Psychopharm Depressive Disorders

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問題一覧

How do you switch to and from an MAOI to another antidepressant?

Waiting at least 5 half lives after discontinuing antidepressant before starting MAOI

What is unique about tapering Fluoxetine to an MAOI?

It has a very long half life and will need to wait at least 5 weeks before starting an MAOI

If you taper from an MAOI to an antidepressant how long should you wait before starting and why?

Wait at least 14 days to start antidepressant because that is the time it takes the liver to produce new MAO enzymes

What foods are okay and not okay to consume while taking MAOIs?

Not okay: "anything fermented" - Dried, aged, smoked, fermented, spoiled, or improperly stored meat, poultry, or fish; broad bean pods ; aged cheese; tap and unpasteurized beer; marmite; sauerkraut and kimchee; soy and tofu; banana peel; tyramine-containing products Okay: processed cheese/yogurts; canned or bottled beer/alcohol; products containing yeast

Comparse and contrast the causes of Serotonin Syndrome vs Hyertensive Crisis (from MAOIs)

Serotonin Syndrome = Excess serotonergic activity, often due to combining serotonergic drugs (e.g., SSRI + MAOI, SNRI + triptan, linezolid, dextromethorphan, MDMA) Hypertensive Crisis = Ingestion of tyramine-rich food or sympathomimetic drugs while on MAOI, especially irreversible MAO-A inhibitors

Compare and contrast the onset of Serotonin Syndrome vs Hyertensive Crisis (from MAOIs)

Serotonin Syndrome: Rapid (within hours of drug ingestion or dose change) Hypertensive Crisis: Rapid (within minutes to a few hours after tyramine exposure)

Compare and contrast the neuromuscular findings of Serotonin Syndrome vs Hyertensive Crisis (from MAOIs)

Serotonin Syndrome: Clonus (esp. inducible or spontaneous), hyperreflexia, tremor, myoclonus, agitation Hypertensive Crisis: May have tremor, agitation, but clonus and hyperreflexia are absent

Compare and contrast autonomic instability of Serotonin Syndrome vs Hyertensive Crisis (from MAOIs)

Serotonin Syndrome: Diaphoresis, hyperthermia, tachycardia, hypertension, dilated pupils Hypertensive Crisis: Severe hypertension, flushing, headache, sweating, nosebleed, possible bradycardia reflex

Compare and contrast the mental status of Serotonin Syndrome vs Hyertensive Crisis (from MAOIs)

Serotonin Syndrome: Altered (agitation, confusion, delirium) Hypertensive Crisis: Usually preserved until BP reaches critical levels

Compare and contrast the body temperature of Serotonin Syndrome vs Hyertensive Crisis (from MAOIs)

Serotonin Syndrome: Often elevated (can exceed 104°F) Hypertensive Crisis: May have low-grade fever or be afebrile

Compare and contrast the management strategies of Serotonin Syndrome vs Hyertensive Crisis (from MAOIs)

Serotonin Syndrome: -Stop all serotonergic agents immediately -Supportive care: IV fluids, cooling, benzodiazepines for agitation -For moderate to severe cases: Cyproheptadine (5HT2A antagonist) -Avoid antipyretics (ineffective in central hyperthermia) -ICU care if temp >106°F or vital instability Hypertensive Crisis: -Immediate discontinuation of MAOI -Administer phentolamine (alpha-blocker) or nifedipine (CCB) for BP control -ICU monitoring if end-organ damage suspected (e.g., stroke symptoms) -Strict diet education to prevent recurrence

This group consists of fluoxetine, sertraline, paroxetine, fluvoxamine, citalopram, and escitalopram. All selectively and potently inhibit SERT allowing more 5HT to be available in the synaptic space.

SSRIs

This group consists of venlafaxine, desvenlafaxine, duloxetine, and levomilnacipran. All inhibit both SERT & NET. They also act on DA in the PFC without inhibiting DAT (blocking NET enhances/increases DA specifically/only in the PFC). Leads to increases in BP, diaphoresis, & urinary retention. More prone to discontinuation syndrome.

SNRIs

This group consists of phenelzine, tranylcypromine, and isocarboxazid. They were the 1st antidepressants. They inhibit both MAO-A & MAO-B increasing 5HT, NE, & DA by inhibiting their enzymatic breakdown. They are the only antidepressant directly increase neurotransmission for all 3 monoamine neurotransmitters. They non-selectively inhibit MAO irreversibly.

