Struma ovarii pathophysiology: Difference between revisions
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==Microscopic Pathology== | ==Microscopic Pathology== | ||
On microscopic histopathological analysis the tumor was initially diagnosed as granulosa cell tumor in frozen study but finally turned out to be Struma Ovarii which is the characteristic finding of Struma ovarii. <ref name="pmid22436494">{{cite journal |vauthors=Mostaghel N, Enzevaei A, Zare K, Fallahian M |title=Struma ovarii associated with Pseudo-Meig's syndrome and high serum level of CA 125; a case report |journal=J Ovarian Res |volume=5 |issue= |pages=10 |year=2012 |pmid=22436494 |pmc=3350392 |doi=10.1186/1757-2215-5-10 |url=}}</ref> | |||
[[File:Struma_ovarii_Microscopic_appearance_of_the_resected_tumor.jpg|thumb|none|450px| Microscopic appearance of the resected tumor.]] | [[File:Struma_ovarii_Microscopic_appearance_of_the_resected_tumor.jpg|thumb|none|450px| Microscopic appearance of the resected tumor.]] | ||
Revision as of 23:07, 10 August 2017
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Struma ovarii Microchapters |
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Diagnosis |
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Treatment |
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Struma ovarii pathophysiology On the Web |
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Risk calculators and risk factors for Struma ovarii pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:
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].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Pathophysiology
Pathogenesis
- 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].
- [Pathogen name] is usually transmitted via the [transmission route] route to the human host.
- Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
- [Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
- The progression to [disease name] usually involves the [molecular pathway].
- The pathophysiology of [disease/malignancy] depends on the histological subtype.
Genetics
- [Disease name] is transmitted in [mode of genetic transmission] pattern.
- Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
- The development of [disease name] is the result of multiple genetic mutations.
Associated Conditions
- Adenomatous or colloid cervical goiters. [1]
- Hyperthyroidism in postmenopausal woman. [2]
- Pseudo-Meig's syndrome [3]
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis the tumor was initially diagnosed as granulosa cell tumor in frozen study but finally turned out to be Struma Ovarii which is the characteristic finding of Struma ovarii. [3]
References
- ↑ Kempers RD, Dockerty MB, Hoffman DL, Bartholomew LG (1970). "Struma ovarii--ascitic, hyperthyroid, and asymptomatic syndromes". Ann. Intern. Med. 72 (6): 883–93. PMID 5448747.
- ↑ Nonne N, Ameyar-Zazoua M, Souidi M, Harel-Bellan A (2010). "Tandem affinity purification of miRNA target mRNAs (TAP-Tar)". Nucleic Acids Res. 38 (4): e20. doi:10.1093/nar/gkp1100. PMC 2831319. PMID 19955234.
- ↑ 3.0 3.1 Mostaghel N, Enzevaei A, Zare K, Fallahian M (2012). "Struma ovarii associated with Pseudo-Meig's syndrome and high serum level of CA 125; a case report". J Ovarian Res. 5: 10. doi:10.1186/1757-2215-5-10. PMC 3350392. PMID 22436494.