Hyperthyroidism

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Introduction0:00–0:24

In hyperthyroidism, ‘hyper’ refers to having too much, and ‘thyroid’ refers to thyroid hormone, so hyperthyroidism refers to a condition where there’s excess thyroid hormones.
The condition is also called thyrotoxicosis, and is generally due to overproduction from the thyroid gland. Normally, the hypothalamus, which is located at the base of the brain, detects low blood levels of thyroid hormones and releases thyrotropin-releasing hormone into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary.

Physiology0:24–2:21

The anterior pituitary then releases thyroid-stimulating hormone, also called thyrotropin or simply TSH. TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”.
The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells. Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4.
Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins. Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body.
Once inside the cell T­4 is mostly converted into T3, where it can exert its effect. T3 speeds up the cell’s basal metabolic rate.
So as an example, the cell might produce more proteins and burn up more energy in the form of sugars and fats. It’s as if the cells are in a bit of frenzy.
T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response.
Thyroid hormone is important - and the occasional increase can be really useful when you need a boost to get through the final rounds of a sporting competition or when you’re trying to stay warm during a snowstorm!

Pathology2:21–4:12

Now, hyperthyroidism can happen a few different ways - all of them result in too much thyroid hormone and a hypermetabolic state, where cellular reactions are happening faster than normal.
The most common primary cause is Graves disease, an autoimmune disorder where B cells produce antibodies against several thyroid proteins.
These autoantibodies include thyroid-stimulating immunoglobulins, which bind to the TSH receptor on follicular cells and imitate TSH.
This results in growth of the thyroid gland and stimulates the follicular cells to produce excess thyroid hormone. Another primary cause is toxic nodular goiter, where one or more follicules start generating lots of thyroid hormone - in some cases it’s because of a mutated TSH receptor that inappropriately keeps these follicular cells active.
A different cause is a hyperfunctioning thyroid adenoma, where the follicular cells start growing uncontrollably forming a benign tumor and making excess thyroid hormones.
Also, anytime the thyroid gets inflamed or damaged, there can be a large release of pre-formed thyroid hormones. There’s also Jod-Basedow syndrome, or iodine-induced thyrotoxicosis, which can develop soon after an iodine-deficient person gets a hefty dose of iodine.
And finally neonatal hyperthyroidism, which is when newborns who have mothers with Graves disease start generating too much thyroid hormone in response to thyroid-stimulating immunoglobulin that crosses the placenta and enters the baby.
A secondary cause of hyperthyroidism is when there’s a healthy thyroid that generates a lot of thyroid hormone in response to a TSH-secreting tumor in the anterior pituitary.

Symptoms4:12–5:15

The symptoms of hyperthyroidism include weight loss despite an increase in appetite because of the higher basal metabolic rate; heat intolerance because the body is producing more heat; and rapid heart rate, sweating, hyperactivity, anxiety and insomnia because of the effect of thyroid hormones on the sympathetic nervous system.
Sympathetic overstimulation of muscles that control eye movements also makes the eyes appear more open than normal, so you see more of the “white” of the eyes.
If the hyperthyroidism has been on-going for a long time, there is a risk of developing congestive heart failure and osteoporosis.
A thyroid storm is a life-threatening complication of hyperthyroidism where the body goes into a state of severe hypermetabolism.
It can develop when someone with hyperthyroidism stops their treatment, develops an infection, or has surgery. All of the normal symptoms of hyperthyroidism become exaggerated - for example heat intolerance turns to high fever and rapid heart rate turns into cardiac arrhythmia.

Diagnosis5:15–5:47

Diagnosing hyperthyroidism is done by measuring blood levels of TSH, T3, and T4. If it’s due to a primary cause, TSH will be low and unbound thyroid hormones will be high.
Once hyperthyroidism is confirmed, a radioactive iodine uptake test and a thyroid scan help determine the specific cause of the disorder.
If blood levels of TSH are normal or high, this points to a pituitary tumor, which can be confirmed with an injection of thyrotropin-releasing hormone.

Treatment5:47–6:11

Treatment varies based on the exact cause of hyperthyroidism, but generally involves drugs like beta-blockers, to treat the immediate symptoms, and anti-thyroid drugs, to block thyroid hormone production and release.
Radioiodine therapy can be used to partially or completely destroy thyroid function, followed by replacement hormone therapy.
In a few cases, the thyroid is removed with surgery. Alright, as a quick recap, hyperthyroidism refers to any one of a number of disorders where there is an excess of thyroid hormones.

Review6:11–6:35

It is mostly caused by over-functioning of the thyroid gland, but is sometimes caused instead by a pituitary tumor or inflammation of the thyroid.
The result is a hypermetabolic state, which causes symptoms like weight loss, heat intolerance, rapid heart rate, and hyperactivity.