Central nervous system depressants opioids

Central nervous system depression is the usual effect of morphine, and sedation and drowsiness are frequently observed with therapeutic doses. When given in the absence of pain morphine may sometimes produce dysphora—an unpleasant sensation of fear and anxiety. The most important stimulatory effects of morphine in man are emesis and miosis. Miosis, due to stimulation of the Edinger-Westphal nucleus of the third nerve, occurs with all opioids. The combination of pinpoint pupils, coma, and respiratory depression are classical signs of morphine overdosage. Stimulation of the solitary nuclei may also be responsible for depression of the cough reflex (antitussive effect). Pharmacokinetics and metabolism... 

The most commonly abused prescription drugs are opioids and opiates such as oxycodone and morphine, central nervous system depressants such as barbiturates and benzodiazepines, and stimulants such as dextroamphetamine and methylphenidate. Brand-name painkillers such as Vicodin and OxyContin, depressants such as Valium and Xanax, and stimulants such as Ritalin and Dexedrine are commonly abused (as are some OTC cough remedies). Although helpful and safe when used appropriately, these drugs can cause serious harm when taken in unapproved ways. 

In four cases of overdose with up to 1000 mg there was significant central nervous system depression and miosis after acute overdosage of olanzapine (258). Olanzapine concentrations were over 250, 59, 54, and 151 ng/ml. All four patients recovered with supportive care and two required advanced airway support. The authors pointed out that all the patients had marked miosis and depressed mental status, findings that are usually associated with intoxication with opioids or alpha2-adrenoceptor agonists. 

Interactions. Morphine (also pethidine and possibly other opioids) is potentiated by monoamine oxidase inhibitors. Any central nervous system depressant (including alcohol) will have additive effects. Patients recently exposed to neuromuscular blocking agents (unless this is adequately reversed, e.g. by neostigmine) are particularly at risk from the respiratory depressant effects of morphine. The effect of diuretic drugs may be reduced by release of antidiuretic hormone by morphine. Useful interactions include the potientating effect on pain relief of tricyclic antidepressants and of dexamfetamine. 

The toxic effects of illicit fentanyl derivatives include rapid onset respiratory and central nervous system depression. Patients often present comatose and apneic. Other signs and symptoms consistent with opioid intoxication such as bradycardia, hypotension, miosis, and decreased gastrointestinal motility also occur. 

Heroin s primary toxic principle is its profound ability to depress the central nervous system (CNS). Opioid analgesics bind with stereospecific receptors at many sites within the CNS. Heroin, similar to other opioids, exerts its pharmacologic effect by acting at mu, kappa, and delta receptors in the brain. Although the precise sites and mechanisms of action have not been fully determined, alterations in the release of various neurotransmitters from afferent nerves sensitive to painful stimuli may be partially responsible for the analgesic effect. Activities associated with the stimulation of opiate receptors are analgesia, euphoria, respiratory depression, miosis, and reduced gastrointestinal motility. 

A. Benzodiazepines will potentiate the central nervous system-depressant effects of opioids, ethanol, and other sedative-hypnotic and depressant drugs. 

Drug interactions morphine has additive effects when used in conjunction with alcohol, other opioids, or illicit drugs that cause central nervous system depression because respiratory depression, hypotension, and profound sedation or coma may result. 

Hydromorphone should be used with caution if other central nervous system depressants are given concomitantly. These drugs are other opioids, general anesthetics, phenothiazine, tricyclic antidepressants, sedative-hypnotics, and other central nervous system depressants (including ethanol). 

Concurrent use of butorphanol with central nervous system depressants (e.g. alcohol, barbiturates, tranquilizers, and antihistamines) may result in increased central nervous system depressant effects. When used concurrently with such drugs, the dose of butorphanol should be the smallest effective dose and the frequency of dosing reduced as much as possible when administered concomitantly with drugs that potentiate the action of opioids. 

Side effects are similar to those observed with opioids constipation nausea central nervous system depression seizures (in conditions with lower seizure threshold)... 

The behavioral effects of nicotine have been defined as both stimulant and depressant, effects that are influenced by the present mental status and expectations of the smoker. Smokers may feel alert and relaxed. Nicotine produces myriad effects on the central nervous system (CNS), almost all of which appear to be mediated through nicotinic receptors. Additionally, nicotine influences multiple neuronal systems. One of its most prominent effects is stimulated release of dopamine, particularly in the nucleus accumbens, which is a major component of the reward system. Nicotine also stimulates the release of endogenous opioids and glucocorticoids. 

There are three major classes of prescription drugs of abuse opioids, central nervous system (CNS) depressants, and stimulants. Opioids are medications often prescribed to treat pain. They work on special parts of the brain to relieve... 

Drugs and chemicals are known to cause activated interaction. The depressant action of opioid drugs is enhanced by drugs acting on the central nervous system (CNS) such as alcohol, anesthetics, anxiolytics, hypnotics, tricyclic antidepressants, and antipsychotics. Concomitant administration of opioid analgesics and monoamine oxidase inhibitors (MAOIs) should be avoided, or extra care should be taken if such a therapy is inevitable. Fatal reactions are reported when treated along with selegiline. Interactions also are reported with cyclizine, cimetidine, mexiletine, cisapride, metoclopramide, or domperidone. 

Like Rohypnol, GHB is a central nervous system (CNS) depressant, which, when tested on animals, induces a sleep-like state in doses ranging from 0.1 to 1.5 milligrams per kilogram.33 Although many neurotransmitter systems are affected by treatment with GHB, evidence supports the hypothesis that GHB itself acts as a neurotransmitter. This implies that GHB is a naturally occurring chemical in the body that is necessary for normal nervous system functions. Administered as a drug, GHB has been shown to temporarily inhibit the release of dopamine in the brain.34 This inhibition is followed by a marked increase in the release of both dopamine and naturally occurring opioids, such as endorphins.35... 

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