Instruct: Given a question, retrieve passages that answer the question.
Query: What hormones does the thyroid produce?
Thyroid hormones are two hormones produced and released by the thyroid gland, namely triiodothyronine (T3) and thyroxine (T4). They are tyrosine-based hormones that are primarily responsible for regulation of metabolism. T3 and T4 are partially composed of iodine. A deficiency of iodine leads to decreased production of T3 and T4, enlarges the thyroid tissue and will cause the disease known as simple goitre. The major form of thyroid hormone in the blood is thyroxine (T4), which has a longer half-life than T3.[1] In humans, the ratio of T4 to T3 released into the blood is approximately 14:1.[2] T4 is converted to the active T3 (three to four times more potent than T4) within cells by deiodinases (5'-iodinase). These are further processed by decarboxylation and deiodination to produce iodothyronamine (T1a) and thyronamine (T0a). All three isoforms of the deiodinases are selenium-containing enzymes, thus dietary selenium is essential for T3 production. Edward Calvin Kendall was responsible for the isolation of thyroxine in 1915.[3]
Normal thyroid hormone function requires normal thyroid hormone transport across cell membrane, appropriate deiodination, thyroid hormone nuclear receptor, thyroid hormone response elements, co-activators, co-repressors, and normal histone acetylation. Any abnormalities in this chain can result in thyroid hormone resistance and it has not been as well studied as the various forms of insulin resistance.
The most common and helpful way to diagnose thyroiditis is first for a physician to palpate the thyroid gland during a physical examination. Laboratory tests allow doctors to evaluate the patient for elevated erythrocyte sedimentation rates, elevated thyroglobulin levels, and depressed radioactive iodine uptake (Mather, 2007). Blood tests also help to determine the kind of thyroiditis and to see how much thyroid stimulating hormone the pituitary gland is producing and what antibodies are present in the body. In some cases a biopsy may be needed to find out what is attacking the thyroid.
Thyroid hormone resistance (sometimes Refetoff syndrome) describes a rare syndrome in which the thyroid hormone levels are elevated but the thyroid stimulating hormone (TSH) level is not suppressed, or not completely suppressed as would be expected. The first report of the condition appeared in 1967. Essentially this is decreased end organ responsiveness to thyroid hormones. A new term "impaired sensitivity to thyroid hormone" has been suggested in March 2014 by Refetoff et al.
The hypothalamus senses low circulating levels of thyroid hormone (Triiodothyronine (T3) and Thyroxine (T4)) and responds by releasing thyrotropin-releasing hormone (TRH). The TRH stimulates the anterior pituitary to produce thyroid-stimulating hormone (TSH). The TSH, in turn, stimulates the thyroid to produce thyroid hormone until levels in the blood return to normal. Thyroid hormone exerts negative feedback control over the hypothalamus as well as anterior pituitary, thus controlling the release of both TRH from hypothalamus and TSH from anterior pituitary gland.
In vertebrate biology, iodine's primary function is as a constituent of the thyroid hormones, thyroxine (T4) and triiodothyronine (T3). These molecules are made from addition-condensation products of the amino acid tyrosine, and are stored prior to release in an iodine-containing protein called thyroglobulin. T4 and T3 contain four and three atoms of iodine per molecule, respectively; iodine accounts for 65% of the molecular weight of T4 and 59% of T3. The thyroid gland actively absorbs iodine from the blood to produce and release these hormones into the blood, actions which are regulated by a second hormone, called thyroid-stimulating hormone (TSH), which is produced by the pituitary gland. Thyroid hormones are phylogenetically very old molecules which are synthesized by most multicellular organisms, and which even have some effect on unicellular organisms.
The thyroid gland is an auxiliary organ to the hypothalamus-pituitary system. Thyrotropin-releasing hormone (TRH) produced by the hypothalamus signals to the pituitary to release thyroid-stimulating hormone (TSH), which then stimulates the thyroid to secrete T and T thyroid hormones. Secondary hypothyroidism occurs when TSH secretion from the pituitary is impaired, whereas tertiary hypothyroidism is the deficiency or inhibition of TRH. 
If there is a deficiency of dietary iodine, the thyroid will not be able to make thyroid hormone. The lack of thyroid hormone will lead to decreased negative feedback on the pituitary, leading to increased production of thyroid-stimulating hormone, which causes the thyroid to enlarge (the resulting medical condition is called endemic colloid goitre; see goitre).[36] This has the effect of increasing the thyroid's ability to trap more iodide, compensating for the iodine deficiency and allowing it to produce adequate amounts of thyroid hormone.
Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, TSH, or hTSH for human TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T), and then triiodothyronine (T) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone produced by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid. In 1916, Bennett M. Allen and Philip E. Smith found that the pituitary contained a thyrotropic substance.
Findings have suggested that thyroid hormone (T4) is taken up by the hypothalamic glial cells in the infundibular nucleus/ median eminence, and that it is here converted into T3 by the type 2 deiodinase (D2). Subsequent to this, T3 is transported into the thyrotropin-releasing hormone (TRH)-producing neurons in the paraventricular nucleus. Thyroid hormone receptors have been found in these neurons, indicating that they are indeed sensitive to T3 stimuli. In addition, these neurons expressed MCT8, a thyroid hormone transporter, supporting the theory that T3 is transported into them. T3 could then bind to the thyroid hormone receptor in these neurons and affect the production of thyrotropin-releasing hormone, thereby regulating thyroid hormone production.
Higher levels of thyroid hormone suppress GnIH expression, and lower levels of thyroid hormone are associated with higher GnIH levels. The inactivation of GnIH expression prevents delayed puberty caused by hypothyroidism, demonstrating that GnIH mediates interactions between the HPG and HPT (hypothalamic-pituitary-thyroid) axes. Furthermore, thyroid hormone may function in a pathway for photoperiodic regulation of reproduction involving GnIH and energy status. Melatonin modulates thyroid-stimulating hormone (TSH) production in the anterior pituitary, and TSH promotes thyroid hormone production. Thyroid hormone production influences metabolism and GnIH production, both of which impact reproduction.
There are many changes to the body during pregnancy. One of the major changes to help with the development of the fetus is the production of human chorionic gonadotropin (hCG). This hormone, produced by the placenta, has similar structure to TSH and can bind to the maternal TSH receptor to produce thyroid hormone. During pregnancy, there is also an increase in estrogen which causes the mother to produce more thyroxine binding globulin, which is what carries most of the thyroid hormone in the blood. These normal hormonal changes often make pregnancy look like a hyperthyroid state but may be within the normal range for pregnancy, so it necessary to use trimester specific ranges for TSH and free T4. True hyperthyroidism in pregnancy is most often caused by an autoimmune mechanism from Grave's Disease. New diagnosis of hypothyroidism in pregnancy is rare because hypothyroidism often makes it difficult to become pregnant in the first place. When hypothyroidism is seen in pregnancy, it is often because an individual already has hypothyroidism and needs to increase their levothyroxine dose to account for the increased thyroxine binding globulin present in pregnancy.
Individuals with thyroid storm tend to have increased levels of free thyroid hormone, although total thyroid hormone levels may not be much higher than in uncomplicated hyperthyroidism. The rise in the availability of free thyroid hormone may be the result of manipulating the thyroid gland. In the setting of an individual receiving radioactive iodine therapy, free thyroid hormone levels may acutely increase due to the release of hormone from ablated thyroid tissue.
The thyroid gland and every cell that uses thyroid hormone use selenium, which is a cofactor for the three of the four known types of thyroid hormone deiodinases, which activate and then deactivate various thyroid hormones and their metabolites; the iodothyronine deiodinases are the subfamily of deiodinase enzymes that use selenium as the otherwise rare amino acid selenocysteine. (Only the deiodinase, iodotyrosine deiodinase, which works on the last breakdown products of thyroid hormone, does not use selenium.)
There are several hormones that can be measured in the blood to determine how the thyroid gland is functioning. These include the thyroid hormones triiodothyronine (T3) and its precursor thyroxine (T4), which are produced by the thyroid gland. Thyroid-stimulating hormone (TSH) is another important hormone that is secreted by the anterior pituitary cells in the brain. Its primary function is to increase the production of T3 and T4 by the thyroid gland.
The protein encoded by this gene is a nuclear hormone receptor for triiodothyronine. It is one of the several receptors for thyroid hormone, and has been shown to mediate the biological activities of thyroid hormone. Knockout studies in mice suggest that the different receptors, while having certain extent of redundancy, may mediate different functions of thyroid hormone. Defects in this gene are known to be a cause of generalized thyroid hormone resistance (GTHR), a syndrome characterized by goiter and high levels of circulating thyroid hormone (T-T), with normal or slightly elevated thyroid stimulating hormone (TSH). Several transcript variants have been observed for this gene, but the full-length nature of only one has been observed so far.