MAOIs

This group consists of clomipramine, amitriptyline, nortriptyline, imipramine, and doxepin. Have therapeutic levels so you can draw labs to check if patient is within a therapeutic (i.e. effective vs toxic) range. They are considered “old school” SSRIs and SNRIs. Potentially lethal in OD. Also help with neuropathic-type pain.

TCAs

Identify the major receptor sites that are affected by tricyclic antidepressants (including but not limited to, muscarinic 1, alpha 1, histamine 1, and sodium channel) and how action on these receptors translates into side effects of treatment.

M1: blurred vision, dry mouth, constipation, tachycardia, urinary retention, memory dysfunction alpha: orthostatic hypotension and dizziness H1: sedation, drowsiness, weight gain Na+ channel: coma, seizures, cardiac arrhythmias, cardiac arrest/death in OD

-Mechanism of Action: Inhibits SERT and NET; blocks H1, M1, α1, and sodium channels -Neurotransmitters: ↑ Serotonin and norepinephrine -Side Effects: Sedation, anticholinergic effects (dry mouth, constipation), orthostatic hypotension, weight gain -Adverse Reactions: Cardiac arrhythmias (Na+ channel blockade), seizures, lethal in overdose -Interactions: Risk of serotonin syndrome with other serotonergic agents; hypertensive crisis with MAOIs; CYP450 interactions -Lab Tests: EKG for QT prolongation, LFTs, plasma drug levels (if toxicity suspected) -Pregnancy Risk: C; avoid if possible in 3rd trimester due to neonatal withdrawal

Amitriptyline (TCA)

-Mechanism of Action: Inhibits DAT and NET; no direct serotonin effect -Neurotransmitters: ↑ Dopamine and norepinephrine -Side Effects: Insomnia, dry mouth, weight loss, agitation -Adverse Reactions: Seizures (dose-dependent, esp. >450 mg/day or in bulimia), psychosis (rare) -Interactions: CYP2B6 substrate; avoid with MAOIs; can lower seizure threshold if combined with other risk meds -Lab Tests: None routinely needed; seizure threshold monitoring if high risk -Pregnancy Risk: C; consider alternatives unless benefits outweigh risks

Bupropion (NDRI)

-Mechanism of Action: Selective serotonin reuptake inhibitor (SERT blockade) -Neurotransmitters: ↑ Serotonin -Side Effects: Sexual dysfunction, GI upset, fatigue -Adverse Reactions: QT prolongation, serotonin syndrome -Interactions: Avoid with MAOIs; caution with QT-prolonging drugs -Lab Tests: Baseline and periodic EKG in high-risk patients -Pregnancy Risk: C; may be used if benefits outweigh risks

Citalopram (SSRI)

-Mechanism of Action: Strong SERT inhibition > NET; also blocks M1, H1, α1, Na+ channels -Neurotransmitters: ↑ Serotonin (primarily), some norepinephrine -Side Effects: Anticholinergic effects, sedation, sexual dysfunction -Adverse Reactions: Cardiac toxicity, seizures, serotonin syndrome -Interactions: Contraindicated with MAOIs; CYP450 metabolism -Lab Tests: EKG, plasma drug levels, LFTs -Pregnancy Risk: C; caution advised

Clomipramine (TCA, with strong SERT affinity)

-Mechanism of Action: Bupropion inhibits NET/DAT; Dextromethorphan is an NMDA receptor antagonist, sigma-1 agonist, and SERT inhibitor -Neurotransmitters: ↑ Dopamine, NE, serotonin; NMDA antagonism modulates glutamate -Side Effects: Dizziness, dry mouth, somnolence, dissociation -Adverse Reactions: Serotonin syndrome, increased BP, hallucinations at high doses -Interactions: CYP2D6 inhibition; avoid MAOIs, serotonergic drugs -Lab Tests: Baseline BP, possibly LFTs -Pregnancy Risk: Not established; caution recommended

Dextromethorphan-Bupropion (NDMA antagonist + NDRI)

