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4. Pharm III > 1- Antidepressants > Flashcards

1- Antidepressants Flashcards

1
Q

What are the hypotheses for the cause of depression and which is the most relevant?

A

Monoamine (most relevant)- all antidepressants increase amine neurotransmission

(others: neurotrophic, neuroendocrine

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2
Q

How long does it take for antidepressants to have an effect?

A

2-3 weeks due to neuronal plasticity

(reuptake inhibited immediately but effects are delayed)

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3
Q

What is the long-term effect of uptake inhibitors?

A

Antidepressants down-regulate auto-receptors, increasing firing rate of 5-HT neuron

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4
Q

Antipressants only have effects if what?

A

Pt has chemical imbalances

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5
Q

What is the general MOA for TCAs?

A

Inhibit re-uptake of NE and 5-HT, block alpha-adrenergic, histamine, and muscarinic receptors

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6
Q

What is the use of TCAs?

A

Depression (one of last line), neuropathic pain, enuresis (smaller dose)

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7
Q

TCAs are typically well absorbed where and how often are they given?

A

Well absorbed orally, given 1x daily @ bedtime

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8
Q

What metabolizes TCAs?

A

CYP2D6 (drug interactions VERY common)

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9
Q

TCAs + MAOIs has the potential to cause what drug interaction?

A

Serotonin syndrome (severe CNS toxicity)

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10
Q

How do TCAs interact with SSRIs?

A

Compete for metabolism so can be toxic

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11
Q

How do TCAs interact with amphetamine (sympathomimetic drugs)?

A

Cause HTN

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12
Q

How do TCAs interact with alcohol or other CNS depressants?

A

Sedative actions

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13
Q

TCAs can potentiate the effects of what drug class?

A

Anticholinergic

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14
Q

Some of the SEs of TCAs include blockade of what receptors leading to what sxs?

A
  • Histamine receptor blockade: drowsiness, sedation,
  • Cholinergic blockade (PNS): dry mouth, urinary retention, impaired memory
  • 𝜶1 receptor blockade: CV
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15
Q

Aside from receptor blockades, what are the other SEs of TCAs?

A

Weight gain, analgesia, SIADH, sexual dysfunction, decrease is seizure threshold, tolerance

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16
Q

What is the most serious complication a/w toxicity/ overdose of TCAs?

A

Cardiac toxicity (Torsades de pointes)

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17
Q

Aside from cardiac toxicity, what are other effects of toxicity/ overdose with TCAs?

A

Prolonged QT interval, cardiac arrhythmias, respiratory depression

(can be fatal)

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18
Q

Pt presents with toxicity/ overdose with TCAs. What is the tx for the Torsades de pointes?

A

Magnesium, isoproterenol, cardiac pacing

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19
Q

Pt presents with toxicity/ overdose with TCAs. What is the tx for managing arrhythmias/ preventing seizures?

A

Lidocaine, propranolol, phenytoin

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20
Q

Pt presents with toxicity/ overdose with TCAs. What is the tx for restoring acid/ base balance?

A

Sodium bicarb and potassium chloride

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21
Q

Can TCAs be given in pregnancy?

A

YES

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22
Q

Why is there limited use with TCAs?

A

Toxicity and potential overdose

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23
Q

How are TCAs dosed?

A

Start @ low dose then increase → tapered gradually

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24
Q

What is the benefit of using TCAs?

A

No euphoria/ low abuse potential

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25
Q

Due to the fact that all TCAs are equally effective at treating depression, choice of drug is based on what?

A

Adverse effects

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26
Q

Are Amitriptyline and Imipramine secondary or tertiary amines?

A

Tertiary (serotonin > NE)

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27
Q

What is the MOA of Amitriptyline and Imipramine and are they more or less potent than secondary amines?

A

Inhibit 5-HT reuptake

Produce more seizures and more sedating than secondary amines

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28
Q

Are Nortriptyline and Desipramine tertiary or secondary amines?

A

Secondary (NE > serotonin)

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29
Q

What is the MOA for Nortriptyline and Desipramine?

A

Block NE reuptake

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30
Q

What is the MOA for SSRIs?

A

Selectively inhibits 5-HT reuptake

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31
Q

What is the use for SSRIs?

A

Depression (DOC), panic disorder, OCD, social anxiety, bulimia, alcoholism, used in children/ teenagers

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32
Q

What is the DOC (class) for depression)

A

SSRIs

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33
Q

Where are SSRIs well absorbed and what is their half life?

A

Well absorbed by gut, t1/2 = 24-72hrs

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34
Q

What metabolizes SSRIs?

A

Metabolized by and inhibit CYP450s (2D6) = many drug interactions

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35
Q

What is the result of inhibition of CYP3A4 and CYP2D6 with SSRIs?

A

Increased toxicity of TCAs and Phenytoin/ carbamazepine

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36
Q

How do SSRIs interact with MAOIs?

A

Serotonin syndrome

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37
Q

How do SSRIs interact with St Johns wort or amphetamines?

A

Serotonin syndrome

38
Q

How do SSRIs interact with beta blockers?

A

Heart block and hypotension

39
Q

How do SSRIs interact with codeine?

A

Fluoxetine inhibits conversion to active compound

40
Q

How do SSRIs interact with Meperidine?

A

Increases 5-HT (potential for serotonin syndrome)

41
Q

How do SSRIs interact with Tramadol?

