Refers to dyspepsia that occurs in the absence of a clinically identifiable structural lesion.
Refers to a constellation of symptoms referable to the gastrointestinal area of the upper G.I. tract.
Upper gastrointestinal tract symptoms accounts for 5% of all primary care visits.
Dyspepsia symptoms affect up to 40% of the adult population.
A relapsing and remitting process.
Rome III criteria for diagnosis consists of sensation of pain or burning in the epigastric area, early satiety, fullness during or after meal, or a combination of these symptoms.
Disturbances in gastrointestinal function are believed to be causal in the development of symptoms.
Disturbances in gastrointestinal motility and sensory function play key roles in symptoms.
Pathophysiologic factors include changes in gastric motility, visceral hypersensitivity, genetic susceptibility, psychosocial factors and H pylori infection.
Symptoms must be chronic and occur at least weekly over a period of at least six months in the absence of an organic explanation.
Divided into two syndromes: the epigastric pain syndrome and the postprandial distress syndrome.
Epigastric pain syndrome consists of intermittent abdominal pain or burning in the epigastric area that occurs at least once per week.
The postprandial distress syndrome is characterized by occurrence at least several times a week of bothersome postprandial fullness occurring after normal sized meals or by early satiety preventing the person from finishing a regular meal.
Global prevalence is between five and 11%.
Approximately 80% of patients with epigastric pain have a normal endoscopic examination.
Approximately 80% of persons with D report this symptoms are aggravated by the ingestion of a meal.
Gastrointestinal endoscopy can identify most causes of dyspepsia and shows that less than 10% of patients have a peptic ulcer, less than 1% have a gastroesophageal cancer and more than 70% have functional dyspepsia.
Upper gastrointestinal endoscopy has a low rate of identification of organic disease and is not desirable nor realistic to perform this type of testing in all patients with dyspepsia.
Upper G.I. endoscopy is a reasonable first line strategy if there is considerable concern about the presidency of H. Pylori.
Celiac disease is not significantly increased among persons reporting dyspepsia
Medications are usually not implicated in causing dyspepsia.
Functional dyspepsia and gastroparesis have symptoms which frequently overlap and are hard to distinguish.
FD can be confused with G.I. manifestations outside the gastroduodenal region including other functional disorders.
Mechanisms include antral hypomotility, impaired stomach accommodation, disordered gastric electrical activity, and visceral hypersensitivity.
Associated with anxiety, depression and neuroses.
Symptoms are not able to reliably distinguish between organic disease and functional forms of dyspepsia.
Negatively affects attendance and productivity.
Costs associated in 2009 in excess of $18 billion.
Treatment is unsatisfactory with present agents such as histamine H2 receptor antagonists, proton pump inhibitors, antacids or the eradication of H. pylori organisms.
Cisapride demonstrated superiority to placebo in these patients but is no longer available in the U.S.
Itopride improves pain and fullness symptoms exerting prokinetic effects by way of antidopaminergic and antiacetylcholinesterase actions.
Acid suppression with PPI therapy has moderate efficacy, and this may be secondary to the treatment of atypical gastroesophageal reflux disease.
H pylori eradication provide significant benefits in patients with functional dyspepsia(HEROES Trial).