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📖PHARM: Psych, RA & Gout > 2-16 Anti-Depressants > Flashcards

2-16 Anti-Depressants Flashcards

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1
Q

Name the MAOI’s (4)

A
  1. Phenelzine
  2. Isocarboxazid
  3. Tranylcypromine
  4. Selegiline
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2
Q

Name the TCA’s (6)

A
  1. Amitriptyline
  2. Nortriptyline
  3. Doxepin
  4. Imipramine
  5. Desipramine
  6. Clomipramine

“AND IDC (i dont care)”

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3
Q

Name the SSRI’s (6) (Selective Serotonin Reuptake Inhibitors)

A
  1. Fluoxetine
  2. Fluvozamine
  3. Citalopram
  4. Sertraline
  5. Escitalopram
  6. Paroxetine
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4
Q

Name the SNRI’s (Selective Norepinephrine Reuptake Inhibitors) (3)

A
  1. Duloxetine
  2. Venlavaxine
  3. Desvenlafaxine

I pop SNRI’s and watch DVD’s

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5
Q

MAO-A vs MAO-B (which is primary?)

  1. What does MAO-A do?
  2. What does MAO-B do?
  3. What function do they have in common?
A
  1. MAO-A: metabolizes catecholamine (NE, Epi), 5HT (Key type)
  2. MAO-B: metabolizes trace amines
  3. MAO-A/B: both metabolize tyramine and DA
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6
Q

Name the irreversible MAOIs (3)

What does it mean for them to be irreversible?

A
  1. Phenelzine
  2. Tranylcypromine
  3. Selegiline

Once bound to MAO, enzyme must be replaced (takes 10-14 days)

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7
Q

Reversible MAOI’s (1) How is it used here in the US?

How does their duration of action compare to irreversible MAOI’s

A

There is only meclobemide and it is not used in the US. It shows a shorter duration than irreversible MAO-I’s

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8
Q

Key MAO AE’s (2)

  1. What happens and why?
  2. Potential clinical consequences?
A

HTN Crisis: “Cheese reaction” : Foods w/ high amounts of tyramine (aged cheeses, wines, cured meats) because they are normally metabolized by live MAO’s and if not metabolized serves as a pressor.

Must be careful if patient is on rec. drugs or already hypertensive (risk of ruptured aneurysm, stroke, etc.)

Serotonin Syndrome: MAO’s +SSRI’s/SNRI (or TCA’s)

Increased reflexes, myoclonus, autonomic dysfunction etc.

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9
Q

How can selegiline be administered in order to minimize the “cheese reaction”?

A

Via transdermal patch

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10
Q

What is the therapeutic site of action for TCA’s and in general, how do TCA’s differ from each other?

A

All TCAs block the reuptake pumps of both 5-HT and NE thus preventing their reuptake. Different TCAs differ in the magnitude of the re-uptake blockade of these amines.

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11
Q
  1. What is a T_ertiary TCA?_
  2. Name them (2)
  3. Compare how well they block 5-HT and NE
A
  1. TCAs w/ 2 methyl groups of N
  2. Imipramine and Amitriptyline
  3. Equally block 5-HT and NE reuptake
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12
Q
  1. What is a Secondary TCA?
  2. Name them (2)
  3. Compare how well they block 5-HT and NE
A
  1. TCA having 1 methyl group on N
  2. Despramine and Nortriptyline
  3. Preferentially blocks NE re-uptake vs 5-HT
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13
Q

What is unique about the TCAs Clomipramine and Doxepin?

A

They are both tertiary TCAs but act like secondary.

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14
Q

TCA Pharmacokinetics

  1. Lipid solubility, protein binding, and volume of distribution (high or low?)
  2. Is absorption rapid or slow?
  3. T 1/2
A
  1. High lipid solubility, high protein binding, large Vd
  2. Rapid absorption: serum concentrations peak w/in a few hours
  3. T 1/2 = 8-36 hrs
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15
Q

Prominent TCA side-effects are due to their blocking actions on which receptors (3)? What are the key SE’s for blocking of each receptor?

A
  1. H1 histamine receptors: sedation, weight gain
  2. M1 muscarinic receptors: sedation, confusion
  3. a1 adrenergic receptors: sedation, orthostatic hypotension, dizziness
  4. SNRIs: sexual dysfunction (due to increased serotonin) and HTN and Diaphoresis (due to increased NE)
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16
Q

Put the following (5) effects in order of least to greatest, in terms of the concentration of TCA needed to bring about the particular effect:

CNS toxicity, peripheral Ach receptor blockade, Antidepressant efficacy, CVS toxicity, Histamine receptor blockade

A
  1. Histamine receptor blockade
  2. Peripheral Ach receptor blockade
  3. Antidepressant efficacy
  4. CNS toxicity
  5. CVS toxicity
17
Q

What (2) populations must you be careful with when prescribing TCAs?

A
  1. Elderly- more sensitive to TCA side effects so minimize prescribing them
  2. Pts w/ substance abuse issues- TCAs have an additive effect w/ CNS depressants (like alcohol, barbituates, opiates, and benzos)
18
Q

How large is the therapeutic window for TCAs?

Describe the clinical presentation of TCA overdose based on the receptors/ channels effected (4).

