Next, what we’re going to do here is begin
at the level of the hypothalamus and quickly,
just reiterate those releasing hormones for
In the first portion of endocrinology, I then
walked you through the group of releasing
hormones and I gave you a picture.
But, what I’m going to add in here as well
is some clinical applications and integrations.
So, let’s go and dive into this a little
bit further, shall we?
First, growth hormone releasing hormone.
It works upon the anterior pituitary to release
I’m sorry I can’t hear you.
Growth hormone, good.
What inhibits growth hormone?
Somatostatin, why is that important?
Analog of somatostatin could be used in what
kind of patient?
Well, the medicine available include what’s
known as your tesamorelin.
Keep that in mind.
This is a growth hormone releasing hormone
Somatostatin, I just gave you a couple of
examples in which you inhibit or you wish
to inhibit growth hormone release… acromegaly.
Welcome to your drug octreotide.
Do not confuse this with somatotrophs or somatomammotropins.
Corticotropin-Corticotropin releasing hormone.
Now, a couple of things here that you want
to pay attention to.
Remember, your boards current day practice
and current day boards is not about you memorizing,
you’re only going to get so far with memorization.
Obviously, the 200 and 205 you’ll be desperate
for residency program; 227 you’re competitive…
you’re competitive; 240/250, you own, haha,
this residency programs, right?
They want you, you’re not begging.
So, what do you want to do on this exam?
Think… critical thinking.
You can’t memorize this stuff.
Corticotropin releasing hormone, I can give
you a lot of angles so that you can get your
240 and 250 and that’s why you’re here.
CRH promotes ACTH.
Okay, no big deal, but the next one’s interesting.
Cortico-Corticotropin releasing hormone stimulation
test to distinguish, you fill in the gap,
you fill in the gap between primary, secondary,
adrenal insufficiency, right?
If it’s primary adrenal insufficiency, I
don’t… and-and you give… you give corticotropin
releasing hormone, primary.
You’re going to release ACTH, but there’s
no effect because the adrenals are dead, right?
Next, corticotropin releasing hormone in secondary
adrenal insufficiency, where is my problem?
Anterior pituitary, secondary.
You with me?
What does primary mean?
Primary from med school means that primary
organ is never able to release that hormone.
Where should cortisol come from?
Adrenal cortex, Addison’s is a primary.
So, no matter how much CRH did you give, ACTH
will be released, but you’re not going to
In secondary, my problem is in the anterior
pituitary, it gives corticotropin releasing
Now, at this point, your ACTH is not going
to be released; it will be decreased.
In both cases of primary and secondary adrenal
insufficiency, your cortisol levels will be
depressed, but for different reasons, right?
Because you know in primary, your ACTH levels
are elevated whereas in secondary, even with
a CRH stimulation test, you find your ACTH
to be depressed.
If you’re still not good with that, that’s
okay, I’m just introducing the concept that
you need to make sure that you iron out properly.
And as we go into details of the adrenal cortex,
I’ll point it out one more time or plus
repeat, haha, and then listen to what I just
Alright, let’s go on to TRH.
Where are these coming from, these hormones?
Where are they working?
Good, in the anterior pituitary.
All over the place, huh?
And you need to be sport about that.
TRH works upon where?
Once again anterior pituitary.
What are you going to release?
Stop, that’s the easy part.
Let’s say that you give TRH… not give
TRH, your patient has elevated levels of TRH.
Think Hashimoto… primary hypothyroidism.
What’s your TRH-TRH levels?
What about prolactin?
Welcome to hyperprolactinemia, right?
Do not forget that, TRH.
Not only does it release TSH, also releases
prolactin, therefore it’s a female.
Tell me about her menstrual cycle, present
or not present?
Good, not present.
Clinically, we call this amenorrhea.
Next, theoretically, once again, another angle,
huh, maybe a pathophysiology question.
Theoretical confirmation of secondary and
What does that mean to you?
What if you give TRH here and it’s secondary
What do you mean secondary?
If it’s secondary hypothyroidism, where
is my problem?
Once again, it will be the anterior pituitary,
Where’s primary hypothyroidism?
It will be the problem in the anterior pituitary.
You give a TRH stimulation test and guess
You are not able to properly stimulate my
anterior pituitary to release TSH.
So, you want to walk through that.
Now, technically speaking, tertiary means
the third place where you can have a problem
with decreased T3/T4.
The first place, primary, thyroid; second
place, anterior pituitary; third place, tertiary
would be where?
Be able to think through all of endocrinology
and really all of medicine and there’s no
way that the boards can really fool you.
Maybe one or two questions here and there
just because you got tired, you know, but
apart from that though, you’ll be okay.
Let’s take a Gn...
Let’s take a look at GnRH, gonadotropin
What’s interesting about a lot of these
hormones, I will tell you, is the fact that
A lot of these are pulsatile in nature, what
does that mean?
Remember I told you that a lot of your hormones
are being released at night when you’re
sleeping including growth hormone that’s
why you use IGF1?
Also GnRH pulsatile, what does that mean?
[sound] It’s like a beat… boom, boom,
boom, boom… just like a drum.
And every time you hit that drum is when you
release that hormone, pulsatile in nature.
That’s important for you to know, isn’t
Oh yeah, watch this.
Before we begin though, GnRH, releasing hormone,
come from hypothalamus, working where?
What it releasing?
LH and FSH.
Depending as to what gender?
If it’s a male, obviously the testes; if
it’s a female, it will be the ovaries, right?
Now, when it’s a short-acting analog is
known as a gonadorelin, the brandname... look
at this, it’s called Lutrepulse, why the
Now you know.
Why the “L”?
Well, you know because this wasn’t before
releasing LH and such.
Gonadorelin is important.
You also have a long-acting analog.
This is the one that you definitely want to
This is leuprolide.
Now, what does this mean?
Remember pulsatile, that is perfect, optimum
Here you are in the rhythms of studying, right?
All of a sudden there is a bulldozer coming
through the… coming through your home [sound],
And so, now, at this point, it completely
disrupts your rhythm and so, therefore, whatever
studying that you’ve been doing is down
What I mean by that is literally, if you were
to step your foot on the pedal, long-acting...
at first, you’re going to have increased
stimulation, but please know that everything
in the anterior pituitary is going to be destroyed
or slowed down if you continue pressing on
This is leuprolide.
In order for you to inhibit the release of
LH and FSH from the anterior pituitary, you
do not give an antagonist... or excuse me,
you can give an agonist... yes, you can give
an antagonist, but you give an agonist so
that you lose the pulsatile rhythm of release
and you have constitutive down regulation
of your receptors.
Thus LH and FSH will be decreased, but initially,
you’re going to have a stimulus, initially.
So, that stimulates and suppresses FSH and
LH release respectively.
That statement should be very clear to you
now and you’re not just memorizing it.
Yes, initially transient.
What’s your ultimate goal?
Obviously to suppress.
Why is this important?
Well, in management and pharmacology and such,
you’ve talked about things such as prostate
cancer and you’ve talked about management
of polycystic ovarian syndrome and so, therefore,
leuprolide is a drug to suppress release of
LH and FSH.
Interesting, isn’t it?
Then you have other drugs here.
A pure gonadotropin releasing hormone antagonist
and this is your Degarilex.