Thyroid storm, what happens here?
Let’s say that the colloid gets destroyed.
When it does, it may then result in massive
release of T3, T4 into circulation.
Characterized by fever, sever tachy-.
All that thyroid hormone sensitizing the heart
and therefore, making it easier for catecholamines
to work on beta-1 receptors to the point where
the palpitations and arterial fibrillation
might be taking place.
There might be so much issue then which now
you might then cause delirium or to the point
of even coma.
Quite dangerous – thyroid storm.
Usually, precipitated by severe physiologic
stress (childbirth, surgery), lots of stress
in a patient with uncontrolled hyperthyroidism.
Look for stresses in which the… results
in massive release of T3, T4 into circulation.
With the thyroid storm, you want to try to
get in there as quickly as possible, because
you’re worried about the patient becoming
Antithyroid drugs are the main therapy – should
be started at least several hours prior to
any, any iodine.
PTU is preferred mainly due to, once again,
its inhibition of conversion of T4 into T3.
You’re worried about the palpitations, tachycardia
and arterial fibrillation and therefore you’re
thinking about giving beta blockade and “stress
dose” of glucocorticoid coverage, because,
remember, what is the precipitating event
that is leading up to a thyroid storm?
Extreme stress, such as childbirth.
And therefore, during this stress, maybe it
will be in the best interest of the patient
to therefore supplement the patient with more
Potassium iodide can be used in the treatment. It is taken up by the thyroid and blocks the release of additional thyroid hormone.
It is a slow mechanism, so initially treatment must include PTU or methimazole.
Supportive measures, fluid and electrolyte
management, address underlying stress (such
as infection, maybe the childbirth we were talking about earlier) and make sure that
you monitor the underlying issue before you completely relieve the patient of any therapeutic
Acetaminophen for that fever, not aspirin,
because what does aspirin do with your thyroid
It may displace…
Aspirin, NSAIDs may displace your thyroid
hormone T4 from your TBG.
We’ve talked about that particular issue
being called euthyroid hypothyroxinemia.
Cooling blankets, because there’s fever
here quite high.
Sedatives for agitation.
Let’s talk about subclinical hyperthyroidism.
What does it define as biochemically?
Constellation of, well, there’s suppressed
TSH with normal free T4 and T3 levels that
Exogenous type – look at the number of patients
that you might be exposed to in the US suffering
from subclinical hyperthyroidism.
10 million in US, 200 million worldwide who
take thyroid hormone are at risk.
So, those individuals…
Hypothyroidism – extremely common.
Taking your Synthroid and such may result
with subclinical hyperthyroidism.
The benefit of inducing subclinical hyperthyroidism
to suppress TSH in patients with thyroid cancer,
nodular thyroid, head and neck irradiation
outweigh the risk of administering thyroid
So, often times, the benefit of inducing subclinical
hyperthyroidism is to make sure that you suppress
some of that TSH, as you expect to find here
biochemically, especially in those patients
that have thyroid cancer, nodules.
We’ve talked about multi nodular and head
and neck irradiation outweigh the risks of
administering thyroid hormone therapy itself.
The endogenous type – most common cause
(mcc) would mean autonomously functioning
thyroid adenoma or multinodular goiter.
Contribute to osteopenia, atrial fibrillation
risk in the elderly.
Treatment is recommended in most patients
with TSH<0.1, selected patients and especially
those at high risk for osteoporosis and cardiac
Subclinical hyperthyroidism is an area that
you want to pay attention to, only because
of its frequency found in our society.
Work-up of hyperthyroidism, step by step.
What would the presenting symptoms be in hyperthyroidism?
Tachycardia, palpitations perhaps, tremors,
anxiety, decreased weight.
If it’s a primary hyperthyroidism, you’d
expect there to be suppression of your TSH
with elevated levels of free T4.
Next, radioactive uptake and scan.
What you’re going to find?
Let’s do the following.
If your thyroid gland is being destroyed,
and we’ve talked about thyroiditis, and
it would be in your best interest to make
sure you go back in your organising your thoughts
Is it Graves’ disease?
