Silent thyroiditis pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]
Overview
The exact pathogenesis of [disease name] is not fully understood.
OR
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
OR
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
OR
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
OR
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
OR
The progression to [disease name] usually involves the [molecular pathway].
OR
The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
The control, synthesis, and release of the thyroid hormone is usually controlled by hypothalamus and pituitary gland.[1][2]
- 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.
- Secretion of thyroid hormones follows upper control from the hypothalamus and the pituitary. Thyroid releasing hormone (TRH) acts on thyrotropes releasing cells in the pituitary causing them to release thyroid stimulating hormone (TSH).
- 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.
- Iodine is essential for the synthesis of thyroid hormones. Iodide is up taken through a special Na/I transporter found in the membrane of thyroid follicular cell. After the iodide uptake, 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.
- 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 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.
- 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.
- The higher regulation of thyroxine 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 thyroxine will stimulate TRH and TSH secretion). This is useful in diagnosing the cause of hyperthyroidism.
- TSH will be low in primary hyperthyroidism where the gland is the source of the excess hormones. In secondary hyperthyroidism, TSH will be high as the pituitary or the hypothalamus are the sources of the disease.
Pathogenesis
- The exact pathogenesis of silent thyroiditis is not fully understood. It is thought that silent thyroiditis is the result of an autoimmune phenomenon. The following evidences are suggestive of an autoimmune pathogenesis of silent thyroiditis.[3][4][5][6]
- Lymphocytic infiltration of the thyroid gland
- Presence of antithyroid antibodies
- Association with HLA-DR3 and DR5
- Presence of anti-DNA antibodies
- Activated matured T (HLA-DR+CD3+), activated helper/inducer T (HLA-DR+CD4+) and activated suppressor/cytotoxic T (HLA-DR+CD8+) cells were higher in patients with silent thyroiditis as compared to the healthy controls. It indicates that the activation of T cells, especially of helper/inducer T cells, might have an important role in the pathogenesis of silent thyroiditis.[7]
Genetics
Silent thyroiditis is associated with the following HLA genes.[5]
- HLA-DR3
- HLA-DR5
Associated Conditions
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- Microscopic histopathological findings in silent thyroiditis include:[3][8]
- Diffuse lymphocytic infiltrate
- Lack of Hurthle cells (Askanazy cells) and germinal centers
- Lack of fibrosis
References
- ↑ De Groot LJ, Chrousos G, Dungan K, Feingold KR, Grossman A, Hershman JM, Koch C, Korbonits M, McLachlan R, New M, Purnell J, Rebar R, Singer F, Vinik A, Rousset B, Dupuy C, Miot F, Dumont J. "Thyroid Hormone Synthesis And Secretion". PMID 25905405.
- ↑ Kirsten D (2000). "The thyroid gland: physiology and pathophysiology". Neonatal Netw. 19 (8): 11–26. doi:10.1891/0730-0832.19.8.11. PMID 11949270.
- ↑ 3.0 3.1 Volpé R (1988). "Is silent thyroiditis an autoimmune disease?". Arch. Intern. Med. 148 (9): 1907–8. PMID 3415401.
- ↑ Samuels MH (2012). "Subacute, silent, and postpartum thyroiditis". Med. Clin. North Am. 96 (2): 223–33. doi:10.1016/j.mcna.2012.01.003. PMID 22443972.
- ↑ 5.0 5.1 Farid NR, Hawe BS, Walfish PG (1983). "Increased frequency of HLA-DR3 and 5 in the syndromes of painless thyroiditis with transient thyrotoxicosis: evidence for an autoimmune aetiology". Clin. Endocrinol. (Oxf). 19 (6): 699–704. PMID 6606505.
- ↑ Tajiri J, Higashi K, Morita M, Ohishi S, Umeda T, Sato T (1986). "Elevation of anti-DNA antibody titer during thyrotoxic phase of silent thyroiditis". Arch. Intern. Med. 146 (8): 1623–4. PMID 3488044.
- ↑ Kushima K, Ban Y, Taniyama M, Itoh K (1994). "Circulating activated T lymphocyte subsets in patients with silent thyroiditis". Endocr. J. 41 (6): 663–9. PMID 7704090.
- ↑ Mittra ES, McDougall IR (2007). "Recurrent silent thyroiditis: a report of four patients and review of the literature". Thyroid. 17 (7): 671–5. doi:10.1089/thy.2006.0335. PMID 17696838.