A

Increased seizure risk

42
Q

What are the SEs (although mild) of SSRIs?

A

CNS stimulation, sexual disinterest/ dysfunction, photosensitivity

43
Q

Amitriptyline and Imipramine drug class?

A

TCAs

44
Q

Nortriptyline and Desipramine drug class?

A

TCAs

45
Q

Fluoxetine drug class?

A

SSRIs

46
Q

Sertraline drug class?

A

SSRIs

47
Q

Paroxetine drug class?

A

SSRIs

48
Q

Citalopram drug class?

A

SSRIs

49
Q

Escitalopram drug class?

A

SSRIs

50
Q

What is the DOC for depression?

A

Citalopram

51
Q

What is the use of Paroxetine?

A

OCD and social anxiety

52
Q

T1/2 of Sertraline is how long and what is important about its elimination?

A

26 hours, extensive first pass metabolism

53
Q

What drug in the SSRI class has the fewest drug interactions?

A

Sertraline

54
Q

What SSRI is preferred in elderly?

A

Sertraline

55
Q

Does Fluoxetine or Norfluoxetine (active metabolite of Fluoxetine) have a longer half life?

A

Fluoxetine = 2-3 days

Norfluoxetine = 7-9 days)

56
Q

What SSRI is most likely to inhibit CYP450 enzymes (CYP2D6)/ has the most drug interactions (ex. pain meds)?

A

Fluoxetine

57
Q

Use of Fluoxetine should be cautioned in what patient population?

A

Diabetic pts (impairs blood glucose levels)

58
Q

Venlafaxine drug class?

A

SNRIs

59
Q

Duloxetine drug class?

A

SNRIs

60
Q

What is the MOA for MAOIs?

A

Irreversibly inhibi MAOs (which metabolize NE, DA, 5-HT)

61
Q

MAO-A metabolizes what and where (location)?

A

NE, DA, and 5-HT in both CNS and periphery

62
Q

MAO-B metabolizes what and where (location)?

A

Selectively metabolizes DA in CNS but NOT in GI tract

63
Q

What is the use of MAOIs?

A

Refractory depression (class of last choice)

64
Q

What is the half life of MAOIs?

A

Long (effects persist after discontinuing drug)

65
Q

How do MAOIs interact with sympathomimetic amines?

A

Severe hypertension (OTC cold/ cough meds)

66
Q

How do MAOIs interact with any other drug that releases serotonin?

A

Serotonin syndrome → hyperpyrexia

67
Q

What do MAOIs inhibit?

A

CYP450 enzymes (2D6)

68
Q

What are the SEs of MAOIs?

A
  • Hypertensive crisis (phenelzine), avoid foods w/ tyramine
  • Orthostatic hypotension
  • Weight gain (very common)
  • Anticholinergic
69
Q

Phenelzine drug class?

A

MAOIs

70
Q

Selegiline drug class?

A

MAOIs

71
Q

What is the MOA of Phenelzine?

A

Inhibits both MAO-A and MAO-B → increases NE and 5-HT

72
Q

What is true about the drug action of Phenelzine?

A

Actions persist longer than serum levels

73
Q

Phenelzine is a substrate for what?

A

MAOs

74
Q

What is the use of Phenelzine?

A

Refractory depression (drug of last choice due to serious SEs)

75
Q

What is the MOA of Selegiline?

A

Selectively inhibits MAO-B → increases DA

76
Q

What is true about the SEs of Selegiline?

A

Fewer than other MAOIs

77
Q

In addition to depression, Selegiline can also be used for what?

A

Parkinson’s (lower dose)

78
Q

What is the MOA of Bupropion?

A

Inhibits DA reuptake

79
Q

What is the use of Bupropion?

A

ADHD, alcoholism (decreases craving), ER for smoking cessation

80
Q

What are the pharmacokinetics of Bupropion?

A

Extensive first pass metabolism, high protein binding, active metabolites

81
Q

What are the SEs of Bupropion?

A

Seizures, CNS effects, cardiac

82
Q

What is the MOA of Mirtazapine?

A

Blocks presynaptic alpha-2 receptors → increases release of NE and 5-HT

83
Q

What is the use for Mirtazapine?

A

Eliminates SEs a/w SSRIs (anxiety, insomnia, nausea, sexual dysfunction)

84
Q

What are the pharmacokinetics of Mirtazapine?

A

Metabolized by CYP450s, t1/2 = 20-40 hrs

85
Q

What are the SEs of Mirtazapine?

A

Drowsiness/ sedation (may be advantage in depressed pts with insomnia and anxiety?

86
Q

What is the MOA of Atomoxetine?

A

Selective inhibitor of NE reuptake

87
Q

What is the use of Atomoxetine?

A

ADHD (first non-stimulant for tx), increase memory and attention

Does not cause euphoria = good choice for addicts

88
Q

What are the SEs of Atomoxetine?

A

GI distress, insomnia, liver damage (possible but rare)

89
Q

What is the MOA for Trazodone?

A

5-HT2A receptor antagonist

90
Q

What is the use of Trazodone?

A

Sleep aid, pain management

91
Q

What are the pharmacokinetics of Trazodone?

A

Short t1/2, high first pass metabolism

92
Q

What are the SEs of Trazodone?

A

Sedating (not good antidepressant), priapism (rare but serious)

4. Pharm III (16 decks)

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