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Irritable bowel syndrome (IBS): Pathophysiology

Last updated on October 1, 2021

Irritable bowel syndrome (IBS): PathophysiologyIrritable bowel syndrome (IBS) was historically described using the terminology spastic colon, nervous stomach, and colitis, among others. These descriptions are no longer considered accurate or acceptable. IBS is currently defined as lower abdominal pain, disturbed defecation, and bloating in the absence of identifiable or known structural or biochemical abnormalities that might account for symptoms. Although the pathogenesis of irritable bowel syndrome (IBS) is multifactorial and not fully understood, symptoms appear to be caused by abnormal gastrointestinal (GI) motility and enhanced pain sensitivity within the GI tract.

For example, patients with diarrhea-predominant IBS have accelerated transit in the small bowel, whereas those with constipation-predominant IBS have a delay in transit time. Further, irritable bowel syndrome (IBS) patients report pain and awareness at lower levels of pressure and volume than healthy patients do when parts of the gastrointestinal (GI) tract are distended by a balloon. The cause of these abnormalities in motility and pain sensitivity within the GI tract is currently under investigation.

Normal gastrointestinal (GI) function involves integration of the enteric nervous system (ENS), central nervous system (CNS), and peripheral, sensory, motor, and autonomic nerves. The connection between these systems, referred to as the brain-gut axis, is a mechanism by which the CNS receives input and sends feedback to regulate and alter GI function. Many neurotransmitters are involved in this regulation, including, but not limited to, substance P, the opioid enkephalins, calcitonin-gene-related polypeptide (CGRP), nitric oxide, cholecystokinin, and 5-hydroxytryptamine (5-HT). Over 95% of 5-HT (i.e., serotonin) in the body is located within the gastrointestinal tract, where its actions as a neurotransmitter and signaling molecule are critical to intestinal motility and pain sensitivity.

Dysregulating 5-HT may result in nausea, vomiting, and abnormal motor or secretory intestinal actions. Recently, the discovery of several subtypes of 5-HT receptors has improved the level of understanding of GI physiology. The 5-HT3 receptor subtype is believed to modulate GI motility and perception of pain. Another subtype, 5-HT4, is also involved in gastrointestinal (GI) motility as well as stimulation of release of other neurotransmitters. The latest research suggests that defects in the coordination of activity by the brain-gut axis, possibly caused by abnormalities in neurotransmitters such as 5-HT, may result in the irregular GI motility and enhanced pain sensitivity observed in irritable bowel syndrome (IBS) patients. As a result, newer therapies for IBS are focusing on neurotransmitter activity.

Irritable bowel syndrome (IBS): PathophysiologyIt is believed that the physiologic irregularities in irritable bowel syndrome (IBS) patients are modified by psychosocial influences. A biopsychosocial model was introduced, which represents the concept that although psychosocial symptoms are not essential for the diagnosis of IBS, they may influence the experience and management of the disorder. In fact, the reactivity of the intestines in IBS patients is modifiable by emotional state, and patients who poorly manage stress typically have a higher perception of symptoms, decreased coping skills, and a poor clinical outcome.

In addition to the etiology of irritable bowel syndrome (IBS) previously discussed, it appears that prior infection, antibiotic use, or food sensitivity may be associated with development of the disorder. Up to 33% of patients with diarrhea-predominant IBS have a positive history of gastrointestinal infection. The inflammation induced by the infection may alter nerve endings in the gastrointestinal (GI) tract and affect the brain-gut axis and 5-HT activity.

Originally posted 2010-02-21 01:50:36. Republished by Blog Post Promoter

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