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Functional gastroduodenal disorders / Functional dyspepsia
Functional dyspepsia
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Gastroduodenal visceral hypersensitivity (of both the proximal and distal stomach) to acid or mechanical distention. Hypersensitivity to gastric distension, present in 34% of patients with FD, is associated with postprandial pain, belching, and weight loss(8). Basal gastric acid secretion is within normal limits in patients with FD, but acid-related symptoms (perhaps due to gastric or duodenal hypersensitivity) may arise in a subgroup of patients(1). |
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Postprandial motor disturbances (accelerated gastric emptying, antral-fundic incoordination or proximal-distal gastric dystony, and abnormal phasic contractions). Several studies have documented the presence of gastric dysrhythmias especially in the postprandial period in patients with FD(1). - Fundus: Postprandial impaired relaxation, with unsuppressed phasic contractility. It is present in a small subset of patients with functional dyspepsia, and clinically associated with relevant and severe bloating and H. pylori infection but also with the absence of nausea(9) - Antrum: Postprandial antral hypomotility(10), with overdistention. |
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Decreased fundic accommodation. Tack and colleagues(11) have identified decreased volume response of the gastric fundus after a meal in up to 40% of patients with functional dyspepsia. This impaired accommodation was associated with early satiety and weight loss, but was not related to delayed gastric emptying, presence of H. pylori , or hypersensitivity to gastric distension. |
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Delayed gastric emptying of solids and liquids. Recent studies have shown that less than 25% of patients with FD have delayed gastric emptying. "Gastric emptying was definitely delayed (t1/2 > 192 min) in 24% of patients with functional dyspepsia"(12), . In a trial performed by Sarnelli et al, delayed gastric emptying of solids was constantly associated with postprandial fullness and with vomiting, whereas postprandial fullness and severe early satiety are associated with delayed liquid emptying(13). Moreover, Piessevaux et al found in another study that there is an association between abnormal intragastric distribution patterns and symptomatic profiles, which might be related to different pathophysiological mechanisms. Early satiety was associated with early distal redistribution of the liquid phase and fullness was associated with late proximal retention(14). |
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Alterations of neurohormonal mechanisms in response to a meal8. |
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Previous acute gastroenteritis. About 10% of subjects having an Salmonella's acute gastroenteritis will have a FD.(15) |
Psychological and psychosocial factors undoubtedly contribute to the clinical course of FD . Abnormalities of several psychosocial dimensions were found to be associated with epigastric pain and with hypersensitivity to gastric distension in FD(1,6) And it has been established an association of FD with anxiety and depression(7). Psychological factors may be responsible for visceral sensation-processing disturbances via the central and enteric nervous systems, playing a role in the etiology of FD.
A different approach was based on attempts to identify pathophysiology-based subgroups. Thus, associations were shown between symptomatic patterns and delayed gastric emptying, impaired fundic accommodation, and visceral hypersensitivity.
Although particular mechanisms are differentially associated with particular symptoms, these associations are not consistent.]
The underlying physiopathological mechanisms associated with FD are unclear, although traditionally, delayed gastric emptying, visceral hypersensitivity to acid or mechanical distention, and impaired gastric accommodation have been implicated as putative physiologic disturbances, and more than one mechanism may be operational in a particular individual. So, several different mechanisms may contribute to the pathophysiology of FD, including(8):
