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Pharmacology II Exam 1 > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q 
When treating depression with SSRIs, like fluoxetine or sertraline, side effects include: agitation & insomnia. Which receptor is related to these side effects?
A. 5-HT3
B. 5-HT2
C. 5-HT1a/2a
D. 5-HT5/7
A

B (tolerance develops to most)

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2
Q 
When treating depression with SSRIs, like fluoxetine or citalopram, side effects include: EPSE & initial anxiety/panic attacks. Which receptor is related to these side effects?
A. 5-HT3
B. 5-HT2
C. 5-HT1a/2a
D. 5-HT5/7
A

B (tolerance develops to most, long-term effect is anxiolytic)

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3
Q 
When treating depression with SSRIs, like fluoxetine or sertraline, sexual dysfunction occurs in 30-50% of patients. Which receptor is related to these side effects, which include DELAYED ORGASM and decreased libido?
A. 5-HT3
B. 5-HT2
C. 5-HT1a/2a
D. 5-HT5/7
A

B (no tolerance, may persist after discontinuation)

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4
Q

How does sexual dysfunction related to SSRI use affect males vs. females?

A

More common in males, but more severe in females

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5
Q 
When treating depression with SSRIs, like fluoxetine or citalopram, side effects include: nausea & GI distress. Which receptor is related to these side effects?
A. 5-HT3
B. 5-HT2
C. 5-HT1a/2a
D. 5-HT5/7
A

A (usually transient, tolerance develops)

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6
Q 
When treating depression with SSRIs, like fluoxetine or citalopram, side effects include: diarrhea. Which receptor is related to these side effects?
A. 5-HT3
B. 5-HT2
C. 5-HT1a/2a
D. 5-HT5/7
A

A (tolerance develops)

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7
Q

2 DDIs to know with SSRIs

A

MAOIs (serotonin syndrome) and tamoxifen (2D6 interference, tamoxifen loss of efficacy)

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8
Q

Nancy calls the pharmacy wanting to stop her antidepressant (fluoxetine 80 mg) today because she doesn’t think she needs it. What can you tell her about starting/stopping drugs like fluoxetine?

A

(Obvs an SSRI) Rebound effects can be caused by abrupt discontinuation (dysphoria, agitation, seizures, paranoia)

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9
Q

You are filling prescriptions for Terry, who is on fluoxetine & Eliquis, and see a drug interaction warning. Why is this?

A

Fluoxetine (or any SSRI) impairs platelet aggregation and increases risk of bleeding

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10
Q

What cardiovascular side effect can be caused by fluoxetine (SSRI)?

A

QT interval prolongation

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11
Q

What ocular side effect can be caused by fluoxetine (SSRI)?

A

Mydriasis (pupillary dilation —> precipitate closed-angle glaucoma)

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12
Q

What is nocturnal bruxism and why am i even asking this………….

A

Grinding teeth during the night (there is a point:) causes headache associated with fluoxetine (SSRI)

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13
Q

AE= bone fractures (among others!!)

A

Fluoxetine (SSRI)

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14
Q

Main MOA of trazodone

A

Antagonized 5-HT2a and weakly inhibits SERT

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15
Q

What “off target” actions of trazodone account for some of its side effects?

A

Blocks a1 and H1 receptors (little to no effect on muscarinic receptors)

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16
Q

2 advantages of trazodone use (antagonizes 5-HT2A, weakly inhibits SERT, a1 block, H1 block)

A

5-HT2a antagonism may reduce those side effects (sexual, insomnia, EPSE, agitation), may benefit depressed patients with insomnia

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17
Q

Use: major depressive disorder (not first-line, more so used for treatment-resistant depression)
Might decrease side effects associated with SSRIs

A

Trazodone

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18
Q 
Which of the following is a side effect due to trazodone?
A. Priapism
B. Insomnia 
C. Hypertensive crisis
D. Weight gain
A

A (rare but potentially serious, from a1 blockade)

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19
Q 
Which of the following is a side effect due to trazodone and fluoxetine?
A. Weight loss
B. Bleeding risk
C. Nocturnal bruxism
D. Bone fractures
A

B (impaired platelet aggregation)

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20
Q

Side effects of trazodone include priapism, bleeding risk, ____, and ____.

A

Sedation, orthostatic hypotension

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21
Q

MOA of duloxetine

A

(SNRI) inhibition of SERT and NERT

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22
Q

What are the off-target actions of duloxetine (specifically, a1/h1/M)?

A

Little or no action (like SSRIs!)

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23
Q

Describe the SERT/NERT selectivity of duloxetine, an SNRI.