A
  • Narrow therapeutic window
  • Effects of overdose on…
    1. a1-adrenergic receptors: hypotension, respiratory depression
    2. M1 muscarinic receptors: confusion/delirium/altered mental status; respiratory depression
    3. H1 histamine receptors: confusion/delirium/ AMS; respiratory depression
    4. Blocks sodium channels in myocardium membranes: quinidine-like effects (prolonged action potential/ QRS interval); cardiac conduction defects and severe arrhythmias
19
Q

Which SSRI has a half-life longer than the others? Which has the smallest level of protein binding?

A

Longest half-life: Fluoxetine (1-4d) and its metabolite (7-15d) is signficantly longer than the others

Least protein binding: Escitalopram

20
Q

Which SSRI is the least selective for 5-HT? Which has the highest affinity for 5-HT?

A

least: Fluoxetine

most: paroxetine

21
Q
  1. What (2) SSRIs use CYP2D6 for metabolism?
  2. Which SSRI is the most likely of all SSRIs to have drug-drug interactions and why?
A
  1. Paroxetine and Fluvoxamine both use CYP2D6
  2. Fluvoxamine is the most likely to have DDI becomes it inhibits a number of CYP enzymes (1A2, 2C19, 2D6, and 3A4)
22
Q

What are the (5) potential adverse effects of SSRIs?

A
  1. GI
  2. Anxiety
  3. CNS issues
  4. Sexual Dysfunction
  5. SSRI Discontinuation Syndrome: (dizziness, nausea, HA, insomnia, restlessness, unstable gait, brain “zaps”
23
Q

Which type of SSRI is most likely to lead to an SSRI discontinuation syndrome?

A

Most likely w/ short acting SSRIs.

Paroxetine > (effexor/pristiq)>> fluvoxamine > sertraline > citalopram >> fluoxetine

24
Q

Relative to their antidepressant effect, SSRI adverse effects often occur when?

A

AEs often occur prior to the onset of antidepressant efficacy

25
Q
  1. Which SNRI has the greatest level of protein binding?
  2. Which (2) SNRIs are most likely to cause discontinuation syndrome?
A
  1. Duloxetine (Cymbalta) has the greatest level of protein binding
  2. Venlafaxine and desvenlafaxine are most likely to lead to discontinuation syndrome (they have the shortest half-lives)
26
Q
  1. What is the relationship between Venlafaxine and Desvenlafaxine?
  2. How does this relationship impact metabolism of Desvenlafaxine?
  3. How are the other SNRIs metabolized?
A
  1. Desvenlafaxine is the metabolite of venlafaxine.
  2. Because it is a metabolite, desvenlafaxine only goes through phase II metabolism.
  3. Venlaxine and Duloxetine both are CYP2D6 substrates.
27
Q
  1. SNRI Side Effects are dependent on what?
  2. What are the SEs? (3 main categories)
A
  1. Dose dependent SEs
  2. Same as SSRI SEs + Increased BP and Diaphoresis
28
Q

Name the (2) atypical antidepressants

A

Mirtazapine and Bupropion

29
Q

Mirtazapine

  1. MOA
  2. SEs
  3. Protein binding
A
  1. MOA: Noradrenergic and serotonin a2 adrenergic receptro antagonist (blocks presynaptic autoreceptors on NE and 5HT neurons)
  2. SEs: Because it also blocks histamine, you can see wt gain, dry mouth, and sedation
  3. Highly protein bound (85%)
30
Q

How are the sedation effects of Mirtazapine related to dose?

A

Counterintuitively, while highly sedating at low doses, Mirtazapine is less sedating at high doses and can actually even be stimulating

31
Q

Buproprion

  1. MOA
  2. Metabolism
  3. Protein binding
A
  1. MOA: NE and DA reuptake inhiitor (NDRI)
  2. Strong CYP2d6 inhibitor
  3. Highly protein bound (85%)
32
Q

Buproprion SEs (4)

A
  1. SEIZURES (at high doses)
  2. Dry mouth
  3. Nausea
  4. Insomnia

No risk of weight gain, sexual dysfunction, etc.

33
Q

Nefazodone

  1. MOA
  2. SEs (1)
A
  1. MOA: Blocks 5-HT reuptake
  2. SE: Mild sedation
34
Q

Vilazodone

  1. MOA
  2. SEs (1)
A
  1. MOA: Blocks 5HT reuptake (partial agonist of 5-HT1A receptors)
  2. SEs: GI (N/V/D) and Insomnia
35
Q

Vortioxetine

  1. MOA (4)
  2. SEs (1)
A
  1. MOA:
  • Blocks 5HT reuptake
  • Agonist at 5-HT1A
  • Partial agonist at 5-HT1B
  • Antagonist at: 5-HT3 & 5-HT7
  1. SEs: GI (Nausea > vomiting/diarrhea)
36
Q
  1. What do you have to consider when switching from one MAOI to another?
  2. What do you have to consider when switiching from any other antidepressant to an MAOI?
A
  1. When moving from one irreversible MAOI to another, you need to wait for neurons to regenerate MAO enzymes (usually 10-14 day).
  2. When moving from any other antidepressant to an MAOI, you need to wait 5 half-lives before starting the MAOI

📖PHARM: Psych, RA & Gout (6 decks)

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