L50. Depression Pharmacology

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Why aren't Monoamino Oxidase Inhibitors (MAOIs) used as frequently?

MAOIs indirectly activate amines (including norepinephrine, serotonin, dopamine, and dietary tyramine). A build up of tyramine can lead to excessively high levels of norepinephrine ---> HTN Crisis

Modern examples of MAOIs

Isocarboxazid, Phenelzine, Selegiline

Clomipramine

TCA used for OCD - targets serotonin transporter

Amitriptyline

TCA used for depression and pain management

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Commonly used SSRIs

Escitalopram, Fluoxetine, Paroxetine, and Sertraline

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MOA for SSRI's

SSRI's block the serotonin transporter, thus inhibiting its reuptake into the neuron and letting it stay in the synaptic cleft for longer thus potentiating serotonin's effect on the brain/body. This is effective for depression as pt's with depression usually have lo levels of serotonin.

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MOA for SNRIs

SSRI's block the serotonin AND norepinephrine transporter, thus inhibiting their reuptake into the neuron and letting it stay in the synaptic cleft for longer thus potentiating serotonin's effect on the brain/body.

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Commonly used SNRIs

Venlafaxine and Duloxetine

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Atomoxetine

SNRI used for ADHD

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Drugs used for rapid antidepressant response

Ketamine Esketamine (this one approved for tx-resistant depression)

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Tx for mania

Carbamazepine Valproic Acid Lithium

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T or F: SSRIs are SERT blockers

TRUE - SSRIs block the serotonin transporter (SERT)

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Clorimipramine, Fluoxetine, Fluvoxamine, Paroxetine are examples of SSRis that...

Can be used to tx OCD

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Buspirone

Selective 5-HT1A serotonin agonist used for GAD

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A pt comes to you with severe anxiety, complaining of frequent episodes that need to be alleviated soon given her demanding job. What drugs are good options?

Benzos - alprazolam, clonazepam --> rapid acting anxiolytics but high dependence/tolerance

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Drugs used for situational anxiety

B-blockers to block autonomic manifestation of anxiety-induced SANS activation (fight or flight response) ---> e.g. feeling like you are going to vomit before exam

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MOA for tricyclic antidepressants (TCA)

TCAs work by inhibiting serotonin and norepinephrine reuptake --> they block SERT (serotonin transporter) and NET (norephinephrine transporter) to allow these neurotransmitters to stay in the synaptic cleft for longer.

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Mechanism of action for MAO inhibitors

Inhibit monoamine oxidase (which is the enzyme that typically breaks down dopamine, norepinephrine, and serotonin) --> thus the levels of these neurotransmitters build up in the neuron and there will be more to release at the synapse

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Differences between the mechanism of action for imipramine, despramine, clomipramine (Hint: they are all TCAs)

Imipramine: equally targets SERT and NET (serotonin and norepinephrine build up in synaptic cleft) Despramine: preferentially targets NET (norepinephrine builds up more) Clomipramine: preferentially targets SERT (serotonin builds up more)

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