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Functional dyspepsia (FD) is a common gastrointestinal disorder defined by symptoms emanating from the gastroduodenal region in the absence of an underlying organic disease that may easily explain the symptoms. Characteristic symptoms include epigastric burning, epigastric pain, postprandial fullness, and early satiety. FD was formerly known as non-ulcer dyspepsia, as opposed to "organic dyspepsia" with underlying conditions of gastritis, peptic ulcer disease, or cancer. The exact cause of functional dyspepsia is unknown however there has been many theories regarding the mechanisms. Risk factors for developing functional dyspepsia include female sex, smoking, non-steroidal anti-inflammatory medication use, and H pylori infection. Gastrointestinal infections can trigger the onset of functional dyspepsia. Theories behind the pathophysiology of functional dyspepsia include gastroduodenal motility, gastroduodenal sensitivity, intestinal microbiota, immune dysfunction, gut-brain axis dysfunction, abnormalities of gastric electrical rhythm, and autonomic nervous system/central nervous system dysregulation. Functional dyspepsia is diagnosed based off clinical criteria and symptoms. Depending on the symptoms present patients may need blood work, imaging, or endoscopies to confirm the diagnosis of functional dyspepsia. Functional dyspepsia is further classified into two subtypes, postprandial distress syndrome (PDS) and epigastric pain syndrome (EPS). Functional dyspepsia can be managed with medications such as prokinetic agents, fundus-relaxing drugs, centrally acting neuromodulators, and proton pump inhibitors. Up to 15-20% of patients with functional dyspepsia experience persistent symptoms. Functional dyspepsia is more common in women than men. In Western nations the prevalence is believed to be 10-40% and 5-30% in Asian nations. Signs and symptoms Symptoms of functional dyspepsia include epigastric burning, epigastric pain, postprandial fullness (often described as bloating by patients), and early satiety. Food consumption frequently makes dyspeptic symptoms worse. Although functional dyspepsia is typically chronic, the symptoms are generally sporadic, even during periods of severe symptoms. Patients 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. While nausea and heartburn are still possible co-occurring symptoms, they are no longer regarded as major dyspeptic symptoms and may originate from different processes. When certain symptoms occur, such as vomiting, a coexisting or alternative condition, like gastroparesis, needs to be evaluated. Causes Functional dyspepsia has a wide range of complex etiologies. Gastric motor function abnormalities have long been linked to functional dyspepsia. However, a study revealed that there was no relationship between symptoms and stomach physiological abnormalities. The symptoms are significantly modulated by meal consumption, and genetic factors may also play a part. Risk factors 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. On the other hand, the Kyoto consensus indicates that H pylori infection is an organic cause of dyspepsia, sometimes known as H pylori-associated dyspepsia. However, this phrase is controversial because the general consensus also indicates that the patient should be diagnosed with functional dyspepsia if symptoms continue or return following successful elimination. In one long-term investigation, a high body mass index was an independent predictor of the emergence of functional dyspepsia. 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. 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. According to two Australian longitudinal investigations, there are reciprocal effects between the stomach and the brain. Specifically, people who had functional dyspepsia at baseline were more likely than those who did not experience anxiety or depression during follow-up. Triggers Acute gastroenteritis can lead to the development of post-infection functional dyspepsia. According to a meta-analysis of 19 papers, exposed people had nearly three times the chance of developing functional dyspepsia over the course of more than six months following an infection compared to non-exposed people. Mechanism Because functional dyspepsia symptoms are complicated and heterogeneous, the underlying pathophysiology of the disorder is still unknown despite a great deal of research. The causes of dyspeptic symptoms have been attributed to a number of pathophysiologic processes. These include gastroduodenal motility, gastroduodenal sensitivity, intestinal microbiota, immune dysfunction, gut-brain axis dysfunction, abnormalities of gastric electrical rhythm, and autonomic nervous system/central nervous system dysregulation. Gastroduodenal motility Patients with functional dyspepsia frequently have sensorimotor abnormalities of the gastroduodenum, including altered motility and pathological reactions to mechanical and chemical stimuli. One of the main pathophysiologic mechanisms thought to underlie the symptoms of functional dyspepsia is delayed stomach emptying. Several studies have looked into the connection between the pattern and intensity of symptoms and delayed stomach emptying. The proportion of dyspeptic individuals with delayed stomach emptying varies from 20% to 50%, depending on the study. In response to gastric balloon distension during fasting and following meal intake, patients with functional dyspepsia demonstrate impaired proximal stomach accommodation. Due to the poor accommodation, there is a disproportional volume distribution, with the fundus volume being less and the antral volume being bigger than usual. Furthermore, individuals suffering from functional dyspepsia exhibit compromised fundus accommodation in reaction to duodenal distension. Gastroduodenal sensitivity In functional dyspepsia, the stomach's sensitivity to chemical and mechanical stimuli is changed. After fasting and meal consumption, patients with functional dyspepsia exhibit visceral hypersensitivity following gastric fundus distension. Following stomach distension, even patients with normal accommodation experience discomfort. Additionally, some individuals exhibit hypersensitivity to distension of the duodenum, jejunum, or rectal cavity, indicating a more widespread sensitization of the central and autonomic nervous systems. In.... Discover the Alan J Talley popular books. Find the top 100 most popular Alan J Talley books.