Hyperthyroidism classification: Difference between revisions

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==Overview==


==Classification==
==Classification==


*Graves' disease: An autoimmune disorder resulting from  thyroid-stimulating immunoglobulins, which stimulate thyroid gland growth and hormone synthesis .Its prominent features including pretibial myxedema and Ophthalmopathy are autoimmune in origin. Graves' disease is the most common cause of hyperthyroidism . <ref name="pmid18550875">{{cite journal | author = Brent GA | title = Clinical practice. Graves' disease | journal = [[The New England Journal of Medicine]] | volume = 358 | issue = 24 | pages = 2594–605 | year = 2008 | month = June | pmid = 18550875 | doi = 10.1056/NEJMcp0801880 | url = }}</ref> High iodine intake, stressful events may be a risk factor.
*[[Graves' disease]]: An autoimmune disorder resulting from  thyroid-stimulating immunoglobulins, which stimulate [[thyroid gland]] growth and [[hormone]] synthesis. It's prominent features, including [[pretibial myxedema]] and ophthalmopathy, are autoimmune in origin. Graves' disease is the most common cause of hyperthyroidism.<ref name="pmid18550875">{{cite journal | author = Brent GA | title = Clinical practice. Graves' disease | journal = [[The New England Journal of Medicine]] | volume = 358 | issue = 24 | pages = 2594–605 | year = 2008 | month = June | pmid = 18550875 | doi = 10.1056/NEJMcp0801880 | url = }}</ref> High [[iodine]] intake and stressful events may be risk factors.


*Toxic adenoma and toxic multinodular goiter: It results from focal or diffuse hyperplasia of thyroid follicular cells which are independent of regulation by TSH. Activating somatic mutations of the genes for the TSH receptor have been found in both these. Mutations of the TSH-receptor gene are most common; they were found in 15 of 31 toxic adenomas in one study.{{cite journal |author=Führer D, Holzapfel HP, Wonerow P, Scherbaum WA, Paschke R |title=Somatic mutations in the thyrotropin receptor gene and not in the Gs alpha protein gene in 31 toxic thyroid nodules |journal=J. Clin. Endocrinol. Metab. |volume=82 |issue=11 |pages=3885–91 |year=1997 |month=November |pmid=9360556 |doi= |url=}}
*[[Toxic adenoma]] and [[toxic multinodular goiter]]: It results from focal or diffuse hyperplasia of thyroid follicular cells which are independent of regulation by [[TSH]]. Activating somatic mutations of the genes for the TSH receptor have been found in both of these. Mutations of the TSH-receptor gene are most common; they were found in 15 of 31 toxic adenomas in one study.<ref>{{cite journal |author=Führer D, Holzapfel HP, Wonerow P, Scherbaum WA, Paschke R |title=Somatic mutations in the thyrotropin receptor gene and not in the Gs alpha protein gene in 31 toxic thyroid nodules |journal=J. Clin. Endocrinol. Metab. |volume=82 |issue=11 |pages=3885–91 |year=1997 |month=November |pmid=9360556 |doi= |url=}}</ref>


*Hashitoxicosis:It has two phases,initially it presents with hyperthyroidism and a high radioiodine uptake caused by TSH-receptor antibodies.This is followed by infiltration of the gland with lymphocytes resultating in autoimmune-mediated destruction of thyroid tissue leading to the development of hypothyroidism.
*Hashitoxicosis: It has two phases, initially it presents with hyperthyroidism and a high radioiodine uptake caused by TSH-receptor antibodies. This is followed by infiltration of the gland with [[lymphocyte]]s resulting in autoimmune-mediated destruction of thyroid tissue leading to the development of [[hypothyroidism]].


*Iodine-induced hyperthyroidism: Develop after an iodine load or iodine-rich drugs such as amiodarone.
*Iodine-induced hyperthyroidism: Develop after an iodine load or iodine-rich drugs such as [[amiodarone]].