Thyroid's secretory capacity (GT, also referred to as thyroid's incretory capacity, maximum thyroid hormone output, T4 output or, if calculated from levels of thyroid hormones, as SPINA-GT) is the maximum stimulated amount of thyroxine that the thyroid can produce in a given time-unit (e.g. one second).
Yet, since discovery of resistance to thyroid hormones in the absence of thyroid hormone receptor beta mutations, lack of a mutation in a patient does not rule out resistance. 
The thyroid is a small gland in the front of the neck. The thyroid makes hormones called T3 and T4 that regulate how the body uses energy. Thyroid hormone levels are controlled by the pituitary gland, which is a pea-sized gland in the brain. It makes thyroid stimulating hormone (TSH), which triggers the thyroid to make thyroid hormone.
Thyroid hormones play an instrumental role during the early development of the fetus's brain. Therefore, mothers suffering from thyroid-related issues and altered thyroid hormone levels may inadvertently trigger structural and functional changes in the fetal brain. The fetus is able to produce its own thyroid hormones from the onset of the second trimester; however, maternal thyroid hormones are important for brain development before and after the baby is able to synthesize the hormones while still in the uterus. Due to this, the baby may experience an increased risk of neurological or psychiatric diseases later in life.
Goiter is the general enlargement of the thyroid that can be associated with many thyroid diseases. The main reason this happens is because of increased signaling to the thyroid by way of TSH receptors to try to make it produce more thyroid hormone. This causes increased vascularity and increase in size (hypertrophy) of the gland. In hypothyroid states or iodine deficiency, the body recognizes that it is not producing enough thyroid hormone and starts to produce more TSH to help stimulate the thyroid to produce more thyroid hormone. This stimulation causes the gland to increase in size to increase production of thyroid hormone. In hyperthyroidism caused by Grave's Disease or toxic multinodular goiter, there is excess stimulation of the TSH receptor even when thyroid hormone levels are normal. In Grave's Disease this is because of a autoantibodies (Thyroid Stimulating Immunoglobulins) which bind to and activate the TSH receptors in place of TSH while in toxic multinodular goiter this is often because of a mutation in the TSH receptor that causes it to activate without receiving a signal from TSH. In more rare cases, the thyroid may become enlarged because it becomes filled with thyroid hormone or thyroid hormone precursors that it is unable to release or because of congential abnormalities or because of increased intake of iodine from supplementation or medication.
There are three main treatments for Hürthle cell adenomas. Once the adenoma is detected most often the nodules removed to prevent the cells from later metastisizing. A total thyroidectomy is often performed, this results in a complete removal of the thyroid. Some patients may only have half of their thyroid removed, this is known as a thyroid lobectomy. Another treatment option includes pharmacological suppression of thyroid hormone. The thyroid gland is responsible for producing the thyroid hormones triiodothyronine (T3) and thyroxine (T4). Patients with suppressed thyroid function often require oral thyroid replacement (e.g. levothyroxine) in order to maintain normal thyroid hormone levels. The final treatment option is RAI ablation (radioactive iodine ablation). This treatment option is used to destroy infected thyroid cells after total thyroidectomy. This treatment does not change prognosis of disease, but will diminish the recurrence rate. Also, Hürthle cells do not respond well to RAI. However, often doctors suggest this treatment to patients with Hürthle cell adenoma and Hürthle cell carcinoma because some Hürthle cells will respond and it will kill remaining tissue.
Thiamazole is a drug used to treat hyperthyroidism such as in Graves' disease, a condition that occurs when the thyroid gland begins to produce an excess of thyroid hormone. The drug may also be taken before thyroid surgery to lower thyroid hormone levels and minimize the effects of thyroid manipulation. Additionally, thiamazole is used in the veterinary setting to treat hyperthyroidism in cats.
Thyroid disease is a medical condition that affects the function of the thyroid gland. The thyroid gland is located at the front of the neck and produces thyroid hormones that travel through the blood to help regulate many other organs, meaning that it is an endocrine organ. These hormones normally act in the body to regulate energy use, infant development, and childhood development.
Hormonal output from the thyroid is regulated by thyroid-stimulating hormone (TSH) secreted from the anterior pituitary gland, which itself is regulated by thyrotropin-releasing hormone (TRH) produced by the hypothalamus.