Let’s talk about sellar masses.
So, whenever you have a mass within the sella,
things that you’re always looking for symptomatically
are your neurologic issues, especially headaches
and visual impairment.
We talked about this just now.
Often times these sellar masses are incidental
on-on MRIs and may often times be known as
incidentalomas microadenomas in normal population.
So, this might have been there the whole time,
Hormonal abnormalities may also occur, obviously
if there are sellar masses.
Here, I want to show you a second messenger
system that you want to be clear about.
We have GTP beta and gamma.
This, as you remember from biochemistry, is
What must you have so that you can have proper
activation of your enzyme?
You have to make sure that you hold on to
your alpha, right?
So, you then become an alpha, active G-protein
and when you do so, you might then stimulate
an enzyme called adenylyl cyclase.
And that adenylyl cyclase will convert your
ATP into cyclic AMP.
And if you remember correctly that at some
point in time, you will then remove a phosphate
so that you can inactivate it and then turn
into your GDP.
Now, with all that said, let’s get into
our topic of what’s known as MEN1, multiple-multiple
endocrine neoplasia type 1.
Your first thing that you want to do is, well,
identify your patient.
Usually, family history is taking place and
when you deal with MEN1, it is a triade.
The triade here is going to be called pan-para-pit,
as we’ll talk about later.
You’ll have pancreatic tumour, you’ll
have a hyperparathyroid, hence the hypercalcemia
and the kidney stone.
So, some of the things that you want to pay
attention to right off the bat with MEN1 is
family history and whether or not kidney stones
of calcium type.
In addition is pancreas and then when you
say pituitary, you’ll have prolactin levels
In your female, may result in galactorrhea
and she’s going to be amenorrheic.
The reason that we went through the G-protein
in great detail is the following.
Understand that these adenomas and these tumours
that you’re going to find in MEN1 often
tend to be constitutive activation of your
Gs and hopefully, what you remember is that
of all of the hormones that you’re going
to release pathologically from a functioning
Remember, up until now, our discussion earlier
was... has been a dysfunctional or a non-functional
In non-functioning adenoma, the first hormone
to be knocked out is growth hormone hence,
we walked through dwarfism.
Whereas if it’s a functioning adenoma, the
number one hormone to come out would be your
So, here, when we talk about 40% of somatotroph
adenomas, that’s exactly right because the
prolactin or prolactin is a somatotropin,
So, therefore, you can expect there not only
to be prolactin, but at times maybe excess
What’s my problem?
Biochemically and genetically, there might
be an issue with my Gs-protein.
What does Gs mean to you?
In order for you to be active, you have to
have the alpha sub-unit.
Pituitary transforming genes, something called
Pituitary transforming genes - associated
and also fibroblast growth factor receptor-4.
I would make sure that to memorize some of
these growth factors here and some of these
genes and something that you already know
from biochemistry with these G-proteins so
that you have constitutive activation.
Let’s do classification of our pituitary
If it’s less than 1, it’s microadenoma.
If it’s greater than 1, we call it a macroadenoma.
Gonadotrophs adenomas usually present clinically
as a non-functioning sellar mass.
That’s interesting, isn’t it?
Thyrotroph adenomas may present clinically
as non-functioning sellar mass that secrete
only alpha or TSHbeta sub-unit and may cause
hyperthyroidism due to increased secretion
of intact TSH.
So, what we’ll do here as we’re going
through our topics of adenomas is, well, specifically
what kind of hormone are you producing from
40%, do not forget, would be what kind?
So, that would include both prolactin and
Now, we have gonadotrophs, thyrotrophs, corticotrophs,
lactotrophs and somatotrophs.
The combination adenomas are well recognized
to clinical syndrome of both prolactin and
Do not forget that.
And naturally, your emphasis should be when
you talk about functioning adenomas, the bottom
two statements here.
In the meantime though, when you have a functioning
adenoma, always pay attention to your patient
in your stem and is your patient in fact suffering
from Cushing’s disease.
You’ll notice Cushing’s disease and not
Cushing’s disease is specifically increased
cortisol due to ACTH coming from the anterior
We’ll talk more about this when the time
is right, but at this point, it is imperative
that you specifically know the difference
between Cushing’s disease and Cushing’s
syndrome, as we shall see, or otherwise you
will miss a question unnecessarily.
What we’re seeing here would be a pituitary
adenoma and with an MRI, you’ll find enlargement
of the pituitary compressing the optic chiasm
resulting in visual disturbances.
The topic prolactin, just to make sure we’re
We saw this in the very beginning where I
walked you through many types of releasing
hormones above the dash line representing
the hypothalamus and the various anterior
pituitary hormones below the line.
I also had you pay attention to dopamine,
normally inhibiting the prolactin and, as
you can see here on the side branch, thyrotropic
releasing hormone stimulating prolactin release.
One step further, I also gave an example where
you can have a non-functioning adenoma in
the sella which is then compressing the stock,
diminishing or delaying the delivery of dopamine
to your prolactin, thus increasing release
Do not ever forget that.
Prolactin, what does it do?
Lactation in women.
Now, is this the hormone when the infant is
suckling on the mother’s nipple?
Is this the hormone that’s responsible for
ejection of milk?
This, however, is the hormone that’s responsible
for synthesis of milk.
Now, don’t be so black and white where you’re
thinking, “Well, if I have a prolactinoma,
if I have a hyperprolactinemia, if it’s
not physiologically responsible for ejection…”
I don’t want you to think that you wouldn’t
Listen, if you have too much prolactin for
whatever reason, either prolactinoma or functioning
adenoma in the anterior pituitary, maybe it’s
due to antipsychotics, maybe it’s lesions
in the stalk, maybe compression of the stalk,
whatever it may be, that hyperprolactinemia
is going to have so much milk synthesis and
which, at some point, of course, you’ll
Regulation, we talked about TRH stimulating
And so, therefore, it is extremely high in
Dopamine inhibits prolactin release.