A

SERT > NERT 5x (others in the class have 10X selectivity for SERT)

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24
Q

Use: major depressive disorder
Anxiety
Pain syndromes
Stress incontinence

A

Duloxetine (SNRI- pain= diabetic neuropathy/fibromyalgia/musculoskeletal pain)

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25
Q

T/F: Duloxetine has similar side effects & drug interactions as SSRIs - except the sexual dysfunction.

A

False (including the sexual dysfunction!!)

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26
Q

Why are TCAs not as commonly used as SSRIs or SNRIs?
A. They are less studied
B. Side effects & potential for lethal overdose
C. They are not as effective
D. Rebound depression upon discontinuation

A

b

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27
Q

MOA of amitriptyline

A

Inhibits SERT and NERT (tricyclic antidepressant)

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28
Q

Describe the SERT/NERT selectivity of amitriptyline

A

SERT < NERT 8x

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29
Q

What are the off-target actions of amitriptyline (specifically, a1/h1/M)?

A

Antagonized all of them (side effects!!)

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30
Q

Uses: major depressive disorder

Pain syndromes

A

Amitriptyline (TCA- pain= migraine prophylaxis, diabetic neuropathy, IBS)

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31
Q

List the side effects of amitriptyline related to its off target blockade

A

M - tachycardia, a1- orthostatic hypotension and drowsiness, h1- sedation and weight gain

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32
Q

Sexual dysfunction side effects of amitriptyline are 5-HT___(number) receptor-related.

A

2

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33
Q 
Which of the following describes the symptoms of TCA (amitriptyline) overdose toxicity? Select all that apply.
A. Agitation/delirium
B. Hypotension
C. GI cramping
D. Hyperpyrexia
A

A and B (neurological and CV)

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34
Q 
Which of the following describes the symptoms of TCA (amitriptyline) overdose toxicity? Select all that apply.
A. Severe insomnia
B. Arrhythmias
C. Vomiting, diarrhea
D. Seizures
A

B and D (neuro & CV)

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35
Q 
Which of the following describes the symptoms of TCA (amitriptyline) overdose toxicity? Select all that apply.
A. Muscle rigidity
B. Excessive salivation &amp; sweating
C. Loss of consciousness 
D. Severe tachycardia
A

C and D (neuro & CV)

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36
Q

List 2 atypical antidepressants that are alternatives when patients are not responsive to, or cannot tolerate, SSRIs/SNRIs.

A

Bupropion, mirtazepine

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37
Q

Which of the following describes bupropion’s conjectured MOA?
A. Antagonizes 5-HT2 and weakly inhibits DAT
B. Inhibits NERT > SERT
C. Presynaptic a2 auto-receptor antagonist, increasing the release of 5-HT and NE
D. Inhibition of NET and DAT, increases release of NE/DA from nerve terminals

38
Q 
Which of the following is bupropion associated with? Select all that apply.
A. Weight gain
B. Sexual dysfunction
C. Lower seizure threshold
D. Dry mouth
A

C and D (**NOT associated with sexual dysfunction or weight gain)

39
Q

T/F: Bupropion benefits patients who experience MDD and insomnia.

A

False- not associated with somnolence and insomnia is a side effect

40
Q 
Which of the following is bupropion associated with? Select all that apply.
A. Weight loss
B. Sexual dysfunction
C. Mydriasis
D. Nausea
41
Q

Boxed warning for bupropion smoking cessation (Zyban)

A

Neuropsychiatric effects (depression, anxiety, psychosis, suicidal/homicidal ideation)

42
Q

Uses: major depressive disorder - monotherapy or add-on to manage side effects and/or augment anti-depressive activity
Seasonal affective disorder

A

Bupropion (also smoking cessation!, manages SSRI-induced sexual dysfunction)

43
Q

Which of the following does NOT describe mirtazepine’s MOA/off-target effects?
A. Antagonizes 5-HT2 and weakly inhibits DAT
B. H1 blockade, presynaptic 5-HT2 antagonism
C. Presynaptic a2 auto-receptor antagonist, increasing the release of 5-HT and NE
D. Inhibition of NET and DAT, increases release of NE/DA from nerve terminals
E. Postsynaptic 5-HT3 antagonist

A

A and D (blocks: pre a2, pre 5-HT2, post 5-HT3, H1)

44
Q

T/F: Mirtazepine would be beneficial in patients with insomnia and MDD.

A

True (sedative effects)

45
Q 
Which of the following is NOT associated with sexual dysfunction?
A. Amitriptyline
B. Mirtazepine
C. Fluoxetine
D. Duloxetine
A

B (also bupropion)

46
Q

Use: MDD

Might be beneficial to patients with insomnia, sexual dysfunction-induced from other drugs, or cachexia

A

Mirtazepine (off-target H1= sedation & weight gain)

47
Q

T/F: Patients might lose weight while taking mirtazepine.

