Goiter pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
Overview
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 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 is continuous, it leads to goiter.
Pathophysiology
Pathogenesis
Pathogenesis: [1] [2] [3] [4] [5] [6] [7] [8] [9] [10]
- Goiters may can occur as a result of either hypothyroidism, hyperthyroidism, or when the levels of thyroid hormone are normal.
- Thyroid enlargement (goiter) and hypothyroidism may occur due to compensatory responses as a result of a severe underlying disorder.
- When the thyroid gland can't secrete enough thyroid hormone to cater to the metabolic requirements, it may lead to simple goiter.
- 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 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 is continuous, it leads to goiter.
- Thyroid hormone deficiency may be related to iodine deficiency, inborn errors of thyroid hormone synthesis and goitrogens.
- Goiters may from as a result of a 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:
- The effect of thyroid hormone dysfunction
- The effect of enlarged thyroid gland
- The effect of primary disease causing goitre
- 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 → dyspnea
- Effect on the esophagus → dysphagia
- Effect on the superior venacava → distended neck veins
- Effect on the recurrent laryngeal nerve → horsiness 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: [11] [12]
- Thyroglobulin (Tg) gene
- Thyroid-stimulating hormone receptor (TSHR) gene
- Na+/I- symporter (NIS) gene
Associated Conditions
- Grave's disease
- Hashimoto's thyroiditis
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
Microscopic studies that aid in the histopathological analysis:
- Fine needle aspiration cytology (FNAC)
- Open biopsy
Histologic Findings:
- Simple nontoxic 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.
- ↑ 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.