Phenelzine Oral: Uses, Side Effects, Interactions, Pictures, Warnings & Dosing

Drug interactions may change how your medications work or increase your risk for serious side effects. This document does not contain all possible drug interactions. Keep a list of all the products you use (including prescription/nonprescription drugs and herbal products) and share it with your doctor and pharmacist. Do not start, stop, or change the dosage of any medicines without your doctor’s approval.

Some products that may interact with this drug include: other antidepressants (including maprotiline, mirtazapine, nefazodone, TCAs such as amitriptyline/nortriptyline), appetite suppressants (such as diethylpropion), drugs for attention deficit disorder (such as atomoxetine, methylphenidate), apraclonidine, bupropion, buspirone, carbamazepine, cyclobenzaprine, deutetrabenazine, dextromethorphan, certain drugs for high blood pressure (such as guanethidine, methyldopa, beta blockers such as atenolol, clonidine, rauwolfia alkaloids), other MAO inhibitors (isocarboxazid, linezolid, metaxalone, methylene blue, moclobemide, procarbazine, rasagiline, safinamide, selegiline, tranylcypromine), metoclopramide, certain opioid medications (such as fentanyl, meperidine, methadone, tapentadol), certain drugs for Parkinson’s (such as entacapone, levodopa, tolcapone), street drugs (such as LSD, mescaline), stimulants (such as amphetamines, cocaine, dopamine, epinephrine, phenylalanine), tetrabenazine, “triptan” migraine drugs (such as sumatriptan, rizatriptan), tramadol, tyrosine, tryptophan, valbenazine.

The risk of serotonin syndrome/toxicity increases if you are also taking other drugs that increase serotonin. Examples include street drugs such as MDMA/ “ecstasy,” St. John’s wort, certain antidepressants (including SSRIs such as fluoxetine/paroxetine, SNRIs such as duloxetine/venlafaxine), among others. The risk of serotonin syndrome/toxicity may be more likely when you start or increase the dose of these drugs.

Tell your doctor or pharmacist if you are using any of these medications before, during, or within 2 weeks after treatment with phenelzine. Tell your doctor or pharmacist if you have taken fluoxetine during at least 5 weeks before starting phenelzine. Discuss with your doctor how much time to wait between starting or stopping any of these drugs and taking phenelzine.

Tell your doctor or pharmacist if you are taking other products that cause drowsiness such as opioid pain or cough relievers (such as codeine, hydrocodone), alcohol, marijuana (cannabis), drugs for sleep or anxiety (such as alprazolam, lorazepam, zolpidem), muscle relaxants (such as carisoprodol, cyclobenzaprine), or antihistamines (such as cetirizine, diphenhydramine).

Check the labels on all your medicines (such as allergy, cough-and-cold products, decongestants, diet pills) because they may contain dextromethorphan, decongestants, stimulants, or ingredients that cause drowsiness. Ask your pharmacist about the safe use of those products.

It is very important that you follow special dietary restrictions in order to limit the amount of tyramine in your diet. Avoid drinking large amounts of beverages containing caffeine (coffee, tea, colas) or eating large amounts of chocolate. Caffeine can increase the side effects of this medication. Foods and beverages high in tyramine should be avoided while you are taking this medication and for at least 2 weeks after you stop using this medication.

Foods high in tyramine include: aged cheeses (cheddar, camembert, emmenthaler, brie, stilton blue, gruyere, gouda, brick, bleu, roquefort, boursault, parmesan, romano, provolone, liederdranz, colby, edam), aged/dried/fermented/salted/smoked/pickled/processed meats and fish (includes bacon, summer sausage, liverwurst, hot dogs, corned beef, pepperoni, salami, bologna, ham, mortadella, pickled or dried herring), banana peel, beef/chicken liver (stored, not fresh), bouillon cubes, commercial gravies, concentrated yeast extracts, fava beans, Italian green beans, broad beans, fermented bean curd, homemade yeast-leavened bread, kim chee (Korean fermented cabbage), orange pulp, overripe or spoiled fruits, packaged soups, red wine, sauerkraut, sherry, snow pea pods, sourdough bread, soy sauce, soybeans, soybean paste/miso, tofu, tap beer and ale, vermouth.

Moderate-to-low tyramine content foods include: alcohol-free beer, avocados, bananas, bottled beer and ale, chocolate and products made with chocolate, coffee, cola, cultured dairy products (such as buttermilk, yogurt, sour cream), distilled spirits, eggplant, canned figs, fish roe (caviar), green bean pods, pate, peanuts, port wine, raisins, raspberries, red plums, spinach, tomatoes, white wine.

