Hyperthyroidism is the condition in which the total production of thyroid hormone (thyroxine, T4, and triiodothyronine, T3, the more active form) by the thyroid gland is increased, through primary causes in the gland itself or central causes upstream of it, and this leads to the manifestations of thyrotoxicosis.
Thyrotoxicosis is not the same thing. Thyrotoxicosis is the state produced by a high level of thyroid hormone at the tissues, while hyperthyroidism is over-activity of the gland. The two usually overlap, but not always: thyrotoxicosis can also arise when an inflamed gland releases hormone that was already stored, or when thyroid hormone is taken from outside the body, even though the gland’s own production is not raised. Hyperthyroidism is the narrower, more mechanical term.
The causes of thyrotoxicosis fall into a few groups. Graves disease and toxic nodular disease — toxic multinodular goiter and toxic adenoma — raise production because the gland, or part of it, makes hormone without normal feedback from TSH, the pituitary thyroid-stimulating hormone that normally regulates the gland; Graves disease is the most common cause, toxic multinodular goiter the second. An iodine load can push that autonomous tissue into overproduction, which is the Jod-Basedow phenomenon. De Quervain and painless thyroiditis cause thyrotoxicosis by releasing hormone that was already stored in a damaged gland. Factitious thyrotoxicosis comes from levothyroxine taken from outside, and amiodarone disturbs thyroid function through its iodine load.
A sensible route starts with what determines severity and how iodine acts, follows Graves disease from mechanism to management, and then turns to treatment and the remaining causes:
- Determinants of thyrotoxicosis severity and iodine-induced hyperthyroidism — what makes thyrotoxicosis severe in one patient and mild in another, and how an iodine load can set it off.
- Graves disease epidemiology, pathogenesis and ophthalmopathy — how common the disease is, what drives it, and why the orbit is also affected.
- Clinical manifestations of Graves disease — the findings on examination, the general thyrotoxic features, and the eye, skin and nail changes.
- Clinical course of Graves disease — relapse and remission, the late shift to hypothyroidism, and the timelines of the eye and skin changes.
- Diagnosis and management of Graves disease — when to suspect it, the laboratory pattern and the use of scintigraphy, and the recommendations for ophthalmopathy and pregnancy.
- Treatment of thyrotoxicosis — the ways to control and definitively treat an overactive thyroid.
- Subclinical hyperthyroidism — a suppressed TSH with normal hormone levels, and when it needs treatment.
- De Quervain thyroiditis — the painful, seasonal thyroiditis and its two phases.
- Amiodarone-induced thyroid dysfunction and factitious thyrotoxicosis — the two opposite thyroid effects of amiodarone and thyrotoxicosis from levothyroxine misuse.