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Fluoxetine Bupropion

Area of assessment Clinically sedative antidepressants, e.g. amitriptyline, mianserin, trimipramine Less sedative antidepressants, e.g. bupropion, fluoxetin, moclobemide, nefazodone ... [Pg.80]

In contrast to anticonvulsants and alcohol, drugs such as bupropion, fluoxetine, fluvoxamine, nefazodone, quinidine, paroxetine, and some antipsychotics can inhibit specific CYP enzymes (7, 11, 36, 37, 41, 42, 43 and 44). Thus, TCAs, certain BZDs, bupropion, some steroids, and antipsychotics can all have their metabolism inhibited by drugs such as fluoxetine. For example, fluoxetine at 20 mg/day produces on average a 500% increase in the levels of coprescribed drugs which are principally dependent on CYP 2D6 for their clearance. That can lead to serious or even life-threatening toxicity if the drug has a narrow therapeutic index and the dose is not adjusted for the change in clearance caused by the coadministration of fluoxetine. [Pg.37]

D6 Tricyclic antidepressants (TCAs), benztropine, perphenazine, clozapine, haloperidol, codeine/oxycodone, risperidone, class Ic antiarrhythmics, 3 blockers, trazodone, paroxetine, maprotiline, amoxapine, duloxetine, mirtazapine (partly), venlafaxine, bupropion Fluoxetine, paroxetine, duloxetine, hydroxybupropion, methadone, cimetidine, haloperidol, quinidine, ritonavir Phenobarbital, rifampin... [Pg.668]

Bupropion + fluoxetine ( other SSRIs) —> delirium and possible grand-mal seizures. Bupropion + lithium —> seizures can occur. [Pg.460]

Preskorn SH. Comparison of fhe folerabilify of bupropion, fluoxetine, imipramine, nefazodone, paroxefine, sertraline, and venlafaxine. J Clin Psychiafry f 995 56(Suppl 6) f2-2f. [Pg.228]

Selective serotonin reuptake inhibitors (SSRIs) are frequently prescribed medications. Their therapeutic actions are diverse, ranging from efficacy in depression to obsessive-compulsive disorder, panic disorder, bulimia, and other conditions. They include bupropion, fluoxetine, nefazodone, paroxetine, and miscellaneous other drugs. [Pg.1271]

After ingestion of a meal that included sardines, cheese, and red wine, a patient taking an antidepressant drug experiences a hypertensive crisis. The drug most likely to be responsible is (A) Bupropion Fluoxetine Imipramine Phenelzine Trazodone... [Pg.593]

The mechanism of action of most of the miscellaneous antidepressants is not clearly understood. Examples of this group of drugs include fluoxetine (Prozac) and bupropion (Wellbutrin). [Pg.282]

Adverse reactions with administration of bupropion include citation, dry mouth, insomnia, headache, nausea, constipation, anorexia, weight loss, and seizures. Fluoxetine administration may result in headache, activation of mania or hypomania, insomnia, anxiety, nervousness, nausea, vomiting, and sexual dysfunction. Trazodone administration may cause the following adverse reactions drowsiness, skin disorders, anger, hostility, anemia, priapism, nausea, and vomiting. Additional... [Pg.282]

Antidepressants Desipramine, imipramine, sertraline, fluoxetine, paroxetine, venlafaxine, bupropion, nefazodone, mirtazapine, gepirone, amineptine Mixed findings suggest that better designed studies may find a niche for some of these drugs. Amineptine was effective for withdrawal symptoms. [Pg.196]

At the last visit, MW s fluoxetine was changed to bupropion, pergolide was started and gradually increased to 0.25 mg three times daily, and a dandruff shampoo was started. Since that time his skin condition, attitude, apathy, stiffness, rigidity, handwriting, tremor, slowness, and kicking have improved. The UPDRs score is 5 while "on". [Pg.484]

