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Haloperidol alcohol

There is an increased central nervous system (CNS) depressant effect when the skeletal muscle relaxants are administered with other CNS depressants, such as alcohol, antihistamines, opiates, and sedatives. There is an additive anticholinergic effect when cyclobenzaprine is administered with other drugs with anticholinergic effects (eg, antihistamines, antidepressants, atropine, haloperidol). See Chapter 30 for information on diazepam. [Pg.191]

Conversion of haloperidol to reduced haloperidol (a secondary alcohol) Glutathine dependent reduction of disulfiram to deithyldithiocarbamate Thioredoxin dependent of sulindac to sulindac sulfide DT diaphorase reduction of menadione to hydroquinone Conversion of pentabromoethane to tetra bromoethane (releasing free bromide ion)... [Pg.707]

Recently, three papers have reported the determination of risperidone and its active metabolite 9-hydroxyrisperidone using LLE and SPE technologies. The analytical columns used to separate these compounds were C4 or C18 bonded phases of 3 pm or 5 pm particle sizes with UV/VIS detection. Mobile phases consisted of phosphate bufiers (pH 3-4) in acetonitrile. The sample volumes used ranged from 200 pi to 1 ml, with extraction recoveries averaging 90%. The limits of quantitation ranged from 0.5 to 10 ng/ml in human plasma (Nagasaki et al., 1999 Avenso et al., 2000 Titier et al., 2002). A study by Titier showed the simultaneous determination of clozapine, olanzapine, haloperidol, risperidone, and its active metabolites by RP-HPLC in human plasma. The assay involved LLE with a hexane/isoamyl alcohol mixture... [Pg.34]

Drugs that affect nefazodone include general anesthetics, sibutramine, sumatriptan, buspirone, carbamazepine, and propranolol. Drugs that may be affected by nefazodone include alcohol, benzodiazepines, buspirone, carbamazepine, cisapride, digoxin, haloperidol, HMG-CoA reductase inhibitors, MAOIs, propranolol, St. John s wort, cyclosporine, and tacrolimus. [Pg.1067]

Drugs that may be affected by SSRIs Drugs that may be affected by SSRIs include alcohol, benzodiazepines, beta blockers, buspirone, carbamazepine, cisapride, clozapine, cyclosporine, diltiazem, digoxin, haloperidol, hydantoins, lithium, methadone, mexiletine, nonsedating antihistamines, NSAIDs, olanzapine, phenothiazines, phenytoin, pimozide, procyclidine, ritonavir, ropivacaine, sumatriptan, sulfonylureas, sympathomimetics, tacrine, theophylline, tolbutamide, tricyclic antidepressants, and warfarin. [Pg.1086]

Clinical signs and symptoms include sudden onset of irrational, combative, or destructive behavior after ingesting relatively small amounts of alcohol. The behavior is atypical of the individual when not drinking, and usually begins within minutes to hours. After the acute outburst, the patient usually lapses into deep sleep and upon awakening has only fragmentary memory or total amnesia for the episode. Treatment should attempt to diminish stimulation as much as possible, and antipsychotics, such as haloperidol (2 to 5 mg orally, i.m., or i.v.) may reduce combative or destructive behavior. [Pg.296]

Haloperidol A concentrated solution of haloperidol (5 mg/mL) is incompatible with heparin sodium (in sodium chloride or glucose solutions), sodium nitroprusside (in glucose solutions), cefmetazole sodium, diphenhydramine, and sargramostim. Solutions of haloperidol precipitate if diluted with a 0.9% sodium chloride solution.158,159 Photodegradation of haloperidol could be prevented using benzyl alcohol and vanillin.160... [Pg.354]

The functional capacity of the brain is impaired. Irreversible damage may manifest in a measurable fallout of neuronal cell bodies. Often delirium tremens develops (usually triggered by alcohol withdrawal), which can be managed with intensive therapy (clomethiazole, haloperidol, among others). In addition, alcoholic hallucinations and Wernicke-Korsakow syndrome occur. All of these are desolate states. [Pg.344]

A 34-year-old alcoholic man with acute pancreatitis was given continuous intravenous infusion of haloperidol (2 mg/hour) for agitation after 7 hours he received a bolus dose of haloperidol 10 mg for worsening agitation and 20 minutes later, QT interval was 560 ms (420 ms before treatment) (131). He developed torsade de pointes and ventricular fibrillation, which resolved with electric defibrillation. He was a smoker and was also taking tiapride and alprazolam for depression, in addition to pantoprazole, piperazilline + tazobactam, paracetamol, and vitamins Bi, B6, and B 12-... [Pg.201]

A 39-year-old man died suddenly 1 hour after taking a single oral dose of haloperidol 5 mg (14). He had myasthenia, alcoholic hepatitis, and electrolyte abnormalities due to inadequate nutritional state. His electrocardiogram showed prolongation of the QTC interval (460 ms). Autopsy showed a cardiomyopathy but no explanation for sudden death. [Pg.296]

Haloperidol increased blood alcohol concentrations (45). Anticoagulants... [Pg.297]

A 37-year-old man who had abused metamfetamine, paint thinner, psychotomimetic drugs, and alcohol for 20 years was given chlorpromazine, haloperidol, and fluni-trazepam just before surgery. After spinal anesthesia he was given propofol 5 mg/kg/hour intravenously. However, euphoria and excitement occurred 10 minutes after the start of the infusion and he had excitement, hallucinations, and delirium. His symptoms were suppressed by intravenous haloperidol 5 mg. [Pg.692]

