Duodenal atresia pathophysiology: Difference between revisions
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===Pathogenesis=== | ===Pathogenesis=== | ||
*It is thought that duodenal atresia is the result of failure of re-canalization of the duodenum in 8 to 10 weeks of fetal development.<ref name="pmid6028984">{{cite journal| author=Boyden EA, Cope JG, Bill AH| title=Anatomy and embryology of congenital intrinsic obstruction of the duodenum. | journal=Am J Surg | year= 1967 | volume= 114 | issue= 2 | pages= 190-202 | pmid=6028984 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6028984 }} </ref> | *It is thought that duodenal atresia is the result of failure of re-canalization of the duodenum in 8 to 10 weeks of fetal development.<ref name="pmid6028984">{{cite journal| author=Boyden EA, Cope JG, Bill AH| title=Anatomy and embryology of congenital intrinsic obstruction of the duodenum. | journal=Am J Surg | year= 1967 | volume= 114 | issue= 2 | pages= 190-202 | pmid=6028984 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6028984 }} </ref> | ||
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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].
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
Pathogenesis
- It is thought that duodenal atresia is the result of failure of re-canalization of the duodenum in 8 to 10 weeks of fetal development.[1]
- Duodenal atresia arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
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
Duodenal atresia is commonly associated with the following:[2][3]
- Down syndrome in 25 %to 40% of cases
- VATER
- Vertebral defects
- Anal anomalies
- Esophageal atresia
- Renal abnormalities
- Malrotation
- Annular pancreas
- Biliary tract abnormalities
- Cardiac
- Mandibulofacial anomalies
Gross Pathology
- On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Boyden EA, Cope JG, Bill AH (1967). "Anatomy and embryology of congenital intrinsic obstruction of the duodenum". Am J Surg. 114 (2): 190–202. PMID 6028984.
- ↑ Freeman, SB; Torfs, CP; Romitti, PA; Royle, MH; Druschel, C; Hobbs, CA; Sherman, SL (2009). "Congenital gastrointestinal defects in Down syndrome: a report from the Atlanta and National Down Syndrome Projects". Clinical Genetics. 75 (2): 180–184. doi:10.1111/j.1399-0004.2008.01110.x. ISSN 0009-9163.
- ↑ Morris, Grant; Kennedy, Alfred; Cochran, William (2016). "Small Bowel Congenital Anomalies: a Review and Update". Current Gastroenterology Reports. 18 (4). doi:10.1007/s11894-016-0490-4. ISSN 1522-8037.