Sandbox: hyperthyroidism landing: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
No edit summary
m (Bot: Automated text replacement (-{{columns-list|3| +{{columns-list|))
 
(22 intermediate revisions by one other user not shown)
Line 1: Line 1:
__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.


==Patient information==
==Causes==


===Overview===
<div style="-webkit-user-select: none;">
Hyperthyroidism is a disorder that the thyroid gland makes too much [[thyroid hormone]]. About 1 percent of the U.S. population has hyperthyroidism. Some diseases, such as [[Graves’ disease]], thyroid nodules and [[thyroiditis]], are associated with the cause of hyperthyroidism. Hyperthyroidism can affect your metabolism. Usual signs and symptoms include [[goiter]], increased appetite but [[weight loss]], [[palpitation]], [[hypertension]], increased sensitivity to heat and perspiration, [[nervousness]] and hand [[tremors]]. The Thyroid-Stimulating Hormone (TSH) test is a very sensitive and useful test to identify the disorder. Other examinations include the [[T3]] and [[T4]] test, radioactive iodine uptake test and thyroid scan. Treatment options of hyperthyroidism depends on the cause, age, physical condition and the severity of symptoms. Usual treatment measures are medications, radioactive iodine and [[thyroidectomy]]. The common [[side effect]] of radioactive iodine and [[thyroidectomy]] is [[hypothyroidism]]. The patient will need to take thyroid hormone supplement to restore normal hormone levels.
Major causes in humans are:
*[[Graves disease|Graves' disease]]  
*[[Toxic thyroid adenoma]]
*[[Toxic multinodular goitre]]


===What are the symptoms of Hyperthyroidism?===
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.
Symptoms of hyperthyroidism vary from person to person. Usual signs include the following:
   
*[[Goiter]]
*Increased appetite, but [[weight loss]]
*[[Palpitation]]
*[[Hypertension]]
*Increased sensitivity to heat and perspiration
*[[Nervousness]], anxiety or irritability, difficulty sleeping
*Hand [[tremors]]
*[[Fatigue]], [[muscle weakness]]
*Changes in menstrual patterns (usually lighter flow, less frequent periods) in women


Other health problems may also cause these symptoms. Only a doctor can tell for sure. A person with any of these symptoms should tell the doctor so that the problems can be diagnosed and treated as early as possible.
[[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.


===Who is at highest risk?===
===Life Threatening Causes===
*[[Graves’ disease]]
*[[Adenocarcinoma]]
*Thyroid nodules
*[[Choriocarcinoma]]
*[[Thyroiditis]]
*Metastatic follicular thyroid cancer
*Too much [[iodine]] ingestion
*[[Pituitary tumor]]
*Over-medicating with synthetic [[thyroid hormone]]
*[[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


===Diagnosis===
===Common Causes===
*Thyroid-Stimulating Hormone (TSH) test: This is a very sensitive and useful test and usually used as the first test to identify the disorder. The TSH test is based on the feedback between TSH and thyroid hormone. Patients with hyperthyroidism may show a lower reading than normal people.
*[[Graves disease|Graves' disease]]  
*T3 and T4 test: This test may show the levels of T3 and T4 in your blood. In patients with hyperthyroidism, the levels of one or both of these hormones in your blood will be higher than normal.
*[[Toxic thyroid adenoma]]
*Thyroid-stimulating immunoglobulin (TSI) test: This test may help diagnose [[Graves' disease]], which has this kind of antibody.
*[[Toxic multinodular goitre]]
*Radioactive [[iodine uptake]] test: This test can detect the iodine uptake function of your [[thyroid gland]] and help diagnose the cause of hyperthyroidism. For example, low levels of iodine uptake might be a sign of [[thyroiditis]], whereas high levels could indicate [[Graves’ disease]].
*Thyroid scan: This test may also help diagnose the cause of hyperthyroidism by providing images of nodules and other possible thyroid irregularities.


