OXYMORPHONE HYDROCHLORIDE Drug Interactions
Also known as: Oxymorphone Hydrochloride
OXYMORPHONE HYDROCHLORIDE (brand name: Oxymorphone Hydrochloride) is a Opioid Analgesics. 1 INDICATIONS AND USAGE Oxymorphone hydrochloride tablets are indicated for the management of acute pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Limitations of Use Because of the risks of addiction, abuse, misuse, overdose, and death, which…OXYMORPHONE HYDROCHLORIDE has 17 documented drug interactions in our database, including 6 contraindicated, 11 major, 0 moderate, and 0 minor interactions.
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Contraindicated
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Moderate
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Concomitant use can lead to severe and potentially fatal respiratory depression, profound sedation, coma, and death. Patients may exhibit decreased level of consciousness, hypoventilation, bradycardia, hypotension, and miosis. The risk is heightened in opioid-naïve individuals, elderly patients, or those with underlying respiratory compromise.
Mechanism
Oxymorphone, a mu-opioid receptor agonist, and lorazepam, a gamma-aminobutyric acid (GABA)-A receptor positive allosteric modulator, both cause central nervous system (CNS) depression. Their co-administration leads to additive and synergistic CNS depressant effects, primarily by enhancing the inhibitory neurotransmission in the brainstem respiratory centers and other CNS areas. This leads to profound depression of ventilatory drive and reduced arousal.
Clinical Management
Concomitant use of opioids and benzodiazepines is contraindicated due to the high risk of severe adverse outcomes. If co-administration is unavoidable and no alternative treatment options are adequate, prescribers must limit dosages and duration to the minimum necessary and monitor patients closely for signs of respiratory depression and sedation. Naloxone should be readily available, and patients/caregivers must be educated on the risks and symptoms.
The concurrent use of oxymorphone and diazepam can lead to profound sedation, respiratory depression, coma, and death. Patients may experience decreased level of consciousness, hypoventilation, apnea, hypotension, and psychomotor impairment. This interaction significantly increases the risk of accidental overdose and life-threatening adverse events.
Mechanism
Oxymorphone, an opioid agonist, and diazepam, a benzodiazepine, both depress the central nervous system (CNS). Opioids primarily act on mu-opioid receptors to inhibit GABAergic interneurons, leading to disinhibition of dopamine neurons and respiratory depression. Benzodiazepines enhance the effect of the inhibitory neurotransmitter GABA at the GABA-A receptor, increasing chloride ion influx and hyperpolarizing neurons. The synergistic CNS depressant effects of these two drug classes significantly amplify respiratory depression, sedation, and psychomotor impairment.
Clinical Management
Concomitant use of oxymorphone and diazepam is contraindicated due to the high risk of respiratory depression, profound sedation, coma, and death. If co-administration is unavoidable, which should be rare and only considered when alternative treatment options are inadequate, dosages of both drugs should be reduced, and patients must be closely monitored for signs of respiratory depression and sedation. Naloxone should be readily available, and patients should be educated on the risks.
The primary clinical effects include severe respiratory depression, profound sedation, somnolence, coma, and potentially death. Patients may exhibit decreased respiratory rate, shallow breathing, hypoxemia, hypotension, and impaired psychomotor function.
Mechanism
Oxymorphone, an opioid agonist, and oxazepam, a benzodiazepine, both exert central nervous system (CNS) depressant effects. The co-administration leads to an additive and synergistic depression of the CNS, primarily affecting the gamma-aminobutyric acid (GABA) system for benzodiazepines and opioid receptors for oxymorphone, resulting in profound respiratory depression and sedation.
Clinical Management
Concurrent use of oxymorphone and oxazepam is generally contraindicated due to the high risk. If co-administration is unavoidable, the lowest effective doses of both drugs should be used for the shortest possible duration, with close monitoring for respiratory depression and sedation. Consider alternative therapies that do not involve co-prescribing an opioid and a benzodiazepine.
The concurrent use of oxymorphone and temazepam significantly increases the risk of severe adverse effects, including profound sedation, respiratory depression, coma, and death. Patients may experience decreased level of consciousness, hypoventilation, bradycardia, and hypotension, which can progress rapidly.