Is thyroiditis dealing with pain or is it
And if it is painful thyroiditis, is it acute,
perhaps due to bacteria commonly?
Or is it sub-acute, maybe due to mumps and
Or is it painless?
In any case, whenever there’s thyroiditis,
that means the thyroid gland has been destroyed.
And remember that graph that I showed you
with a spectrum of symptoms that your patient
may present and this may include what?
Hyperthyroidism initially and then you get
into euthyroid state transiently; may then
get into hypothyroid and if it’s an infection
may then result in recovery.
Point is this, if the thyroid gland is not
functioning, how in the world is that thyroid
gland going to take up radioactive iodine
or any iodine at all?
Decreased uptake in thyroiditis, but your
patient’s presenting how?
With hypothyroidism, sub-acute or silent with
Iodine-induced, meaning to say that iodine
has been administered.
You increase production of T3, T4.
TSH is going to drop.
The TSH receptor is not being fully stimulated.
The radioactive iodine is therefore diminished.
Why struma ovarii?
The ovary in a female has an ovarian tumor
known as cystic teratoma.
This teratoma is then going to directly release
Your patient is then going to present how?
It will supress TSH.
TSH receptor is sub-optimal functioning.
Decreased radioactive iodine uptake.
Exogenous, iatrogenic, factitious – all
of it means synonymously that the patient
is now taking T3, T4.
Maybe the doctor has prescribed Synthroid.
Maybe an athlete might be taking some derivative
of T3, T4.
TSH receptor not working.
What about radioactive iodine uptake?
Do you see the similarities between iodine-induced,
struma ovarii, exogenous administration?
All resulting in decreased TSH receptor activity.
Let’s go on to the other side where now
we have normal or elevated uptake of radioactive
Now, remember, this is not for therapy.
This is for what?
This is for diagnostic purposes.
If you only find focal regions within your
thyroid gland taking up your iodine, this
to you means a “hot” nodule.
A “hot” nodule is benign, as far as you’re
It is not a cancer.
It’s that black and white for you right
Whereas if you had a nodule that is not taking
up any iodine at all, how would that appear
on an imaging study?
An imaging study known as a scintigram, which
show you a lucent area of being black.
That is a “cold” nodule and that to you
should mean maybe your patient is suffering
from cancer and the most common of all of
your thyroid cancer would be a papillary cancer
of your thyroid.
Localised focal regions of uptake.
Our next topic is what if the entire darn
thyroid gland was taking up the iodine?
The entire thyroid gland.
That means that every single TSH receptor
is being stimulated, stimulated, stimulated,
That means the entire thyroid gland pathologically
is successfully taking iodine.
So, therefore, what do you call this?
A diffuse uptake.
Is that clear?
Versus a focal uptake, “hot”.
Other possibilities, apart from Graves’
disease, would include: you can have choriocarcinoma
and then with the choriocarcinoma you can
either have the placental or the gestational
cancer that you know of, or you’re going
to have non-gestational choriocarcinoma and
that choriocarcinoma would be a germ-cell
tumor of either the testes or the ovaries.
With choriocarcinoma, when the time is right,
you should know you divide that in gestational
My point is this, in either case, chorio-
You’re going to be releasing beta hCG in
All that beta hCG shares a similarity structurally
with what, what hormone?
Therefore, that beta hCG that’s being produced
excessively in choriocarcinoma will then bind
to TSH receptors, therefore cause what kind
A diffuse uptake.
Rare, but my goodness, isn’t that a good
And then you have a secondary hyperthyroidism.
You have a pituitary tumor that is now a functioning
adenoma producing too much TSH.
Now, you tell me: increased TSH receptor activity,
increased radioactive iodine uptake – is
it focal region or is it diffuse?
Really, the TSH, it’s coming out of the
It’s not going to discriminate.
It will bind to as many TSH receptors as it
needs to, on the thyroid gland.
Welcome to diffuse uptake.
How important is this algorithm for hyperthyroidism?
Obviously, you want to spend time here and
make sure that you have a full and complete
understanding before walking into your board
exam or walking into the wards of your hospital.
If this is in your head, can you see your
patient literally falling into one of these
That’s the way that you want to approach