Other diseases with similar symptoms:
===Causes by Organ System===
*Autonomic nerve dysfunction
{| style="width:80%; height:100px" border="1"
*[[Coronary artery disease]]
| style="width:25%" bgcolor="LightSteelBlue" ; border="1" |'''Cardiovascular'''
*[[Goiter]]
| style="width:75%" bgcolor="Beige" ; border="1" | No underlying causes
*[[Schizophrenia]]
|-
*[[Thyroid cancer]]
| bgcolor="LightSteelBlue" | '''Chemical/Poisoning'''
| bgcolor="Beige" | No underlying causes
|-
|- bgcolor="LightSteelBlue"
| '''Dental'''
| bgcolor="Beige" | No underlying causes
|-
|- bgcolor="LightSteelBlue"
| '''Dermatologic'''
| bgcolor="Beige" | [[Hydatidiform mole]]
|-
|- bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
| bgcolor="Beige" | [[Amiodarone ]] ,  [[Atezolizumab]],  [[Levothyroxine and indinavir interaction]],  [[Nivolumab]],  [[Potassium iodide]],  [[Pramipexole]],  [[Sorafenib]],  [[Thyroxine]]
|-
|- bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
| bgcolor="Beige" | No underlying causes
|-
|- bgcolor="LightSteelBlue"
| '''Endocrine'''
| bgcolor="Beige" | [[Anterior pituitary hyperhormonotrophic syndrome]],  [[Autoimmune enteropathy]],  [[Autoimmune thyroid disease]],  [[Autonomous thyroid tissue ]] ,  [[Choriocarcinoma]],  [[De quervain thyroiditis]],  [[Excessive replacement therapy]],  [[Exogenous thyroid hormone intake]],  [[Factitious thyroiditis ]] ,  [[Graves' disease ]] ,  [[Hashimoto's thyroiditis]],  [[Jod-basedow thyrotoxicosis]],  [[Metastatic follicular thyroid cancer]],  [[Pituitary tumor]],  [[Polyendocrinopathy]],  [[Polyostotic fibrous dysplasia]],  [[Postpartum thyroiditis]],  [[Suppurative thyroiditis]],  [[Thyroid adenoma]],  [[Thyroid carcinoma]],  [[Thyroid nodule]],  [[Thyroid stimulating globulin]],  [[Thyroid tumor]],  [[Thyroiditis]],  [[Thyrotropinoma]],  [[Toxic adenoma]],  [[Toxic multinodular goiter]],  [[Toxic thyroid adenoma]],  [[Tsh hypersecretion]],  [[Tsh-mediated hyperthyroidism]],  [[Tsh-producing pituitary adenoma]]
|-
|- bgcolor="LightSteelBlue"
| '''Environmental'''
| bgcolor="Beige" | No underlying causes
|-
|- bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
| bgcolor="Beige" | [[Enteropathy]]
|-
|- bgcolor="LightSteelBlue"
| '''Genetic'''
| bgcolor="Beige" | [[Glutaricaciduria type 3]],  [[Ipex syndrome ]] ,  [[Mccune-albright syndrome ]] ,  [[Troell-junet syndrome]]
|-
|- bgcolor="LightSteelBlue"
| '''Hematologic'''
| bgcolor="Beige" | [[Diabetes mellitus]]
|-
|- bgcolor="LightSteelBlue"
| '''Iatrogenic'''
| bgcolor="Beige" | [[Excessive replacement therapy]],  [[Exogenous thyroid hormone intake]],  [[Intentional suppressive therapy]],  [[Iodine overuse ]]
|-
|- bgcolor="LightSteelBlue"
| '''Infectious Disease'''
| bgcolor="Beige" | [[Hashitoxicosis]],  [[Thyrotoxicosis factitia]]
|-
|- bgcolor="LightSteelBlue"
| '''Musculoskeletal/Orthopedic'''
| bgcolor="Beige" | No underlying causes
|-
|- bgcolor="LightSteelBlue"
| '''Neurologic'''
| bgcolor="Beige" | No underlying causes
|-
|- bgcolor="LightSteelBlue"
| '''Nutritional/Metabolic'''
| bgcolor="Beige" | [[Diabetes mellitus]],  [[Diarrhea]]
|-
|- bgcolor="LightSteelBlue"
| '''Obstetric/Gynecologic'''
| bgcolor="Beige" | [[Hyperemesis gravidarum]],  [[Teratoma]],  [[Trophoblastic disease]]
|-
|- bgcolor="LightSteelBlue"
| '''Oncologic'''
| bgcolor="Beige" | [[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]]
|-
|- bgcolor="LightSteelBlue"
| '''Ophthalmologic'''
| bgcolor="Beige" | No underlying causes
|-
|- bgcolor="LightSteelBlue"
| '''Overdose/Toxicity'''
| bgcolor="Beige" | [[Iodine overuse ]]
|-
|- bgcolor="LightSteelBlue"
| '''Psychiatric'''
| bgcolor="Beige" | No underlying causes
|-
|- bgcolor="LightSteelBlue"
| '''Pulmonary'''
| bgcolor="Beige" | No underlying causes
|-
|- bgcolor="LightSteelBlue"
| '''Renal/Electrolyte'''
| bgcolor="Beige" | No underlying causes
|-
|- bgcolor="LightSteelBlue"
| '''Rheumatology/Immunology/Allergy'''
| bgcolor="Beige" | [[Autoimmune enteropathy]],  [[Autoimmune thyroid disease]],  [[Autonomous thyroid tissue ]] ,  [[Immune dysregulation]],  [[Intentional suppressive therapy]],  [[Polyostotic fibrous dysplasia]]
|-
|- bgcolor="LightSteelBlue"
| '''Sexual'''
| bgcolor="Beige" | No underlying causes
|-
|- bgcolor="LightSteelBlue"
| '''Trauma'''
| bgcolor="Beige" | No underlying causes
|-
|- bgcolor="LightSteelBlue"
| '''Urologic'''
| bgcolor="Beige" | [[Testicular cancer]]
|-
|- bgcolor="LightSteelBlue"
| '''Miscellaneous'''
| bgcolor="Beige" | No underlying causes
|-
|}