Mechanism
Oxymorphone, an opioid agonist, and temazepam, a benzodiazepine, both exert central nervous system (CNS) depressant effects by acting on distinct receptors. Oxymorphone primarily acts on mu-opioid receptors, while temazepam enhances the activity of gamma-aminobutyric acid (GABA) at GABA-A receptors. The co-administration leads to an additive and synergistic depression of the CNS, including respiratory drive and consciousness.
Clinical Management
Concomitant use of oxymorphone and temazepam is contraindicated due to the high risk of severe respiratory depression and death. If no alternative treatments are adequate, and co-prescription is deemed absolutely necessary, the lowest effective doses should be used for the shortest possible duration, with close monitoring for respiratory depression and sedation. Patients should be educated on the risks and advised against driving or operating machinery.
Patients may experience severe sedation, profound respiratory depression, coma, and death. Other effects can include hypotension, psychomotor impairment, and increased risk of accidental overdose.
Mechanism
Both oxymorphone, an opioid agonist, and triazolam, a benzodiazepine, are central nervous system (CNS) depressants. Their concomitant use leads to additive pharmacodynamic effects, primarily by enhancing GABAergic neurotransmission (benzodiazepine) and activating mu-opioid receptors (oxymorphone), resulting in profound CNS and respiratory depression.
Clinical Management
Concomitant use of oxymorphone and triazolam is generally contraindicated. If co-prescription is absolutely unavoidable, use the lowest effective doses and shortest possible duration, and closely monitor patients for signs of respiratory depression and sedation. Consider alternative non-opioid or non-benzodiazepine treatments when possible.
The concurrent use of oxymorphone and chlordiazepoxide significantly increases the risk of severe respiratory depression, profound sedation, coma, and death. Patients may exhibit decreased level of consciousness, hypoventilation, pinpoint pupils, and hypotension.
Mechanism
Both oxymorphone, an opioid agonist, and chlordiazepoxide, a benzodiazepine, are central nervous system (CNS) depressants. Their co-administration leads to synergistic depression of the CNS, primarily by enhancing GABAergic neurotransmission, which results in profound respiratory depression and sedation.
Clinical Management
Concomitant use of opioids and benzodiazepines is generally contraindicated due to the high risk of severe adverse outcomes. If no alternative treatments are adequate, and the benefits outweigh the risks, prescribe the lowest effective doses for the shortest duration possible, and monitor patients closely for respiratory depression and sedation. Consider naloxone availability and patient education on overdose symptoms.
Patients may experience profound sedation, somnolence, dizziness, and impaired psychomotor function. The most serious clinical effect is an increased risk of respiratory depression, which can be life-threatening, along with hypotension and coma.
Mechanism
Both oxymorphone, an opioid agonist, and cyclobenzaprine, a centrally acting muscle relaxant with anticholinergic properties, cause central nervous system (CNS) depression. Their co-administration leads to an additive depressant effect on the brain and spinal cord, exacerbating sedation and respiratory depression.
Clinical Management
Avoid concomitant use if possible. If co-administration is necessary, initiate both drugs at the lowest effective doses and titrate slowly. Closely monitor patients for signs of respiratory depression, excessive sedation, and altered mental status, especially during initiation or dose escalation. Educate patients about the risks and advise against operating heavy machinery or driving.
Patients may experience profound sedation, respiratory depression, hypotension, and psychomotor impairment. This can lead to an increased risk of falls, accidental injury, and potentially life-threatening respiratory arrest. Symptoms such as dizziness, confusion, and difficulty breathing should be closely monitored.
Mechanism
Oxymorphone, an opioid agonist, exerts its primary effects through binding to mu-opioid receptors in the central nervous system (CNS), leading to analgesia, sedation, and respiratory depression. Methocarbamol is a centrally acting skeletal muscle relaxant whose mechanism of action is not fully elucidated but involves general CNS depression. The co-administration of these agents results in an additive depressant effect on the CNS.
Clinical Management
Avoid concomitant use of oxymorphone and methocarbamol if possible. If co-administration is necessary, initiate both drugs at the lowest effective dose and titrate slowly while closely monitoring for signs of CNS and respiratory depression. Educate patients about the risks and advise against operating heavy machinery or driving.
