Central nervous system depressants interactions

Toluene (methylbenzene) does not possess the myelotoxic properties of benzene, nor has it been associated with leukemia. It is, however, a central nervous system depressant and a skin and eye irritant. It is also fetotoxic. See Table 56-1 for the TLVs. Exposure to 800 ppm can lead to severe fatigue and ataxia 10,000 ppm can produce rapid loss of consciousness. Chronic effects of long-term toluene exposure are unclear because human studies indicating behavioral effects usually concern exposures to several solvents. In limited occupational studies, however, metabolic interactions and modification of toluene s effects have not been observed in workers also exposed to other solvents. Less refined grades of toluene contain benzene. 

PCP has a sedative effect on certain systems in the body and interactions with other central nervous system depressants such as alcohol and benzodiazepines may lead to coma or accidental overdose. 

Pharmacodynamic alcohol interactions are also of great clinical significance. Additive central nervous system depression with other sedative-hypnotics is most important. Alcohol also potentiates the pharmacologic effects of many nonsedative drugs, including vasodilators and oral hypoglycemic agents. There is some evidence that alcohol also enhances the antiplatelet action of aspirin. 

Procarbazine 50-200 mg/d orally Nausea and vomiting, flu-like syndrome, drug interactions Bone marrow depression, central nervous system depression, leukemogenic... 

Central nervous system depression is multiplied when BZDs are taken with other downers interaction with alcohol can be lethal, even after only a few pills and a couple of drinks. The drugs last for a very long time in the body tis sues, and people may not be aware that even a short-acting sleeping pill such as Halcion can have aftereffects the next day. Longer-acting BZDs can last for several days. 

FLUOXETINE, FLUVOXAMINE, PAROXETINE BZDs - ALPRAZOLAM, DIAZEPAM, MIDAZOLAM t in plasma concentrations of these BZDs. Likely t sedation and interference with psychomotor activity Alprazolam, diazepam and midazolam are subject to metabolism by CYP3A4. Fluvoxamine, fluoxetine and possibly paroxetine are inhibitors of CYP3A4 sertraline is a weak inhibitor. SSRIs are relatively weak compared with ketoconazole, which is possibly 100 times more potent as an inhibitor Warn patients about risks associated with activities that require alertness. Consider use of alternatives such as oxazepam, lorazepam and temazepam, which are metabolized by glucuronidation >- For signs and symptoms of CNS depression, see Clinical Features of Some Adverse Drug Interactions, Central nervous system depression... 

Central nervous system depressant drugs including benzodiazepines, several Hj-receptor antihistamines, alcohol, phenothiazines, antiepilepsy drugs interact to augment their sedative effects. 

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. 

Also note that the potential for an interaction between drugs does not preclude their concurrent use. Certain combinations are routinely prescribed without problems in many patients (as with lithium and antipsychotics), whereas others are contraindicated due to the severity of the interaction (for example, MAOIs and SSRIs). However, whenever psychiatric medications are coadministered, the additive potential of central nervous system depression and anticholinergic effects must be considered. 

The mechanism by which 1,1,1-trichloroethane and other organic solvents depress the central nervous system is poorly understood, but is thought to involve interactions of the parent compound with lipids and/or proteinaceous components of neural membranes (Evans and Balster 1991). No known methods specifically counteract the central nervous system effects of 1,1,1-trichloroethane. Because the specific cellular or biochemical nature of central nervous system depression is poorly understood, it is difficult to propose any method to interfere with this effect of 1,1,1 -trichloroethane, other than to prevent further exposure to the compound so that it can be cleared from the body. 

Patients with coexisting cardiovascular and pulmonary conditions (e.g., ARDS, pulmonary infection, pulmonary aspiration) may be more susceptible to the toxic effects or complications of tricyclic antidepressant poisoning. The influence of chronic exposure to tricyclic antidepressants on the risks of an acute overdose is unclear. Tricyclic antidepressants interact with other central nervous system depressant drugs, which together may lead to increased central nervous system and respiratory depression. 

Procarbazine inhibits RNA and DNA synthesis and interferes with mitosis. It is a drug that interacts with alcohol and generally increases the effects of central nervous system depressants and can produce hypertension. 

CICLOSPORIN BZDs-ALPRAZOLAM, MIDAZOLAM, DIAZEPAM Likely t plasma concentrations and risk of t sedation These BZDs are metabolized primarily by CYP3A4, which is moderately inhibited by cidosporin Warn patients about t sedation. Consider using alternative drugs, e.g. ffurazepam, quazepam. Warn about activities requiring attention For signs and symptoms of CN5 depression, see Qinkal Features of Some Adverse Drug Interactions, Central nervous system depression... 

Although workers are often exposed to a variety of solvents with Stoddard solvent, there are no available studies specifically characterizing the interactions of Stoddard solvent with other chemicals. Since Stoddard solvent may have adverse effects on the nervous system, it may compound the effects of other chemicals that cause central nervous system depression, such as alcohol, barbiturates, benzodiazepines, or medical anesthetics. Guinea pigs with a diet high in vitamin C survived a high exposure to Stoddard solvent vapors better than those with a diet low in vitamin C (Jenkins et al. 1971) however, it is not known how vitamin C levels might affect humans exposed to Stoddard solvent. 

Ativan can interact with alcohol, increasing central nervous system depression. The client should not consume alcohol at all. 

In addition to pharmacokinetic drug-drug interactions, pharmacodynamic effects have been reported as well. Halothane increases the susceptibility to ventricular arrhythmias under theophylline therapy as a result of increased sensitivity of the myocardium to endogenous catecholamine release by theophylUne. Ketamine lowers the theophyUine seizure threshold. Benzodiazepines Uke midazolam, diazepam, lorazepam, and Uurazepam increase the central nervous system concentration of adenosine, a potent central nervous system depressant. As theophyUine also blocks adenosine receptors, it counteracts benzodiazepine-induced sedation, resulting in increased dosage requirements for these compounds. ... 

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. 

Ginseng interacts with phenelzine, a drug used to treat depression, stimulating the central nervous system. 

Inhaled (volatile) anesthetics potentiate the neuromuscular blockade produced by nondepolarizing muscle relaxants in a dose-dependent fashion. Of the general anesthetics that have been studied, inhaled anesthetics augment the effects of muscle relaxants in the following order isoflurane (most) sevoflurane, desflurane, enflurane, and halothane and nitrous oxide (least) (Figure 27-9). The most important factors involved in this interaction are the following (1) nervous system depression at sites proximal to the neuromuscular junction (ie, central nervous system) (2) increased muscle blood flow (ie, due to peripheral vasodilation produced by volatile anesthetics), which allows a larger fraction of the injected muscle relaxant to reach the neuromuscular junction and (3) decreased sensitivity of the postjunctional membrane to depolarization. 

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