Disposition in the Body. Readily absorbed after oral administration bioavailability about 65%. Haloperidol is localised in the tissues and rapidly taken up by the brain. It is slowly excreted in the urine, about 40% of a dose being eliminated in 5 days with only about 1% of the dose as unchanged drug about 15% of a dose is excreted in the bile. Metabolites which have been identified in urine are 4-fluorobenzoylpropionic acid and 4-fluorophenylaceturic acid (the glycine conjugate of 4-fluoro-phenylacetic acid), both of which are inactive. Haloperidol is also metabolised by reduction of the ketone group to a secondary alcohol. [Pg.648]

Thoma and Klimek (115) also found that the natural food colorant curcumin as well as Fast Yellow, chrysoine, apocarotinol, and, cochineal Red A photostabi-lized solutions of nifedipine and nitrofurazone. They also found that vanillin and methyl gallate could stabilize solutions of dihydroergotamine. These authors also found that furosemide was stabilized by the addition of vanillin, haloperidol by benzyl alcohol, and vanillin and thiothixene by quinosol and vanillin. [Pg.366]

When treating alcoholic liver diseases, it should be taken into account that one is generally dealing with chronic alcoholics. Therefore, one should be aware of the fact that a withrawal syndrome might occur, possibly requiring the application of clomethiazole, haloperidol or clonidine. In this complicated phase, the administration of zinc is likewise recommended. (138)... [Pg.536]

Clinically important, potentially hazardous interactions with alcohol, amiodarone, amphotericin B, cisapride, clonidine, digitalis, diltiazem, disopyramide, erythromycin, glucocorticoids, halofantrine, haloperidol, hypokalemic diruretics, imipramine antidepressants, levodopa, lithium, pentamidine, pimozide, quinidine, sotalol, stimulant laxatives, tetracosactides, thioridazine... [Pg.544]

Haloperidol undergoes extensive metabolism to form a myriad of primary and secondary metabolites (479-486). The principal phase I reactions involve the following oxidative N-dealkylation to initially form 4-fluoro-phenylbenzoylpropionaldehyde (which is rapidly oxidized to the acid) and 4-(4-chlorophenyl)-4-hydroxypiperidine (479,480, 483-485) N-oxidation to form haloperidol-iV-oxide (485) and reversible reduction of the carbonyl group to the alcohol, or reduced haloperidol (481,487). A phase II metabolite, hal-operidol-O-glucuronide, accounts for as much... [Pg.637]

Factors that inhibit or alter the activity of the mixed function oxidase enzymes may increase the risk from exposure to the indicator compounds in the aromatic EC5-EC9 fraction (the BTEXs), the aromatic EC>16-EC35 fraction (the carcinogenic PAHs in this fraction) and a constituent of the aliphatic I < C5IiCH fraction (//-hexane). For example, concurrent alcohol consumption may increase the risk of central nervous system depression from the BTEXs, ototoxicity from toluene, and hematotoxicity from benzene. Acetone exposure may increase the risk of peripheral neuropathy of n-hexane. People who take haloperidol, acetaminophen, or aspirin, or who have a nutritionally inadequate diet, may also be more susceptible to the toxicity of these agents. ATSDR (1995f) noted that a substantial percentage of children consume less than the recommended dietary allowances of certain nutrients. [Pg.206]

Although phenothiazines, clonidine, carbamazepine, y-hydroxybutyric acid, and valproic acid may reduce symptoms of alcohol withdrawal, their ability to prevent seizures or delirium tremens has yet to be proven, and in fact, the phenothiazines may lower the seizure threshold. Other drugs used to treat symptoms of alcohol withdrawal include other barbiturates, alcohol itself, sympatholytics such as atenolol, thiamine, magnesium, and other neuroleptics such as haloperidol. At the time of this writing, gabapentin is being compared to lorazepam for acute alcohol withdrawal in a phase II clinical trial. [Pg.1196]

Haloperidol IM (oily vehicle) 1.2% Benzyl alcohol in sesame oil... [Pg.344]

Procyclidine may reduce the antipsychotic effectiveness of haloperidol and phenothiazines, possibly by direct CNS antagonism related to its anticholinergic properties. Haloperidol and phenothiazine exert their effects in part by blocking the hyperactivity of dopaminergic transmission in the mesocortical and mesolimbic systems. Concomitant use with phenothiazine derivatives, especially thioridazine having pronounced anticholinergic effects, also increases the risk of anticholinergic adverse effects. Paralytic ileus may result from concomitant use with phenothiazines or tricyclic antidepressants. Concomitant use with alcohol and other CNS depressants increases procyclidine s sedative effects. [Pg.592]

The use of alcohol to treat patients in alcohol withdrawal or obstetrical patients with premature contractions is no longer recommended. Some medical centers continue to use alcohol to prevent or reduce the risk of alcohol withdrawal in postoperative patients, but administering a combination of a benzodiazepine with haloperidol or clonidine may be more appropriate. [Pg.380]


See other pages where Haloperidol alcohol is mentioned: [Pg.532]    [Pg.194]    [Pg.1024]    [Pg.186]    [Pg.195]    [Pg.88]    [Pg.37]    [Pg.1250]    [Pg.1399]    [Pg.272]    [Pg.353]    [Pg.781]    [Pg.408]    [Pg.75]    [Pg.3362]    [Pg.1579]    [Pg.51]    [Pg.72]    [Pg.493]    [Pg.43]    [Pg.483]    [Pg.627]    [Pg.307]    [Pg.314]    [Pg.191]    [Pg.193]   
See also in sourсe #XX -- [ Pg.297 ]




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Haloperidol

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