Risk factors for developing functional dyspepsia include female sex, smoking, non-steroidal anti-inflammatory medication use, and H pylori infection.
Depending on the symptoms present people suspected of having FD may need blood work, imaging, or endoscopies to confirm the diagnosis of functional dyspepsia.
Functional dyspepsia can be managed with medications such as prokinetic agents, fundus-relaxing drugs, centrally acting neuromodulators, and proton pump inhibitors.
[6] Those with FD typically refer to early satiety as a vague abundance of gas after eating or discomfort, but in reality, what they truly mean is that they find it difficult to finish a normal-sized meal because they are uncomfortable or feel full.
[12] Several epidemiological studies have demonstrated a moderate correlation between dyspepsia in the general population and female sex, smoking, non-steroidal anti-inflammatory medication use, and H pylori infection.
[14] Since the brain and gut communicate through the hypothalamic-pituitary-adrenal axis and the enteric nerve system, psychological comorbidity plays a significant influence in the development of functional dyspepsia.
[15] Anxious participants had an eight-fold increased risk of developing functional dyspepsia compared to those without anxiety in a population-based survey conducted in Sweden.
[5][12][15] Patients with functional dyspepsia frequently have sensorimotor abnormalities of the gastroduodenum, including altered motility and pathological reactions to mechanical and chemical stimuli.
[22][23] In response to gastric balloon distension during fasting and following meal intake, patients with functional dyspepsia demonstrate impaired proximal stomach accommodation.
[29] Additionally, some individuals exhibit hypersensitivity to distension of the duodenum,[30] jejunum,[29] or rectal cavity,[31] indicating a more widespread sensitization of the central and autonomic nervous systems.
[33] On the other hand, a decrease in primary bile acid levels may have an impact on the small intestine's microbial diversity, which may promote the proliferation of proinflammatory bacteria and low-grade inflammation, both of which may result in the breakdown of the epithelial barrier.
Through the hypothalamic-pituitary-adrenal axis, changes in epithelial barrier function brought on by immune system and gastrointestinal microbiota disruptions can control gut-brain connections.
[41] This impact has been demonstrated in controlled trials including healthy volunteers under stress as well as in animal models of functional dyspepsia.
[44][45] Additionally, there is proof that up to two thirds of patients with functional dyspepsia have anomalies in the underlying stomach myoelectrical activity, as determined by cutaneous electrogastrography.
Alarm symptoms include dysphagia, especially if progressive, or odynophagia, overt gastrointestinal bleeding, such as melena or hematemesis, persistent vomiting, unintentional weight loss, family history of gastric or esophageal cancer, palpable abdominal or epigastric mass or abdominal adenopathy, and signs of iron-deficiency anemia.
[55] There is no validated diagnostic algorithm, and current guidelines and the Rome committee oppose routine laboratory testing in all patients.
Liver function tests are needed if there is concern regarding a potential hepatobiliary cause of severe episodic epigastric discomfort.
[58] The most recent guidelines for managing dyspepsia prohibit endoscopic use in patients under 60 years of age because its low yield, even in cases where alarm symptoms are present.
[59][60] Because of the low yield, routinely requesting an abdominal ultrasound or CT scan in the absence of alarm symptoms or signs is not advised.
[15] For individuals with functional dyspepsia who are infected, H. pylori eradication treatment is recommended in all guidelines because it can potentially alleviate symptoms and reduce the risk of developing stomach cancer and peptic ulcers.
It makes sense to advise patients to eat smaller, more frequent meals and to steer clear of foods that worsen their symptoms.
[67][68] Prokinetic medications are effective in treating functional dyspepsia by stimulating the contractions of the stomach's smooth muscle and have been suggested as initial treatments for PDS.
Its reasoning stems from the common occurrence of psychiatric comorbidity and the theory that visceral hypersensitivity may react to centrally active neuromodulators and play a role in the development of symptoms.
[12] When administered at a modest dosage in the evening, the antidepressant mirtazapine has demonstrated effectiveness in treating early satiety and nausea in individuals with functional dyspepsia who have lost weight and do not exhibit clinically significant co-occurring depression or anxiety.