Antidepressants MAOI SSRIs TCAs

ANTI EPILEPTICS 1. ANTIMALARIALS -chloroquine, mefloquine 2. ANTIDEPRESSANTS-MAOIs, SSRIs, TCAs 3. ANTIPSYCHOTICS t risk of seizures These drugs lower seizure threshold Care with co-administration. Watch for t fit frequency warn patient of this risk when starting these drugs and take suitable precautions. Consider increasing dose of antiepileptic... 

Each antidepressant has a response rate of approximately 60% to 80%, and no antidepressant medication or class has been reliably shown to be more efficacious than another 22 MAOIs may be the most effective therapy for atypical depression, but MAOI use continues to wane because of problematic adverse effects, dietary restrictions, and possibility of fatal drug interactions.22,28 There is some evidence that dual-action antidepressants, such as TCAs and SNRIs, may be more effective for inpatients with severe depression than are the single-action drugs such as SSRIs,22,28 but the more general assertion that multiple mechanisms of action confer efficacy advantages is quite controversial.33... 

SSRIs, selective serotonin reuptake inhibitors TCAs, tricyclic antidepressants MAOI, monoamine oxidase inhibitor. 

Newer Generation Antidepressants. All SSRIs have been shown effective in the treatment of panic disorder. Of these, flnoxetine (Prozac), paroxetine (Paxil), and sertraline (Zoloft), as well as the SNRI venlafaxine ER (Effexor XR), have received FDA approval for the treatment of panic disorder. Because they are safer and easier to tolerate, SSRls/SNRls have largely supplanted the MAOIs and TCAs as standard treatments (along with benzodiazepines) for panic disorder. 

Antidepressants MAOIs, TCAs, SSRIs, SNRIs, mirtazapine, venlafaxine Amphetamines, phentermine, methylphenidate, sibutramine... 

The field of antidepressant research was revolutionized in the late 1980s by the introduction of selective serotonin reuptake inhibitors (SSRIs), exemplified by fluoxetine (9). In addition to their antidepressant action, SSRIs have also proven effective for a broad range of psychiatric illnesses, and, more importantly, they demonstrated an improved tolerability profile as compared to TCAs and MAOIs due to their increased selectivity. On the other hand, SSRIs proved inferior to TCAs and MAOIs in their reduced antidepressant effects, slower onset of action, lower remission rates, and decreased ability to control the physical symptoms associated with depression. 

Note. ECT=electroconvulsive therapy OCD=obsessive-compulsive disorder SSRI=selective serotonin reuptake inhibitor TCA=tricyclic antidepressant MAOI=monoamine oxidase inhibitor. 

Note. SSRIs=selective serotonin reuptake inhibitors TCAs=tricyclic antidepressants MAOIs=monoamine oxidase inhibitors. 

There are clear biological distinctions between OCD and PD. For example, panic attacks are produced by CO 2 inhalation, lactate infusion, yohimbine administration, psychostimulants, isoproterenol, and mCPP. By contrast, none of these agents except mCPP exacerbates obsessions or compulsions. Furthermore, OCD is benefited most by clomipramine or SSRIs, whereas panic attacks are helped by a variety of antidepressants (e.g., TCAs, SSRIs, MAOIs). 

The metabolic profile of anxiolytic agents has important ramifications for their clinical use. This section discusses the metabolism of the benzodiazepinesand buspirone in some detail. The metabolism of the SSRIs, TCAs, and MAOIs is covered in the chapter on antidepressants. 

Another major difference with Effexor as compared to many other antidepressants is that it does not last long in the body. With SSRIs, MAOIs, and TCAs, days or even weeks are needed to wash out the drugs from the body. Effexor, on the other hand, has a half-life of 5 hours, meaning that after the drug is ingested half of it will be eliminated 5 hours later. If for some reason the drug is not well tolerated, the side effects of Effexor will subside in a matter of hours. This makes Effexor extremely tolerable and risk free. To sustain its therapeutic effects, however, Effexor must be taken several times a day. 

MAOI, monoamine oxidase inhibitor SARI, serotonin antagonist and reuptake inhibitor SNRI, serotonin and norepinephrine reuptake inhibitor SSRI, selective serotonin reuptake inhibitor TCA, tricyclic antidepressant. 

The clinician should bear in mind the toxic potential for the various antidepressant medications when patients already have or develop suicidality. The TCAs and MAOIs have narrow therapeutic indices, whereas the SSRIs, SNRIs, nefa-zodone, and mirtazapine have wide therapeutic indices.22... 

If the depressive symptoms do not resolve when treatment with one of the aforementioned mood stabilizers has been maximized, adjunctive therapy with an antidepressant or second mood stabilizer should be considered. SSRIs and bupropion are well tolerated by bipolar patients and appear to hold less potential to induce mania than TCAs. Nevertheless, treatment with any antidepressant should not be started until it has been confirmed that the patient s mood stabilizer is at a therapeutic level. If treatment with two or more of these first-line antidepressants is unsuccessful, a MAOI should be considered. 

Figure 6.8. Changes that occur following the chronic administration of antidepressants. SSRIs and MAOIs desensitize the inhibitory S-HT a somato dendritic receptors. SSRIs and MAOIs desensitize the inhibitory S-HT b/S-HTid inhibitory auto receptor on the presynaptic terminal. After acute administration, the TCAs and the SSRIs inhibit the uptake of 5-HT into the nerve terminal by binding to the...