-Mechanism: Inhibits SERT and NET -Neurotransmitters: ↑ Serotonin, norepinephrine -Side Effects: Nausea, dry mouth, fatigue, insomnia, increased BP -Adverse Reactions: Hepatotoxicity (rare), serotonin syndrome -Interactions: Avoid with MAOIs; CYP2D6 inhibitor -Lab Tests: LFTs at baseline and during treatment -Pregnancy Risk: C; caution advised

Duloxetine (SNRI)

-Mechanism: Pure SERT inhibition (S-enantiomer only) -Neurotransmitters: ↑ Serotonin -Side Effects: Sexual dysfunction, insomnia, GI upset -Adverse Reactions: Serotonin syndrome, QTc prolongation (less than citalopram) -Interactions: Fewer CYP450 issues than other SSRIs -Lab Tests: ECG in high-risk cardiac patients -Pregnancy Risk: C

Escitalopram (SSRI)

-Mechanism: Noncompetitive NMDA receptor antagonist; indirect activation of AMPA signaling -Neurotransmitters: ↑ Glutamate, downstream effects on BDNF -Side Effects: Dissociation, sedation, nausea, increased BP -Adverse Reactions: Abuse potential, cognitive/perceptual disturbances -Interactions: Caution with other CNS depressants -Lab Tests: Monitor BP before and after dosing -Pregnancy Risk: Not recommended in pregnancy

Esketamine (NMDA Antagonist)

-Mechanism: SERT inhibition + 5HT2C antagonist + weak NET inhibition -Neurotransmitters: ↑ Serotonin, disinhibition of dopamine and norepinephrine -Side Effects: Insomnia, sexual dysfunction, anxiety, GI upset -Adverse Reactions: Long half-life → increased risk of serotonin syndrome when switching -Interactions: CYP2D6 inhibitor; long washout needed before starting MAOIs -Lab Tests: None routinely -Pregnancy Risk: C

Fluoxetine (SSRI)

-Mechanism: SERT inhibition + potent sigma-1 receptor binding -Neurotransmitters: ↑ Serotonin -Side Effects: Sedation, nausea -Adverse Reactions: Serotonin syndrome, drug-drug interactions -Interactions: Strong CYP1A2 and CYP3A4 inhibitor; many drug interactions -Lab Tests: Consider liver function in long-term use -Pregnancy Risk: C

Fluvoxamine (SSRI)

-Mechanism: α2 antagonist, 5HT2A/2C and 5HT3 antagonist, H1 antagonist -Neurotransmitters: ↑ Norepinephrine and serotonin -Side Effects: Sedation, weight gain, increased appetite -Adverse Reactions: Rare agranulocytosis -Interactions: Sedation worsened by other CNS depressants -Lab Tests: CBC if signs of infection -Pregnancy Risk: C

Mirtazapine (NaSSA)

-Mechanism: SERT inhibition + 5HT2A antagonist + α1 antagonist -Neurotransmitters: ↑ Serotonin, modulates norepinephrine -Side Effects: Sedation, orthostatic hypotension -Adverse Reactions: Hepatotoxicity (boxed warning) -Interactions: Potent CYP3A4 inhibitor -Lab Tests: LFTs regularly -Pregnancy Risk: C; rarely used due to liver risk

Nefazodone (SARI)

-Mechanism: SERT inhibition + M1 antagonist + weak NET inhibition + NOS inhibition -Neurotransmitters: ↑ Serotonin, weak ↑ norepinephrine -Side Effects: Sedation, anticholinergic effects, sexual dysfunction, weight gain -Adverse Reactions: Discontinuation syndrome, serotonin syndrome -Interactions: CYP2D6 inhibitor -Lab Tests: None routinely -Pregnancy Risk: D – associated with cardiac malformations

Paroxetine (SSRI)

-Mechanism: SERT inhibition + weak DAT inhibition + sigma-1 binding -Neurotransmitters: ↑ Serotonin, possibly ↑ dopamine -Side Effects: GI upset, sexual dysfunction, insomnia -Adverse Reactions: Serotonin syndrome, activation in panic disorder -Interactions: Fewer CYP450 interactions than fluoxetine or paroxetine -Lab Tests: None routinely -Pregnancy Risk: C

Sertraline (SSRI)

