Goiter pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Reddy Kothagadi M.B.B.S[2]
Overview
When the thyrotrophin releasing hormone-thyroid stimulating hormone axis (TRH-TSH thyroid hormone axis) is interfered, it results in structural and functional changes in the thyroid gland. Increased TSH production is trigerred by a deficiency in thyroid hormone synthesis or intake. In order to normalize thyroid hormone levels, the increase in TSH leads to increased cellularity and hyperplasia of the thyroid gland and when this process occurs continuously, it leads to goiter.
Pathophysiology
Pathogenesis:[1][2][3][4][5][6][7][8][9][10][11]
- Goiters may occur as a result of either hypothyroidism, hyperthyroidism, or even with normal levels of thyroid hormone.
- Thyroid enlargement (goiter) and hypothyroidism may occur due to compensatory responses as a result of a severe underlying disorder.
- When the thyroid gland cannot secrete enough thyroid hormone to cater to the metabolic requirements, it may lead to simple goiter (smooth enlargement).
- In order to compensate for inadequate hormone synthesis, the thyroid gland enlarges, this type of compensation overcomes mild to moderate hormonal impairment.
- When the TRH-TSH thyroid hormone axis is interfered, it results in the structural and functional changes of the thyroid gland.
- Increased TSH production is triggered by a deficiency in thyroid hormone synthesis or intake.
- In order to normalize thyroid hormone levels, the increase in TSH leads to increased cellularity and hyperplasia of the thyroid gland and when this process is continuous, it leads to goiter.
- Thyroid hormone deficiency may occur secondary to to iodine deficiency, inborn errors of thyroid hormone synthesis and goitrogens.
- Goiters may form as a result of many TSH receptor agonists. The TSH receptor gets stimulated under the following conditions:
- Adenoma of the pituitary
- Adenoma of the hypothalamus
- Pituitary resistance to thyroid hormone
- TSH receptor antibodies
- Tumors producing hCG (human chorionic gonadotropin)
- The pathophysiological consequences of goitres results from one of the following:
- Thyroid hormone dysfunction
- Enlarged thyroid gland
- The effect of primary disease causing goiter
- The effect of thyroid hormone dysfunction:
- Thyroid hyperfunction (hyperthyroidism) → Features of hyperthyroidism
- Thyroid hypofunction (hypothyroidism) → Features of hypothyroidism
- The effect of enlarged thyroid gland:
- Effect on the trachea results in dyspnea
- Effect on the esophagus results in dysphagia
- Effect on the superior vena cava results in distended neck veins
- Effect on the recurrent laryngeal nerve results in hoarseness of voice
- The effect of primary disease causing goitre:
- The effect depends on the underlying disease
Genetics
- Goiter may be caused by a mutation in the following genes which vary from one family to the other: [12][13][14][15][16][17]
- Thyroglobulin (Tg) gene
- Thyroid-stimulating hormone receptor (TSHR) gene
- Sodium-iodine (Na+/I-) symporter (NIS) gene [18]
Associated Conditions
The following conditions are associated with goiter:[19][20]
Gross Pathology
- On gross pathology the following features are observed:[21][22][23]
- Enlarged thyroid gland
- Multiple nodules lacking fibrous capsule
- Secondary changes such as hemorrhage, calcification and cystic degeneration are observed
Microscopic Pathology
Goiter histologic findings:
- Simple non-toxic goiters demonstrate:
- Hyperplasia
- Colloid accumulation
- Nodularity
- Nodular hyperplasia is commonly seen in multinodular goiter. Cytologic findings include:
- Benign appearing follicular cells
- Abundant colloid, macrophages
- Hürthle cells (occasionally)
References
- ↑ Rapoport, Basil (1991). "Pathophysiology of Hashimoto's Thyroiditis and Hypothyroidism". Annual Review of Medicine. 42 (1): 91–96. doi:10.1146/annurev.me.42.020191.000515. ISSN 0066-4219.
- ↑ Larsen, P.R. (1972). "Triiodothyronine: Review of recent studies of its physiology and pathophysiology in man". Metabolism. 21 (11): 1073–1092. doi:10.1016/0026-0495(72)90038-8. ISSN 0026-0495.
- ↑ Gaitan, Eduardo; Wahner, Heinz W.; Cuello, Carlos; Correa, Pelayo; Jubiz, William; Gaitan, Jorge E. (1969). "Endemic Goiter in the Cauca Valley: II. Studies of Thyroid Pathophysiology1". The Journal of Clinical Endocrinology & Metabolism. 29 (5): 675–683. doi:10.1210/jcem-29-5-675. ISSN 0021-972X.
- ↑ Elte JW, Bussemaker JK, Haak A (1990). "The natural history of euthyroid multinodular goitre". Postgrad Med J. 66 (773): 186–90. PMC 2429462. PMID 2114018.
- ↑ Berghout A, Wiersinga WM, Smits NJ, Touber JL (1990). "Interrelationships between age, thyroid volume, thyroid nodularity, and thyroid function in patients with sporadic nontoxic goiter". Am. J. Med. 89 (5): 602–8. PMID 2239979.