The combined CNS depressant effects can lead to profound sedation, respiratory depression, hypotension, psychomotor impairment, and coma. Patients may experience dizziness, confusion, decreased level of consciousness, and impaired coordination, significantly increasing the risk of falls and accidental injury. The risk of life-threatening respiratory depression is particularly elevated.
Mechanism
Oxymorphone, an opioid agonist, produces central nervous system (CNS) depression by binding to mu-opioid receptors. Carisoprodol, a centrally acting skeletal muscle relaxant, also causes CNS depression, primarily through its active metabolite meprobamate, which acts as a GABA-A receptor positive allosteric modulator. The co-administration of these agents results in an additive depressant effect on the CNS.
Clinical Management
Concomitant use of oxymorphone and carisoprodol should generally be avoided due to the high risk of severe CNS and respiratory depression. If co-administration is unavoidable, the lowest effective doses of both drugs should be used, and patients must be closely monitored for signs of respiratory depression and excessive sedation. Consider alternative muscle relaxants with less CNS depressant activity or non-opioid analgesics.
Patients may experience increased sedation, dizziness, confusion, and psychomotor impairment. The most significant risk is profound respiratory depression, which can be life-threatening. Other effects include hypotension and coma.
Mechanism
Oxymorphone is an opioid analgesic that acts as a mu-opioid receptor agonist, causing central nervous system (CNS) depression. Baclofen is a gamma-aminobutyric acid (GABA) analogue that acts as a GABA-B receptor agonist, also producing CNS depressant effects. The co-administration of these two agents results in an additive depressant effect on the CNS.
Clinical Management
Avoid concomitant use if possible. If co-administration is necessary, initiate both drugs at the lowest effective doses and titrate slowly. Closely monitor patients for signs of respiratory depression, sedation, and altered mental status, especially during initiation or dose adjustments. Educate patients about the risks and advise against operating machinery or driving.
Patients may experience severe sedation, profound respiratory depression, coma, and even death. Other potential effects include impaired psychomotor function, dizziness, confusion, and hypotension, which can increase the risk of falls and accidents.
Mechanism
Oxymorphone is an opioid agonist that produces central nervous system (CNS) depression through its action on mu-opioid receptors. Tizanidine is an alpha-2 adrenergic agonist that also causes significant CNS depression, muscle relaxation, and sedation. The co-administration of these two agents results in an additive depressant effect on the CNS.
Clinical Management
Avoid concomitant use of oxymorphone and tizanidine due to the high risk of additive CNS and respiratory depression. If co-administration is unavoidable, reduce the starting dose of one or both medications, monitor patients closely for signs of sedation and respiratory depression, and educate them on the risks. Consider alternative non-opioid analgesics or non-pharmacological treatments for pain or muscle spasms.
Patients may experience profound sedation, respiratory depression, hypotension, coma, and even death. Impaired psychomotor function, dizziness, and confusion are also common, increasing the risk of falls and accidents.
Mechanism
Oxymorphone, an opioid agonist, produces central nervous system (CNS) depression by binding to mu-opioid receptors. Metaxalone, a centrally acting skeletal muscle relaxant, also causes generalized CNS depression. The concurrent use of these agents results in an additive depressant effect on the CNS.
Clinical Management
Avoid concomitant use of oxymorphone and metaxalone if possible. If co-administration is necessary, initiate both drugs at the lowest effective doses and titrate carefully, monitoring closely for signs of respiratory depression and excessive sedation. Educate patients about the risks and advise against driving or operating heavy machinery.
Patients may experience increased sedation, dizziness, confusion, and psychomotor impairment. The most serious clinical effect is an enhanced risk of respiratory depression, which can be life-threatening. Other effects include profound sedation and impaired motor function.
Mechanism
Oxymorphone is an opioid agonist that produces central nervous system (CNS) depression by binding to mu-opioid receptors. Chlorzoxazone is a centrally acting skeletal muscle relaxant that also causes generalized CNS depression. The concurrent use of these agents results in an additive depressant effect on the CNS.