-Mechanism: 5HT2A/2C antagonist, weak SERT inhibitor, α1 and H1 antagonist -Neurotransmitters: ↑ Serotonin modulation -Side Effects: Sedation, dizziness, orthostasis -Adverse Reactions: Priapism, cardiac arrhythmia at high doses -Interactions: Additive sedation with CNS depressants -Lab Tests: ECG if cardiac history -Pregnancy Risk: C

Trazodone (SARI)

-Mechanism: SERT inhibition at low doses, NET inhibition at higher doses -Neurotransmitters: ↑ Serotonin (low dose), ↑ NE (high dose) -Side Effects: Nausea, insomnia, elevated BP -Adverse Reactions: Hypertension, serotonin syndrome -Interactions: Avoid MAOIs -Lab Tests: Monitor BP, especially at high doses -Pregnancy Risk: C

Venlafaxine (SNRI)

-Mechanism: SERT inhibition + 5HT1A partial agonist -Neurotransmitters: ↑ Serotonin -Side Effects: Diarrhea, nausea, insomnia, sexual dysfunction -Adverse Reactions: Serotonin syndrome -Interactions: Avoid MAOIs; CYP3A4 substrate -Lab Tests: None routinely -Pregnancy Risk: C

Vilazodone (SPARI)

-Mechanism: SERT inhibition + 5HT1A agonist, 5HT1B partial agonist, 5HT3/7/1D antagonist -Neurotransmitters: ↑ Serotonin, indirect ↑ dopamine, acetylcholine, norepinephrine -Side Effects: Nausea, dizziness, sexual dysfunction -Adverse Reactions: Serotonin syndrome, hyponatremia -Interactions: CYP2D6 substrate; avoid with strong CYP2D6 inhibitors -Lab Tests: Sodium levels in elderly or those on diuretics -Pregnancy Risk: C

Vortioxetine (Multimodal Antidepressant)

What is a significant finding of the STAR-D study?

That the first antidepressant treatment has the highest change of working

This meds unique properties cause TrkB stimulation to increase BDNF and mTOR stimulation to increase neural plasticity

Esketamine

NMDA + u receptors cause antidepressant effect, and also has anti-suicidal properties

Ketamine

What is unique about Dextromethorphan/Bupropion (Auvelity)?

Dextromethorphan is a CYP2D6 substrate and Bupropion is a CYP2D6 inhibitor which allows Dextromethorphan to work

Compare Dextromethorphan to Ketamine

Dextromethorphan has greater NMDA antagonism and sigma-1 agonism than Ketamine, and also has a unique nACh alpha4-beta4 receptor

What receptor on Ketamine is associated with antidepressant effects?

Mu receptor

What does the mTOR pathway cause?

Increase in spine density/formation

Glutamate Receptor Modulators

Dextromethorphan/Bupropion (Auvelity) and Esketamine (Spravato)

What is unique about TCA toxicity?

The wider the QRS, the greater level of toxicity

-Considered "dirty" drugs, and potentially lethal in overdose. Help with neuropathic pain. Can draw a level to know if treatment is in effective or toxic range. -H1 blockade - sedation and weight gain -M1 blockade - anticholinergic -Alpha-1 blockade - orthostatic hypotension -Voltage-senstivie sodium channel blockade (VSSCB) - coma, seizures, arrythmias, death

TCAs

Switching from a serotonergic drug to MAOI

Wait 5 half lives (5-7 days for most drugs, and 5 weeks for fluoxetine)

Switching from an MAOI to serotonergic drug

Wait at least 14 days

Phenelzine (Nardil), tranylcypromine (Parnate), isocarboxazid (Marplan)

MAOIs

-Inhibit two different enzymes that leads to increase in all 3 monoamines (5HT, NE, and DA) -Only antidepressants that directly increase neurotransmission for all 3 monoamine neurotransmitters -Two week washout period while new enzymes are made in the liver -Many dietary restrictions and drug-drug interactions!

MAOIs

What are the side effects of MAOIs?