- ↑ Soto, Roberto J.; Imas, Berta; Brunengo, Ana M.; Goldberg, David; Burian, Rosa; Gnocchi, Luisa (1967). "Endemic Goiter in Misiones, Argentina: Pathophysiology Related to Immunological Phenomena". The Journal of Clinical Endocrinology & Metabolism. 27 (11): 1581–1587. doi:10.1210/jcem-27-11-1581. ISSN 0021-972X.
- ↑ Gärtner R, Dugrillon A (1998). "[From iodine deficiency to goiter. Pathophysiology of iron deficiency goiter]". Internist (Berl) (in German). 39 (6): 566–73. PMID 9677510.
- ↑ Peteiro-Gonzalez, D.; Lee, J.; Rodriguez-Fontan, J.; Castro-Piedras, I.; Cameselle-Teijeiro, J.; Beiras, A.; Bravo, S. B.; Alvarez, C. V.; Hardy, D. M.; Targovnik, H. M.; Arvan, P.; Lado-Abeal, J. (2010). "New Insights into Thyroglobulin Pathophysiology Revealed by the Study of a Family with Congenital Goiter". The Journal of Clinical Endocrinology & Metabolism. 95 (7): 3522–3526. doi:10.1210/jc.2009-2109. ISSN 0021-972X.
- ↑ Capen, C.C. (1992). "Pathophysiology of chemical injury of the thyroid gland". Toxicology Letters. 64-65: 381–388. doi:10.1016/0378-4274(92)90211-2. ISSN 0378-4274.
- ↑ Maceri, Dennis R.; Sullivan, Michael J.; McClatchney, Kenneth D. (1986). "AUTOIMMUNE THYROIDITIS". The Laryngoscope. 96 (1): 82???86. doi:10.1288/00005537-198601000-00015. ISSN 0023-852X.
- ↑ Neumann, Susanne; Willgerodt, Helmut; Ackermann, Frank; Reske, Andreas; Jung, Martin; Reis, André; Paschke, Ralf (1999). "Linkage of Familial Euthyroid Goiter to the Multinodular Goiter-1 Locus and Exclusion of the Candidate Genes Thyroglobulin, Thyroperoxidase, and Na+/I−Symporter1". The Journal of Clinical Endocrinology & Metabolism. 84 (10): 3750–3756. doi:10.1210/jcem.84.10.6023. ISSN 0021-972X.
- ↑ Brix TH, Hegedüs L (2000). "Genetic and environmental factors in the aetiology of simple goitre". Ann. Med. 32 (3): 153–6. PMID 10821321.
- ↑ Dohán O, De la Vieja A, Paroder V, Riedel C, Artani M, Reed M, Ginter CS, Carrasco N (2003). "The sodium/iodide Symporter (NIS): characterization, regulation, and medical significance". Endocr. Rev. 24 (1): 48–77. doi:10.1210/er.2001-0029. PMID 12588808.
- ↑ Targovnik, Héctor M.; Esperante, Sebastián A.; Rivolta, Carina M. (2010). "Genetics and phenomics of hypothyroidism and goiter due to thyroglobulin mutations". Molecular and Cellular Endocrinology. 322 (1–2): 44–55. doi:10.1016/j.mce.2010.01.009. ISSN 0303-7207.
- ↑ Spitzweg, Christine; Morris, John C. (2010). "Genetics and phenomics of hypothyroidism and goiter due to NIS mutations". Molecular and Cellular Endocrinology. 322 (1–2): 56–63. doi:10.1016/j.mce.2010.02.007. ISSN 0303-7207.
- ↑ Moreno, José C.; Visser, Theo J. (2010). "Genetics and phenomics of hypothyroidism and goiter due to iodotyrosine deiodinase (DEHAL1) gene mutations". Molecular and Cellular Endocrinology. 322 (1–2): 91–98. doi:10.1016/j.mce.2010.03.010. ISSN 0303-7207.
- ↑ Fraser GR (1969). "The genetics of thyroid disease". Prog Med Genet. 6: 89–115. PMID 4980080.
- ↑ Portulano C, Paroder-Belenitsky M, Carrasco N (2014). "The Na+/I- symporter (NIS): mechanism and medical impact". Endocr Rev. 35 (1): 106–49. doi:10.1210/er.2012-1036. PMC 3895864. PMID 24311738.
- ↑ Girgis CM, Champion BL, Wall JR (2011). "Current concepts in graves' disease". Ther Adv Endocrinol Metab. 2 (3): 135–44. doi:10.1177/2042018811408488. PMC 3474632. PMID 23148179.
- ↑ "Hashimoto's Thyroiditis - Endotext - NCBI Bookshelf".
- ↑ MORTENSEN JD, WOOLNER LB, BENNETT WA (1955). "Gross and microscopic findings in clinically normal thyroid glands". J Clin Endocrinol Metab. 15 (10): 1270–80. doi:10.1210/jcem-15-10-1270. PMID 13263417.
- ↑ "Reorganized text". JAMA Otolaryngol Head Neck Surg. 141 (5): 428. 2015. doi:10.1001/jamaoto.2015.0540. PMID 25996397.
- ↑ Hegedüs L, Bonnema SJ, Bennedbaek FN (2003). "Management of simple nodular goiter: current status and future perspectives". Endocr Rev. 24 (1): 102–32. doi:10.1210/er.2002-0016. PMID 12588812.