Tell your doctor or pharmacist right away if you notice symptoms of high blood pressure such as fast/slow heartbeat, vomiting, sweating, headache, chest pain, sudden vision changes, weakness on one side of the body, or trouble speaking.

Contact your healthcare professionals (such as doctor, pharmacist, dietician) for more information, including recommendations for your diet.

Does Phenelzine SULFATE interact with other drugs you are taking?

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Phenelzine Interactions Checker – Drugs.com

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There are 534 drugs known to interact with
phenelzine, along with
25 disease interactions, and 1 alcohol/food interaction.

Of the total drug interactions,
151 are major, 377 are moderate, and 6 are minor.

Does phenelzine interact with my other drugs?

Enter other medications to view a detailed report.

• View all 534 medications that may interact with phenelzine
• View phenelzine alcohol/food interactions (1)
• View phenelzine disease interactions (25)

Most frequently checked interactions

View interaction reports for phenelzine and the medicines listed below.

• Major
• Moderate
• Minor
• Unknown

• Abilify (aripiprazole)
• Adderall (amphetamine / dextroamphetamine)
• Alcohol (contained in alcoholic beverages) (ethanol)
• Aspirin Low Strength (aspirin)
• Ativan (lorazepam)
• Benadryl (diphenhydramine)
• Cardizem LA (diltiazem)
• Celexa (citalopram)
• Cipro (ciprofloxacin)
• Cymbalta (duloxetine)
• Depakote (divalproex sodium)
• Effexor (venlafaxine)
• Elavil (amitriptyline)
• Fentanyl Transdermal System (fentanyl)
• Fish Oil (omega-3 polyunsaturated fatty acids)
• Klonopin (clonazepam)
• Lamictal (lamotrigine)
• Latuda (lurasidone)
• Lexapro (escitalopram)
• Lithium Carbonate ER (lithium)
• Omega-3 (omega-3 polyunsaturated fatty acids)
• Paracetamol (acetaminophen)
• Prozac (fluoxetine)
• Seroquel (quetiapine)
• Trintellix (vortioxetine)
• Tylenol (acetaminophen)
• Viibryd (vilazodone)
• Vitamin B12 (cyanocobalamin)
• Vitamin D3 (cholecalciferol)
• Vyvanse (lisdexamfetamine)

Phenelzine alcohol/food interactions

There is 1 alcohol/food interaction with phenelzine.

Phenelzine disease interactions

There are 25 disease interactions with phenelzine which include:

• blood pressure
• carcinoid syndrome
• headaches
• hyperthyroidism
• liver disease
• pheochromocytoma
• renal dysfunction
• alcohol
• depression
• hypertension/CVD
• liver disease
• pheochromocytoma
• severe renal disease
• hypoglycemia
• parkinsonism
• schizophrenia/bipolar
• seizures
• angina
• bipolar disorder screening
• diabetes
• hypotension
• renal disease
• schizophrenia
• seizures
• glaucoma

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Drug Interaction Classification

These classifications are only a guideline. The relevance of a particular drug interaction to a specific individual is difficult to determine. Always consult your healthcare provider before starting or stopping any medication.

Major	Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit.
Moderate	Moderately clinically significant. Usually avoid combinations; use it only under special circumstances.
Minor	Minimally clinically significant. Minimize risk; assess risk and consider an alternative drug, take steps to circumvent the interaction risk and/or institute a monitoring plan.
Unknown	No interaction information available.

Further information

Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.

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Antidepressants: pharmacological group

Description

Drugs specifically for depression appeared in the late 1950s. In 1957, iproniazid was discovered, which became the ancestor of the group of antidepressants – MAO inhibitors, and imipramine, on the basis of which tricyclic antidepressants were obtained.

According to modern concepts, depression is accompanied by a decrease in serotonergic and noradrenergic synaptic transmission. Therefore, the accumulation of serotonin and norepinephrine in the brain caused by them is considered an important link in the mechanism of action of antidepressants. MAO inhibitors block monoamine oxidase, an enzyme that causes oxidative deamination and inactivation of monoamines. Currently, two forms of MAO are known – type A and type B, which differ in the substrates exposed to them. Type A MAO causes mainly the deamination of noradrenaline, adrenaline, dopamine, serotonin, tyramine, and type B MAO causes the deamination of phenylethylamine and some other amines. Allocate inhibition competitive and non-competitive, reversible and irreversible. Substrate specificity can be observed: a predominant effect on the deamination of various monoamines. All this significantly affects the pharmacological and therapeutic properties of various MAO inhibitors. So, iproniazid, nialamide, phenelzine, tranylcypromine irreversibly block MAO type A, and pirlindol, tetrindole, metralindol, eprobemide, moclobemide, etc. have a selective and reversible effect on it.