Orthostatic hypotension, weight gain, insomnia, sexual dysfunction, and edema

Inhibits both NE and DA reuptake (helps with decreasing positive affect) • Lacks significant SERT activity • No sexual side effects or weight gain • Stimulating (similar to adderall) • Approved for smoking cessation • Seizure risk (especially with IR formulation) (contraindication – anything that increases risk for seizures) • Comes in 3 formulations: IR, SR, XL (SR and XL preferred)

Bupropion

Alpha-2 antagonism and does not block any transporters (SERT, NET) makes it unique! • Alpha-2 antagonism increases norepinephrine release by blocking its ability to turn itself off 5HT2C activity – increase NE and DA • Alpha-2 antagonism enhance serotonin release by blocking norepinephrine’s ability to block serotonin’s release • Alpha-2 antagonism stimulates serotonin release via alpha-1 receptor 5HT2C antagonism + H1 action = weight gain • Thus Alpha-2 antagonism cuts the breaks and steps on the gas!

Mirtazapine

Explain the interplay of these receptors in Mirtazapine: 5-TH2A, 5-HT2C, H1, and 5-HT3

5-HT2A and 5-HT2C together re-sync circadian rhythm and enhance sleep (sedating), 5-TH2C increases NE and DA, 5-HT2C and H1 together cause weight gain, H1 by itself is sedating, and 5-HT3 prevents N/V and diarrhea by blockng the chemoreceptor trigger zone

Explain the receptor binding of Vortioxetine and what are its unique effects?

Works on numerous serotonin pathways in unique ways (5TH1A, 5HT1B, 5HT1D, 5HT3, and 5HT7) - seems to be weight neutral - much lower incidence of sexual side effects - may have a "pro-cognitive" effect? - notorious for causing nausea - Use cautiously with Wellbutrin (max dose when combined with Wellbutrin is 10 mg)

SARIs

Trazadone and Nefazadone

-Blocks 5HT2A, 5HT2C, and SERT – also works on NET -NOT associated with priapism -Rare incidence of spontaneous live failure - rarely used now because of this

Nefazadone

Blocks 5HT2A and 5HT2C which is unique • Behaves differently depending on the dose • Higher doses – antidepressant action (150-600 mg) • Lower doses – sedative/hypnotic (25-150 mg - 5HT2A, H1, and sigma properties making it very sedating so it is mainly used as a sleep aid for this reason) • Priapism is a serious side effect risk that you must warn patients about

Trazodone

NET > SERT (used as a 2nd option after Wellbutrin) • May be better for cognitive symptoms, fatigue, anergia, anhedonia • May increase sweating, urinary hesitancy, hypertension • Doesn’t affect CYP-450 in significant way

S-milnacipran

SERT > NET (slightly - not as dose related as venlafaxine) • Changed the way we think about pain (psychic vs somatic) • Avoid in patients with liver problems (e.g.: alcoholism, hepatitis, etc).

Duloxetine

SNRIs

Venlafaxine, Desvenlafaxine, Duloxetine, S-milnacipran

An active metabolite of venlafaxine • Has greater NET vs 5HT compared to venlafaxine (but also dose related) • Very few CYP-450 and CYP-2D6 interactions

Desvenlafaxine

Blocks 5HT and NET, and the degree of 5HT vs NET is dose dependent • Lower doses are primarily 5HT (less than 200 mg) • Higher doses affect NET (greater than 200 mg) -NOTORIOUS for withdrawal reactions if abruptly stopped -Metabolized by CYP2D6 (why IR is never used, and ER is always Rx)

Venlafaxine

Work like SSRIs in that they all inhibit SERT • Each also inhibits norepinephrine transport (NET) to various degrees (leads to increase of Dopa in PFC) • Also act on dopamine specifically in the prefrontal cortex without inhibiting dopamine transporter (DAT) • Blocking NE enhances and increases DA in the prefrontal cortex • Less likely to have weight gain • May increase blood pressure, urinary retention, sweating • As a class, tend to be more prone to discontinuation syndrome

SNRIs

5HT1A partial agonism is unique to this class • 5HT1A action can be achieved without adding another drug • Lower incidence of sexual side effects • Tends to have more GI side effects (due to rapid elevation of 5HT) • Must be taken with food per package insert (no calorie amount specified) • bioavailability is 72% with food, decreases by 50-60% without food.

Vilazodone

SPARIs

Vilazodone

Nausea, dizziness, "the zaps", flu-like symptoms, anxiety, vertigo, depression, mania, insomnia, GI upset, sweats, sensitivity to light

SSRI Withdrawl Syndrome

What drug is most associated with SSRI Discontinuation Syndrome?