===When to seek urgent medical care?===
===Causes in Alphabetical Order===
Call your health care provider if symptoms of hyperthyroidism develop. If you experience either of the following symptoms, seeking urgent medical care as soon as possible:
{{columns-list|
*[[Palpitation]]
*[[Adenocarcinoma]]
*Severe [[hypertension]]
*[[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]]
}}
</div>


===Treatment options===
==Calssification==
Usual treatment measures of hyperthyroidism include medications, radioactive iodine, and surgery. Treatment options depends on the cause, age, physical condition and the severity of symptoms.
Hyperthyroidism can be classified according to the results of iodine uptake test into:
*Medications: Antithyroid medications, such as [[methimazole]] (Tapazole) and [[propylthiouracil]] (PTU), are used to block the production of thyroid hormone. Symptoms may begin to improve in 6 to 12 weeks and the whole treatment period may last for at least a year. [[Beta blockers]], for example [[propranolol]], may be used to relieve symptoms such as [[palpitation]], [[nervousness]],[[hypertension]], [[sweating]] and [[shaking]].
*Radioactive iodine: This kind of treatment may destroy the thyroid gland and stop the excess production of [[hormone]]s. During this period, the patient takes radioactive iodine by mouth. A common [[side effect]] is permanent hypothyroidism, which needs thyroid supplements.
===High iodine uptake===
*[[Surgery]]: Thyroidectomy is another type of treatment option. The possible side effect after surgery is hypothyroidism. Patients need to take [[thyroid hormone]] supplements to restore normal hormone levels.


===Contraindicated medications===
{{MedCondContrPI


|MedCond =hyperthyroidism|Levothyroxine|Phentermine}}


===Where to find medical care for Hyperthyroidism?===
*Grave’s disease
[http://maps.google.com/maps?f=q&amp;hl=en&amp;geocode=&amp;q={{urlencode:{{#if:{{{1|}}}|{{{1}}}|hyperthyroidism}}}}&amp;sll=37.0625,-95.677068&amp;sspn=65.008093,112.148438&amp;ie=UTF8&amp;ll=37.0625,-95.677068&amp;spn=91.690419,149.414063&amp;z=2&amp;source=embed Directions to Hospitals Treating Hyperthyroidism]
*Toxic multinodular goiter
*Toxic thyroid adenoma


===Prevention===
[[Image:Graves-disease-thyroid-scintigraphy-2.jpg|400px|Thyroid scan of a Grave's disease patient showing increaed iodine uptake and visualization of the pyramidal lobe (which is not normally seen) - Case courtesy of Dr Arshdeep Sidhu, <a href="https://radiopaedia.org/">Radiopaedia.org</a>. From the case <a href="https://radiopaedia.org/cases/21945">rID: 21945</a>]]
*For hyperthyroidism caused by too much iodine ingestion, the method of prevention is decreasing iodine ingestion and a regular check of thyroid hormone levels in the blood.
===High or normal uptake:===
*For hyperthyroidism caused by over-medicating with synthetic thyroid hormone, giving the appropriate dose to patients and a regular check of thyroid hormone levels in the blood may be important.


