Duodenal atresia pathophysiology: Difference between revisions

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{{Duodenal atresia}}
{{Duodenal atresia}}


{{CMG}}; {{AE}}  
{{CMG}}; {{AE}} {{HQ}}
==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
It is thought that duodenal atresia is the result of failure of [[Nervous system|neural]] cell migration during the 8th to 10th week of [[Duodenum|duodenal]] re-canalization. It is associated with [[down syndrome]], [[Vertebra|vertebral]] defects, [[Anus|anal]] anomalies, [[esophageal atresia]], [[annular pancreas]], [[Intestinal malrotation|malrotation]], [[Kidney|renal]] abnormalities, [[cardiac]] causes, and mandibulofacial anomalies.  


OR
==Pathophysiology==


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].
===Pathogenesis===
 
*[[Duodenum]] starts developing during the 6th and 7th week of [[gestation]].<ref name="pmid10436237">{{cite journal| author=Ando H, Kaneko K, Ito F, Seo T, Harada T, Watanabe Y| title=Embryogenesis of pancreaticobiliary maljunction inferred from development of duodenal atresia. | journal=J Hepatobiliary Pancreat Surg | year= 1999 | volume= 6 | issue= 1 | pages= 50-4 | pmid=10436237 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10436237  }} </ref><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>
OR
**Re-canalization occurs during the 8th to 10th week of [[gestation]].
 
*It is thought that duodenal atresia is the result of failure of re-canalization of the [[duodenum]] in 8 to 10 weeks of [[Fetus|fetal]] development.
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
**This is due to failure of [[Neural crest|neural]] cell migration
 
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==
[[File:Duodenum anatomy.jpg|thumb|none|372x372px|Duodenum Anatomy.[https://www.wikidoc.org/images/0/0b/Duodenum_anatomy.jpg Source: Libre Pathology]]]


===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==
==Genetics==
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
*Duodenal atresia is not transmitted [[Genetics|genetically]].
*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==
==Associated Conditions==
Duodenal atresia is commonly associated with the following:<ref name="FreemanTorfs2009">{{cite journal|last1=Freeman|first1=SB|last2=Torfs|first2=CP|last3=Romitti|first3=PA|last4=Royle|first4=MH|last5=Druschel|first5=C|last6=Hobbs|first6=CA|last7=Sherman|first7=SL|title=Congenital gastrointestinal defects in Down syndrome: a report from the Atlanta and National Down Syndrome Projects|journal=Clinical Genetics|volume=75|issue=2|year=2009|pages=180–184|issn=00099163|doi=10.1111/j.1399-0004.2008.01110.x}}</ref><ref name="MorrisKennedy2016">{{cite journal|last1=Morris|first1=Grant|last2=Kennedy|first2=Alfred|last3=Cochran|first3=William|title=Small Bowel Congenital Anomalies: a Review and Update|journal=Current Gastroenterology Reports|volume=18|issue=4|year=2016|issn=1522-8037|doi=10.1007/s11894-016-0490-4}}</ref>


==Gross Pathology==
* [[Down syndrome]] in 25 %to 40% of cases
*On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
* VATER
 
**[[Vertebra|Vertebral]] defects
==Microscopic Pathology==
**[[Anus|Anal]] anomalies
*On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
**[[Esophageal atresia]]
**[[Kidney|Renal]] abnormalities
*[[Intestinal malrotation|Malrotation]]
*[[Annular pancreas]]
*[[Bile duct|Biliary]] tract abnormalities
*[[Heart|Cardiac]] anomalies
*Mandibulofacial anomalies


==References==
==References==
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[[Category:Up-To-Date]]

Latest revision as of 15:55, 2 January 2018

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hamid Qazi, MD, BSc [2]

Overview

It is thought that duodenal atresia is the result of failure of neural cell migration during the 8th to 10th week of duodenal re-canalization. It is associated with down syndrome, vertebral defects, anal anomalies, esophageal atresia, annular pancreas, malrotation, renal abnormalities, cardiac causes, and mandibulofacial anomalies.

Pathophysiology

Pathogenesis

  • Duodenum starts developing during the 6th and 7th week of gestation.[1][2]
    • Re-canalization occurs during the 8th to 10th week of gestation.
  • 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.
    • This is due to failure of neural cell migration
Duodenum Anatomy.Source: Libre Pathology


Genetics

Associated Conditions

Duodenal atresia is commonly associated with the following:[3][4]

References

  1. Ando H, Kaneko K, Ito F, Seo T, Harada T, Watanabe Y (1999). "Embryogenesis of pancreaticobiliary maljunction inferred from development of duodenal atresia". J Hepatobiliary Pancreat Surg. 6 (1): 50–4. PMID 10436237.
  2. 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.
  3. 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.
  4. 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.

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