*TSH-mediated hyperthyroidism:It is because of increased TSH production.It has two forms, neoplastic and non-neoplastic.Neoplastic include TSH-producing pituitary adenoma. Almost all of these patients have a goiter,40 percent have defects in their filed of vision, and one-third of women have galactorrhea. All patients have high serum thyroid hormone concentrations.Non-neoplastic TSH-mediated hyperthyroidism is due to resistance of the effect of thyroid hormone on pituitary TSH.
*TSH-mediated hyperthyroidism: It is because of increased TSH production. It has two forms, neoplastic and non-neoplastic. Neoplastic includes TSH-producing pituitary adenoma. Almost all of these patients have a [[goiter]], 40 percent have defects in their field of vision, and one-third of women have [[galactorrhea]]. All patients have high serum thyroid hormone concentrations. Non-neoplastic TSH-mediated hyperthyroidism is due to resistance of the effect of [[thyroid hormone]] on pituitary TSH.
 
*Trophoblastic disease and germ cell tumors:Hyperthyroidism can occur in women with a hydatidiform mole or choriocarcinoma and in men with testicular germ cell tumors.


*Trophoblastic disease and germ cell tumors: Hyperthyroidism can occur in women with a [[hydatidiform mole]] or [[choriocarcinoma]] and in men with testicular germ cell tumors.


==References==
==References==
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[[Category:Thyroid disease]]
[[Category:Endocrinology]]
[[Category:Endocrinology]]
[[Category:Emergency medicine]]
[[Category:Emergency medicine]]
[[Category:Intensive care medicine]]
[[Category:Disease]]
[[Category:Mature chapter]]
[[Category:Otolaryngology]]
[[Category:Otolaryngology]]
[[category:Primary care]]
[[Category:Needs content]]
[[Category:Needs overview]]
[[Category:Needs overview]]
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Latest revision as of 22:17, 29 July 2020

Hyperthyroidism Microchapters

Patient Information

Overview

Classification

Differentiating hyperthyroidism from other diseases

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Farman Khan, MD, MRCP [2]

Overview

Classification

  • Graves' disease: An autoimmune disorder resulting from thyroid-stimulating immunoglobulins, which stimulate thyroid gland growth and hormone synthesis. It's prominent features, including pretibial myxedema and ophthalmopathy, are autoimmune in origin. Graves' disease is the most common cause of hyperthyroidism.[1] High iodine intake and stressful events may be risk factors.
  • Toxic adenoma and toxic multinodular goiter: It results from focal or diffuse hyperplasia of thyroid follicular cells which are independent of regulation by TSH. Activating somatic mutations of the genes for the TSH receptor have been found in both of these. Mutations of the TSH-receptor gene are most common; they were found in 15 of 31 toxic adenomas in one study.[2]
  • Hashitoxicosis: It has two phases, initially it presents with hyperthyroidism and a high radioiodine uptake caused by TSH-receptor antibodies. This is followed by infiltration of the gland with lymphocytes resulting in autoimmune-mediated destruction of thyroid tissue leading to the development of hypothyroidism.
  • Iodine-induced hyperthyroidism: Develop after an iodine load or iodine-rich drugs such as amiodarone.
  • TSH-mediated hyperthyroidism: It is because of increased TSH production. It has two forms, neoplastic and non-neoplastic. Neoplastic includes TSH-producing pituitary adenoma. Almost all of these patients have a goiter, 40 percent have defects in their field of vision, and one-third of women have galactorrhea. All patients have high serum thyroid hormone concentrations. Non-neoplastic TSH-mediated hyperthyroidism is due to resistance of the effect of thyroid hormone on pituitary TSH.
  • Trophoblastic disease and germ cell tumors: Hyperthyroidism can occur in women with a hydatidiform mole or choriocarcinoma and in men with testicular germ cell tumors.

References

  1. Brent GA (2008). "Clinical practice. Graves' disease". The New England Journal of Medicine. 358 (24): 2594–605. doi:10.1056/NEJMcp0801880. PMID 18550875. Unknown parameter |month= ignored (help)
  2. Führer D, Holzapfel HP, Wonerow P, Scherbaum WA, Paschke R (1997). "Somatic mutations in the thyrotropin receptor gene and not in the Gs alpha protein gene in 31 toxic thyroid nodules". J. Clin. Endocrinol. Metab. 82 (11): 3885–91. PMID 9360556. Unknown parameter |month= ignored (help)

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