fib. And you're kind of like, no, not
necessarily because my airway and protecting my bronchioles
like I would be in chronic bronchitis is better than all
the other side effects where I can actually take care of needs,
taking care of their appetite, their blood pressure, their
blood glucose level, bone density, calcium and vitamin D
to help with the bone density, weight bearing exercises, so on,
so forth, versus keeping our bronchioles away from that
inflammation with long term corticosteroid injections and or
consumption. So again, that's kind of the the
difference between that in Addison's disease is adrenal
insufficiency. So in this situation, we've
knocked out all three layers of the adrenals.
So there's no aldosterone, there's no cortisol, there's no
sex androgens. And some of the reasons why that
happens is infections, because of hemorrhaging, things of that
nature. Cons now is primary
hyperaldosteronism. So in Christians we had
hypercortisolism in cons. On the outer portion is where
aldosterone is made. So now we've got
hyperaldosteronism. Now what do we know about
aldosterone? I talk about the RAAS all the
time. It is renin, angiotensin,
aldosterone system. So remember when I talk about
potassium spraying diuretics or aldosterone, aldosterone
antagonists or we talk about ACE inhibitors, angiotensin
converting enzyme inhibitor, these are all things that are
affecting this Reenin, angiotensin, aldosterone system.
Same thing with Addison's. We're affecting the aldosterone,
no aldosterone. In cons, we are actually the
opposite, increasing aldosterone.
So what happens with increased aldosterone?
Well, aldosterone is going to control salt, increase
aldosterone, increase salt. If I increase salt, what follows
it? Water hyperaldosteronism or
cons? We are increasing aldosterone,
which increases salt and water follows it.
If I've got increased salt, then what happens?
In an inverse relationship? We have that sodium potassium
pump, which means that I get hypokalemia.
All right, let's dive into cons a little bit more.
If I've got increased sodium from hyperaldosteronism and
water follows it, what is the one thing that's going to happen
right away? High blood pressure, because now
my body's consistently making excess aldosterone.
So now my blood pressure stays elevated and not just elevated
little bit. I mean, it stays to the point
where it's resistant to treatment.
Because if the problem is aldosterone and we're not able
to control that, then it's kind of hard to get a medication to
work. What we've got to do is treat
the underlying cause, which is that primary hyperaldosteronism.
And usually that's going to happen with a tumor just like we
saw in Cushing's, but where cortisol is made or that
hyperplasia like we saw in Cushing's in that cortisol area
put down the aldosterone area of the adrenals of the adrenal
cortex. So with hypokalemia, because of
that inverse proportion, we've now got one of ASGRAF.
So if I've got something with Khan syndrome, then I'm looking
not only at that elevated blood pressure, which again, we kind
of talked about that yesterday with strokes, right, both
hemorrhagic and ischemic strokes, the underlying cause is
hypertension as one of the main causes, and it is that silent
killer. So now we're thinking about
something that can cause stroke, which is one of ASGRAF.
And then now we've got hypokalemia, which with
hypokalemia, we've now got one of Asgraf as well too, that
change in potassium hypo versus hyperkalemia.
So again, very important to understand the difference
between the three. OK, So I'm going to take it one
step further with cons. Cons Hyperaldosteronism increase
sodium, decrease potassium, blood pressure is high, usually
caused by some sort of a growth in the adenoma, some sort of
cancer, some sort of tumor, some sort of hyperplasia.
So the initial thing is to stop the aldosterone, let's use
aldosterone antagonist. So what drug have I talked about
extensively where I break down the RAAS and I talked about an
aldosterone antagonist and we see this now we're trying in
endocrine all the way with cardio.
Day one of cardio I talked about diuretics and I said potassium
sparing diuretic is what we call it as lay terms.
But in fact the class of drug of potassium sparing diuretics like
spironolactone Aplarenon amylaride Miller known is that
their aldosterone antagonist. If the problem here is in fact
too much aldosterone, can I not initially look at the word I
used initially use an aldosterone antagonist?
Yes. Can I use the ones that help the
RAA system? Yes.
So things like ACE inhibitors, Arbs, angiotensin receptor
blockers still affecting that development of aldosterone, just
one step ahead. Instead of renin, we work on the
angiotensin and then with the aldosterone, we work with an
aldosterone antagonist. So you see medications that can
work that are going to help with that increased aldosterone, but
ultimately that's just putting a Band-Aid on a cut.
That's all that's doing. Band-Aid on a cut.
I'm OK, aldosterone antagonist, Aldosterone antagonist.
I keep taking my spironolactone. I take an ACE inhibitor, I take
an ARB. I'm just putting a Band-Aid on a
cut, on a cut, on a cut, on a cut.
And I'm not treating the underlying cause.
So what is the best action in order for this to be resolved?
Well, our ultimate resolution in this situation is going to be
removal of the tumor or the adenoma or control that
cancerous growth or whatever it is that's actually causing it.
So ultimately the progression is again finding that the fact that
this person has that resistant hypertension, maybe we get some
imaging, maybe we get ACT, maybe an MRI, we get some imaging in
order for us to see that there is infected growth on the
adrenal glands. And when we look more in depth,
we're looking at it, we're saying, OK, wow, just kind of in
the up outer portion of the cortex.
And now we're seeing the signs and symptoms with hypokalemia,
hypernatremia, high blood pressure, maybe some
dysrhythmias, both electrolytes causing dysrhythmias.
So now we're concerned about again that V fib.
Then we look at the treatment and again, we can put a Band-Aid
on the cut, but ultimately the resolution is going to be
surgery. So that is Khan's disease with
the brief comparison to Cushing's and to adrenal
insufficiency or Addison's. But ultimately the way that you
want to know all three of these is 100% the way that I would ask
it. And I always tell you, if I say
I would ask it this way, that's probably how the boards are
going to ask it or the boards will ask it in a matrix or grid
because endocrine, again, similar signs and symptoms
dealing with the adrenals, 100%. A great way to ask a case study
matrix grade or even a bow tie because now I can give you a
straight up diagnosis and you got to choose one of the three.
I'll probably throw in a fourth one like hyperthyroidism, which
can also elevate things as well too, like blood pressure, heart
rate, skin issues. So you see, I can take all of
these different topics and I can create them into one big case
study or one big bow tie.