Hyperthyroidism is an increase in the total thyroid hormone production by the thyroid gland. The hormones are thyroxine (T4) and triiodothyronine (T3, the more active form). Hyperthyroidism leads to the manifestations of thyrotoxicosis, the state produced by a high level of thyroid hormone at the tissues.
The two words usually overlap, but not always. Hyperthyroidism describes the over-activity of the gland, so it is the narrower, more mechanical term. Thyrotoxicosis describes what the tissues receive, whatever the source. That is why the source of the extra hormone is what sorts the cases.
How did the excess reach the tissues?
This is the question the whole topic hangs on. The state at the tissues is the same whatever the cause, so the causes are sorted by the route the extra hormone takes. Hyperthyroidism itself has primary causes in the gland and central causes upstream of it. The gland normally answers TSH from the pituitary. So some causes work through the gland, and others bypass it.
Causes of thyrotoxicosis fall into a few groups.
Does the gland make more hormone?
The first route is the gland making more, and it holds the most common causes. Graves disease and toxic nodular disease (toxic multinodular goiter and toxic adenoma) raise hormone production. In both, the gland or part of it makes hormone without normal TSH feedback. Graves disease is the most common cause of thyrotoxicosis. Toxic multinodular goiter is the second most common.
Can iodine push the gland?
Iodine can push the gland itself. An iodine load can push autonomous tissue into overproduction, the Jod-Basedow phenomenon. Amiodarone disturbs thyroid function through its iodine load, and it has two opposite thyroid effects.
Can stored hormone escape?
A second route works by release rather than extra production: the gland lets out hormone it already holds. Thyrotoxicosis can arise when an inflamed gland releases hormone that was already stored. De Quervain and painless thyroiditis cause thyrotoxicosis this way, by releasing hormone already stored in a damaged gland. De Quervain thyroiditis is painful and seasonal, with two phases.
Can hormone come from outside?
The third route bypasses the gland. Thyrotoxicosis can arise when thyroid hormone is taken from outside the body, though the gland’s own production is not raised. Factitious thyrotoxicosis comes from levothyroxine taken this way, and it is covered alongside the amiodarone effects.
Where to start
One case sits apart from these routes: subclinical hyperthyroidism, where TSH is suppressed but the hormone levels are normal. The notes below follow the routes in learning order.
- Determinants of thyrotoxicosis severity and iodine-induced hyperthyroidism: what sets how severe thyrotoxicosis is, and how an iodine load can switch on overproduction. Start here.
- Graves disease epidemiology, pathogenesis and ophthalmopathy: the pathogenesis of the most common cause, and the eye changes.
- Clinical manifestations of Graves disease: the general and eye, skin and nail signs of the disease.
- Clinical course of Graves disease: relapse, remission and the later hypothyroidism, with the eye and skin on their own timelines.
- Diagnosis and management of Graves disease: how the blood pattern points to it, and the planning in pregnancy.
- Treatment of thyrotoxicosis: how thyrotoxicosis is managed, from symptom control to definitive treatment.
- Subclinical hyperthyroidism: normal hormone levels, suppressed TSH, and when that matters.
- De Quervain thyroiditis (subacute thyroiditis): a painful thyroid inflammation that runs in two phases.
- Amiodarone-induced thyroid dysfunction and factitious thyrotoxicosis: the iodine effects of amiodarone and thyrotoxicosis from levothyroxine taken from outside.
In the case you have in mind, which route did the extra hormone take?