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Pharmacology serotonin reuptake

There is, however, a unique risk in the bipolar form that antidepressant treatment may trigger a switch into mania. This may occur either as the natural outcome of recovery from depression or as a pharmacological effect of the drug. Particular antidepressants (the selective serotonin reuptake inhibitors) seem less liable to induce the switch into mania than other antidepressants or electroconvulsive therapy. Treatment for mania consists initially of antipsychotic medication, for instance the widely used haloperidol, often combined with other less specific sedative medication such as the benzodiazepines (lorazepam intramuscularly or diazepam orally). The manic state will usually begin to subside within hours and this improvement develops further over the next 2 weeks. If the patient remains disturbed with manic symptoms, additional treatment with a mood stabilizer may help. [Pg.71]

When treating anxiety one should of course first treat any reversible medical condition. When pharmacological treatment is necessary SSRI is most often drug of choice. Selective serotonin reuptake inhibitors are both effective and safe. Benzodiazepines that have been widely used are drugs with a relative high risk of adverse effects (see Chapter 4). Risks for dependence and abuse must always be considered for benzodiazepines. [Pg.86]

Preskorn S. (1997). Clinically relevant pharmacology of selective serotonin reuptake inhibitors. Clinical Pharmacokinetics. 32 1-21. [Pg.514]

Pharmacology These agents are potent and selective inhibitors of neuronal serotonin reuptake and they also have a weak effect on norepinephrine and dopamine neuronal reuptake. [Pg.1081]

The pharmacological inhibition of the serotonin eliminating enzyme MAO is used in the therapy of depression and hypertension. Tranylcypromine is an irreversible unselective MAO inhibitor which displays numerous interactions with amine-containing food and monoamine-related drugs, resulting in evenmally fatal hypertensive crisis, cranial hemorrhage, arrhythmias and seizure can occur. The coadministration with speciflc serotonin reuptake inhibitors (SSRI) can result in similar effects and is therefore contraindicated. Moclobemide, on the other hand, is a reversible inhibitor of MAOa, one of the two enzyme subtyppes (MAOa, MAOb) which is void of most interactions see with tranylcypromine. [Pg.315]

Hiemke C. and S. Harther (2000). Pharmacokinetics of selective serotonin reuptake inhibitors. Pharmacology and Therapeutics 85 11-28. [Pg.265]

Leonard, H.L., March, J., Rickler, K.C., and Allen, A.J. (1997) Pharmacology of the selective serotonin reuptake inhibitors in children and adolescents. / Am Acad Child Adolesc Psychiatry 36 725-736. [Pg.281]

Preskorn, S.H. (2000) The adverse effect profiles of the selective serotonin reuptake inhbitors relationship to in vitro pharmacology. J Psychiatri Practi 6 153-157. [Pg.282]

FIGURE 43.1 Pharmacologic treatment algorithm for full syndrome pediatric PTSD. Based on a snythesis of consensus data and clinical reports in the adult and child literature. The author hers no responsibility for the use of this guideline by third parties. SSRI, selective serotonin reuptake inhibitor NEE, nefaza-done SIB, self injurious behavior VLF, venlafaxine VPA, valproic acid. [Pg.583]

Hirano, Kazufumi, Ryohei Kimura, Yumi Sugimoto, Jun Yamada, Shinya Uchida, Yasuhiro Kato, Hisakuni Hashimoto, and Shizuo Yamada. Relationship Between Brain Serotonin Transporter Binding, Plasma Concentration and Behavioural Effect of Selective Serotonin Reuptake Inhibitors. British Journal of Pharmacology 144 (2005) 695-702. The researchers show that SSRIs begin to act on serotonin transporters within hours. [Pg.102]

The prevalence of anxiety disorders has spurred the search for pharmacological ways to treat these pathologies. To date, doctors have found that drugs from two broad classes—the benzodiazepines and selective serotonin reuptake inhibitors. [Pg.110]

In this chapter, we review the pharmacology of several selective serotonin reuptake inhibitors [SSRIs] and other drugs that act on the serotonergic system. That these developments have enhanced safety and tolerability is now beyond dispute, but it is also clear that these agents are no more effective than the old-style tricyclic antidepressants [TCAs]. [For a comprehensive discussion of serotonergic medication, see Montgomery, Chapter 12, in this volume.] Here, several compounds are discussed in detail. [Pg.213]

Basic pharmacology. Fluvoxamine is an effective serotonin reuptake inhibitor with an ICjg value of 0.3 pmol/L comparable ICjg values for desipramine and fluoxetine are 0.8 jmol/L and 1.3 omol/L, respectively [Bradford 1984]. The ICjo values for NA and dopamine were 100 times higher than those for serotonin [Bradford 1984]. In vitro data indicate that fluvoxamine has little or no affinity for Oj, a, Pi, P2, Dj, S-HTj, muscarinic, or histaminergic receptors [Benfield and Ward 1986]. Fluvoxamine has a total of 11 metabolites, and the 2 principal ones have little or no pharmacological activity [Claassen 1983]. [Pg.215]


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