Pharmacology inhibitors MAOIs

Synergy of unwanted pharmacological effect ginseng and its products will inhibit the central nervous system (CNS) when they are applied with luminal, chloral hydrate, or ephedrine, which can increase the release of dopamine, noradrenaline, and serotonin in the CNS thus inducing a hypertensive crisis if monoamine oxidase inhibitors (MAOIs) are given simultaneously. 

Maintenance/Continuation/Extended treatment There is no evidence to indicate how long the depressed patient should be treated with nefazodone. However, it is generally agreed that pharmacologic treatment for acute episodes of depression should continue for at least 6 months. Whether the dose of antidepressant needed to induce remission is identical to the dose needed to maintain euthymia is unknown. In clinical trials, more than 250 patients were treated for at least 1 year. Switching to or from a monoamine oxidase inhibitor (MAOi) At least 14 days should elapse between discontinuation of an MAOI and initiation of therapy with nefazodone. In addition, wait at least 7 days after stopping nefazodone before starting an MAOI. 

Antidepressants were first introduced into the market in the 1950s with the serendipitous discovery of the antidepressant effect of two drugs initially evaluated for other medical uses Iproniazide, a monoamine oxidase inhibitor (MAOI), and Imipramine, a tricyclic antidepressant (TCA). Since then, a whole new generation of chemically and pharmacologically unrelated compounds have been introduced, which appear to be safer and better tolerated due to a more specific mechanism of action. These include selective serotonin reuptake inhibitors (SSRIs), serotonin and... 

There are three main pharmacological classes of antidepressant compounds tricyclic antidepressants (TCA), monoamine oxidase inhibitors (MAOI) and serotonin reuptake inhibitors (SSRI). Members of each class have been tried in BN. According to a survey of 19 controlled clinical trials, all are more effective than placebo, with little to choose between them in terms of efficacy (Bacaltchuk and Hay 2003). 

The antidepressant drugs are generally classified according to their chemical structure (e.g., tricyclic antidepressants [TCA]) or according to their pharmacological action (e.g., monoamine oxidase inhibitors [MAOI] serotonin reuptake inhibitors [SSRI]). Certain other antidepressants, which do not fall into the above categories, are sometimes referred to as atypical antidepressants (see below). 

Newer generations of antidepressants have provided pharmacological interventions that are effective and better tolerated than older agents like the tricyclic antidepressants (TCAs) and the monoamine oxidase inhibitors (MAOIs). In addition, substantial efforts have been undertaken to improve the ability of clinicians to recognize the signs and symptoms of depression and to treat. This chapter focuses exclusively on the diagnosis and treatment of major depressive disorder. 

Monoamine oxidase inhibitors and many pharmacological agents are synergistic, sometimes resulting in a hypertensive crisis. The agents with which the MAOIs may be synergistic include amphetamine, dextroamphetamine, methyl amphetamine, ephedrine, procaine preparations (which usually contain norepinephrine), epinephrine, methyldopa, and phenylpropanolamine (over-the-counter cold preparations). 

It was initially believed that the antidepressant effectiveness of MAOIs was the direct result of MAO inhibition. This acute effect decreases degradation of monoamines (e.g., norepinephrine, serotonin, or dopamine) stored in presynaptic neurons, thereby resulting in an increased amount of these neurotransmitters available at the synapse. More recent research indicates that this model does not fully explain the mechanism of MAOIs efficacy. For example, the positive (h-) stereoisomer of tranylcypromine is a poor antidepressant despite inhibiting MAO. The main pharmacologic difference between the negative (-) and + isomers of tranylcypromine is that the former has much weaker effects as a norepinephrine reuptake inhibitor in relation to its potency as an MAOI. The other MAOIs may also block the reuptake of selected neurotransmitters. However, like the non-MAOI uptake inhibitors, these acute effects often precede clinical antidepressant effects by weeks. More consistent with the 2- to 4-week lag in therapeutic effect, chronic treatment with a diverse number of MAOIs has been shown to reduce the number of a2- and P-adrenergic and serotonin (5-HT2) postsynaptic binding sites in the brain. 

Selegiline [(/ )(-)-W,a-dimethyl-W-(2-propynyl)benzeneethanamine, Elde-pryl. Deprenyl, 1] is a phenethylamine derivative which is pharmacologically active in the levo form. It is indicated as adjuvant treatment with levo-dopa in Parkinson s disease, and is supplied as a 5 mg tablet of selegiline hydrochloride. It belongs to the class of type B inhibitors of monoamine oxidase (MAOI-B). At high doses (>40 mg/day in man), selegiline loses its MAOI-B specificity and also inhibits MAO-A. 

In 1987, the United States Food and Dmg Administration (FDA) approved the use of fluoxetine for the treatment of depression and this derivative is now considered to be the prototype of a dmg class called selective serotonin reuptake inhibitors (SSRIs). As the name suggests, this term refers to the reuptake blockage of serotonin into the pre-synaptic membrane in order to indirectly increase neurotransmitter availability. A number of these derivatives showed beneficial effects for the treatment of a variety of additional conditions such as obsessive-compulsive disorders (OCD), bulimia nervosa, anxiety disorders, obesity, anorexia, post-traumatic stress disorders (PTSD) and others. SSRIs have become the first-line therapy for depression, which is based on improved side effect profiles when compared with TCA derivatives or MAOIs. A number of adverse effects are described in the pharmacological literature and include sexual dysfunction. 

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