Citalopram is a selective serotonin re-uptoke inhibitor (SSRI). These tend to have fewer ontimuscarinic effects than tricyclic antidepressant (TCA) drugs, such as dry mouth and constipation however, SSRIs tend to cause gastrointestinal effects, such as nausea and vomiting. MAOIs are monoamine oxidase inhibitors. 

The growth during the 1990s in the use of antidepressants, particularly selective serotonin reuptake inhibitors (SSRIs), for the treatment of anxiety disorders represented a major advance in the pharmacotherapy of anxiety. The efficacy of tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs) had been established alongside their antidepressantw actions several decades... 

With the introduction of the SSRIs, the safety and tolerability of antidepressants improved remarkably. As a class, these medications have little or no affinity for cholinergic, (3-adrenergic or histamine receptors and do not interfere with cardiac conduction. They are well tolerated by patients with heart disease and by the elderly, who are especially sensitive to the anticholinergic and orthostatic effects of the tricyclic antidepressant agents (TCAs) and monoamine oxidase inhibitors (MAOIs). 

Most child and adolescent studies published thus far have focused on the effects of the tricyclic antidepressants (TCAs) and, more recently, the SSRIs. A few open studies have also shown that monoamine oxidase inhibitors (MAOIs) can be used safely with children and adolescents (Ryan et ah, 1988b), but noncompliance with dietary requirements may present a significant problem for minors. Other antidepressants, including the heterocyclics (HTC) (e.g., amoxapine, maprotiline), buproprion, venlafaxine, and nefazodone, have been found to be efficacious for the treatment of depressed adults (APA, 2000), but they have not been well studied for the treatment of MDD in children and adolescents. Therefore, this chapter mainly describes the use of SSRIs and TCAs for youth with MDD. 

In adults, mood stabilizers reduce the risk of cycling and have modest antidepressant effects (APA, 1994b). For patients with bipolar depression who do not respond to mood stabilizers alone, an antidepressant should be added to the treatment. It appears that bipolar depressed patients may be less likely to respond to TCAs than patients with unipolar depressions, who may show a more favorable response to bupropion, SSRI, or MAOIs. Furthermore, some studies, but not all, have also suggested that bupropion and the MAOIs are less likely to produce mania and less rapid cycling (APA, 1994b Compton and Nemeroff, 2000). 

In contrast, a less extensive but still convincing database has identified important clinical differences in efficacy for antidepressants used to treat patients with atypical or comorbid depression. Individuals with atypical depression (distinct quality of mood, hyperphagia, hypersomnia, psychomotor retardation, rejection sensitivity, and such unusual atypical features as chocolate craving] have superior responses to monoamine oxidase inhibitors (MAOIs], selective serotonin reuptake inhibitors (SSRIs), and perhaps venlafaxine, and most do not respond well to tricyclic antidepressants (TCAs] (Davidson et al. 1982 Liebowitz et al. 1988 Quitkin et al. 1988, 1991). Despite these data, TCAs unfortunately have been the first choice for most atypical patients until SSRIs were introduced. 

The commonly used classes of antidepressants are discussed in the following sections, and information about doses and half-lives is summarized in Table 2-1. The antidepressant classes are based on similarity of receptor effects and side effects. All are effective against depression when administered in therapeutic doses. The choice of antidepressant medication is based on the patient s psychiatric symptoms, his or her history of treatment response, family members history of response, medication side-effect profiles, and comorbid disorders (Tables 2-2 and 2-3). In general, SSRIs and the other newer antidepressants are better tolerated and safer than TCAs and MAOIs, although many patients benefit from treatment with these older drugs. In the following sections, clinically relevant information is presented for the antidepressant medication classes individually, and the pharmacological treatment of depression is also discussed. The use of antidepressants to treat anxiety disorders is addressed in Chapter 3. 

Although more stimulating antidepressants (e.g., bupropion, SSRIs, venlafaxine, or certain MAOIs) do not potentiate alcohol, they can produce insomnia. To minimize this problem, the dose may be given earlier in the day. TCAs may cause episodes of excitement (rare), confusion, or mania, usually in patients with an underlying psychotic illness, suggesting that a preexisting disorder must be present for these drugs to exert any psychotomimetic effects. 

There is a great disparity of current knowledge regarding the effects of antidepressants on GYP enzymes. There have been almost no studies to test the potential effects of TCAs, MAOIs, and trazodone on GYP enzymes. There has only been one study with bupropion but it demonstrated that bupropion produces substantial inhibition of GYP 2D6 comparable with the effect of fluoxetine and paroxetine. In contrast to studies in these antidepressants, there have been extensive in vitro and in vivo studies of SSRIs, nefazodone, and venlafaxine. 

As previously noted, all currently available antidepressants enhance monoamine neurotransmission by one of several mechanisms. The most common mechanism is inhibition of the activity of SERT, NET, or both monoamine transporters (Table 30-2). Antidepressants that inhibit SERT, NET, or both include the SSRIs and SNRIs (by definition), and the TCAs. Another mechanism for increasing the availability of monoamines is inhibition of their enzymatic degradation (the MAOIs). Additional strategies for enhancing monoamine tone include binding presynaptic autoreceptors (mirtazapine) or specific postsynaptic receptors (5-HT antagonists and mirtazapine). Ultimately, the increased availability of monoamines for... 

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