Endocardial cushion defect pathophysiology: Difference between revisions

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* AV canal connects the atria to the ventricles.<ref name="pmid3343065">{{cite journal |vauthors=Wenink AC, Zevallos JC |title=Developmental aspects of atrioventricular septal defects |journal=Int. J. Cardiol. |volume=18 |issue=1 |pages=65–78 |date=January 1988 |pmid=3343065 |doi=10.1016/0167-5273(88)90031-9 |url=}}</ref>
* AV canal connects the atria to the ventricles.<ref name="pmid3343065">{{cite journal |vauthors=Wenink AC, Zevallos JC |title=Developmental aspects of atrioventricular septal defects |journal=Int. J. Cardiol. |volume=18 |issue=1 |pages=65–78 |date=January 1988 |pmid=3343065 |doi=10.1016/0167-5273(88)90031-9 |url=}}</ref>
* At four to five weeks of gestation, the superior and inferior endocardial cushions of the common AV canal fuse  
* At four to five weeks of gestation, the superior and inferior endocardial cushions of the common AV canal fuse.<ref name="pmid13924605">{{cite journal |vauthors=VAN MIEROP LH, ALLEY RD, KAUSEL HW, STRANAHAN A |title=The anatomy and embryology of endocardial cushion defects |journal=J. Thorac. Cardiovasc. Surg. |volume=43 |issue= |pages=71–83 |date=January 1962 |pmid=13924605 |doi= |url=}}</ref>
* Contribute to the formation of the mitral and tricuspid valve and the AV septum
* Results in the formation of the mitral and tricuspid valve and the AV septum.


=== Pathophysiology ===
=== Pathophysiology ===

Revision as of 08:22, 20 April 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti 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

Physiology

  • AV canal connects the atria to the ventricles.[1]
  • At four to five weeks of gestation, the superior and inferior endocardial cushions of the common AV canal fuse.[2]
  • Results in the formation of the mitral and tricuspid valve and the AV septum.

Pathophysiology

Genetics

  • Chromosome 21 has been designated an AV canal critical region.
  • Trisomy 21 have an AV canal defect, usually the complete form

Associated Conditions

Common cardiac conditions associated with endocardial cushion defect include:[4][5]

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

  1. Wenink AC, Zevallos JC (January 1988). "Developmental aspects of atrioventricular septal defects". Int. J. Cardiol. 18 (1): 65–78. doi:10.1016/0167-5273(88)90031-9. PMID 3343065.
  2. VAN MIEROP LH, ALLEY RD, KAUSEL HW, STRANAHAN A (January 1962). "The anatomy and embryology of endocardial cushion defects". J. Thorac. Cardiovasc. Surg. 43: 71–83. PMID 13924605.
  3. Korenberg JR, Bradley C, Disteche CM (February 1992). "Down syndrome: molecular mapping of the congenital heart disease and duodenal stenosis". Am. J. Hum. Genet. 50 (2): 294–302. PMC 1682442. PMID 1531166.
  4. Peoples WM, Moller JH, Edwards JE (1983). "Polysplenia: a review of 146 cases". Pediatr Cardiol. 4 (2): 129–37. doi:10.1007/BF02076338. PMID 6878069.
  5. Karl TR (January 1997). "Atrioventricular septal defect with tetralogy of Fallot or double-outlet right ventricle: surgical considerations". Semin. Thorac. Cardiovasc. Surg. 9 (1): 26–34. PMID 9109222.

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