In this lecture we're going to talk about
hypothyroidism and hyperthyroidism in children.
Let's start with hyperthyroidism.
So there are many causes of hyperthyroidism in children.
By far, the most common is the autoimmune disease, Grave's disease.
Where patient's are having antibodies directed against their thyroid
that are causing the thyroid to spit out too much thyroid hormone.
Also, patients might have Hashimoto's Thyroiditis,
and in the early phases, they can have a toxic effect
where there is an excessive excretion called Hashitoxicosis,
certainly that could be causing hyperthyroidism in children as well.
Subacute thyroiditis is seen, it's usually cause by viruses
and usually it's a more mild malingering sort of condition.
The toxic nodule is possible, we sometimes see this in patients
where there is one nodule that just secreting quiet a bit of thyroid hormone.
Multinodular goiter is possible in children,
we see that more commonly in people
with certain conditions such as McCune-Albright.
Certain drugs can cause hyperthyroidism, of course we think of things like
excessive iodine or excessive thyroid hormone medication.
Very rarely a patient can have a TSH producing adenoma,
which cause a secondary hyperthyroidism in a child.
After radiation therapy for thyrotoxicosis,
patients can be transiently hyperthyroid.
And very rarely, patients can have a selective pituitary thyroid resistance,
so when that feedback loop, the pituitary doesn't respond to specifically T3,
and does there's an excessive production of TSH,
which is then stimulating the thyroid hormone to make more thyroid.
So let's focus however on Grave's disease,
which is our most common cause of this condition.
Grave's disease is an autoimmune attack
of the TSH receptors on thyroid follicular cells.
It can be associated with other autoimmune diseases
such as myasthenia gravis, diabetes, or Addison's disease.
It's more common in girls than it is in boys,
and there is a familial disposition.
In other words, if it runs in the family the child is at risk for it too.
So the symptoms of hyperthyroidism as you expect,
include anxiety and restlessness.
They include an increased appetite.
These patients will have sweating, diarrhea, and perhaps some weight loss.
There maybe a rapid growth in height,
especially in that first year of life when thyroid hormone
is one of the premier factors in how children grow rather than growth hormone.
Patients typically will have tremor and tachycardia as a side effect.
And on exam you may feel a goiter.
Remember the best way to palpate a thyroid gland
is from behind with both fingers over the thyroid
and then ask the patient to swallow.
So, on exam we will see exopthalmos sometimes
but that's really is more common in adults.
However, if you see bilateral exopthalmos,
that's likely to be hyperthyroidism.
Remember, this condition can be permanent,
so we want to correct the condition before we encounter the exopthalmos.
Also remember unilateral exophthalmos is unlikely to be thyroid disease,
but it's more likely to be a mass or a tumor
such as seen in neurofibromatosis.
Symptoms and severe cases of hyperthyroidism include behavioral problems,
psychosis, and also patients can have a thyrotoxic crisis
which is essentially being so ramped up
that their vital signs are abnormally affected and they may develop shock.
So hyperthyroidism, to understand it and to diagnose,
we should understand the basics of the thyroid gland.
Remember, the pituitary makes thyroid stimulating hormone,
which then convinces the thyroid to start making free T4.
The T4 then goes up and inhibits the pituitary in a negative feedback loop
to prevent excessive thyroid production.
So when we suspect thyroid and hyperthyroidism,
we're going to check both a TSH and a free T4,
or more commonly, we'll just check a TSH first.
If that's low, then we'll reflexively check a T4,
and if that's high, we've sense the diagnosis.
The total T4 includes both the bioactive component of T4
called the free T4 and the T4 that's bound and is not bioactive.
You may see the phrase, free T4 by dialysis or free T4.
And that's the best way to measure what is free T4.
The dialysis were first how they do the test in the lab,
it has nothing to do whether the patient is on dialysis.
So, if you suspect hyperthyroidism, we're going to get that TSH
and we're gonna get a T4.
We can also get a free T3
and under certain circumstances that maybe beneficial.
Imaging, if we suspect hyperthyroidism
and we think it's the thyroid gland itself
we'll wanna image that thyroid gland.
We can use a radionuclide scan
to look for activity of the gland using radioactive iodine.
Increased uptake for, occurs in hyperthyroidism from Grave's.
Decreased uptake for destruction-mediated hyperthyroidism is seen
such as radiation or thyroiditis.
And a hot nodule will show up specifically toxic nodular disease,
so the scan can really be helpful in distinguishing the cause.
Typically, in patients with hyperthyroidism we're gonna manage
some of their symptoms with betablockers,
and this is a high yield fact for your exam.
The beta blockers will block a lot of the symptomalogic response
of being hyperthyroid.
So if a patient is profoundly hyperthyroid,
we start off with beta blockers while we then proceed to figure out
what's going on and how to manage this condition more thoroughly.
We can also use thionamides as a way to control their hyperthyroidism.
Specifically, methimazole is generally our first line agent.
Outisde of the United States, some people use carbimazole,
but that is not accepted in the United States by the FDA at this time.
We treat to normalize the T4 and the TSH,
so we're gonna continue get titers
and find the place where this child should be.
In about 30% of patients will go into remission using methimazole.
Iodine has a fast onset of action and is really used for the thyroid storm.
We're gonna use that to basically prepare for the patient to go to surgery,
we want that patient to be iodine-replete,
when they go to surgery to prevent the thyroid storm.
Radioactive iodine, this is another way to treat hyperthyroidism.
It goes directly to the thyroid, and it essentially irradiates the gland
and the area where there's excessive production.
This is useful for Grave's disease, and also for a toxic nodule.
However, the side effect ironically can be hyperthyroidism,
and a thyroiditis 2 to 3 weeks later.
They also can get hypothyroidism 2 to 4 months later,
and they may require a second dose.
And for all these reasons,
this is not our first line agent for management of this condition.
Some patients will have a surgical excision for their hyperthyroidism.
This is generally indicated with a toxic nodule,
and in other selected cases of Grave's disease
that were having a hard time controlling,
where conservative treatment it doesn't seem to be working.
The reason we like to limit our surgical excisions,
is that a large resection can result in a lifelong hypothyroidism
and need for taking synthetic thyroid hormone for the rest of their lives.
Again, before we have the surgery,
we're going to give iodine and make the patient euthyroid
so as to prevent a post-operative thyroid storm.