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__NOTOC__ | __NOTOC__ | ||
{{Hyperthyroidism landing}} | {{Hyperthyroidism landing}} | ||
{{CMG}};{{AE}}{{AY}} | {{CMG}};{{AE}}{{AY}} | ||
==Overview== | ==Overview== | ||
''Hyperthyroidism'' is the clinical [[syndrome]] caused by an excess of circulating free [[thyroxine]] (T4) or free [[triiodothyronine]] (T3), or both. Hyperthyroidism may be caused by either central disorders in the hypothalamus or the pituitary producing an excess of TSH or TRH, primary causes in the thyroid gland as grave's disease or toxic adenoma, or remote production from extra thyroid tissue such as struma ovarii. Manifestations of hyperthyroidism mimic those of catecholamine excess such as palpitations, excessive sweating, insomnia, and anxiety. | |||
Hyperthyroidism is | |||
==Causes== | ==Causes== | ||
| Line 93: | Line 13: | ||
*[[Toxic thyroid adenoma]] | *[[Toxic thyroid adenoma]] | ||
*[[Toxic multinodular goitre]] | *[[Toxic multinodular goitre]] | ||
Excess thyroid hormone from pills can also cause hyperthyroidism. [[Amiodarone]], a heart medication, can sometimes cause hyperthyroidism. Hamburger toxicosis is a condition that occurs sporadically and is associated with ground beef contaminated with thyroid hormone. | Excess thyroid hormone from pills can also cause hyperthyroidism. [[Amiodarone]], a heart medication, can sometimes cause hyperthyroidism. Hamburger toxicosis is a condition that occurs sporadically and is associated with ground beef contaminated with thyroid hormone. | ||
| Line 238: | Line 156: | ||
===Causes in Alphabetical Order=== | ===Causes in Alphabetical Order=== | ||
{{columns-list | {{columns-list| | ||
*[[Adenocarcinoma]] | *[[Adenocarcinoma]] | ||
*[[Amiodarone ]] | *[[Amiodarone ]] | ||
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==Calssification== | ==Calssification== | ||
Hyperthyroidism can be classified according to the results of iodine uptake test into: | Hyperthyroidism can be classified according to the results of iodine uptake test into: | ||
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===High or normal uptake:=== | ===High or normal uptake:=== | ||
{| style="float: right; width: 350px" | |||
{| style="float: right; width: 350px | | [[Image:Thyroid scan.jpg|right|300px|Normal thyroid scan - Myohan at en.wikipedia [CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons]] | ||
| [[Image:Thyroid scan.jpg|right| | |||
|} | |} | ||
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*Subacute thyroiditis | *Subacute thyroiditis | ||
*Hyperthyroidism due to ectopic thyroid tissue | *Hyperthyroidism due to ectopic thyroid tissue | ||
<br> | |||
<br> | |||
<br> | |||
==Pathophysiology== | ==Pathophysiology== | ||
Thyroid hormones (T3 and T4) are regulating basal metabolic rate, influence oxygen consumption by tissues. They are crucial for normal development of the brain and growth of the body especially in prepubertal period | * Thyroid hormones (T3 and T4) are regulating basal metabolic rate, influence oxygen consumption by tissues. They are crucial for normal development of the brain and growth of the body, especially in prepubertal period. | ||
==== Hypothalamic-pituitary-thyroid axis ==== | |||
* Secretion of thyroid hormones follows upper control from the hypothalamus and the pituitary. Thyroid releasing hormone (TRH). TRH acts on thyrotropes releasing cells in the pituitary causing them to release thyroid stimulating hormone (TSH). | |||
{| style="float: right; width: 350px;" | {| style="float: right; width: 350px;" | ||
| [[Image:Thyroid system.png|right|400px|Hypothalamic–pituitary–thyroid axis - By Mikael Häggström - All used images are in public domain., Public Domain, https://commons.wikimedia.org/w/index.php?curid=8567011]] | | [[Image:Thyroid system.png|right|400px|Hypothalamic–pituitary–thyroid axis - By Mikael Häggström - All used images are in public domain., Public Domain, https://commons.wikimedia.org/w/index.php?curid=8567011]] | ||
|} | |} | ||
* TSH acts on thyroid gland by binding to specific membrane receptors and activating an intracellular pathway involving cAMP that ends in the formation and secretion of thyroid hormones. | |||
* The higher regulation of thyroxin secretion follows the negative feedback role, meaning that high levels of T3 and T4 will suppress TRH and TSH secretion and vice versa (Low levels of thyroxins will stimulate TRH and TSH secretion). This is useful in diagnosing the cause of hyperthyroidism (in secondary hyperthyroidism where the pituitary or the hypothalamus are the sources of the disease. TSH will be high, while in primary hyperthyroidism where the gland is the source of the excess hormones, TSH will be low). | |||
