Irritable bowel syndrome pathophysiology
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Differentiating Irritable bowel syndrome from other Diseases |
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Diagnosis |
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Irritable bowel syndrome pathophysiology On the Web |
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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
- The exact pathogenesis of Irritable Bowel Syndrome (IBS) is not fully understood.
- It is thought that IBS is caused by the interaction of various factors:
- Gastrointestinal motor abnormalities- IBS is referred to as ‘spastic colon’ due to changes in colonic motor function. Manometry recordings in studies from the transverse, descending and sigmoid colon showed that spastic colon led to changed patterns of colonic and small intestinal motor function. Peak amplitude of high-amplitude propagating contractions (HAPCs) in diarrhea-prone IBS patients were found to be higher, compared to healthy subjects. This led to increased responses to ingestion, CRH(Corticotropin releasing hormone), CCK(cholecystokinin) and were associated with abdominal discomfort and accelerated transit through the colon. On the other hand, constipation prone IBS patients showed fewer HAPCs, delayed transit through the colon and decreased motility. One study showed that >90% of HAPCs were associated with abdominal pain.
- CNS dysregulation- IBS is considered as a brain-gut disorder.
- Psychosocial factors- anxiety and depression lead to alteration of the central processing of afferents
- Visceral hypersensitivity- Both central and peripheral mechanisms are implicated.
- Immune activation and mucosal inflammation
- Altered gut microbiota
- Gastrointestinal infections- leads to post inflammatory neuroplastic changes and visceral hypersensitivity
- Abnormal serotonin pathways
- Neuroimmune factors
- Genetic factors- Mutations in SCN5A encode alpha subunit of voltage gated sodium channel NaV1.5
- Bile acid malabsorption- causes alteration of the function of an apical ileal bile acid transporter
Genetics
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].