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What opioid agonists are contraindicated in patients taking MAO inhibitors?
Wiki User
∙ 11y ago
morphine, demerol
Wiki User
∙ 11y ago
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Doe your eys dialate on suboxone?
No, all opioid drugs, agonists and partial agonists alike, cause constriction of the pupil. The only time the pupil will dialate is when the person is going through withdrawls.
Will liquid methadone block effects of oxycodone if taken together?
no, the two will potentiate each other seeing as how they're both opioid agonists
Is Prozac an opioid?
No. Lexapro (escitalopram oxalate) is in the class of antidepressants called SSRIs (selective serotonin reuptake inhibitors).
Is Xanax a morphine derivative?
Yes. Most Benzodiazepine's are derived from opioid oxidase inhibitors. Which are formed from a protein synthesis of the amino acids.
What is the recommended dosage of Opioid analgesics?
Recommended doses vary, depending on the type of opioid analgesic and the form in which it is being used. Doses may be different for different patients
Is hydrocodon an ace inhibitor?
No. It binds to opioid receptors in the central nervous system mainly in the brain. The placing of the receptors affect the action of the opioid. They act as CNS depressives. ACE inhibitors have effect on blood pressure and renal elimination. It has no similarities with painkillers such as Hydrocodone
How does oxycodone interact with Wellbutrin?
In theory, concurrent use of a CYP2D6 inhibitor, such as bupropion, may inhibit the conversion of oxycodone to oxymorphone. so you get increasd level of oxycodone. In addition, concurrent use with a CYP2D6 inhibitor may increase the adverse effects of oxycodone. Close monitoring for pronounced opioid effects is advisable. Excessive use of opioid agonists (e.g., opiate addiction) is associated with an increased seizure risk; seizures may be more likely to occur during concurrent use of bupropion in these patients since bupropion is associated with a dose-related risk of seizures.
Can you abuse embeda?
Embeda contains morphine, an opioid agonist, and is a Schedule II controlled substance. Opioid agonists have the potential for being abused and are sought by drug abusers and people with addiction disorders and are subject to criminal diversion. Morphine can be abused in a manner similar to other opioid agonists, legal or illicit. This should be considered when prescribing or dispensing Embeda in situations where the physician or pharmacist is concerned about an increased risk of misuse, abuse, or diversion. Abuse of Embeda by crushing, chewing, snorting, or injecting the dissolved product will result in the uncontrolled delivery of the opioid and pose a significant risk to the abuser that could result in overdose and death. Concerns about abuse and addiction should not prevent the proper management of pain. Healthcare professionals should contact their State Professional Licensing Board or State Controlled Substances Authority for information on how to prevent and detect abuse of this product.
Is neurontin an opioid?
Neurontin is not an opioid
What receptors does heroin effect?
Heroin (diacetyl-morphine) by itself has very little effect on receptors in the brain. It's main physiological effects are attributed to the conversion of heroin by the body to its metabolites morphine and/or 6-monoacetylmorphine (depending upon the route of administration of heroin). But for all intents and purposes, this is a just a pharmacological technicality, as most drugs (such as codeine) are not very active in their own right and depend upon metabolism by the liver or other organs to produce the specific effects of the drug.Heroin is an opioidergic drug and thus affects endogenous opioid receptors, acting as an agonist (meaning it plugs into and activates these receptors). It has the highest affinity for the μ-opioid (or "mu-opioid") sub receptor. This specific opioid-receptor is mainly responsible for providing all the classical narcotic effects of most opiate/opioid painkillers, including: pain relief, relaxation of smooth muscle (in the gut), euphoria, and central nervous system depression (which causes reduction in anxiety and hypertension).Like most other opiates, heroin also binds to two other opioid receptors as an agonist. First, it has moderate affinity for the δ- (or "delta-") opioid receptor. The physiological effects of δ opioid receptor agonists is not as fully