==== Thyroxin synthesis and secretion ==== | |||
* Iodine is essential for the synthesis of thyroid hormones. The daily iodide need is about 100mcg / day. Iodide is uptaken through a special Na/I transporter found in the membrane of thyroid follicular cell. After uptaking iodide, it goes through a series of organic reactions ending in the formation of the two forms of thyroid hormones: T3 and T4. T3 and T4 remain stored in the thyroglobulin of the follicles and are released in response to further stimulation by TSH to the thyroid follicles. | |||
Iodine is essential for synthesis of thyroid hormones. The daily iodide need is about 100mcg / day. | [[Image:Thyroid hormone synthesis.png|400px|Thyroid hormone synthesis - By Mikael Häggström.When using this image in external works, it may be cited as:Häggström, Mikael (2014). "Medical gallery of Mikael Häggström 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.008. ISSN 2002-4436. Public Domain.orBy Mikael Häggström, used with permission. - Mainly Own workSource image for nucleus derivative:(Public Domain license), CC0, https://commons.wikimedia.org/w/index.php?curid=15534147]] | ||
Iodide is uptaken through a special Na/I transporter found in the membrane of thyroid follicular cell. After uptaking iodide, it goes through a series of organic reactions ending in the formation of the two forms of thyroid hormones :T3 and T4. | * While T3 is 3 to 5 times more potent than T4, it represents only one-fourth of the total hormone secretion. T3 is thought to be the biologically active form of the of the two forms of the hormone. Most of the circulating T3 is due to peripheral conversion of T4 in the liver and peripheral tissues while only a small percentage is secreted directly from the thyroid gland itself. | ||
T3 and T4 remain stored in the thyroglobulin of the follicles and are released in response to further stimulation by TSH to the thyroid follicles. | * The majority of circulating T3 and T4 are bound to plasma proteins and thus not active (T4 is mostly bound to thyroxine binding globulin and T3 is mostly bound to transthyretin). Conditions that impair the production of thyroid binding globulins (such as pregnancy, liver failure, and certain drug administration) cause a change in the total serum thyroxins but the free T3 and T4 remain normal and the patient remains euthyroid (this carries only laboratory significance). | ||
* T3 and T4 act on nuclear receptors (DNA binding proteins) and cause the regulate the transcription of many proteins to regulate the metabolic rate of the body. | |||
[[Image:Thyroid hormone synthesis.png| | * In grave’s disease, the most common cause of hyperthyroidism. The disorder lies in the secretion of thyroid stimulating antibodies (TSI) that work on thyroid follicular cells causing an excessive uncontrolled release of the thyroxins. TSI responsible for many other aspects of the disease such as ophthalmopathy and the skin manifestations. This is thought to be due to the epitopic similarity between antigens on the surface of these cells and the thyroid receptors. | ||
While T3 is 3 to 5 times more potent than T4, it represents only one fourth of the total hormone secretion. | |||
T3 is thought to be the biologically active form of the of the two forms of the hormone. Most of the circulating T3 is due to peripheral conversion of T4 in the liver and peripheral tissues while only a small percentage is secreted directly from the thyroid gland itself. | |||
T3 and T4 act on nuclear receptors (DNA binding proteins) and cause the regulate the transcription of many proteins to regulate the metabolic rate of the body. | |||
==Historical perspective== | |||
*In 1786, the association between goiter and [[exophthalmos]] was first described by Caleb Hillier Parry. However, his observation was first published in 1825. | |||
*In 1835, Robert James Graves gave his name to the [[autoimmune disease]] causing [[exophthalmos]] and [[goiter]].<ref name="urlHyperthyroidism - Wikipedia">{{cite web |url=https://en.wikipedia.org/wiki/Hyperthyroidism#History |title=Hyperthyroidism - Wikipedia |format= |work= |accessdate=}}</ref> | |||
*In 1840, the same classic description was described by von Basedow. | |||
*In 1884, [[Thyroidectomy|thyroidectomies]] were tried successfully for treatment of [[goiter]]. | |||
*In 2000 [[Thyroidectomy|thyroidectomies]] performed by Kocher in the 19th century, the mortality rate was reported as 5%. | |||
