Toxic megacolon pathophysiology
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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 believed that oxic megacolon is the result of defective smooth muscle contraction, lowered basal pressure in the colonic lumen, and an inhibited gastro-colic reflex is caused by changes in colonic response to vasoactive intestinal polypeptide, substance P, neurotensin, leukotrienes, and nitric oxide.[1][2]
- The progression to toxic megacolon usually is caused by soluble inflammatory mediators, that had downstream inhibitory effects on colonic muscle tone. Nitric oxide is the the most important nonadrenergic, noncholinergic neurotransmitter induces colonic smooth muscle relaxation.[3][4]
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, dilated colon, eroded mucosa, and pseudomembranes are characteristic findings of toxic megacolon.[5][6]
Microscopic Pathology
- On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
References
- ↑ Template:Citejournal
- ↑ Gan, S. Ian; Beck, P. L. (2003). "A new look at toxic megacolon: an update and review of incidence, etiology, pathogenesis, and management". The American Journal of Gastroenterology. 98 (11): 2363–2371. doi:10.1111/j.1572-0241.2003.07696.x. ISSN 0002-9270.
- ↑ Latella G, Vernia P, Viscido A, Frieri G, Cadau G, Cocco A, Cossu A, Tomei E, Caprilli R (2002). "GI distension in severe ulcerative colitis". Am. J. Gastroenterol. 97 (5): 1169–75. doi:10.1111/j.1572-0241.2002.05691.x. PMID 12014723.
- ↑ Boeckxstaens GE, Pelckmans PA, Herman AG, Van Maercke YM (1993). "Involvement of nitric oxide in the inhibitory innervation of the human isolated colon". Gastroenterology. 104 (3): 690–7. PMID 8095033.
- ↑ Kobayasi S, Mendes EF, Rodrigues MA, Franco MF (1992). "Toxic dilatation of the colon in Chagas' disease". Br J Surg. 79 (11): 1202–3. PMID 1467905.
- ↑ Seltman AK (2012). "Surgical Management of Clostridium difficile Colitis". Clin Colon Rectal Surg. 25 (4): 204–9. doi:10.1055/s-0032-1329390. PMC 3577611. PMID 24294121.