Clinical Management
Avoid concomitant use of oxymorphone and chlorzoxazone if possible. If co-administration is necessary, use the lowest effective doses for the shortest duration possible, and monitor patients closely for signs of respiratory depression, sedation, and mental status changes. Educate patients and caregivers about the risks and symptoms of CNS depression.
Patients may experience profound sedation, respiratory depression, hypotension, and psychomotor impairment. This can lead to increased risk of falls, accidental injury, and potentially life-threatening respiratory compromise, especially in opioid-naive individuals or those with underlying respiratory conditions.
Mechanism
Oxymorphone is an opioid agonist that produces central nervous system (CNS) depression through its action on mu-opioid receptors. Orphenadrine is an anticholinergic muscle relaxant with significant CNS depressant and sedative properties. The co-administration of these two agents results in an additive depressant effect on the CNS.
Clinical Management
Avoid concomitant use of oxymorphone and orphenadrine if possible. If co-administration is necessary, initiate both medications at the lowest effective dose and titrate slowly while closely monitoring for signs of CNS and respiratory depression. Educate patients about the risks and advise against operating heavy machinery or driving.
The co-administration of oxymorphone and clonazepam significantly increases the risk of severe adverse outcomes including profound sedation, respiratory depression, coma, and death. Patients may experience decreased level of consciousness, hypoventilation, bradycardia, and hypotension. This interaction poses a life-threatening risk, particularly in opioid-naive individuals or those with underlying respiratory compromise.
Mechanism
Oxymorphone, an opioid agonist, and clonazepam, a benzodiazepine, both depress the central nervous system (CNS). Opioids bind to mu-opioid receptors, while benzodiazepines enhance the effect of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) at GABA-A receptors. The synergistic CNS depressant effects of these two drug classes lead to profound respiratory depression, sedation, and hypotension.
Clinical Management
Avoid concomitant use of oxymorphone and clonazepam due to the high risk of severe adverse effects, as highlighted by an FDA Black Box Warning. If co-prescription is unavoidable, use the lowest effective doses for the shortest possible duration, and monitor patients closely for signs of respiratory depression and sedation. Consider alternative treatments that do not involve concurrent opioid and benzodiazepine use.
Patients may experience severe respiratory depression, profound sedation, coma, and potentially death. Other symptoms include dizziness, confusion, psychomotor impairment, and hypotension. The risk of these adverse effects is significantly increased when these drugs are used concomitantly.
Mechanism
Both oxymorphone (an opioid agonist) and alprazolam (a benzodiazepine) are central nervous system (CNS) depressants. Oxymorphone acts primarily on mu-opioid receptors, while alprazolam enhances the effect of gamma-aminobutyric acid (GABA) at GABA-A receptors. The synergistic CNS depressant effects lead to profound respiratory depression, sedation, and hypotension.
Clinical Management
Concomitant use should generally be avoided due to the high risk. If co-prescription is absolutely necessary and no alternatives exist, use the lowest effective doses for the shortest possible duration, and closely monitor patients for respiratory depression and sedation. Educate patients and caregivers on the risks and symptoms, and consider prescribing naloxone for overdose reversal.
Concomitant use can lead to profound sedation, respiratory depression, coma, and death. Patients may exhibit decreased level of consciousness, hypoventilation, hypoxia, and hypotension. The interaction can also impair psychomotor function and increase the risk of accidental injury.
Mechanism
Oxymorphone, an opioid agonist, primarily acts on mu-opioid receptors in the central nervous system (CNS), leading to dose-dependent CNS depression, including respiratory depression. Midazolam, a benzodiazepine, enhances the inhibitory effects of gamma-aminobutyric acid (GABA) at GABA-A receptors, also resulting in CNS depression. The synergistic CNS depressant effects of both drugs significantly increase the risk of respiratory depression and profound sedation.
Clinical Management
Avoid concomitant use of oxymorphone and midazolam whenever possible due to the high risk of severe adverse outcomes. If co-administration is absolutely necessary, use the lowest effective doses for the shortest duration possible, and closely monitor patients for respiratory depression and sedation. Have naloxone and flumazenil readily available, and educate patients and caregivers on the risks and symptoms of overdose.
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