Hyperthyroidism is characterized by excessive secretion of thyroid hormones: the most common cause is the autoimmune disorder Graves' disease.

The thyroid gland is a butterfly-shaped organ composed of two lobes, left and right, connected by a narrow tissue band, called an "isthmus".

The follicular lumen is filled with colloid, a concentrated solution of thyroglobulin and is the site of synthesis of the thyroid hormones thyroxine (T4) and triiodothyronine (T3).

[17] In the development of the embryo, at 3–4 weeks gestational age, the thyroid gland appears as an epithelial proliferation in the floor of the pharynx at the base of the tongue between the tuberculum impar and the copula linguae.

[20] The fetus needs to be self-sufficient in thyroid hormones in order to guard against neurodevelopmental disorders that would arise from maternal hypothyroidism.

[23] Aberrations in prenatal development can result in various forms of thyroid dysgenesis which can cause congenital hypothyroidism, and if untreated this can lead to cretinism.

[31][32] In addition to these actions on DNA, the thyroid hormones also act within the cell membrane or within cytoplasm via reactions with enzymes, including calcium ATPase, adenylyl cyclase, and glucose transporters.

[38] The production of thyroxine and triiodothyronine is primarily regulated by thyroid-stimulating hormone (TSH), released by the anterior pituitary gland.

However, calcitonin seems far less essential than PTH, since calcium metabolism remains clinically normal after removal of the thyroid (thyroidectomy), but not the parathyroid glands.

General practitioners, and internal medicine specialists play a role in identifying and monitoring the treatment of thyroid disease.

[46][47] Hyperthyroidism often causes a variety of non-specific symptoms including weight loss, increased appetite, insomnia, decreased tolerance of heat, tremor, palpitations, anxiety and nervousness.

[51] Surgery does however carry a risk of damage to the parathyroid glands and the recurrent laryngeal nerve, which innervates the vocal cords.

Typical symptoms are abnormal weight gain, tiredness, constipation, heavy menstrual bleeding, hair loss, cold intolerance, and a slow heart rate.

These antibodies activate the receptor, leading to development of a goitre and symptoms of hyperthyroidism, such as heat intolerance, weight loss, diarrhoea and palpitations.

[58] Graves' disease can be diagnosed by the presence of pathomnomonic features such as involvement of the eyes and shins, or isolation of autoantibodies, or by results of a radiolabelled uptake scan.

Graves' disease is treated with anti-thyroid drugs such as propylthiouracil, which decrease the production of thyroid hormones, but hold a high rate of relapse.

Surgical removal of the gland with subsequent thyroid hormone replacement may be considered, however this will not control symptoms associated with the eye or skin.

[67][68] Because of the prominence of the thyroid gland, cancer is often detected earlier in the course of disease as the cause of a nodule, which may undergo fine-needle aspiration.

[74] Mucinous, clear secretions may collect within these cysts to form either spherical masses or fusiform swellings, rarely larger than 2 to 3 cm in diameter.

Segments of the duct and cysts that occur high in the neck are lined by stratified squamous epithelium, which is essentially identical to that covering the posterior portion of the tongue in the region of the foramen cecum.

[84] They are however not always accurate, particularly if the cause of hypothyroidism is thought to be related to insufficient thyrotropin releasing hormone (TRH) secretion, in which case it may be low or falsely normal.

[90] The thyroid gland received its modern name in the 1600s, when the anatomist Thomas Wharton likened its shape to that of an Ancient Greek shield or thyos.

[91] In 1600 BCE burnt sponge and seaweed (which contain iodine) were used within China for the treatment of goitres, a practice which has developed in many parts of the world.

[96] French chemist Bernard Courtois discovered iodine in 1811,[92] and in 1896 Eugen Baumann documented it as the central ingredient in the thyroid gland.

[104] In larval lampreys, the thyroid originates as an exocrine gland, secreting its hormones into the gut, and associated with the larva's filter-feeding apparatus.

In the adult lamprey, the gland separates from the gut, and becomes endocrine, but this path of development may reflect the evolutionary origin of the thyroid.

For instance, the closest living relatives of vertebrates, the tunicates and amphioxi (lancelets), have a structure very similar to that of larval lampreys (the endostyle), and this also secretes iodine-containing compounds, though not thyroxine.

Iodine and T4 trigger the change from a plant-eating water-dwelling tadpole into a meat-eating land-dwelling frog, with better neurological, visuospatial, smell and cognitive abilities for hunting, as seen in other predatory animals.

A similar phenomenon happens in the neotenic amphibian salamanders, which, without introducing iodine, do not transform into land-dwelling adults, and live and reproduce in the larval form of aquatic axolotl.

In amphibian metamorphosis, thyroxine and iodine also exert a well-studied experimental model of apoptosis on the cells of gills, tail, and fins of tadpoles.