Many neurotransmitters are inactivated by a combination of enzymic and non-enzymic methods. The monoamines - dopamine, noradrenaline and serotonin (5-HT) - are actively transported back from the synaptic cleft into the cytoplasm of the presynaptic neuron. This process utilises specialised proteins called transporters, or carriers. The monoamine binds to the transporter and is then carried across the plasma membrane it is thus transported back into the cellular cytoplasm. A number of psychotropic drugs selectively or non-selectively inhibit this reuptake process. They compete with the monoamines for the available binding sites on the transporter, so slowing the removal of the neurotransmitter from the synaptic cleft. The overall result is prolonged stimulation of the receptor. The tricyclic antidepressant imipramine inhibits the transport of both noradrenaline and 5-HT. While the selective noradrenaline reuptake inhibitor reboxetine and the selective serotonin reuptake inhibitor fluoxetine block the noradrenaline transporter (NAT) and serotonin transporter (SERT), respectively. Cocaine non-selectively blocks both the NAT and dopamine transporter (DAT) whereas the smoking cessation facilitator and antidepressant bupropion is a more selective DAT inhibitor. [Pg.34]

Tricyclic drugs have, as the name implies, a three-ring structure, and interfere with reuptake of norepinephrine and/or serotonin into axon terminals. Tricyclic drugs include imipramine (Tofranil), amitriptyline (Elavil), clomipramine (Anafranil), and nortriptyline (Pamelor, Aventil). Tricyclics have the occasional but unfortunate cardiovascular side effects of arrhythmia and postural hypotension. Newer, nontricyclic antidepressants have been developed that are collectively referred to as SSRIs. These have a potent and selective action on serotonin, and lack the cardiovascular side effects of the tricyclics. These include fluoxetine (Prozac), paroxetine (Paxil), sertraline (Zoloft), and fluvoxamine (Luvox). A fifth SSRI, citalopram (Celexa) has been used in Europe and has recently been approved in the United States. Venlafaxine (Effexor) blocks reuptake of norepinephrine and serotonin, while bupropion (Wellbutrin) acts on both dopamine and norepinephrine. [Pg.251]

Antidepressants. In the early 1980s, the recognition that depression is a frequent comorbid feature of BN coupled with the observation that appetite changes are a common feature of depression led researchers to evaluate antidepressant treatment for BN. Since that time, a series of controlled studies have demonstrated efficacy for a wide assortment of antidepressants including the TCAs imipramine (Tofranil) and desipramine (Norpramin), the MAOl phenelzine (Nardil), the SSRl fluoxetine (Prozac), and the atypical antidepressants trazodone (Desyrel) and bupropion (Wellbutrin). Overall, approximately two-thirds of antidepressant-treated patients with bulimia experience symptomatic improvement while nearly one-third achieves complete remission of binging and purging. In addition, the improvement in the symptoms of BN is not dependent on the presence of comorbid depression. [Pg.221]

Beta agonists (terbutaline, albuterol) Theophylline Antidepressants Bupropion Citalopram Escitalopram Duloxetine Fluoxetine Fluvoxamine... [Pg.265]

There are four classes of antidepressants tricyclic antidepressants (imipramine, trimipramine, amitriptyline, doxepin, desipramine, protriptyline, nortriptyline, amoxapine, maprotiline) monoaminooxidase (MAO) inhibitors (phenelzine, isocarboxazid, tranylcypromine) second-generation antidepressants or atypical antidepressants, which are a chemically dissimilar group of recently proposed drugs (bupropion, trazodone, fluoxetine) and amphetamines and other stimulators of the CNS (dextroamphetamine, methylphenidate). [Pg.103]

Bupropion is an a-aminoketone that is structurally related to amphetamines, and it exhibits unique activity comparable to that of other antidepressants. It is believed that bupropion restores the total amount of norepinephrine in the body. This compound is a poor reuptake inhibitor of dopamine, and does not exhibit anticholinergic activity or inhibit MAO. Its efficacy as an antidepressant is comparable to that of tricyclic antidepressants, and as a serotonin uptake inhibitor it is comparable to fluoxetine. It is preferable to use amoxapine. Synonyms of bupropion are amphebutamon and wellbutrin. [Pg.113]

