Miosis, opioids causing

Miosis Morphine causes constriction of the pupil by a direct action on the parasympathetic nerve. Miosis is pathognomonic of opioid (specifically ju agonist) overdose, but mydriasis occurs with respiratory suppression and asphyxiation. 

Opioids cause miosis (pinpoint pupils) in a dose-dependent manner. Sedation and hearing loss are also coimnon at higher doses of opioids. 

Major gastrointestinal effects include decreased gut motility and changes in secretion of gastric and intestinal fluids. Morphine and most p receptor agonists cause pupillary constriction. Some tolerance to this effect may develop, but addicts with high opioid levels will still have miosis. Respiratory depression is the usual cause of death from opioid overdose. 

The answer is c. (Hardman, p 527. Katzung, p 516.) Naloxone is a pure opioid antagonist at the (1, K, and 5 receptors. j,-receptor stimulation causes analgesia, euphoria, decreased gastrointestinal (Gl) activity, miosis, and respiratory depression. K-receptor stimulation causes analgesia, dysphoria, and psychotomimetic effects. 5-receptor stimulation is not fully understood in humans, but is associated with analgesia and antinociception for thermal stimuli. 

Sedatives, opioids and ethanol cause signs that may include respiratory depression, miosis, hypo-reflexia, coma, hypotension and hypothermia. 

In overdose, methadone causes CNS and respiratory depression, miosis, bradycardia, hypotension, circulatory collapse, hypothermia, coma, seizures, and pulmonary edema (although less frequently than morphine). Treatment for methadone overdose includes supportive measures to maintain adequate respiration and blood pressure, and the administration of the opioid antagonist naloxone to reverse the effects of methadone. If repeated administration of naloxone is required, patients should be monitored for 48 to 72 hours following overdose. Dialysis is not an effective treatment modality, because methadone has a large volume of distribution (Vj = 4 to 5 L/kg) and is highly protein bound (87%). ... 

MIOSIS Morphine and most /i and )Cagonists cause constriction of the pupil by an excitatory action on the parasympathetic nerve innervating the pupd. After toxic doses of jX agonists, the miosis is marked, and pinpoint pupils are pathognomonic however, marked mydriasis occurs if asphyxia intervenes. Some tolerance to the miotic effect develops, but addicts with high circulating levels of opioids continue to have constricted pupils. Therapeutic doses of morphine increase accommodation and lower intraocular pressure in normal and glaucomatous eyes. 

Hydromorphone binds to mu and delta opiod receptors in the central nervous system. It has no effect at the kappa, sigma, or epsilon opioid receptors. Activity at the mu receptors causes analgesia, but also miosis, urinary retention, constipation, hyperthermia, and euphoria. Other side effects such as respiratory depression, pruritus, nausea, vomiting, and development of tolerance are due to binding at both mu and delta receptors. Hydromorphone, unlike other opioids, also has a direct depressant effect on the respiratory brainstem center and the cough center in the medulla. 

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