Monoamine oxidase inhibitors drug administration

The hypotensive effects of most antihypertensive dru are increased when administered with diuretics and other antihypertensives. Many dnigp can interact with the antihypertensive drugs and decrease their effectiveness (eg, antidepressants, monoamine oxidase inhibitors, antihistamines, and sympathomimetic bronchodilators). When the ACE inhibitors are administered with the NSAIDs, their antihypertensive effect may be decreased. Absorption of the ACE inhibitors may be decreased when administered with the antacids. Administration of potassium-sparing diuretics or potassium supplements concurrently with the ACE inhibitors may cause hyperkalemia. When the angiotensin II receptor agonists are administered with... 

Virtually all types of drug that have been shown to be effective in major depression exert profound effects on the functioning of the serotoninergic or noradrenergic systems, or both. Although some treatments have been shown to decrease the sensitivity of certain postsynaptic 5-HT and NE receptors, it is generally believed that it is an enhancement of neurotransmission in these systems that is responsible for the improvement of the core symptoms of depression. For instance, long-term administration of tricyclic antidepressants (TCAs) or monoamine oxidase inhibitors (MAOIs) decreases the density of (3-adrenoceptors and cortical 5-HT2 receptors (Blier and Abbott 2003). 

Serendipity has played a major role in the discovery of most classes of psychotropic drugs. For example, the observation that the first antidepressants, the tricyclic antidepressants and the monoamine oxidase inhibitors, impeded the reuptake of biogenic amines into brain slices, or inhibited their metabolism, following their acute administration to rats, provided the experimenter with a mechanism that could be easily investigated in vitro. Such methods led to the development of numerous antidepressants that differed in their potency, and to some extent in their side effects (for example, the selective serotonin reuptake inhibitors) but did little to further the development of novel antidepressants showing greater therapeutic efficacy. The accidental discovery of atypical antidepressants such as mianserin led to the broadening of the basis of the animal models... 

Hypersensitivity to the drug seizure disorder current or prior diagnosis of bulimia or anorexia nervosa concurrent administration of a monoamine oxidase inhibitor (MAOl) (at least 14 days should elapse between discontinuation of an MAOl and initiation of treatment with bupropion) in patients being treated with other bupropion products (eg, for smoking cessation) in patients undergoing abrupt discontinuation of alcohol or sedatives (including benzodiazepines). 

R.L. Sherry, R.T. Courts, G.B. Baker, Fluorotranylcypromine, a novel monoamine oxidase inhibitor. Neurochemical effects in rat brain after short- and long-term administration. Drug Dev. Res. 48 (1999) 61-69. 

ECT is superior in efficacy when compared with placebo, sham ECT, and active drug therapy. Upon the introduction of effective pharmacotherapy for severe depression, the relative efficacy of drug versus ECT was frequently studied. Our review of the relevant literature led to an extrapolation of the data from selected studies (primarily class I or II designs) for a quantitative analysis of the efficacy of ECT versus other treatments for an acute depressive episode ( 53). The comparisons with ECT included simulated (or sham) ECT, placebo, the standard tricyclic antidepressants, and the monoamine oxidase inhibitors [ Table 8-1 (54, 55, 56, 57, 58 and 59), Table 8 2 (0g 6i 62 and 63), Table 8-3 (56, 61, 62, 63, 64, 65 and 66), and Table 8-4 (55, 60, 61, 62 and 63)]. We also compared the relative efficacy of the bilateral versus the UNID forms of administration [Table 8-5 (42, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77 and 78)]. A meta-analysis was... 

The positive effects of the monoamine oxidase inhibitor isoniazid and the amine reuptake blocker imipramine were both discovered by accident. Isoniazid was being used as an antitubercular drug when patients reports of elation led Nathan Kline to test and to demonstrate its antidepressant power. Ronald Kuhn had synthesized imipramine, a tricyclic molecule, as a possible me-too analog of chlorpromazine. When Kuhn found that it had little or no antipsychotic potential, he tried it out on depressives, and voila They got better. After a while, that is. As with isoniazid, imip-ramine s antidepressant action was evident only after one to four weeks of administration. 

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. 

Adverse effects Large doses of meperidine cause tremors, muscle twitches, and rarely, convulsions. The drug differs from opioids in that in large doses it dilates the pupil and causes hyperactive reflexes. Severe hypotension can occur when the drug is administered postoperatively. When used with major neuroleptics, depression is greatly enhanced. Administration to patients taking monoamine oxidase inhibitors (see p. 123) can provoke severe reactions such as convulsions and hyperthermia. Meperidine can cause dependence, and can substitute for morphine or heroin in use by addicts. Cross-tolerance with the other opioids occurs. 

AKC = atopic keratoconjunctivitis FDA = U.S. Food and Drug Administration GI = gastrointestinal GPC = giant papillary conjrmctivitis OTC = over the cormter VKC = vernal keratoconjunctivitis URI = upper respiratory infection MAOI = monoamine oxidase inhibitor... 

The most frequent side effect for diazepam is somnolence dizziness, ataxia, headache, nervousness, euphoria, and rash occur iess frequently. Excessive use of rectai diazepam may produce rebound seizures (63). Intravenous administration may produce infrequent respiratory depression and hypotension. Other sedative drugs, such as barbiturates, valproate, narcotics, phenothiazines, monoamine oxidase inhibitors, and antidepressants, can potentiate the effects of diazepam. 

Metabolic inactivation, whether taking place in the e,r, or at other sites, is often accidentally inhibited by other drugs. Thus many patients have died as a result of the simultaneous administration of an inhibitor of monoamine oxidase (an enzyme present in mitochondria) and an amine drug which is not toxic on its own. These monoamine oxidase inhibitors, such as tranylcypromine 9,47), are prescribed as mood-elevators in depressive illnesses. Until their synergistic properties were realized, they caused many deaths after usually safe doses of amphetamine, pethidine, and amitriptyline, or after the patient had consumed food rich in pressor amines such as tyramine such foods are red wine, meat-extract, yeast-extract, broad beans, and particularly cheese. These are examples of unfortunate synergism, but many favourable cases are known, examples of which will now be given. 

Drug interactions bupivacaine solutions containing epinephrine or norepinephrine administered to patients receiving monoamine oxidase inhibitors or tri-cychc antidepressants may produce severe, prolonged hypertension. Concurrent administration of vasopressor drugs added to bupivacaine/vasoconstrictor solutions and of ergot-type oxytocic drugs may cause severe, persistent hypertension or cerebrovascular accidents. 

Advanced arteriosclerosis symptomatic cardiovascular disease moderate to severe hypertension hyperthyroidism hypersensitivity or idiosyncrasy to the sympathomimetic amines glaucoma agitated states history of drug abuse during or within 14 days following administration of monoamine oxidase (MAO) inhibitors (hypertensive crises may result). 

Interactions The vitamin pyridoxine (B6) increases the peripheral breakdown of levodopa and diminishes its effectiveness (Figure 8.6). Concomitant administration of levodopa and monoamine oxidase (MAO) inhibitors, such as phenelzine (see p. 124), can produce a hypertensive crisis caused by enhanced catecholamine production therefore, caution is required when they are used simultaneously. In many psychotic patients, levodopa exacerbates symptoms, possibly through the buildup of central amines. In patients with glaucoma, the drug can cause an increase in intraocular pressure. Cardiac patients should be carefully monitored because of the possible development of cardiac arrhythmias. Antipsychotic drugs are contraindicated in parkinsonian patients, since these block dopamine receptors and produce a parkinsonian syndrome themselves. 

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