Paroxetine

Only the “S” enantiomer and no antihistaminic properties • No dose restrictions, "no QTc prolongation risk" • Works purely on SERT • Tends to be best tolerated SSRI, very few CYP-450 interactions (good for patients on multiple drugs)

Escitalopram

Has 2 enantiomers (R & S) and mild antihistaminic properties (H1 receptor = sedating) • Inconsistent therapeutic action at lower doses, thus often requires higher doses • Higher doses (> 40mg) associated with QTc prolongation (FDA black box warning) • In adults older than 60y/o, recommended max dose is 20mg

Citalopram

Equivalent dose of Escitalopram to Citalopram

Equivalent dose of Escitalopram is ½ the dose of Citalopram (eg: 40 mg of Citalopram = 20 mg of Escitalopram)

Like sertraline in that it works on Sigma-1 (similar to Sertraline but more potent) • No FDA indication for depression -used off label (manily treats OCD) • Inhibits CYP 1A2 and 3A4 • Several drug-drug interactions (inhibits metabolism of clozapine -> can lead to toxicity) • Inhibits metabolism of Caffeine (affects sleep)

Fluvoxamine

Weak NET inhibition, inhibits nitric oxide synthesis, and mild anticholinergic action (M1) are unique to med • Tends to be calming, potentially sedating (M1 receptor) • VERY POTENT CYP 2D6 inhibitor (potential for notable drug-drug interactions) • Weight gain/sexual side effects are common • NOTORIOUS for withdrawal reactions if stopped suddenly • May be due to anticholinergic rebound?

Paroxetine

Dopamine transport and Sigma-1 receptor binding are unique to drug • May be helpful for atypical depressive symptoms such as hypersomnia, anergia, and mood reactivity • Sigma-1 may help with anxiolytic effects and addressing psychotic/delusional depression • Moderate inhibitor of CYP2D6 (only at doses >150mg), so potential for drug-drug interactions but less so compared to other SSRIs • Tends to be the agent of choice for pregnant/breastfeeding women

Sertraline

5HT2C antagonism is unique to drug • Blocking 5HT2C enhances the release of NE and DA • May be activating/energizing (not good for active patients but good for low mood/energy) • Improve concentration/motivation • VERY long half-life (2 weeks) • Good for noncompliant patients • Bad in that it takes a long time to clear completely -Fairly potent inhibitor of CYP 2D6, so has potential for notable drug-drug interactions

Fluoxetine

Sertraline, Paroxetine, Citalopram, Escitalopram, Fluoxetine, Fluovoxamine

SSRIs

Side effects of SSRIs (remember SSSS)

-Stomach upset -Sexual dysfunction -Serotonin syndrome -Suicidal thoughts

Explain the MOA for SSRIs

SSRIs block SERT then causes initial increase of serotonin in the somatodentritic area but minimal serotonin in the synapse. The abundance of serotonin in the somatodentriti stimulates 5-HT1A autoreceptors. Then 5-HT1A receptors are downregulated and since they are the gatekeepers this allows greater release of serotonin at the axon terminal. Then upregulated post-synaptic receptors are downregulated thought to cause therapeutic effect.

What receptors are associated with nausea?

5-HT3 agonism

What receptors are associated with GI disturbances/Activating effects

5-HT reuptake inhibition

What receptors are associated with dry mouth, urinary retention, activating effects, tremor-CV issues

NE reuptake inhibition

What receptors are associated with sexual dysfunction, activating effects

5-HT2 agonism

What receptors are associated with psychomotor activation and psychosis

DA reuptake inhibition

What receptors are associated with postrual hypotension, dizziness, and reflex tachycardia

alpha-2 antagonism

What receptors are associated with sedation, drowsiness, weight gain

H1 antagonism

What receptors are associated with priapism

alpha-1 antagonism

What receptors are associated with blurred vision, dry mouth, constipation, sinus tachycardia, urinary retention, memory dysfunction

Ach antagonism

Comparse and contrast the body temperature of Serotonin Syndrome vs Hyertensive Crisis (from MAOIs)

Serotonin Syndrome: Often elevated (can exceed 104°F) Hypertensive Crisis: May have low-grade fever or be afebrile

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