A topic that you want to be extremely comfortable
with is called euthyroid conditions in laboratory
As simple as this may seem, there are certain
things that you want to take at a dissection
that is going to help you differentiate one
type of thyroid pathology from the another.
Do not underestimate what I have to tell you
This brings us to our first discussion of
Break it up.
Eu- prefix – normal.
A pathology is going to lie within hyperthyroxinemia.
Break this up.
When you say thyroxinemia, referring to your
T4 in your blood; in this case, we have hyper.
So, how could you possibly have a normal thyroid
state and be hyperthyroxinemic?
The discussion now brings us back to our physiologic
point of view of thyroid binding globulin.
Remember the definition of total?
Total is bound plus free.
What is the component that makes up majority
of your total?
It is the bound.
So, therefore, euthyroid hyperthyroxinemia,
due to, in general, increased binding protein.
What is this specifically for thyroid hormone?
Thyroid binding globulin.
Coming from where?
Your emphasis and focus should be on, well,
what is then causing liver to increase is
thyroid binding globulin.
Before we go at there, abnormalities.
T4 - binding.
Majority of your T4 is bound thyroid binding
Albumin rounds it all up to approximately
The most common cause - MCC of hyperthyroxinemia
would be TBG excess.
What is that going to do to your total?
What then binds to my TBG?
I’ll show you this.
Remember, the majority of your thyroid hormone
being released into circulation is T4.
It has to be bound to TBG.
Whenever TBG is found to be in excess, you
would then expect there to be a total in T4.
What about that T3?
Well, as far as the normal functioning, or
the functioning of the body, it is within
It could be hereditary.
Whenever you find a patient in a hyperestrogenic
state, such as pregnancy or contraceptive
pills that may contain estrogen…
Estrogen works in liver to increase glycosylation
When you increase your TBG, you’re going
to then decrease the clearance.
So, therefore, with all this TBG that resides
within your circulation, guess what it’s
going to bind to.
So, you increase in the bound faction of your
thyroid hormone, thus, what do you do to your
You’re increasing it.
Keep your bound and total separate.
Resulting in hyperthyroxinemia.
What other conditions might then result in
increase or excess TBG?
Drugs such as Methadone, tamoxifen; a porphyria
pathology, in biochemistry that you’ve heard
it called acute intermittent porphyria - often
times you’ll find euthyroid hyperthyroxinemia;
reduced thyroxin deiodination, such as amiodarone
or propranolol, could all result in euthyroid
What do you mean by deiodination?
The conversion of T4 to T3.
It’s not taking place effectively.
I want to show you a picture here of what’s
important to you clinically.
You’re going to use this picture so that
you can then first understand normal, then
understand what’s happening in a state here
of euthyroid hyperthyroxinemia and truly when
you read a stem of a question or you’re
dealing with the patient and you’re having
discussion with your attending, you know what
he or she is referring to.
Let’s begin on the left here where it’s
The huge blocks that you’re seeing here,
the blocks is your TBG – thyroid binding
Coming from where?
What is that TBG going to bind to?
Now, you’re left with T3.
You’re going to be using clinically or interpreting
what’s known as a thyroid hormone binding resin.
You want to keep your resin, which is what
you’re going to interpret clinically, separate
from your TBG, which are these blocks that
you’re seeing bound to T4.
As long as you’re within normal state and
you have adequate and normal amounts of TBG,
then the resin is going to bind exactly as
to what it needs to with T3.
Let us now move on to the right side of this
And the right half is then showing you euthyroid
What is the difference between the pathology
on the right versus the physiology on the left?
You’ll notice, please, that you have increased
number of these blocks.
How did this occur?
Oh, maybe it was estrogen or a patient that
was in a hyperestrogenism state.
When you increase your TBG, you’re going
to bind more T4.
When you bind more T4, what faction of your
total have you increased?
What happens to total?
It increases it.
Therefore, what do you call this?
But, why is it euthyroid?
You’re still euthyroid because even though
you’re robbing your T4 out of circulation,
your thyroid gland and your anterior pituitary,
the axis, is going to respond accordingly
to start increasing thyroid hormone production
to bring it back to normal.
What do I mean by that?
What is the active form of most hormones?
Free thyroid hormone.
So, when you rob your free faction, this is
then interpreted as being hypo.
Your feedback mechanism in your axis is immediately
going to respond so that it can replenish the free.
Your state of euthyroid.
That picture on the right is probably one
of the most important pictures that you want
to be able to interpret.
In pregnancy, in pregnancy, with the increased
estrogen, you’re then going to increase your TBG.
You’re going to then bind and remove the
free faction of T4 out of circulation.
Are you picturing that?
Thus, immediately during pregnancy, the mother
is then going to start increasing her production
of her thyroid hormone so that you bring or
she brings the thyroid hormone back, free
faction back up to normal.
And of course, that is absolutely critical
to occur or otherwise the foetus is going
to feel the effects of hypothyroidism and
you cannot have that.
Last little point that I’ll make here.
I want you to focus upon the resin there.
And at the end of this section, I’m going
to walk you through a table where that resin,
which is binding T3 will then tell you what’s
actually happening in a patient that is differentials
Understand these two pictures for now.
I’m going to build and build and build upon
these until we finally come to a table where
I’ll summarize everything for you clearly.