Tricyclic antidepressants are named because of their characteristic tricyclic structure. The mechanism of their action is associated with inhibition of the reuptake of neurotransmitter monoamines by presynaptic nerve endings, resulting in the accumulation of mediators in the synaptic cleft and activation of synaptic transmission. Tricyclic antidepressants, as a rule, simultaneously reduce the capture of various neurotransmitter amines (norepinephrine, serotonin, dopamine). Recently, antidepressants have been created that block predominantly (selectively) the reuptake of serotonin (fluoxetine, sertraline, paroxetine, citalopram, escitalopram, etc. ).

There are also so-called “atypical” antidepressants that differ from the “typical” ones both in structure and mechanism of action. Preparations of a bi- and four-cyclic structure appeared, in which no pronounced effect was found either on the capture of neurotransmitters or on the activity of MAO (mianserin, etc.).

A common feature of all antidepressants is their thymoleptic effect, that is, a positive effect on the affective sphere of the patient, accompanied by an improvement in mood and general mental state. Different antidepressants differ, however, in the amount of pharmacological properties. So, in imipramine and some other antidepressants, the thymoleptic effect is combined with a stimulating one, while in amitriptyline, pipofezin, fluacizine, clomipramine, trimipramine, doxepin, a sedative component is more pronounced. In maprotiline, the antidepressant effect is combined with anxiolytic and sedative. MAO inhibitors (nialamide, eprobemide) have stimulating properties. Pirlindol, removing the symptoms of depression, exhibits nootropic activity, improves “cognitive” (“cognitive”) functions of the central nervous system.

Antidepressants have found application not only in psychiatric practice, but also for the treatment of a number of neurovegetative and somatic diseases, chronic pain syndromes, etc. 10 or more days after the start of treatment. This is explained by the fact that the development of the antidepressant effect is associated both with the accumulation of neurotransmitters in the region of nerve endings, and with slowly appearing adaptive changes in the circulation of neurotransmitters and in the sensitivity of brain receptors to them.

Monoamine oxidase inhibitors

A special group are drugs for the treatment of depression, the therapeutic effect of which is associated with inhibition of the activity of the mitochondrial enzyme monoamine oxidase, accompanied by a decrease in the breakdown of catecholamines, as well as indole amines. Most monoamine oxidase inhibitors (MAOIs) act indiscriminately and therefore increase the level of not only catecholamines and serotonin, but also dopamine.

Monoamine oxidase inhibitors (iproniazid), like tricyclic antidepressants, appeared in the 1950s, in the process of finding drugs needed to treat tuberculosis.

There are conflicting opinions about the effectiveness of these antidepressants. In some cases, they are effective in depressions resistant to other antidepressants, with increased appetite, drowsiness, and an atypical course of depression.

The effect of MAOIs on arterial arterial pressure is unpredictable, since these drugs increase the level of norepinephrine and adrenaline in the blood, then blood pressure numbers increase. At the same time, MAOIs inhibit vasomotor centers and thereby reduce sympathetic activity (Anthony P., et al., 2002). The first signs of an increase in blood pressure may be pain in the occipital region, heaviness in the region of the heart, a tense pulse, and fainting.

In order to prevent a sharp increase in blood pressure while taking these drugs, certain medications (desensitizing agents, anesthetics and painkillers), as well as foods containing tyramine (cheese, pizza, sour cream, smoked beef, sauerkraut) should be excluded , legumes, avocados, yeast products, soy sauce, etc.), drinks (champagne, beer, whiskey, coffee, chocolate). Normally, tyramine is destroyed by MAOI even before absorption, while under conditions of inhibition of monoamine oxidase activity, tyramine contained in food is absorbed. In the future, it is captured by adrenergic neurons, participates in synthetic processes and turns into a “false mediator” – octopamine, which in turn leads to a massive release of norepinephrine and can cause a hypertensive crisis (Anthony P., et al., 2002). MAOI preparations are metabolized in the liver and, if this organ is diseased, can cause its toxic damage.

According to L. Elkin et al. (1989), non-selective MAO inhibitors are secondary in the treatment of depression and are used only for simple and mild depression and when other, safer methods of treatment do not help. These are old, currently rarely used inhibitors – phenelzine (Nardil), isocarboxazid (Marplan), tranylcypromine (Parnate).

Combining MAO inhibitors with TCAs has been shown to be effective in depression refractory to the latter drugs (Pande A., et al., 1991). Non-selective MAO inhibitors can also be effective in atypical depressions (hyperphagia, hypersomnia, anxiety and phobias) (Puzhinskiy S., 2000). It is believed that MAOIs are more effective than TCAs in the treatment of atypical depression.

