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Nausea and vomiting accompany a variety of illnesses. Symptoms may be the direct result of primary GI disorders such as bowel obstruction or gastroenteritis. However, it may also represent pathology of the central nervous system (CNS) (increased intracranial pressure, tumor), psychiatric conditions (bulimia nervosa, anxiety), endocrine or metabolic abnormalities (diabetic ketoacidosis, hyponatremia), or iatrogenic causes (medications, toxins). Also, acute symptoms may be the result of severe pain, myocardial infarction, sepsis, or other systemic illnesses. A comprehensive history and physical examination, as well as the use of various diagnostic modalities, are needed to determine the cause and its complications.

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In the U.S., the most common cause of acute nausea and vomiting is viral gastroenteritis. Drug side effects are among the most common causes of nausea and vomiting in adults, but this cause is difficult to diagnose.1 In young women, pregnancy is an important consideration, with the incidence of nausea and vomiting of pregnancy occurring in 70% to 80% of pregnancies.2

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Vomiting is a complex physiologic process that is coordinated at the level of the medulla oblongata. Multiple neurons in this area are activated in a sequential fashion to induce vomiting. A major site involved in activation of the vomiting center is the chemoreceptor trigger zone, located in the area postrema of the fourth ventricle. Chemoreceptors in this area are outside the blood–brain barrier and stimulated by circulating medications and toxins, including dopaminergic antagonists (levodopa, bromocriptine), nicotine, digoxin, and opiate analgesics. Another important peripheral pathway for emesis is mediated through vagal afferents. Vagal activation is triggered by direct gastric mucosal irritants (such as NSAIDs) or increased luminal distention (gastric outlet obstruction, gastroparesis). Vagus activation stimulates neurons in the area postrema and nucleus tractus solitarius. These areas are rich in serotonin receptors and are a major site of action of antiemetic drugs, such as granisetron and odansetron.3 Similar receptors are found throughout the GI tract, as well as the cortex and limbic system, vestibular system, heart, and genitalia. The anatomic locations and receptor-mediated triggering factors in emesis are shown in Table 75-1.

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Table 75-1 Anatomic Locations of Receptor-Mediated Triggering Factors in Emesis
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