Chapter 039. Nausea, Vomiting, and Indigestion (Part 1)

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Harrison's Internal Medicine Chapter 39. Nausea, Vomiting, and Indigestion Nausea, Vomiting, and Indigestion: Introduction Nausea is the subjective feeling of a need to vomit. Vomiting (emesis) is the oral expulsion of gastrointestinal contents resulting from 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 stomach contents, which may be rechewed and reswallowed. In contrast to vomiting, these phenomena often exhibit volitional control. Indigestion is a nonspecific term that encompasses a variety of upper abdominal complaints including nausea, vomiting, heartburn, regurgitation, and dyspepsia (the...

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Chapter 039. Nausea, Vomiting, and Indigestion (Part 1) Harrison's Internal Medicine > Chapter 39. Nausea, Vomiting, and Indigestion Nausea, Vomiting, and Indigestion: Introduction Nausea is the subjective feeling of a need to vomit. Vomiting (emesis) is the oral expulsion of gastrointestinal contents resulting from 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 stomach contents, which may be rechewed and reswallowed. In contrast to vomiting, these phenomena often exhibit volitional control. Indigestion is a nonspecific term that encompasses a variety of upper
abdominal 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 discomfort, or pain. Others with dyspepsia experience a constellation of symptoms including postprandial fullness, early satiety (an inability to complete a meal due to premature fullness), bloating, eructation (belching), and anorexia. Nausea and Vomiting Mechanisms Vomiting is coordinated by the brain stem and is effected by neuromuscular responses in the gut, pharynx, and thoracoabdominal wall. The mechanisms underlying nausea are poorly understood but likely involve the cerebral cortex, as nausea requires conscious perception. This is supported by electroencephalographic studies showing activation of temporofrontal cortical regions during nausea. Coordination of Emesis
Several brain stem nuclei—including the nucleus tractus solitarius, dorsal vagal and phrenic nuclei, medullary nuclei that regulate respiration, and nuclei that control pharyngeal, facial, and tongue movements—coordinate the initiation of emesis. Neurotransmitters involved in this coordination are uncertain; however, roles for neurokinin NK1, serotonin 5-HT3, and vasopressin pathways are postulated. Somatic and visceral muscles exhibit stereotypic responses during emesis. Inspiratory thoracic and abdominal wall muscles contract, producing high intrathoracic and intraabdominal pressures that facilitate expulsion of gastric contents. The gastric cardia herniates across the diaphragm and the larynx moves upward to promote oral propulsion of the vomitus. Under normal conditions, distally migrating gut contractions are regulated by an electrical phenomenon, the slow wave, which cycles at 3 cycles/min in the stomach and 11 cycles/min in the duodenum. With emesis, there is slow-wave abolition and initiation of orally propagating spike activity, which evokes retrograde contractions that assist in oral expulsion of intestinal contents. Activators of Emesis
Emetic stimuli act at several sites. Emesis provoked by unpleasant thoughts or smells originates in the cerebral cortex, whereas cranial nerves mediate vomiting after gag reflex activation. Motion sickness and inner ear disorders act on the labyrinthine apparatus, whereas gastric irritants and cytotoxic agents such as cisplatin stimulate gastroduodenal vagal afferent nerves. Nongastric visceral afferents are activated by intestinal and colonic obstruction and mesenteric ischemia. The area postrema, a medullary nucleus, responds to bloodborne emetic stimuli and is termed the chemoreceptor trigger zone. Many emetogenic drugs act on the area postrema, as do bacterial toxins and metabolic factors produced during uremia, hypoxia, and ketoacidosis. Neurotransmitters that mediate induction of vomiting are selective for these anatomic sites. Labyrinthine disorders stimulate vestibular cholinergic muscarinic M1 and histaminergic H1 receptors, whereas gastroduodenal vagal afferent stimuli activate serotonin 5-HT3 receptors. The area postrema is richly served by nerve fibers acting on 5-HT3, M1, H1, and dopamine D2 receptor subtypes. Transmitter mediators in the cerebral cortex are poorly understood, although cortical cannabinoid CB 1 pathways have been characterized. Optimal pharmacologic management of vomiting requires understanding of these pathways.