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So for the most part I don't 
typically teach endocrine 

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anymore. 
I think mine is on demand 

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correct? 
If I'm not mistaken mine is on 

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demand. 
But this was something that I 

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wanted to add in as a for a long
time is I've been wanting to 

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compare the difference between 
Cushing's, Addison's, and Khan 

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syndrome. 
Cushing's being 

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hypercortisolism, Addison's 
being adrenal insufficiency. 

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Remember the ADI and Addison's 
and adrenal insufficiency, and 

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then Kahn's syndrome, which is 
primary hyperaldosteronism. 

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So again, all of these are kind 
of working in the adrenals. 

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That's where the confusion comes
in. 

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Briefly we'll go over Cushing's,
then briefly we'll go over 

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Addison's and then I'm going to 
dive into Kahn's because that is

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something that I don't really 
cover anywhere else. 

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So that way everyone here is 
able to see exactly the 

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difference between Kahn's, 
Addison's and Cushing's disease.

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So just kind of a recap on 
Cushing's and the recap on 

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Cushing's is that it is 
hypercortisolism. 

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Now we think about cortisol and 
we think about the adrenals. 

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Remember it's the the peripheral
portion of the adrenal. 

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So the cortex, not the medulla. 
I call the medulla not the 

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medulla, right. 
So it's not the middle portion 

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of it or the medulla, it's the 
cortex. 

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And remember the deeper you get,
the sweeter get. 

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So it goes salt, sugar and then 
sex hormones. 

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So the salt is that aldosterone,
that sugar is that cortisol. 

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And then are sex, androgens, 
testosterone and estrogen right 

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in the bottom there before we 
hit the medulla. 

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So in Cushing's, we can have a 
tumor in the adrenals in that 

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middle portion of the cortex. 
That's where that cortisol 

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producing area is. 
So now we've got excess cortisol

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being made because we have some 
sort of a growth hyperplasia 

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tumor which is causing cortisol 
to be elevated. 

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We know that when cortisol is 
elevated, a big fib, appetite, 

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blood pressure increase, insulin
resistance increase, 

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gluconatogenesis increase and 
then fib, the fibroblast 

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decrease, immune system decrease
and our bone density decrease. 

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So again a big fib. 
But that's not the only place 

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that can happen with increase 
cortisol. 

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As far as tumor goes, we can 
have it in the pituitary. 

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Just as a recap. 
You have it in the pituitary 

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where we're producing too much 
ACTH, ACTH, adrenocorticotropin 

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hormone is going to increase 
cortisol production. 

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So tumor in the brain, so 
secondary in the brain in the 

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pituitary, too much ACTH, in 
turn too much cortisol, that's 

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secondary primaries in the 
adrenals. 

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And then our third one is 
exogenous where again, think 

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about long term and we talked 
about this in respiratory 

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chronic bronchitis where we're 
taking steroids over and over 

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and over again for a long 
duration. 

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And we're kind of like, wait, 
it's not going to hurt our body 

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with a big fib. 
And you're kind of like, no, not

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necessarily because my airway 
and protecting my bronchioles 

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like I would be in chronic 
bronchitis is better than all 

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the other side effects where I 
can actually take care of needs,

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taking care of their appetite, 
their blood pressure, their 

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blood glucose level, bone 
density, calcium and vitamin D 

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to help with the bone density, 
weight bearing exercises, so on,

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so forth, versus keeping our 
bronchioles away from that 

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inflammation with long term 
corticosteroid injections and or

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consumption. 
So again, that's kind of the the

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difference between that in 
Addison's disease is adrenal 

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insufficiency. 
So in this situation, we've 

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knocked out all three layers of 
the adrenals. 

