Gastroenterology clinics of North America
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Gastroenterol. Clin. North Am. · Jun 2005
ReviewThe role of food intolerance in irritable bowel syndrome.
Irritable bowel syndrome patients frequently believe that food intolerances are to blame for many of their symptoms, although not uncommonly this is caused by the nonspecific increase in gut motility that occurs with food ingestion. Nevertheless, dietary manipulation may result in substantial improvement in IBS symptomatology provided it is individualized to the particular patient. By further understanding the mechanisms involved in dietary intolerance, it should be possible to optimize the benefits of this approach to treatment.
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Gastroenterol. Clin. North Am. · Jun 2005
ReviewBrain responses to visceral and somatic stimuli in irritable bowel syndrome: a central nervous system disorder?
In healthy subjects, the brain regions most consistently activated in visceral and somatic pain are the key regions in the central pain matrix,including the mid/anterior insula, subregions of the ACC, PFC, thalamus,and in some cases, pontine regions such as the dorsal pons and PAG. Functional neuroimaging studies have demonstrated evidence of altered regional brain activation responses during visceral and somatic stimuli in IBS that have been associated with perceptual differences. Although perceptual studies have shown increased sensitivity to rectosigmoid distension in IBS, most somatic pain studies have demonstrated normal or decreased sensitivity compared with controls; however, a recent study showed increased sensitivity to thermal heat. ⋯ With regard to differences in cortical processing of visceral versus somatic stimuli in IBS, there have been only two studies. Greater activations of the dorsal ACC, thalamus, and PFC have been shown with visceral stimuli compared with somatic stimuli in IBS. A plausible hypothesis for the observations from brain imaging studies is that IBS patients demonstrate a compromised activation of pain inhibition circuits including those of the cortico-pontine circuit but increased activation of limbic and paralimbic circuits that may be related to pain facilitation.
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Nonvariceal UGI bleeding is one of the most common emergencies that gastroenterologists encounter, and continues to be a significant cause of morbidity and mortality. The keys to management are rapid resuscitation and stabilization; appropriate triage based on pre-endoscopic risk factors; early endoscopy to achieve prompt diagnosis and implement hemostatic therapy to high-risk lesions; and aggressive antisecretory therapy (in the case of peptic ulcer bleeding) to reduce the risk of continued or recurrent bleeding.
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The evaluation of dysphagia begins with a careful history, which usually points to the underlying cause in up to 80% of cases. The goals of the history are to distinguish oropharyngeal causes from esophageal causes of dysphagia and to distinguish mechanical from motor disorders of the esophagus in those patients with esophageal dysphagia. ⋯ Esophageal manometry may be an adjunct to the evaluation of patients with esophageal dysphagia, particularly to confirm specific motor disorders, such as achalasia. The management of functional causes of dysphagia is supportive and empiric given the lack of well-controlled treatment studies in this heterogenous group of patients.
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The differential diagnosis of nausea and vomiting is extensive and the underlying cause can be difficult to diagnose. Treatment of nausea and vomiting also can be unsatisfactory because the available pharmacotherapy does not correct the fundamental underlying pathophysiologic abnormalities. ⋯ The spectrum varies from mild nausea to hyperemesis gravidarum. Various treatment approaches are addressed.