The half-life of MAOIs is approximately 2.5 hours, the maximum binding of MAOIs (maximum effectiveness) is observed 14 hours after the absorption of MAOIs, however, the antidepressant effect of these drugs does not appear until 4 weeks after the start of therapy.

Modern selective monoamine oxidase inhibitors that inhibit the activity of an isolated isoenzyme A or B include: selective monoamine oxidase inhibitors of type A – pyrazidol, moclobemide, selective monoamine oxidase inhibitors of type B – selegiline (used in the early stages of Parkinson’s disease).

Pyrazidol

Pyrazidol is a domestic antidepressant of balanced action, it selectively inhibits type A MAO (short-term and completely reversible). The thymoanaleptic effect is manifested in the relief of depressive symptoms, primarily vital anguish, mental anesthesia and psychomotor retardation.

This drug normalizes the metabolism of monoamine neurotransmitters, blocks the deamination of serotonin, to a lesser extent – norepinephrine, and to a small extent – tyramine, partially inhibits the reuptake of monoamines. It exhibits nootropic properties and improves cognitive functions. It should be borne in mind that pyrazidol is mainly used for mild depression or its moderate forms, including neurotic and masked depressions, and may be ineffective in severe depression accompanied by manifestations of agitation (up to 50% of patients with deep depressions of the melancholic type give a positive response to therapy). pyrazidol). The drug is also used for Alzheimer’s disease, “organic” depression, alcohol withdrawal syndrome. Pyrazidol is also used in the treatment of psychosomatic disorders, with astheno-depressive symptoms that have developed against the background of myocardial infarction and cerebral atherosclerosis (the drug goes well with other medicines). The drug has a normalizing effect on the lungs with manifestations of hypoxia.

The therapeutic effect after taking pyrazidol appears after 3-5 days after the start of therapy. The optimal daily dose of the drug is 15-300 mg. (begin treatment with 50-75 mg in two divided doses). With a dosage of the drug over 200 mg. its sedative effect begins to dominate, and more than 400 mg. the drug may have an effect on severe endogenous depression.

The balance of action of pyrazidol is characterized by a combination of an antidepressant effect with an activating effect in adynamia and apathy and a sedative effect in an agitated state. As a result of the foregoing, the drug is effective in mixed, atypical depressions.

In the process of treatment, such comorbid depression symptoms as: manifestations of senesto-hypochondria, obsessive-compulsive states, signs of depersonalization also disappear.

Side effects of pyrazidol are mild and limited to dry mouth, sweating, weakness, tachycardia. More rarely, allergic reactions and dizziness occur. Unlike TCAs, the drug does not have an anticholinergic effect. Contraindications to the appointment of the drug are acute hepatitis and blood diseases.

Moclobemide

The psychotropic profile of a reversible selective MAO inhibitor type A (MAO-A selectively destroys serotonin, norepinephrine and dopamine) – moclobemide approaches TCAs that have a disinhibitory effect (imipramine, desipramine). Indications for the use of moclobemide are depressive states with a predominance of apathy, lethargy, anergy (Fitton A., et al. 1992).

Moclobemide is given at a dose of 300-450 mg. inside once a day after meals. If there is no effect, increase the dosage by 150 mg. per day, at intervals of 2-3 weeks (maximum daily dose – 600 mg twice a day).

Despite the fact that moclobemide inhibits MAO-A, within therapeutic doses, its interaction with sympathomimetics and tyramine-containing products is unlikely, since the main pathway of tyramine metabolism is via monoamine oxidase type B (MAO-B). After the abolition of this antidepressant, MAO-A activity is relatively quickly restored (24-48 hours).

Placebo-controlled studies have shown that moclobemide has a therapeutic effect in major depression and dysthymia. J. Angst, M. Stabl (1992) and J. Angst, F. Jhonson (1994) indicate that moclobemide can be used to treat severe depression.

Due to its low toxicity and good tolerance, moclobemide is the drug of choice in the clinic of depression in the elderly. Moclobemide does not interact with alcohol.

Numerous researchers point to the good tolerability of moclobemide, due in particular to the absence of peripheral and central anticholinergic effects (Fitton A., et al., 1992; Baldwin D., Rudge S., 1994; Pujynski S., Rybakowski J., 1995).

The most common side effects of moclobemide include: dry mucous membranes (especially the oral cavity), dizziness, headaches, drowsiness, nausea, insomnia. Less common are constipation, discomfort in the stomach. Very rarely there are muscle twitches, visual impairment.