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INTRODUCTION

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Nausea is the subjective feeling of a need to vomit. Vomiting (emesis) is the oral expulsion of gastrointestinal contents due to contractions of gut and thoracoabdominal wall musculature. Vomiting is contrasted with regurgitation, the effortless passage of gastric contents into the mouth. Rumination is the repeated regurgitation of food residue, which may be rechewed and reswallowed. In contrast to emesis, these phenomena may exhibit volitional control. Indigestion is a term encompassing a range of complaints including nausea, vomiting, heartburn, regurgitation, and dyspepsia (the presence of symptoms thought to originate in the gastroduodenal region). Some individuals with dyspepsia report predominantly epigastric burning, gnawing, or pain. Others experience postprandial fullness, early satiety (an inability to complete a meal due to premature fullness), bloating, eructation (belching), and anorexia.

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NAUSEA AND VOMITING

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MECHANISMS

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Vomiting is coordinated by the brainstem and is effected by responses in the gut, pharynx, and somatic musculature. Mechanisms underlying nausea are poorly understood but likely involve the cerebral cortex, as nausea requires conscious perception. This is supported by functional brain imaging studies showing activation of a range of cerebral cortical regions during nausea.

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Coordination of Emesis
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Brainstem nuclei—including the nucleus tractus solitarius; dorsal vagal and phrenic nuclei; medullary nuclei regulating respiration; and nuclei that control pharyngeal, facial, and tongue movements—coordinate initiation of emesis. Neurokinin NK1, serotonin 5-HT3, and vasopressin pathways participate in this coordination.

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Somatic and visceral muscles respond stereotypically during emesis. Inspiratory thoracic and abdominal wall muscles contract, producing high intrathoracic and intraabdominal pressures that evacuate the stomach. The gastric cardia herniates above the diaphragm, and the larynx moves upward to propel the vomitus. Distally migrating gut contractions are normally regulated by an electrical phenomenon, the slow wave, which cycles at 3 cycles/min in the stomach and 11 cycles/min in the duodenum. During emesis, the slow wave is abolished and is replaced by orally propagating spikes that evoke retrograde contractions that assist in expulsion of gut contents.

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Activators of Emesis
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Emetic stimuli act at several sites. Emesis evoked by unpleasant thoughts or smells originates in the brain, whereas cranial nerves mediate vomiting after gag reflex activation. Motion sickness and inner ear disorders act on the labyrinthine system. Gastric irritants and cytotoxic agents like cisplatin stimulate gastroduodenal vagal afferent nerves. Nongastric afferents are activated by intestinal and colonic obstruction and mesenteric ischemia. The area postrema, in the medulla, responds to bloodborne stimuli (emetogenic drugs, bacterial toxins, uremia, hypoxia, ketoacidosis) and is termed the chemoreceptor trigger zone.

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Neurotransmitters mediating vomiting are selective for different sites. Labyrinthine disorders stimulate vestibular muscarinic M1 and histaminergic H1 receptors. Vagal afferent stimuli activate serotonin 5-HT3 receptors. The area postrema is served by nerves acting on 5-HT3, M1, H1, and dopamine D2...

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