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

Harrisons Internal Medicine Chapter 39. Nausea, Vomiting, and IndigestionNausea, Vomiting, and Indigestion: IntroductionNausea 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 upperabdominal complaints including nausea, vomiting, heartburn, regurgitation, and dyspepsia (the...
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Chapter 039. Nausea, Vomiting, and Indigestion (Part 1) Chapter 039. Nausea, Vomiting, and Indigestion (Part 1) Harrisons Internal Medicine > Chapter 39. Nausea, Vomiting, andIndigestion Nausea, Vomiting, and Indigestion: Introduction Nausea is the subjective feeling of a need to vomit. Vomiting (emesis) is theoral expulsion of gastrointestinal contents resulting from contractions of gut andthoracoabdominal wall musculature. Vomiting is contrasted with regurgitation,the effortless passage of gastric contents into the mouth. Rumination is therepeated regurgitation of stomach contents, which may be rechewed andreswallowed. In contrast to vomiting, these phenomena often exhibit volitionalcontrol. Indigestion is a nonspecific term that encompasses a variety of upperabdominal complaints including nausea, vomiting, heartburn, regurgitation, anddyspepsia (the presence of symptoms thought to originate in the gastroduodenalregion). Some individuals with dyspepsia report predominantly epigastric burning,gnawing discomfort, or pain. Others with dyspepsia experience a constellation ofsymptoms including postprandial fullness, early satiety (an inability to complete ameal due to premature fullness), bloating, eructation (belching), and anorexia. Nausea and Vomiting Mechanisms Vomiting is coordinated by the brain stem and is effected by neuromuscularresponses in the gut, pharynx, and thoracoabdominal wall. The mechanismsunderlying nausea are poorly understood but likely involve the cerebral cortex, asnausea requires conscious perception. This is supported byelectroencephalographic studies showing activation of temporofrontal corticalregions during nausea. Coordination of Emesis Several brain stem nuclei—including the nucleus tractus solitarius, dorsalvagal and phrenic nuclei, medullary nuclei that regulate respiration, and nuclei thatcontrol pharyngeal, facial, and tongue movements—coordinate the initiation ofemesis. Neurotransmitters involved in this coordination are uncertain; however,roles for neurokinin NK1, serotonin 5-HT3, and vasopressin pathways arepostulated. Somatic and visceral muscles exhibit stereotypic responses during emesis.Inspiratory thoracic and abdominal wall muscles contract, producing highintrathoracic and intraabdominal pressures that facilitate expulsion of gastriccontents. The gastric cardia herniates across the diaphragm and the larynx movesupward to promote oral propulsion of the vomitus. Under normal conditions,distally migrating gut contractions are regulated by an electrical phenomenon, theslow wave, which cycles at 3 cycles/min in the stomach and 11 cycles/min in theduodenum. With emesis, there is slow-wave abolition and initiation of orallypropagating spike activity, which evokes retrograde contractions that assist in oralexpulsion of intestinal contents. Activators of Emesis Emetic stimuli act at several sites. Emesis provoked by unpleasant thoughtsor smells originates in the cerebral cortex, whereas cranial nerves mediatevomiting after gag reflex activation. Motion sickness and inner ear disorders acton the labyrinthine apparatus, whereas gastric irritants and cytotoxic agents suchas cisplatin stimulate gastroduodenal vagal afferent nerves. Nongastric visceral afferents are activated by intestinal and colonicobstruction and mesenteric ischemia. The area postrema, a medullary nucleus,responds to bloodborne emetic stimuli and is termed the chemoreceptor triggerzone. Many emetogenic drugs act on the area postrema, as do bacterial toxins andmetabolic factors produced during uremia, hypoxia, and ketoacidosis. Neurotransmitters that mediate induction of vomiting are selective for theseanatomic sites. Labyrinthine disorders stimulate vestibular cholinergic muscarinicM1 and histaminergic H1 receptors, whereas gastroduodenal vagal afferent stimuliactivate 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 cortexare poorly understood, although cortical cannabinoid CB 1 pathways have beencharacterized. Optimal pharmacologic management of vomiting requiresunderstanding of these pathways.