Antidepressants Flashcards

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1
Q

Therapeutic Use of MAOIs

A

Atypical depression (spending a lot of time in bed, eating a lot, etc)
Treatment-resistant depression
Treatment-resistant panic disorder
Treatment-resistant social anxiety disorder

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2
Q

Two MAOIs that I need to know

A

Phenelzine
Tranylcypromine
Inhibit both MAOA and MAOB

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3
Q

MAOI mechanism of action

A

Inhibit the degradation of biogenic amines in the presynaptic terminals. get an increase in serotonin, NE, DA.

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4
Q

What type of inhibitor are MAOIs?

A

Irreversible inhibitor, so it takes at least 2 weeks for enzymes levels to recover

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5
Q

MAOI side effects

A
Serotonin syndrome (if combined with other serotonergic drugs)
Hypertension/hypertensive crisis (when given adrenergics (decongestants) or stimulants) also caused by tyramine, weight gain, insomnia
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6
Q

Serotonin syndrome

A
Autonomic effects (sweating, tremor, tachycardia)
Mood effects (agitation)
Motor effects (myoclonus, hyperreflexia)
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7
Q

Drugs that, when combined with MAOIs, can lead to serotonin syndrome

A

SSRIs, carbamazepine, meperidine, fentanyl, methadone, tramadol

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8
Q

Tyramine induced hypertensive crisis

A

Can be triggered by the ingestion of tyramine rich foods like cheese, red wine, soy, beer. Tyramine is a catecholamine releasing agent that is broken down by MAOa in gut, if it gets access to sympathetic neurons and will cause release of NE, causing increased BP.

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9
Q

When can somebody who was on MAOIs eat tyramine again?

A

Two weeks after to allow the enzyme to regenerate.

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10
Q

Selegiline transdermal

A

MAOI that is higher dose so it inhibits both MAOA and MAOB.

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11
Q

Why is selegiline better when given transdermally

A

Bypass GI and liver so patients can eat tyramine without having a hypertensive crisis.

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12
Q

Tertiary Amine Tricyclic Antidepressant

A

Amitriptyline (also used in migraine prevention)

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13
Q

Secondary Amine Tricyclic Antidepressants

A

Nortriptyline and Desipramine

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14
Q

Therapeutic uses for TCAs

A

Depression and treatment resistant depression, childhood bedwetting, GAD, Panic disorder, obsessive compulsive disorder, neuropathic pain, fibromyalgia

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15
Q

How do TCAs work?

A

The inhibit the reuptake of NE. Tertiary amines (like amitriptyline) inhibit some 5HT reuptake as well.

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16
Q

Side effects of TCAs?

A
Very dirty drugs:
H1 blockade (weight gain, sedation)
Na channel blockade (anti arrhythmic effects, but can lengthen QT intervals)
M1 blockade (blurry vision, constipation, dry mouth)
Overdose can cause heart block.
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17
Q

When to avoid TCAs?

A

In patients with narrow angle glaucoma, recent cardiac events, prolonged QT. Secondary amines preferable in elderly.

18
Q

Are TCAs lethal in overdose?

A

Yes, absolutely. Cause heart block.

19
Q

Anticholinergic toxicity

A

Red as a beet, dry as a bone, blind as a bat, mad as a hatter, hot as a hare, full as a flask.

20
Q

What happens to tertiary amines when they are broken down by CYPs?

A

Broken down into secondary amines.

21
Q

Can TCAs be given with MAOIs?

A

No way jose. That would be terrible. Cause serotonin syndrome. Wait 14 days for MAOIs to wash out.

22
Q

Dosing of TCAs?

A

Narrow therapeutic index, start low and titrate slowly.

23
Q

SSRI therapeutic uses

A
MDD
GAD
Panic Disorder
PTSD
OCD
PMDD
Bulimia
24
Q

Common side effects with SSRIs

A

GI upset, weight gain, loss of sex drive, headache, akathisia

25
Q

Metabolism of SSRIs

A

Significant first pass metabolism. Metabolized in liver by CYPs

26
Q

SSRIs with most drug interactions

A

Fluvoxamine and fluoxetine

27
Q

SSRIs with the least drug interactions

A

Citalopram and escitalopram

28
Q

SSRI with the longest half life and least withdrawal?

A

Fluoxetine

29
Q

SSRI with the shortest half-life and most withdrawal?

A

Paroxetine

30
Q

Most selective SSRI

A

Escitalopram

31
Q

When does SSRI withdrawal occur and what are the symptoms?

A

Occurs as a result of abrupt discontinuation of SSRI after at least 6 weeks of treatment. Feels like the flu. Usually resolves in 3 weeks.

32
Q

Why are SSRIs preferred over other agents?

A

No cardiac symptoms, simple dosing, typically not lethal. No special diet.

33
Q

SNRIs include

A

Venlafaxine, duloxetine

34
Q

SNRI therapeutic uses. Common problem?

A

MDD
GAD
Neuropathic pain
Fibromyalgia

May increase BP.

35
Q

Venlafaxine mechanism and side effects.

A

At high doses, acts like an SNRI. Low doses, like an SSRI. High doses can cause increase diastolic BP and can cause tachycardia

36
Q

Duloxetine

A

SNRI, for MDD GAD.

37
Q

Buproprion

A

Wellbutrin– Used for MDD and smoking cessation, also can be used for ADHD. Weak NE and DA repute inhibitor, inhibitor of nAChRs. No sexual dysfunction/weight gain.

38
Q

Buproprion adverse effect?

A

May cause seizures. Avoid in patients with eating disorders (who may have electrolyte balances)

39
Q

Mirtazapine

A

Noradrenergic and Specific Serotonergic antidepressant. Antagonizes a2 receptors (enhancing adrenergic transmission because of the auto receptor), indirect agonist of 5HT1 because it blocks 5HT2A and 5HT3, so remaining serotonin shunted to 5HT1A. Weight gain mediated by H1 antagonism, also increased somnolence.

40
Q

Trazodone

A

5HT2A receptor antagonist, mild SNRI, used as sleep aid. Orthostatic hypertension and priapism.

41
Q

Why prescribe a SNRI?

A

If depression with a comorbid pain disorder.