16 The Prescription Drug Abuse Epidemic on GI motility (Kumar, Barker, & Emmanuel, 2014). If the response is insuf- ficient after several classes of medications are used in combination, mu-opioid receptor antagonists may be employed, including methylnaltrexone, alvimo- pan, and naloxegol (Chey et al., 2014 Ford, Brenner, & Schoenfeld, 2013). These agents are specially formulated to not cross the blood-brain barrier, leading to peripheral opioid receptor antagonism without attenuating pain control. In addition to constipation, opioids may also produce nausea and emesis by way of decreased gastric motility, stimulation of the chemoreceptor trig- ger zone, and enhanced vestibular sensitivity. Approximately 25 percent of patients treated with opioids will experience nausea and vomiting (Swegle & Logemann, 2006). Treatment for opioid-related nausea include antihista- mines (e.g., diphenhydramine, hydroxyzine, promethazine) serotonin antagonists (e.g., ondansetron) prokinetic agents (e.g., metoclopramide) and antipsychotics (e.g., prochlorperazine). Respiratory Adverse Effects Although commonly discussed, respiratory depression generally does not occur when opioids are used appropriately at standard doses and titrated slowly. However, respiratory depression is the leading cause of opioid over- dose deaths (Rudd et al., 2016). Respiratory depression caused by opioids is multifactorial. Opioids primarily depress the respiratory drive and rhythm generated in the medullary respiratory center (Pattinson, 2008). Addition- ally, opioids bind to opioid receptors in the pulmonary system, causing dampened respiratory activity, which leads to bradypnea (abnormally slow breathing), decreased volume, and decreased tidal exchange. Ventilatory response to carbon dioxide is decreased, leading to hypercarbia (elevated carbon dioxide levels in the blood) and hypoxemia (low oxygen levels in the blood Lalley, 2008). While rare, respiratory depression may be increased due to several factors (Yaksh & Wallace, 2017). Numerous depressant medications can have additive effects on opioid res- piratory depression. Caution should be used in patients receiving sedatives, anesthetics, alcohol, and other central nervous system (CNS) depressants. Natural sleep can also contribute to respiratory depression due to a dimin- ished sensitivity to carbon dioxide. Older adults are at greater risk due to changes in pulmonary physiology and an increased likelihood of drug inter- actions and comorbid conditions. Comorbid lung diseases, such as COPD, asthma, and sleep apnea, can contribute due to decreased hypoxic drive (Pat- tinson, 2008). Treatment requires opioid dose reduction, with severe respira- tory depression requiring immediate administration of the opioid antagonist naloxone to reverse a potentially fatal overdose (see chapter 13 for more on naloxone and other harm-reduction approaches to opioid misuse).
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