What’s adrenal gland pathology?
Our focus here will be aldosterone, hyper
I highly recommend that you go back and review
your physio because I will go through this
rather quickly, expect you to know the basic
functioning of aldosterone so that we can
walk through the path effectively.
Our topic here is hyperaldosteronism.
Before we begin, you automatically start thinking
about what’s going on with your patient.
There’s going to be increased reabsorption
of sodium, doesn’t matter if it’s primary
In addition, there’s increased reabsorption
of water, thus you’ll have increase in blood
Next, what does aldosterone do with potassium?
It gets rid of it, you secrete it.
If there’s too much aldosterone, either
primary or secondary, your patient is suffering
from hypokalemia, your potassium level will
be less than 3.5.
Next, what do you do with hydrogen?
Or what does aldosterone do with hydrogen?
It secretes it, it gets rid of it.
If you get rid of hydrogen, your PH is going
to increase, your patient is in a state of
What is primary and secondary?
Well, primary hyperaldosteronism will be a
specific tumour in the zona glomerulosa that
is only producing aldosterone… welcome to
What is it going to do to your blood pressure?
It is going to increase it.
Now, be careful, this blood pressure that
you’re increasing, obviously called hypertension,
is it primary or secondary, do you remember?
In the United States, a very common cause
of secondary hypertension is primary hyperaldosteronism.
Interesting, isn’t it?
Do not ever forget that.
Bilateral adrenal hyperplasia, what’s happening
Well, here, you might have increased production
of aldosterone by your adrenal cortex, specifically
the zona glomerulosa.
If you were to find increased levels of aldosterone
primarily, what is its feedback mechanism?
Do not focus upon ACTH clinically, you are
going to be focusing upon plasma renin activity,
Therefore, if there’s increased aldosterone
primarily causing secondary hypertension,
there will be a decrease in rennin.
Is that clear?
You’ll have increased reabsorption of sodium
as mentioned above 145, you’ll have a decrease
in potassium level plasma less than 3.5 and
because you’re getting rid of hydrogen,
your patient is in a state of metabolic alkalosis.
What about secondary, how does secondary work?
All secondary would mean is that, let’s
say that your patient has some type of renal
What do you mean some type?
If I give you a 67 year old male in which,
upon physical examination, you hear renal
Well, that would be atherosclerosis of the
renal artery, correct?
Resulting in renal artery stenosis, what then
Decreased profusion through the afferent arteriole.
What is then elevated here?
Renin, what’s next?
Aldosterone, ah, welcome to secondary hyperaldosteronism.
It wasn’t primary; the inciting event was
decreased profusion to the kidney.
What else may then cause it?
Take a look at the examples here.
CHF, congestive heart failure, you will then
find increase amounts of fluid in your interstitium.
There will be a decreased profusion through
the afferent arterial, you’d be increasing
your renin and therefore causing secondary
Remember, in congestive heart failure, it’s
a vicious cycle, especially if there is right
sided heart failure, what does your patient
This relationship is completely the opposite
Please locate the relationship between renin
and aldosterone in primary.
Increased aldosterone, decreased renin in
primary; in secondary, increased renin, increased
aldosterone… secondary hyperaldosteronism.
What kind of hypertension is this?
You see as to how language becomes really
important for you in medicine, right?
So, both primary and secondary hyperaldosteronism
is causing what kind of hypertension?
That must be understood.
Edema, hypertension, low potassium and alkalosis,
the major factor here or sign that you did
not see in primary hyperaldosteronism was
the edema caused by congestive heart failure
caused by cirrhosis caused by nephrotic syndrome,
In those conditions, don’t you find edema,
decreased profusion through the afferent arterial,
out comes renin and secondary hyperaldosteronism.
Let’s screen for primary hyperaldosteronism.
Plasma aldosterone concentration, PAC, you
want to memorize greater than 15 nanograms,
you do that on your own time, but you know
that it’s already elevated.
Concept first then memorization.
In primary hyperaldosteronism causing secondary
hypertension, where is my lesion?
Is it throughout the cortex of the adrenal
or only in the zona glomerulosa?
That’s a very important question because
that gives you two different diagnoses.
Where is the adenoma located here?
Good, only in the zona glomerulosa.
Give me the diagnosis, if I put the adenoma…
not me, but if pathology puts an adenoma in
the adrenal cortex as a whole, that gives
you Cushing’s, right?
That gives you Cushing’s… simple questions
makes you think, that’s what the exam is
all about, not about memorization.
So, here, we have an increase in aldosterone
and a decrease in renin, take a look at the
Obviously, your plasma aldosterone concentration
is much higher than the plasma renin activity,
that ratio will be increased.
Confirmation of diagnosis, how do you confirm
Non-suppressed 24 hour urine aldosterone after
oral salt loading or non-suppressed plasma
aldosterone concentration after IV saline
Be smart about how do you use your test.
Shouldn’t you be suppressing aldosterone
if you inject your patient with fluid?
What if it doesn’t happen or what if you
give oral salt then what should you be doing
to your aldosterone?
Obviously suppressing it.
Doesn’t this sound an awful lot like oral
glucose tolerance test?
And we had done this for acromegaly.
If you missed that concept, make sure you
go back and take a look at OGTT and acromegaly.
Here, we have oral salt and aldosterone confirmation.
In unclear cases, adrenal vein sampling can
help distinguish unilateral from bilateral
sources of excess aldosterone.
Do not forget that.
Adrenal vein sampling may help you distinguish
between uni and bilateral… an important
slide for screening, confirmation.
If you take a look at this picture of aldosterone,
haha, by that I mean, you can’t tell by
looking at this picture per se that it’s
But, you can definitely tell by looking at
this picture that, my goodness, there is an
adenoma in the adrenal.
So, what are you looking for?
You will be given more information.
Maybe there’s secondary hypertension, maybe
there is decreased potassium and alkalosis
without any effect of Cushing.
So, therefore, this is Conn.
If you find a adenoma such as this and your
patient has moon facies, buffalo hump, trunk
obesity then that would be Cushing, clear?
Things are becoming really interesting for
you, aren’t they?
Primary hyperaldosteronism… surgery for
unilateral source adenoma, use of aldosterone
antagonists… welcome to your spironolactone
Remember that these are drugs or they’re
potassium sparing drugs, aren’t they?
If you antagonize your aldosterone receptors,
obviously you’re going to hold on to your
potassium, but here, we’re using for purposes
because you want to block the effects of the
excess aldosterone for bilateral sources,
hyperplasia; unilateral surgery bilateral