Summary of evidence based guidelines for OSCE explanations
Bhaskar Punukollu, Michael Phelan, Anish Unadkat in MRCPsych Part 1 In a Box, 2019
Here treatment should be attempted along the following steps: First antidepressant (AD).AD and cognitive behavioural therapy (CBT).AD and CBT and lithium.If two ADs have failed start venlafaxine.Augmentation, ie SSRI and mirtazapine.Phenelzine (particularly indicated for atypical depression).Refer to tertiary services.
MAO Inhibitors: Predicting Response/Maximizing Efficacy
Mark S. Gold, R. Bruce Lydiard, John S. Carman in Advances in Psychopharmacology: Predicting and Improving Treatment Response, 2018
Similarly, Paykel et al.26 and Ravaris et al.27 found phenelzine and amitriptyline to be equally effective in outpatient groups characterized as suffering major depressive disorders. Although these studies did not present their data in a way that illustrates the number of individuals meeting a designated level of recovery, they do demonstrate significant and meaningful pre- and post-treatment differences in mean intensity of symptoms. They can be criticized for using a relatively low maximum dose of amitriptyline, choosing a TCA with excessive side effects and without definitive therapeutic blood levels, and not measuring platelet enzyme inhibition (although the dose of phenelzine they used is relatively more adequate than that of amitryptyline). For these reasons generalizability of results is limited. In conclusion, however, it has been impossible to define consistent differences in response to MAOI and TCA when both are used inadequate dosage. There is now substantial evidence that MAOI are effective in endogenous depression.10 We would recommend an initial medication trial with TCA in this group. MAOI remain an effective second line of treatment in those patients that fail to respond.
Stimulants, antidepressants, antimanics, anticonvulsants, and psychotomimetic agents
Bev-Lorraine True, Robert H. Dreisbach in Dreisbach’s HANDBOOK of POISONING, 2001
Repeated administration of any of these drugs causes dizziness, weakness, ataxia, hallucinations, mania, agitation, constipation, dry mouth, urine retention, and excessive rise or fall of blood pressure. Iproniazid and pheniprazine may cause liver injury at any time during drug therapy. Symptoms begin with nausea and lethargy; intractable vomiting indicates rapid progression of liver damage. Pheniprazine has caused impaired vision from bilateral optic tract lesions. Combinations of these drugs or these drugs combined with others such as imipramine or opium derivatives have been more likely to cause extreme reactions, including fatal hyperpyrexia. Tranylcypromine, phenelzine, and related drugs have caused severe hypertension following the ingestion of tyramine containing food (cheese, beer, red wine, pickled herring, fermented sausages, fava beans, chocolate, etc.); and drugs such as meperidine, dextromethorphan, phenylpropranolamine, stimulants, other antidepressants (TCA, SSRI, amphetamine.
N-acetyltransferase: the practical consequences of polymorphic activity in man
Published in Xenobiotica, 2020
Phenelzine (2-phenylethylhydrazine) is a monoamine oxidase inhibitor that has been employed as an antidepressant since the 1960s. It is a simple hydrazine derivative and was first synthesised some 30 years earlier (Votoček & Leminger, 1932). Oxidation is the primary route of metabolism with 70–80% of an orally administered dose being excreted in the urine as phenylacetic acid and p-hydroxyphenylacetic acid. These workers stated that they could not detect any N-acetylated product in urine or plasma samples (Robinson et al., 1985). Although phenelzine has been shown to be a substrate for human N-acetyltransferase in vitro (Tilstone et al., 1979) it is now generally regarded that N-acetylation is a minor pathway (Baker et al., 1999). Before the knowledge of its metabolism was available it was reported that slow acetylators appeared to have an advantage in that they displayed an improved response to antidepressant treatment (Johnstone & Marsh, 1973; Paykel et al., 1982) whereas others did not observe this phenomenon (Marshall et al., 1978; Tyrer et al., 1980)
The use of inactivated brain homogenate to determine the in vitro fraction unbound in brain for unstable compounds
Published in Xenobiotica, 2020
Ramakrishna Nirogi, Parusharamulu Molgara, Gopinadh Bhyrapuneni, Arunkumar Manoharan, Nagasurya Prakash Padala, Veera Raghava Chowdary Palacharla
Dialysis membrane strips (cellulose, MWCO 12 – 14 kDa, batch # 2350 (10–15)) and 96-well equilibrium dialysis (HTD) assembly (Model-HTD96b) used for protein binding studies were procured from HTDialysis, LLC (Galesferry, CT). Rats (Wistar, 5 males) were obtained in-house in accordance with the guidelines and approval by an institutional animal ethics committee. The compounds used in this study and sodium azide were obtained from Sigma-Aldrich (St.Louis, MO). Phenelzine (PNZ) and tranylcypromine (TCP) are reference compounds whereas compound I (Cpd I) and compound II (Cpd II) are internal discovery compounds found to have stability issues in rat brain homogenate. Phenelzine is used as a positive control to test the effect of inactivation of brain homogenate on the stability. All other reagents were obtained from standard suppliers.
Therapeutic strategies for social anxiety disorder: where are we now?
Published in Expert Review of Neurotherapeutics, 2019
Antoine Pelissolo, Sandra Abou Kassm, Lauriane Delhay
The first placebo-controlled RCTs in SAD assessed irreversible monoamine oxidase inhibitors (MAOIs), namely phenelzine. Despite evidence of significant efficacy compared to placebo, phenelzine is not recommended as first or second-line treatment due to its adverse effects profile, dietary limitations and potential for toxicity through food and drug interactions [18]. Moclobemide and brofaromine, two reversible inhibitors of monoamine oxidase A, appeared to be only modestly efficacious in the treatment of SAD, and less effective than SSRIs, venlafaxine, and phenelzine [17]. Other antidepressants have been evaluated for the treatment of SAD with insufficient benefit, such as mirtazapine, or mixed and non-convincing results, such as imipramine, clomipramine, nefazodone, and bupropion [15,18,68].
Related Knowledge Centers
- Antidepressant
- Anxiolytic
- Enzyme Inhibitor
- Major Depressive Disorder
- Hydrazine
- Binding Selectivity
- Monoamine Oxidase Inhibitor
- Tranylcypromine
- Isocarboxazid
- Treatment-Resistant Depression