Anal fistula pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Manpreet Kaur, MD [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

Anatomy

  • The anal canal is a 2 to 4cm in length, starts at the anorectal junction to the end of anal verge.[1]
  • It is divided into an upper and a lower part by transition zone that is seen at the dentate line or pectinate line which is surrounded by longitudinal mucosal folds, called columns of Morgagni.[1]
  • Each of this fold contains anal crypts, each of which contains 3 to 12 anal glands, the distribution of these glands is not uniform with most of the glands present anterior to the position of the anal canal and fewer in the posterior position.[1]

Pathogenesis

  • Anal fistula develops from infection of anal crypts.

There are following steps in the formation of anal fistula:

  • The initial infection occurs in the ducts of the anal glands and the spread of infection results in the formation of the abscess, various theories were put forward to describe the pathogenesis and the most accepted one is the cryptoglandular theory.[2]
  • The crytoglandular theory states that obstruction of anal gland duct results in a infection and due to the presence of these glands deep in relation to the anal canal and sphincter, the infection follows the path of least resistance resulting in abscess formation at the termination of the gland.[3][4]

When the abscess is opened or when it ruptures, a fistula is formed. An anal fistula can have multiple accessory tracts complicating its anatomy

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

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. 1.0 1.1 1.2 "Anatomy and Embryology - Springer".
  2. Rickard MJ (2005). "Anal abscesses and fistulas". ANZ J Surg. 75 (1–2): 64–72. doi:10.1111/j.1445-2197.2005.03280.x. PMID 15740520.
  3. PARKS AG (1961). "Pathogenesis and treatment of fistuila-in-ano". Br Med J. 1 (5224): 463–9. PMC 1953161. PMID 13732880.
  4. Coremans G, Dockx S, Wyndaele J, Hendrickx A (2003). "Do anal fistulas in Crohn's disease behave differently and defy Goodsall's rule more frequently than fistulas that are cryptoglandular in origin?". Am J Gastroenterol. 98 (12): 2732–5. doi:10.1111/j.1572-0241.2003.08716.x. PMID 14687825.

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