*In 1912, [[Hashimoto's thyroiditis|Hashimoto]] disease was described as a cause of hyperthyroidism.<ref name="urlHakaru Hashimoto - Wikipedia">{{cite web |url=https://en.wikipedia.org/wiki/Hakaru_Hashimoto |title=Hakaru Hashimoto - Wikipedia |format= |work= |accessdate=}}</ref> | |||
*In 1956, thyroid stimulating antibodies were discovered in association with [[graves' disease]].<ref name="urlLondon Medical and Surgical Journal : Free Download & Streaming : Internet Archive">{{cite web |url=https://archive.org/details/p2londonmedicals07londuoft |title=London Medical and Surgical Journal : Free Download & Streaming : Internet Archive |format= |work= |accessdate=}}</ref> | |||
*In 1957, [[Antibodies|thyroid antibodies]] were discovered in association with [[Hashimoto's thyroiditis|Hashimoto thyroiditis]]. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
Latest revision as of 22:45, 10 January 2020
Template:Hyperthyroidism landing
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Ahmed Younes M.B.B.CH [2]
Overview
Hyperthyroidism is the clinical syndrome caused by an excess of circulating free thyroxine (T4) or free triiodothyronine (T3), or both. Hyperthyroidism may be caused by either central disorders in the hypothalamus or the pituitary producing an excess of TSH or TRH, primary causes in the thyroid gland as grave's disease or toxic adenoma, or remote production from extra thyroid tissue such as struma ovarii. Manifestations of hyperthyroidism mimic those of catecholamine excess such as palpitations, excessive sweating, insomnia, and anxiety.
Causes
Major causes in humans are:
Excess thyroid hormone from pills can also cause hyperthyroidism. Amiodarone, a heart medication, can sometimes cause hyperthyroidism. Hamburger toxicosis is a condition that occurs sporadically and is associated with ground beef contaminated with thyroid hormone.
Postpartum thyroiditis occurs in about 7% of women during the year after they give birth. PPT typically has several phases, the first of which is hyperthyroidism. Many times, the hyperthyroidism corrects itself within weeks or months without any treatment necessary.
Life Threatening Causes
- Adenocarcinoma
- Choriocarcinoma
- Metastatic follicular thyroid cancer
- Pituitary tumor
- Struma ovarii
- Teratoma
- Testicular cancer
- Thyroid adenoma
- Thyroid carcinoma
- Thyroid nodule
- Thyroid tumor
- Thyrotropinoma
- Toxic adenoma
- Toxic thyroid adenoma
- Trophoblastic disease
- Tsh-producing pituitary adenoma
Common Causes
Causes by Organ System
Causes in Alphabetical Order
- Adenocarcinoma
- Amiodarone
- Anterior pituitary hyperhormonotrophic syndrome
- Atezolizumab
- Autoimmune enteropathy
- Autoimmune thyroid disease
- Autonomous thyroid tissue
- Choriocarcinoma
- De quervain thyroiditis
- Diabetes mellitus
- Diarrhea
- Enteropathy
- Excessive replacement therapy
- Exogenous thyroid hormone intake
- Factitious thyroiditis
- Glutaricaciduria type 3
- Graves' disease
- Hashimoto's thyroiditis
- Hashitoxicosis
- Hydatidiform mole
- Hyperemesis gravidarum
- Immune dysregulation
- Intentional suppressive therapy
- Iodine overuse
- Ipex syndrome
- Jod-basedow thyrotoxicosis
- Levothyroxine and indinavir interaction
- Mccune-albright syndrome
- Metastatic follicular thyroid cancer
- Nivolumab
- Pituitary tumor
- Poems syndrome
- Polyendocrinopathy
- Polyostotic fibrous dysplasia
- Postpartum thyroiditis
- Potassium iodide
- Pramipexole
- Sorafenib
- Struma ovarii
- Suppurative thyroiditis
- Teratoma
- Testicular cancer
- Thyroid adenoma
- Thyroid carcinoma
- Thyroid nodule
- Thyroid stimulating globulin
- Thyroid tumor
- Thyroiditis
- Thyrotoxicosis factitia
- Thyrotropinoma
- Thyroxine
- Toxic adenoma
- Toxic multinodular goiter
- Toxic thyroid adenoma
- Troell-junet syndrome
- Trophoblastic disease
- Tsh hypersecretion
- Tsh-mediated hyperthyroidism
- Tsh-producing pituitary adenoma
Calssification
Hyperthyroidism can be classified according to the results of iodine uptake test into:
High iodine uptake
- Grave’s disease
- Toxic multinodular goiter
- Toxic thyroid adenoma
High or normal uptake:
![Normal thyroid scan - Myohan at en.wikipedia [CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons](/index.php/File:Thyroid_scan.jpg) |
- Iodine caused hyperthyroidism
- Hashitoxicosis
- Germ cell tumors (choriocarcinoma in males and testicular germ cell tumors)
- Pituitary TSH-producing adenoma
Low uptake
- Subacute thyroiditis
- Hyperthyroidism due to ectopic thyroid tissue
Pathophysiology
- Thyroid hormones (T3 and T4) are regulating basal metabolic rate, influence oxygen consumption by tissues. They are crucial for normal development of the brain and growth of the body, especially in prepubertal period.