===What to expect (Outlook/Prognosis)?===
{| style="float: right; width: 350px"
Many cases of hyperthyroidism are generally treatable. Prognosis depends on whether or not the patient has severe complications.
| [[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]]
|}


===Possible Complications===
*Iodine caused hyperthyroidism
 
*Hashitoxicosis
===Sources===
*Germ cell tumors (choriocarcinoma in males and testicular germ cell tumors)
*http://www.endocrine.niddk.nih.gov/pubs/Hyperthyroidism/
*Pituitary TSH-producing adenoma
*http://www.nlm.nih.gov/medlineplus/ency/article/000356.htm
===Low uptake===
{{WH}}
*Subacute thyroiditis
{{WS}}
*Hyperthyroidism due to ectopic thyroid tissue
 
<br>
[[Category:Endocrinology]]
<br>
[[Category:Emergency medicine]]
<br>
[[Category:Otolaryngology]]
==Pathophysiology==
[[Category:Primary care]]
* 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.


[[Category:Needs content]]
==== 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;"
| [[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).


==Causes==
==== 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.
[[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]]
* 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.


==Calssification==


==Pathophysiology==
==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

Common Causes

Causes by Organ System

Cardiovascular No underlying causes
Chemical/Poisoning No underlying causes
Dental No underlying causes
Dermatologic Hydatidiform mole
Drug Side Effect Amiodarone , Atezolizumab, Levothyroxine and indinavir interaction, Nivolumab, Potassium iodide, Pramipexole, Sorafenib, Thyroxine
Ear Nose Throat No underlying causes
Endocrine Anterior pituitary hyperhormonotrophic syndrome, Autoimmune enteropathy, Autoimmune thyroid disease, Autonomous thyroid tissue , Choriocarcinoma, De quervain thyroiditis, Excessive replacement therapy, Exogenous thyroid hormone intake, Factitious thyroiditis , Graves' disease , Hashimoto's thyroiditis, Jod-basedow thyrotoxicosis, Metastatic follicular thyroid cancer, Pituitary tumor, Polyendocrinopathy, Polyostotic fibrous dysplasia, Postpartum thyroiditis, Suppurative thyroiditis, Thyroid adenoma, Thyroid carcinoma, Thyroid nodule, Thyroid stimulating globulin, Thyroid tumor, Thyroiditis, Thyrotropinoma, Toxic adenoma, Toxic multinodular goiter, Toxic thyroid adenoma, Tsh hypersecretion, Tsh-mediated hyperthyroidism, Tsh-producing pituitary adenoma
Environmental No underlying causes
Gastroenterologic Enteropathy
Genetic Glutaricaciduria type 3, Ipex syndrome , Mccune-albright syndrome , Troell-junet syndrome
Hematologic Diabetes mellitus
Iatrogenic Excessive replacement therapy, Exogenous thyroid hormone intake, Intentional suppressive therapy, Iodine overuse
Infectious Disease Hashitoxicosis, Thyrotoxicosis factitia
Musculoskeletal/Orthopedic No underlying causes
Neurologic No underlying causes
Nutritional/Metabolic Diabetes mellitus, Diarrhea
Obstetric/Gynecologic Hyperemesis gravidarum, Teratoma, Trophoblastic disease
Oncologic 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
Ophthalmologic No underlying causes
Overdose/Toxicity Iodine overuse
Psychiatric No underlying causes
Pulmonary No underlying causes
Renal/Electrolyte No underlying causes
Rheumatology/Immunology/Allergy Autoimmune enteropathy, Autoimmune thyroid disease, Autonomous thyroid tissue , Immune dysregulation, Intentional suppressive therapy, Polyostotic fibrous dysplasia
Sexual No underlying causes
Trauma No underlying causes
Urologic Testicular cancer
Miscellaneous No underlying causes

Causes in Alphabetical Order

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

Thyroid scan of a Grave's disease patient showing increaed iodine uptake and visualization of the pyramidal lobe (which is not normally seen) - Case courtesy of Dr Arshdeep Sidhu, <a href="https://radiopaedia.org/">Radiopaedia.org</a>. From the case <a href="https://radiopaedia.org/cases/21945">rID: 21945</a>

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
Normal thyroid scan - Myohan at en.wikipedia [CC BY 3.0 (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons
  • 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).
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
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.

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

  • 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

References

  1. ↑ "Hyperthyroidism - Wikipedia".
  2. ↑ "Hakaru Hashimoto - Wikipedia".
  3. ↑ "London Medical and Surgical Journal : Free Download & Streaming : Internet Archive".
Retrieved from "https://www.wikidoc.org/index.php?title=Sandbox:_hyperthyroidism_landing&oldid=1594901"