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So there's no aldosterone, 
there's no cortisol, there's no 

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sex androgens. 
And some of the reasons why that

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happens is infections, because 
of hemorrhaging, things of that 

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nature. 
Cons now is primary 

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hyperaldosteronism. 
So in Christians we had 

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hypercortisolism in cons. 
On the outer portion is where 

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aldosterone is made. 
So now we've got 

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hyperaldosteronism. 
Now what do we know about 

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aldosterone? 
I talk about the RAAS all the 

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time. 
It is renin, angiotensin, 

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aldosterone system. 
So remember when I talk about 

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potassium spraying diuretics or 
aldosterone, aldosterone 

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antagonists or we talk about ACE
inhibitors, angiotensin 

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converting enzyme inhibitor, 
these are all things that are 

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affecting this Reenin, 
angiotensin, aldosterone system.

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Same thing with Addison's. 
We're affecting the aldosterone,

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no aldosterone. 
In cons, we are actually the 

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opposite, increasing 
aldosterone. 

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So what happens with increased 
aldosterone? 

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Well, aldosterone is going to 
control salt, increase 

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aldosterone, increase salt. 
If I increase salt, what follows

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it? 
Water hyperaldosteronism or 

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cons? 
We are increasing aldosterone, 

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which increases salt and water 
follows it. 

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If I've got increased salt, then
what happens? 

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In an inverse relationship? 
We have that sodium potassium 

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pump, which means that I get 
hypokalemia. 

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All right, let's dive into cons 
a little bit more. 

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If I've got increased sodium 
from hyperaldosteronism and 

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water follows it, what is the 
one thing that's going to happen

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right away? 
High blood pressure, because now

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my body's consistently making 
excess aldosterone. 

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00:06:30,920 --> 00:06:35,440
So now my blood pressure stays 
elevated and not just elevated 

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little bit. 
I mean, it stays to the point 

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where it's resistant to 
treatment. 

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Because if the problem is 
aldosterone and we're not able 

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to control that, then it's kind 
of hard to get a medication to 

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work. 
What we've got to do is treat 

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the underlying cause, which is 
that primary hyperaldosteronism.

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And usually that's going to 
happen with a tumor just like we

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saw in Cushing's, but where 
cortisol is made or that 

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hyperplasia like we saw in 
Cushing's in that cortisol area 

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put down the aldosterone area of
the adrenals of the adrenal 

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cortex. 
So with hypokalemia, because of 

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that inverse proportion, we've 
now got one of ASGRAF. 

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So if I've got something with 
Khan syndrome, then I'm looking 

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not only at that elevated blood 
pressure, which again, we kind 

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of talked about that yesterday 
with strokes, right, both 

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hemorrhagic and ischemic 
strokes, the underlying cause is

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hypertension as one of the main 
causes, and it is that silent 

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killer. 
So now we're thinking about 

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something that can cause stroke,
which is one of ASGRAF. 

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And then now we've got 
hypokalemia, which with 

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hypokalemia, we've now got one 
of Asgraf as well too, that 

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change in potassium hypo versus 
hyperkalemia. 

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So again, very important to 
understand the difference 

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between the three. 
OK, So I'm going to take it one 

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step further with cons. 
Cons Hyperaldosteronism increase

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sodium, decrease potassium, 
blood pressure is high, usually 

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caused by some sort of a growth 
in the adenoma, some sort of 

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cancer, some sort of tumor, some
sort of hyperplasia. 

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So the initial thing is to stop 
the aldosterone, let's use 

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aldosterone antagonist. 
So what drug have I talked about

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extensively where I break down 
the RAAS and I talked about an 

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aldosterone antagonist and we 
see this now we're trying in 

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endocrine all the way with 
cardio. 

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Day one of cardio I talked about
diuretics and I said potassium 

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sparing diuretic is what we call
it as lay terms. 

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But in fact the class of drug of
potassium sparing diuretics like

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spironolactone Aplarenon 
amylaride Miller known is that 

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their aldosterone antagonist. 
If the problem here is in fact 

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too much aldosterone, can I not 
initially look at the word I 

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used initially use an 
aldosterone antagonist? 

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Yes. 
Can I use the ones that help the

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RAA system? 
Yes. 