understood as the other types; but it is thought to play a role in dependence and tolerance; while also providing similar effects to μ-opioid receptors agonists, primarily pain relief and central nervous system depression.Finally, heroin has some-but very low-affinity for the κ-opioid (or "kappa-opioid") receptor. The effects of κ-opioidergic drugs are extremely different than μ- & δ- opioid agonists. Effects include hallucinations, dissociation, delirium, and anesthesia. Most of the effects associated with the μ-opioid receptor do not occur with kappa agonists, including: euphoria, CNS depression, and relaxation of the smooth-muscle in the gut. Opposite to heroin, a substance that strongly binds to κ-opioid receptors, with very little affinity for μ- & δ- receptors, is salvinorin a, the active chemical in Salvia. In the 1970s, κ-opioid agonist drugs were investigated as atypical anesthetics, but were quickly abandoned due to their severely adverse, unpleasant, and hallucinogenic effects. However, heroin's affinity for this opioid receptor is minimal, even at high doses, compared to other opiates such as meperidine, which have far less abuse potential because of kappa-opioid agonist activity at higher doses.Additionally:All drugs that act as μ-opioid agonists, including endogenous endorphins, similarly indirectly impact dopamine and serotonin and induce antidepressant effects. Furthermore, heroin like nearly every other opiate, induces a histamine reaction (it is not known if this is due to an indirect or direct effect at the H1, or histamine, receptors). This can create some-allergic reactions like itchiness. Although other typical allergic-effects like watering-eyes are usually counteracted by μ-opioid agonist effects, which induce dryness in mucus membranes (such as in the mouth and eyes).Note:Unlike other opiates & opioids, heroin has not yet been shown to have any known affinity for other non-opioidergic systems in the brain, such as acting as an antagonist (i.e., a "blocking" agent) at NMDA receptors as seen with methadone (NMDA antagonists reduce glutamate levels and decrease anxiety and in higher doses can cause anesthesia, Ketamine is a potent NMDA antagonist). Heroin also has not been demonstrated to act at nociceptin receptors, like the synthetic-opiate buprenorphine. Nociceptin is a opioid-class receptor, but has opposite physiological effects, acting as an anti-analgesic; however, its overall impact upon opiate pharmacology is not fully understood.
Would there be any interactions between cocaine and hydromorphone in the body?
yes there would be. Monoaminergic drugs can modify opioid withdrawal in nonhumans, and cocaine is reported to attenuate opioid withdrawal in humans. Drug discrimination was used to examine whether s.c. cocaine or other indirect-acting monoamine agonists attenuate morphine (3.2 mg/kg/day) withdrawal induced by naltrexone and by 27 h of morphine deprivation. Naltrexone-precipitated withdrawal was attenuated not only by morphine but also by cocaine, amphetamine, and imipramine. However, reversal of naltrexone-precipitated withdrawal was greater for morphine than for any of the indirect-acting monoamine agonists. Attenuation of the naltrexone discriminative stimulus by indirect-acting monoamine agonists was pharmacologically selective insofar as drugs lacking affinity for monoamine transporters (ketamine and triazolam) were without effect. Twenty-seven hours of morphine deprivation occasioned naltrexone-lever responding and decreased response rate, and both effects were reversed by morphine, cocaine, and amphetamine and not by imipramine, desipramine, ketamine, and triazolam. Thus, indirect-acting monoamine agonists attenuate some (e.g., discriminative) aspects of naltrexone-precipitated withdrawal, whereas only indirect-acting agonists with high affinity for dopamine transporters attenuate deprivation-induced withdrawal. These results suggest that dopamine is differentially involved in naltrexone- and deprivation-induced withdrawal and support the notion that opioid-dependent individuals use stimulants, in part, to attenuate withdrawal.
Can you give stadol to methadone patients?
Uh, NO! Stadol is in a class of partial-agonist, partial antagonist opioid medications that also include Talwin, Nubain and Buprex (the main component in Suboxone) These are contra-indicated with any full agonist opioid medications, taking them concomitantly will be unpleasant, especially in cases of dependence.
