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Clinical Pharmacology for Prescribing$
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Stevan R. Emmett, Nicola Hill, and Federico Dajas-Bailador

Print publication date: 2019

Print ISBN-13: 9780199694938

Published to Oxford Scholarship Online: November 2020

DOI: 10.1093/oso/9780199694938.001.0001

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PRINTED FROM OXFORD SCHOLARSHIP ONLINE (oxford.universitypressscholarship.com). (c) Copyright Oxford University Press, 2021. All Rights Reserved. An individual user may print out a PDF of a single chapter of a monograph in OSO for personal use. date: 03 March 2021



Chapter 6 Gastroenterology
Clinical Pharmacology for Prescribing

Stevan R. Emmett

Nicola Hill

Federico Dajas-Bailador

Oxford University Press

Nausea and vomiting can be defined, respectively, as the urge to or the actual act of expelling undigested food from the stomach. It is thought to be an evolutionary defence mechanism to protect against toxic insult (drugs or mi­crobes) and over- eating, while it can also be triggered during pregnancy, or by unpleasant sights or smells. In some instances, it may be the symptom of a more severe underlying pathology. Severity of nausea and vomiting varies considerably between individuals exposed to the same stimulus and symptoms can be highly detrimental to patient quality of life affecting not only their nutritional intake, but also mood and well- being. Although nausea itself is a subjective term, vomiting is a pathophysiological reflex triggered by the vomiting centre located in the medulla. The vomiting centre re­ceives signals from a number of afferent inputs, i.e. the chemoreceptor trigger zone (CTZ), vestibular nucleus, ab­dominal and cardiac vagal afferents, and cerebral cortex (Table 6.1). It may also be activated by hormonal triggers, which accounts for hyperemesis in pregnancy, and the increased incidence of nausea and vomiting associated with the female gender. As the vomiting centre is located close to centres responsible for salivation and breathing, vomiting is often associated with hypersalivation and hyperventilation. The CTZ is highly vascularized and lo­cated at the floor of the fourth ventricle, just outside the blood– brain barrier and, therefore, is itself directly sensi­tive to chemical stimuli. Afferent inputs activate the vomiting centre through several known neurotransmitter pathways; dopamine (D<sub>2</sub>), serotonin (5- HT<sub>3</sub>, 5- HT<sub>4</sub>), acetylcholine (ACh), and substance P (neurokinin 1; NK<sub>1</sub>). Each of which provides a potential pharmacological target in the management of nausea and vomiting, once the cause has been established. Efferent pathways from the vomiting centre induce autonomic changes, including vasoconstriction, pallor, tachycardia, salivation, sweating, and relaxation of the lower oesophagus and fundus of the stomach. In vomiting, oesophageal relaxation leads to contraction of the pyloric sphincter, thereby emptying the contents of the jejunum, duodenum, and pyloric stomach into the relaxed fundus. Coordination of muscle contraction occurs within the dia­phragm and abdomen, and retrograde contractions from the intestine then expel the contents of the fundus.

Keywords:   adefovir, balsalazide, calcium carbonate, dantron, ecstasy, granisetron, hepatic impairment

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