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So things like ACE inhibitors, 
Arbs, angiotensin receptor 

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blockers still affecting that 
development of aldosterone, just

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one step ahead. 
Instead of renin, we work on the

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angiotensin and then with the 
aldosterone, we work with an 

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aldosterone antagonist. 
So you see medications that can 

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work that are going to help with
that increased aldosterone, but 

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00:09:58,600 --> 00:10:02,080
ultimately that's just putting a
Band-Aid on a cut. 

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That's all that's doing. 
Band-Aid on a cut. 

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I'm OK, aldosterone antagonist, 
Aldosterone antagonist. 

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00:10:08,080 --> 00:10:11,040
I keep taking my spironolactone.
I take an ACE inhibitor, I take 

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an ARB. 
I'm just putting a Band-Aid on a

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cut, on a cut, on a cut, on a 
cut. 

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And I'm not treating the 
underlying cause. 

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So what is the best action in 
order for this to be resolved? 

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Well, our ultimate resolution in
this situation is going to be 

156
00:10:28,320 --> 00:10:32,680
removal of the tumor or the 
adenoma or control that 

157
00:10:33,040 --> 00:10:36,000
cancerous growth or whatever it 
is that's actually causing it. 

158
00:10:36,240 --> 00:10:41,960
So ultimately the progression is
again finding that the fact that

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this person has that resistant 
hypertension, maybe we get some 

160
00:10:46,640 --> 00:10:50,520
imaging, maybe we get ACT, maybe
an MRI, we get some imaging in 

161
00:10:50,520 --> 00:10:53,040
order for us to see that there 
is infected growth on the 

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adrenal glands. 
And when we look more in depth, 

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00:10:56,800 --> 00:10:59,040
we're looking at it, we're 
saying, OK, wow, just kind of in

164
00:10:59,040 --> 00:11:01,240
the up outer portion of the 
cortex. 

165
00:11:01,600 --> 00:11:05,120
And now we're seeing the signs 
and symptoms with hypokalemia, 

166
00:11:05,200 --> 00:11:08,640
hypernatremia, high blood 
pressure, maybe some 

167
00:11:08,640 --> 00:11:12,400
dysrhythmias, both electrolytes 
causing dysrhythmias. 

168
00:11:12,920 --> 00:11:15,400
So now we're concerned about 
again that V fib. 

169
00:11:16,200 --> 00:11:19,680
Then we look at the treatment 
and again, we can put a Band-Aid

170
00:11:19,680 --> 00:11:22,560
on the cut, but ultimately the 
resolution is going to be 

171
00:11:22,560 --> 00:11:27,120
surgery. 
So that is Khan's disease with 

172
00:11:27,120 --> 00:11:32,040
the brief comparison to 
Cushing's and to adrenal 

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00:11:32,040 --> 00:11:36,800
insufficiency or Addison's. 
But ultimately the way that you 

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00:11:36,800 --> 00:11:40,880
want to know all three of these 
is 100% the way that I would ask

175
00:11:40,880 --> 00:11:42,600
it. 
And I always tell you, if I say 

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00:11:42,600 --> 00:11:44,920
I would ask it this way, that's 
probably how the boards are 

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00:11:44,920 --> 00:11:49,080
going to ask it or the boards 
will ask it in a matrix or grid 

178
00:11:49,480 --> 00:11:53,120
because endocrine, again, 
similar signs and symptoms 

179
00:11:53,480 --> 00:11:57,720
dealing with the adrenals, 100%.
A great way to ask a case study 

180
00:11:57,720 --> 00:12:01,280
matrix grade or even a bow tie 
because now I can give you a 

181
00:12:01,280 --> 00:12:03,440
straight up diagnosis and you 
got to choose one of the three. 

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00:12:03,440 --> 00:12:07,200
I'll probably throw in a fourth 
one like hyperthyroidism, which 

183
00:12:07,200 --> 00:12:10,080
can also elevate things as well 
too, like blood pressure, heart 

184
00:12:10,080 --> 00:12:14,240
rate, skin issues. 
So you see, I can take all of 

185
00:12:14,240 --> 00:12:17,920
these different topics and I can
create them into one big case 

186
00:12:17,920 --> 00:12:19,480
study or one big bow tie.