Hypothyroidism is where we are.
Think about your patient walking through the
Anxious, palpitations, sweating, eating quite
a bit of food, but yet is not gaining weight.
What we’ll take a look at with hyperthyroidism
and then differentials for you; in other words,
Something’s causing your thyroid gland to
increase production of T3, T4.
Maybe Graves’, thyroiditis, iodine-induced,
Human chorionic gonadotropin replaces TSH.
Pituitary tumour, what are you releasing?
Struma ovarii, where are you?
How is that causing hyperthyroidism?
Struma ovarii, it’s part of a female teratoma
in the ovaries producing directly T3, T4.
Topic, hyperthyroidism… patient has too
much T3, T4 for whatever reason… look at
Exogenous… absolutely, maybe of an athlete
that was… wishes to increase his or her
Why not take thyroid hormones or perhaps even
you have a patient that has hypothyroidism
taking synthroid excessively resulting in
hyperthyroidic type of symptoms.
We’ll begin our discussion by looking at
Let me set this up for you.
On your left, you see that grey blob?
Hahaha, well, that grey blob; in other words,
that’s your thyroid gland and on your basolateral
membrane, you have a TSH receptor.
Do you remember that?
And that TSH receptor regulates whom?
That’s important known as your sodium-iodide
As long as everything’s perfectly normal,
you have a proper feedback mechanism in place.
The TSH will bind to the receptor and you
will have increased production of one lightning
What does that lightning bolt represent?
Just right so you can maintain normal basal
BMR versus Graves’, what’s happening?
Oh, the TSH is being replaced by whom?
An immunoglobulin antibody known as TSI, thyroid
When you have an immunoglobulin that is then
attacking in this case, remember when I say
attack, it could either destroy it like myasthenia
gravis or it could stimulate it, as you would
So, it’s a type II hypersensitivity.
It is bind to your TSH receptor and what’s
Take a look at the number of lightning bolts…
cute perhaps; if not, whatever.
You are increasing T3,T4 in great excess,
And from head to toe think about your patient
with Graves’ disease.
Stimulates greater production of T4, lots
of free T4… let me take you back to that
important laboratory investigation we talked
about with the resin.
“Oh Dr. Raj, don’t take me there.”
Yes, I will.
So, you have increased T3, T4 and you’re
increasing your total… what’s your total?
Bound plus free.
You’re increasing both of these, aren’t
Yes, you are.
In addition, you’re also increasing the
amount of T3 being produced in Graves’ so
you have a lot more T3 binding to your resin.
So, therefore, your T3 resin uptake will be
Do you see as to how you are now utilizing
and applying that information that I established
earlier with laboratory investigation?
Increase in T4, what’s it going to do?
It’s going to suppress your TSH.
The number one screening hormone that you
are going to take a look at when you’re
assessing your thyroid function…
TSH, TSH, TSH.
You have too much T3, T4 suppressing TSH…
That increase in T3,T4 is going to speed everything
up… welcome to loss of appetite, but you’re
still eating perhaps, but you’re not gaining
weight, that’s for sure.
Weight loss, anxiety, tremors, heat intolerance
is a big one, isn’t it?
Amenorrhea… you completely mess up your
hormonal balance between estrogen, progesterone
and LH and FSH… amenorrhea.
Graves’ disease, autoimmune disease, isn’t
What happens to your eyes?
Bulge out and you have extra ocular muscles
that are undergoing hypertrophic pushing the
What do we call this?
We call this exophthalmos… bug eyes.
Pretibial myxoedema… myxoedema is an important
concept for us.
Let me now slow down here just a tad bit.
Myxoedema, you can find it in hyper; myxoedema,
you can find it in hypo; myxoedema, you can
find it in death.
Three different times which you’re responsible
for right now in medicine with myxoedema…
If it’s Graves’ disease, the myxoedema
will be located… we don’t know exactly
why, but you definitely will most likely find
your myxoedema pretibial.
Where are you?
The leg, the anterior portion, the “shin”…
If it’s hypothyroidism, myxoedema would
be found perhaps in the hands and maybe in
the face giving you the puffy hands and puffy
face that you’re oh so familiar with.
And then finally, why did I say death?
Worst case scenario, later on, we’ll talk
about this of hypothyroidism in which the
patient may actually go into a coma is called
myxoedema coma and your risk of mortality
Three different times in which you will find
I wish to make sure that you are aware where
else you would find it versus just memorizing
Thyroid, what’s known as acropachy and thyroid
bruit all because of increased amounts of
Now, if you have an elderly patient with hyperthyroid
commonly lack these signs and symptoms.
So, therefore called “apathetic hyperthyroidism”.
If there is Grave-like issue in an elderly
patient, the patient… the elderly patient
is not going to behave like your typical,
traditional young patient with anxiety, tremors
and perhaps even loss of weight.
So, the signs and symptoms are not as prevalent,
but you know for a fact that your patient
has hyperthyroidism and doesn’t show you
what you would expect, call this “apathetic
Be very, very aware of this situation because
you do want to pay attention to how old your
patient is whenever you have thyroid disease.
Important points of Graves’.
You’re producing thyroid stimulating immunoglobulin,
This is an IgG versus the TSH receptor.
Now, you tell me, are you stimulating receptor,
are you inhibiting, destroying the receptor?
Good, you’re stimulating… welcome to Graves’.
Autoimmune etiology, definitely want to know
HLA either DR3 and B8.
If I were you, I’d memorize both of those.
More frequent in women, but you know that
autoimmune diseases unfortunately generally
speaking much more prevalent in the female
population than male population.
Associated with exophthalmos, we talked about
how you would then have autoimmune mechanism
independent of hyperfunctioning and if you
were to start correcting Graves’ disease,
which we’ll get into a little bit in management,
that exophthalmos actually starts reverting,
Graves’ opthalmopathy… swelling of the…
what is actually happening is the retroorbital
muscles or extra ocular muscles are undergoing
hypertrophy, you could actually see this,
can be visualized on ultrasound or CT or even
It looks enlarged, pushing the orbit forward
right, bug eyes.
The retroorbital fat is also increased and
retro orbital swelling as you can see here
in the picture beautifully illustrated.
On your left, perfectly normal, pay attention
to the extra ocular retroorbital muscles normal
on the left and on the right, due to excess
T3,T4 undergoing hypertrophy.
Look what it’s doing.
It’s pushing the orbit forward… welcome
to Graves’ opthalmopathy a.k.a exophthalmos.
With Graves’ opthalmopathy, there might
be a lid retraction.
So, therefore, you find more of the orbit
In addition to that, you will find so much
of that orbit moving forward that you might
actually find some of that fat that I was
referring to being quite evident as you see
here in the picture on the right… severe
proptosis in the eye, increased vascularity
of the conjunctiva, enlarged lacrimal gland.
Take a look… take a good look as to what
you can expect with Graves’.
Here, you have a shin or the pretibial region
and with the symptoms of Graves’ without
a doubt this is pretibial myxoedema.
What is it?
It’s thickened area in the pretibial region,
it appears erythematous and could extend down
to the dorsum of the foot.
There might be issues with the skin.
This you would refer to as being dermopathy.
Lesions are firm, non-pitting, typically located
in the pretibial region, all goes hand in
hand with pretibial myxoedema.
So, you want to pay attention to, well, what
exactly are they going for?
Are they asking about the skin or are they
asking about the pretibial myxoedema?