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IBS: Pathophysiology

IBS: PathophysiologyThe pathophysiology of irritable bowel syndrome (IBS) is heterogeneous, involving motor, central nervous system (CNS) and autonomic abnormalities, enhanced visceral sensitivity, and complex psychosocial factors. Patients with IBS may have alterations in gastrointestinal (GI) tract motility in response to both psychological and physical stimuli such as meals, balloon distention, and cholecystokinin, a hormone released from the small-bowel mucosa in response to the ingestion of fats and proteins. Fasting small-bowel motor functions are considerably different from normal in IBS patients.

Abnormalities may be attributed to an impaired gastrocolonic reflex that delays but prolongs activity. Irregularities manifest as decreased spontaneous motor activity, and either spontaneously occurring or exaggerated stress-evoked irregular contractions. Irritable bowel syndrome (IBS) patients have higher than normal colonic resting activity. In stressful situations the differences in colonic motor and myoelectric activity between IBS subjects and normal controls is significant. Gut transit times may be altered in patients with IBS. Patients with diarrhea-predominant disease may have decreased transit times while patients with constipation-predominant disease have increased transit times. However, alterations in transit times do not necessarily correlate with constipation-predominant and diarrhea-predominant variants.

Autonomic function may be implicated in determining which symptoms will be predominant for a given patient. Central nervous system (CNS) modulation of afferent stimuli from the gastrointestinal (GI) tract and subsequent alterations in gastrointestinal motor function are complex processes involving multiple levels of interaction. Patients with diarrhea-predominant irritable bowel syndrome (IBS) have sympathetic adrenergic dysfunction, while constipation-predominant patients have vagal dysfunction.

IBS patients display an enhanced perception of abdominal sensations associated with specific phases of peristalsis as compared with controls. They have greater sensitivity to colon distension even with normal GI motor functions. This may be due to altered nociceptor sensitivity and hyperalgesia stemming from altered afferent conduction or central signal processing. These sensations are frequently reported as tugging or pulling, and may be related to greater sensitivity in gut tension receptors or abnormal gut wall compliance.

About 30% of patients presenting with IBS symptoms have had a recent enteric gastrointestinal (GI) infection. Inflammation of the gut persists, leading to prolonged neuromuscular dysfunction. The likelihood for postinfected patients to present with IBS symptoms is tenfold that of the noninfected patients.

Specific abnormalities or dysfunctions in discrete organs or systems are insufficient to explain symptoms in many patients. Higher cognitive functions, such as thought and emotion also play a role in irritable bowel syndrome (IBS). IBS patients differ psychosocially from IBS “nonpatients” (those with IBS symptoms who have not sought medical attention) and healthy persons. Irritable bowel syndrome (IBS) patients tend to underreport stressful events, express heightened concerns about their health, and require extra reassurance regarding health-related issues. They also have increased colonic motor and electrical activity in response to anger relative to controls. IBS patients also tend to seek health care more often and show less ability to cope with stressful events than do control groups. Compared to nonpatients and healthy people, IBS patients have an increased fear of illness and perceive illness to have a greater impact on daily living. Minnesota Multiphasic Personality Inventory scores for irritable bowel syndrome (IBS) patients are typically high in hypochondria, depression, hysteria, and anxiety disorders, and low in ego strength. IBS nonpatients were not significantly different from healthy patients. For all these reasons, successful management requires managing symptoms and psychosocial influences.

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