E. Nefazodone,fluoxetine,mirtazapine, and venlafaxine have minimal effects on seizure threshold. Bupropion in its original formulation caused seizures in 4 in 1000 patients. Although this has been reduced with the slow release form of the medication (Wellbutrin SR), it remains a contraindication to prescribe this medication to patients with a history of seizures. [Pg.395]

Labbate LA, Pollack MH Treatment of fluoxetine-induced sexual dysfunction with bupropion a case report. Ann Clin Psychiatry 6 13-15, 1994... [Pg.66]

Reports are on hand relating to more recent antidepressants such as bupropion, citalopram (Fairweather ei ul., 1997), fluoxetine (Gelfin et ul.. 1998). moclobemide (Dingemanse et ul., 1998) and paroxetine (Brauer et ul.. 1995). These products, in agreement with their clinical profiles, produce fewer subjective effects and generally less sedation in healthy subjects than the older... [Pg.79]

Although the efficacy of tricyclic antidepressants in the treatment of unipolar depression is beyond reproach, the side-effect profile of these agents makes them less desirable as first-line therapeutic agents. Introduction of selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, paroxetine, sertraline, citalopram and fluvoxamine in the past decade has revolutionized the treatment of depression universally. The side-effect profile of SSRIs, such as nausea, diarrhea and sexual dysfunction, is considerably more benign than that of tricyclic drugs. Multiple controlled trials have proven the efficacy of SSRIs vs. placebo (Nemeroff, 1994). Recently, a number of SNRIs (serotonin and noradrenaline reuptake inhibitors) and so-called atypical antidepressants have been marketed that may have additional advantages over SSRIs, such as more rapid onset of action (venlafaxine. mirtazapine) and low sexual side-effect potential ( bupropion, nefazodone). Additionally, it appears that venlafaxine may be more efficacious in cases of treatment-refractory depression (Clerc et al., 1994 Fatemi et al., 1999). Finally, in a recent report (Thase et al., 2001),... [Pg.276]

The dearth of information on the metabolism of bupropion may initially seem surprising however, this drug is one of the oldest of the newer antidepressants, having entered clinical trials in the mid-1970 s and having been approved before fluoxetine ( 308, 314, 315). Ironically, its marketing was delayed after its approval because of the risk of seizures, which, in turn, is almost undoubtedly a consequence of its complicated pharmacokinetics ( 163). [Pg.138]

As a results of these studies, clinicians have proposed that switching to reboxetine or bupropion might a useful strategy given that these antidepressants share the ability with desipramine and imipramine to block NE uptake. Nevertheless, only one small open label study has been done to test this possibility ( 365). If bupropion is to be used in patients switched from an ineffective trial of fluoxetine, the dose should be kept low for several weeks to allow for the clearance of fluoxetine and norfluoxetine. Case reports indicate that fluoxetine can elevate levels of the active metabolites of bupropion, which, in turn, could mediate an increase risk of adverse effects (366). [Pg.142]

Because reboxetine and bupropion share with desipramine the ability to block the NE uptake pump, some clinician may want to combine them with an SSRI. Bupropion, however, should be used cautiously with fluvoxamine, fluoxetine, and paroxetine because these three antidepressants inhibit one or more CYP enzymes to a substantial degree at their lowest, usually effective antidepressant dose. Therefore, the dose of bupropion should be kept low and TDM could be used to ensure that unusually high levels of bupropion or its active metabolites do not develop. [Pg.143]

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. [Pg.154]


See other pages where Fluoxetine Bupropion is mentioned: [Pg.156]    [Pg.685]    [Pg.161]    [Pg.1138]    [Pg.156]    [Pg.685]    [Pg.161]    [Pg.1138]    [Pg.290]    [Pg.334]    [Pg.577]    [Pg.591]    [Pg.470]    [Pg.778]    [Pg.54]    [Pg.213]    [Pg.303]    [Pg.472]    [Pg.142]    [Pg.63]    [Pg.81]    [Pg.12]    [Pg.138]    [Pg.144]    [Pg.155]    [Pg.157]    [Pg.273]   
See also in sourсe #XX -- [ Pg.1215 ]




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Bupropion

Fluoxetin

Fluoxetine

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