Hypothalamic-pituitary-thyroid axis
- Secretion of thyroid hormones follows upper control from the hypothalamus and the pituitary. Thyroid releasing hormone (TRH). TRH acts on thyrotropes releasing cells in the pituitary causing them to release thyroid stimulating hormone (TSH).
 |
- TSH acts on thyroid gland by binding to specific membrane receptors and activating an intracellular pathway involving cAMP that ends in the formation and secretion of thyroid hormones.
- The higher regulation of thyroxin secretion follows the negative feedback role, meaning that high levels of T3 and T4 will suppress TRH and TSH secretion and vice versa (Low levels of thyroxins will stimulate TRH and TSH secretion). This is useful in diagnosing the cause of hyperthyroidism (in secondary hyperthyroidism where the pituitary or the hypothalamus are the sources of the disease. TSH will be high, while in primary hyperthyroidism where the gland is the source of the excess hormones, TSH will be low).
Thyroxin synthesis and secretion
- Iodine is essential for the synthesis of thyroid hormones. The daily iodide need is about 100mcg / day. Iodide is uptaken through a special Na/I transporter found in the membrane of thyroid follicular cell. After uptaking iodide, it goes through a series of organic reactions ending in the formation of the two forms of thyroid hormones: T3 and T4. T3 and T4 remain stored in the thyroglobulin of the follicles and are released in response to further stimulation by TSH to the thyroid follicles.
- While T3 is 3 to 5 times more potent than T4, it represents only one-fourth of the total hormone secretion. T3 is thought to be the biologically active form of the of the two forms of the hormone. Most of the circulating T3 is due to peripheral conversion of T4 in the liver and peripheral tissues while only a small percentage is secreted directly from the thyroid gland itself.
- The majority of circulating T3 and T4 are bound to plasma proteins and thus not active (T4 is mostly bound to thyroxine binding globulin and T3 is mostly bound to transthyretin). Conditions that impair the production of thyroid binding globulins (such as pregnancy, liver failure, and certain drug administration) cause a change in the total serum thyroxins but the free T3 and T4 remain normal and the patient remains euthyroid (this carries only laboratory significance).
- T3 and T4 act on nuclear receptors (DNA binding proteins) and cause the regulate the transcription of many proteins to regulate the metabolic rate of the body.
- In grave’s disease, the most common cause of hyperthyroidism. The disorder lies in the secretion of thyroid stimulating antibodies (TSI) that work on thyroid follicular cells causing an excessive uncontrolled release of the thyroxins. TSI responsible for many other aspects of the disease such as ophthalmopathy and the skin manifestations. This is thought to be due to the epitopic similarity between antigens on the surface of these cells and the thyroid receptors.
Historical perspective
- In 1786, the association between goiter and exophthalmos was first described by Caleb Hillier Parry. However, his observation was first published in 1825.
- In 1835, Robert James Graves gave his name to the autoimmune disease causing exophthalmos and goiter.[1]
- In 1840, the same classic description was described by von Basedow.
- In 1884, thyroidectomies were tried successfully for treatment of goiter.
- In 2000 thyroidectomies performed by Kocher in the 19th century, the mortality rate was reported as 5%.
- In 1912, Hashimoto disease was described as a cause of hyperthyroidism.[2]
- In 1956, thyroid stimulating antibodies were discovered in association with graves' disease.[3]
- In 1957, thyroid antibodies were discovered in association with Hashimoto thyroiditis.