Goiter pathophysiology: Difference between revisions

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==Gross Pathology==
==Gross Pathology==
*On [[gross pathology]] the following features are observed: <ref name="pmid13263417">{{cite journal| author=MORTENSEN JD, WOOLNER LB, BENNETT WA| title=Gross and microscopic findings in clinically normal thyroid glands. | journal=J Clin Endocrinol Metab | year= 1955 | volume= 15 | issue= 10 | pages= 1270-80 | pmid=13263417 | doi=10.1210/jcem-15-10-1270 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13263417  }} </ref> <ref name="pmid25996397">{{cite journal| author=| title=Reorganized text. | journal=JAMA Otolaryngol Head Neck Surg | year= 2015 | volume= 141 | issue= 5 | pages= 428 | pmid=25996397 | doi=10.1001/jamaoto.2015.0540 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25996397  }} </ref> <ref name="pmid12588812">{{cite journal| author=Hegedüs L, Bonnema SJ, Bennedbaek FN| title=Management of simple nodular goiter: current status and future perspectives. | journal=Endocr Rev | year= 2003 | volume= 24 | issue= 1 | pages= 102-32 | pmid=12588812 | doi=10.1210/er.2002-0016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12588812  }} </ref>
*On [[gross pathology]] the following features are observed:<ref name="pmid13263417">{{cite journal| author=MORTENSEN JD, WOOLNER LB, BENNETT WA| title=Gross and microscopic findings in clinically normal thyroid glands. | journal=J Clin Endocrinol Metab | year= 1955 | volume= 15 | issue= 10 | pages= 1270-80 | pmid=13263417 | doi=10.1210/jcem-15-10-1270 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13263417  }} </ref><ref name="pmid25996397">{{cite journal| author=| title=Reorganized text. | journal=JAMA Otolaryngol Head Neck Surg | year= 2015 | volume= 141 | issue= 5 | pages= 428 | pmid=25996397 | doi=10.1001/jamaoto.2015.0540 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25996397  }} </ref><ref name="pmid12588812">{{cite journal| author=Hegedüs L, Bonnema SJ, Bennedbaek FN| title=Management of simple nodular goiter: current status and future perspectives. | journal=Endocr Rev | year= 2003 | volume= 24 | issue= 1 | pages= 102-32 | pmid=12588812 | doi=10.1210/er.2002-0016 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12588812  }} </ref>
**[[Enlarged thyroid gland]]
**[[Enlarged thyroid gland]]
**Multiple nodules lacking [[fibrous capsule]]
**Multiple nodules lacking [[fibrous capsule]]
Line 62: Line 62:


==Microscopic Pathology==
==Microscopic Pathology==
Microscopic studies that aid in the [[histopathological]] analysis:
'''Goiter histologic findings:'''
*'''[[Fine needle aspiration cytology]] ([[FNAC]])'''
*Simple non-toxic goiters demonstrate:
*'''Open biopsy'''
 
'''Histologic Findings:'''
*Simple nontoxic goiters demonstrate:
**[[Hyperplasia]]
**[[Hyperplasia]]
**Colloid accumulation
**[[Colloid]] accumulation
**Nodularity
**Nodularity


*Nodular hyperplasia is commonly seen in multinodular goiter. Cytologic findings include:
*Nodular hyperplasia is commonly seen in multinodular goiter. [[Cytological|Cytologic]] findings include:
**Benign appearing follicular cells
**Benign appearing [[follicular cells]]
**Abundant colloid, [[macrophages]]
**Abundant [[colloid]], [[macrophages]]
**[[Hurthle cell (patient information)|Hürthle cells]](occasionally)
**[[Hurthle cell (patient information)|Hürthle cells]] (occasionally)





Latest revision as of 15:21, 18 November 2017

Goiter Microchapters

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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]

  • The effect of primary disease causing goitre:
    • The effect depends on the underlying disease

Genetics

Associated Conditions

The following conditions are associated with goiter:[19][20]

Gross Pathology

By Ed Uthman from Houston, TX, USA (Thyroid, Diffuse Hyperplasia) [CC BY 2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons

Microscopic Pathology

Goiter histologic findings:


By Ed Uthman from Houston, TX, USA (Diffuse Thyroid Hyperplasia Uploaded by CFCF) [CC BY 2.0 (http://creativecommons.org/licenses/by/2.0)], via Wikimedia Commons

References

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. 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.
  7. 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.
  8. 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.
  9. 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.
  10. 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.
  11. 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.
  12. Brix TH, Hegedüs L (2000). "Genetic and environmental factors in the aetiology of simple goitre". Ann. Med. 32 (3): 153–6. PMID 10821321.
  13. 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.
  14. 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.
  15. 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.
  16. 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.
  17. Fraser GR (1969). "The genetics of thyroid disease". Prog Med Genet. 6: 89–115. PMID 4980080.
  18. 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.
  19. 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.
  20. "Hashimoto's Thyroiditis - Endotext - NCBI Bookshelf".
  21. 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.
  22. "Reorganized text". JAMA Otolaryngol Head Neck Surg. 141 (5): 428. 2015. doi:10.1001/jamaoto.2015.0540. PMID 25996397.
  23. 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.

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