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Powdered zinc is used in this way in alkaline batteries and the case which also serves as the anode of zinc—carbon batteries is formed from sheet zinc. Zinc is the primary metal in American one cent coins pennies since In , 33, tonnes 36, short tons of zinc were used to produce Major Concomitant use of morphine with other CNS depressants, such as tricyclic antidepressants TCAs , can potentiate the effects of morphine on respiration, blood pressure, and alertness.
Use may cause profound sedation, hypotension, hypoventilation, or coma. Orthostasis may occur in ambulatory patients. Additive effects such as constipation may also occur. Prior to concurrent use of morphine in patients taking a TCA, assess the level of tolerance to CNS depression that has developed, the duration of use, and the patient's overall response to treatment.
If a TCA is used concurrently with morphine, usually, a reduced initial dosage of morphine is to be considered. For example, for extended-release morphine products, start with the lowest possible dose of morphine i. A reduced dosage of the TCA may also be necessary. Monitor patients for sedation, hypotension, reduced GI motility, and respiratory depression.
In addition, because of the potential risk and severity of serotonin syndrome, caution and careful monitoring are recommended when administering TCAs with other drugs that have serotonergic properties such as morphine. Morphine and the TCA should be discontinued if serotonin syndrome occurs and supportive symptomatic treatment should be initiated. Moderate Concomitant use of morphine with other CNS depressants can potentiate the effects of morphine on respiration, blood pressure, and alertness; examples of other CNS depressants include amoxapine.
Moderate Administration of nitrates such as amyl nitrite to patients receiving other hypotension-producing agents, such as opiate agonists, can cause additive hypotensive or orthostatic effects. Moderate Monitor patients for signs of urinary retention or reduced gastric motility when morphine is used concomitantly with an anticholinergic drug.
Opiates increase the tone and decrease the propulsive contractions of the smooth muscle of the gastrointestinal tract. Prolongation of the gastrointestinal transit time may be the mechanism of the constipating effect. Moderate Apomorphine causes significant somnolence.
Concomitant administration of apomorphine and CNS depressants could result in additive depressant effects. Minor Theoretically, apraclonidine might potentiate the effects of CNS depressant drugs such as opiate agonists.
Although no specific drug interactions were identified with systemic agents and apraclonidine during clinical trials, apraclonidine can cause dizziness and somnolence. Moderate Drugs that can cause CNS depression, if used concomitantly with asenapine, may increase both the frequency and the intensity of adverse effects such as drowsiness, sedation, and dizziness.
Caution should be used when asenapine is given in combination with other centrally-acting medications including opiate agonists. Major Concomitant use of opiate agonists with skeletal muscle relaxants may cause respiratory depression, hypotension, profound sedation, and death. Limit the use of opiate pain medications with skeletal muscle relaxants to only patients for whom alternative treatment options are inadequate.
If morphine is initiated in a patient taking a skeletal muscle relaxant, reduced initial dosages are recommended. For extended-release products, start with the lowest possible dose of morphine i. If a skeletal muscle relaxant is prescribed for a patient taking an opiate agonist, use a lower initial dose of the skeletal muscle relaxant and titrate to clinical response. Moderate The plasma concentrations of morphine may be elevated when administered concurrently with cobicistat.
Clinical monitoring for adverse effects, such as oversedation, respiratory depression, and hypotension, is recommended during coadministration. Cobicistat is a P-glycoprotein P-gp inhibitor, while morphine is a P-gp substrate. Moderate Concomitant use of morphine with other CNS depressants, such as neuromuscular blockers, can potentiate the effects of morphine on respiration, alertness, and blood pressure.
A dose reduction of one or both drugs may be warranted. Severe Morphine use is contraindicated in patients who are receiving or who have received monoamine oxidase inhibitors MAOIs within the previous 14 days. Methylene blue is a reversible inhibitor of MAO. Concomitant use of morphine with other serotonergic drugs such as MAOIs may result in serious adverse effects including serotonin syndrome. MAOIs may cause additive CNS depression, respiratory depression, drowsiness, dizziness, or hypotension when used with opiate agonists such as morphine.
Use caution during coadministration. Reduced GI motility when combined with opiate agonists may increase the risk of serious GI related adverse events. Atropine; Hyoscyamine; Phenobarbital; Scopolamine: Moderate Monitor patients for increased side effects if morphine and azithromycin are coadministered. Morphine concentrations could be increased with coadministration. Morphine is a substrate of P-glycoprotein P-gp and azithromycin is a P-gp inhibitor. Belladonna Alkaloids; Ergotamine; Phenobarbital: Major Concomitant use of morphine with opium can potentiate the effects of morphine on respiration, blood pressure, and alertness.
Moderate Bethanechol facilitates intestinal and bladder function via parasympathomimetic actions. Opiate agonists impair the peristaltic activity of the intestine. Thus, these drugs can antagonize the beneficial actions of bethanechol on GI motility. Bismuth Subcitrate Potassium; Metronidazole; Tetracycline: Moderate Additive constipation may be seen with concurrent use of opiate agonists and antidiarrheals.
Opioids increase the tone and decrease the propulsive contractions of the smooth muscle of the gastrointestinal tract. Bismuth Subsalicylate; Metronidazole; Tetracycline: Moderate Close clinical monitoring is advised when administering morphine with boceprevir due to an increased potential for morphine-related adverse events.
If morphine dose adjustments are made, re-adjust the dose upon completion of boceprevir treatment. Although this interaction has not been studied, predictions about the interaction can be made based on the metabolic pathway of morphine. Morphine is a substrate of the drug efflux transporter P-glycoprotein P-gp ; boceprevir is an inhibitor of this efflux protein. Coadministration may result in elevated morphine plasma concentrations. Moderate Due to the CNS effects of brexpiprazole, caution is advisable when brexpiprazole is given in combination with other centrally-acting medications including opiate agonists.
Moderate Based on the sedative effects of brimonidine in individual patients, brimonidine administration has potential to enhance the CNS depressants effects of opiate agonists. Moderate Drowsiness has been reported during administration of carbetapentane. An enhanced CNS depressant effect may occur when carbetapentane is combined with other CNS depressants including morphine. In some cases of acute pain, trauma, or during surgical management, opiate-dependent patients receiving buprenorphine maintenance therapy may require concurrent treatment with opiate agonists, such as morphine.
In these cases, health care professionals must exercise caution in opiate agonist dose selection, as higher doses of an opiate agonist may be required to compete with buprenorphine at the mu-receptor. Management strategies may include adding a short-acting opiate agonist to achieve analgesia in the presence of buprenorphine, discontinuation of buprenorphine and use of an opiate agonist to avoid withdrawal and achieve analgesia, or conversion of buprenorphine to methadone while using additional opiate agonists if needed.
Closely monitor patients for CNS or respiratory depression. When buprenorphine is used for analgesia, avoid co-use with opiate agonists. Buprenorphine may cause withdrawal symptoms in patients receiving chronic opiate agonists as well as possibly potentiate CNS, respiratory, and hypotensive effects. Major Naloxone can antagonize the therapeutic efficacy of morphine in addition to precipitating withdrawal symptoms in patients who are physically dependent on opiate drugs including morphine.
Naloxone should not be administered in the absence of clinically significant respiratory or circulatory depression secondary to morphine overdose. Moderate Excessive use of opioid agonists e. Major When naltrexone is used as adjuvant treatment of opiate or alcohol dependence, use is contraindicated in patients currently receiving opiate agonists. Naltrexone will antagonize the therapeutic benefits of opiate agonists and will induce a withdrawal reaction in patients with physical dependence to opioids.
Also, patients should be opiate-free for at least 7 to 10 days prior to initiating naltrexone therapy. If a patient receives naltrexone, and an opiate agonist is needed for an emergency situation, large doses of opiate agonists may ultimately overwhelm naltrexone antagonism of opiate receptors.
Immediately following administration of exogenous opiate agonists, the opiate plasma concentration may be sufficient to overcome naltrexone competitive blockade, but the patient may experience deeper and more prolonged respiratory depression and thus, may be in danger of respiratory arrest and circulatory collapse.
Non-receptor mediated actions like facial swelling, itching, generalized erythema, or bronchoconstriction may occur presumably due to histamine release. A rapidly acting opiate agonist is preferred as the duration of respiratory depression will be shorter. Patients receiving naltrexone may also experience opiate side effects with low doses of opiate agonists. If the opiate agonist is taken in such a way that high concentrations remain in the body beyond the time naltrexone exerts its therapeutic effects, serious side effects may occur.
Moderate Concomitant use of CNS depressants, such as buspirone, can potentiate the effects of morphine, which may potentially lead to respiratory depression, CNS depression, sedation, or hypotensive responses.
If concurrent use of morphine and buspirone is imperative, reduce the dose of one or both drugs. Major Avoid the concomitant use of butorphanol and opiate agonists, such as morphine. Butorphanol may cause withdrawal symptoms in patients receiving chronic opiate agonists. Concurrent use of butorphanol with other opiate agonists can cause additive CNS, respiratory, and hypotensive effects.
Moderate Monitor for an increase in morphine-related adverse events if concomitant use with cabozantinib is necessary, as plasma concentrations of morphine may be increased.
Cabozantinib is a P-glycoprotein P-gp inhibitor and morphine is a substrate of P-gp; the clinical relevance of this finding is unknown.
Moderate Inducers of CYP3A4 such as carbamazepine may induce the hepatic metabolism of opiate agonists, which may lead to opiate withdrawal or inadequate pain control.
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