A

False (H1 blockade)

48
Q

MOA phenelzine

A

Non-selective, irreversible inhibitor of MAO-A (therapeutic target) and MAO-B, increases 5-HT/NE/DA concentration in nerve terminals

49
Q

Uses: 3rd line for major depressive disorder (mostly for treatment-resistant or atypical depression)

A

Phenelzine (non selective, irreversible MAOI)

50
Q

Which of the following is NOT true about phenelzine?
A. Its onset of action is faster than other antidepressants
B. Associated with multiple drug interactions
C. Its side effects include priapism and bleeding risk
D. The pharmacological effect continues after the drug is cleared

51
Q

Patients taking ____ should avoid wine and cheese (tyramine-containing foods) due to the possibility of this combination causing a(n) ____ ____.

A

Phenelzine (selegiline is MAO-B selective), hypertensive crisis

52
Q

Can patients taking phenelzine expect

  1. Weight loss
  2. Weight gain
  3. No change in weight ?
A
  1. weight gain
53
Q

What are the 2 most common side effects from phenelzine?
A. Hypertensive crisis and priapism
B. Sexual dysfunction, serotonin syndrome
C. Nausea, diarrhea
D. Orthostatic hypotension and sedation

54
Q 
\_\_\_ is noted to cause excessive CNS stimulation (insomnia, euphoria).
A. Phenelzine 
B. Mirtazepine
C. Fluoxetine
D. Bupropion
A

A (MAOI non-selective, irreversible)

55
Q

MOA selegiline

A

Selective MAO-B inhibition at low doses (increases DA) and non-selective MAO-A and MAO-B inhibition at high doses (increases 5-HT/NE/DA)

56
Q

T/F: Selegiline is used at low doses for depression and high doses for Parkinson’s disease.

A

False (low dose= parkinsons, high dose= depression)

57
Q

How might you reduce the dietary restrictions (tyramine foods) associated with selegiline?
A. It is MAO-B selective, so no need to restrict ever.
B. You cannot reduce the restrictions - avoid those foods!
C. Take with water and separate those foods and selegiline by at least 4 hours
D. Use a transdermal patch

A

D (no dietary restrictions needed with the TD patch)

58
Q

Classify this type of depression: weight loss, social disengagement, insomnia, apathy

A

Typical (melancholic) unipolar depression

59
Q

Classify this type of depression: treated with short-term pharmacotherapy, if needed

A

Reactive depression

60
Q

Classify this type of depression: lots of sleeping, weight gain, overly sensitive, brief experiences of happiness

A

Atypical unipolar depression

61
Q

Diagnosis of unipolar depression occurs when patients reports suffering at least____ (number) major depressive episodes lasting at least ____(duration), and have no history or mania or hypomania.

MAJOR SYMPTOMS:
Depressed mood
Anhedonia (inability to experience pleasure)
Insomnia/hyperinsomnia
Change in appetite or weight
Low energy, poor concentration
Thoughts of worthlessness or guilt
Recurrent thoughts of death or suicide
A

One; 2 weeks

62
Q

What are the most common presenting symptoms of unipolar depression? (3)

A

Fatigue, pain, GI complaints (physical)

63
Q

T/F: Unipolar depression has a low rate of recurrence.

A

False (40% of patients with one episode with have another within 2 years)

64
Q

Explain the neurotransmitter receptor theory of depression

A

Low NT release causes low postsynaptic receptor activation & up-regulation of inhibitory presynaptic monoamine receptor density; restoration of transmitter levels results in compensatory down-regulation of autoreceptors that restore normal post-synaptic receptor activity coinciding with therapeutic effect

65
Q

Which depression theory specifically addresses the latency in the onset of antidepressant action?

A

Neurotransmitter receptor theory of depression

66
Q

The neurotrophic theory of depression posits that depression is due to (stimulation/suppression) of neurogenesis in the ____, possibly due to (excess/deficiency) in the __ ___ __ __.

A

Suppression, hippocampus, deficiency, brain-derived neurotrophic factor (BDNF)

67
Q

Patient with chronically activated HPA axis & high cortisol levels would provide evidence for which depression theory?

A

Neurotrophic theory of depression

68
Q

This molecule plays an important role in hippocampal neurogenesis & synaptic connectivity

A

Brain-derived neurotrophic factor (3X reduced in depressed patients)

69
Q

How could the monoamine theory of depression be related to the neurotrophic theory of depression?

A

Monoamines are known to regulate BDNF expression, so monoamine deficiency could lead to BDNF deficiency (takes time to restore)

70
Q

T/F: Psychotherapy is more efficacious than pharmacotherapy, but the latter is faster and cheaper, so more widely used.

A

False- equally efficacious, but the combination is superior (to either alone)

71
Q

T/F: Drug monotherapy may be of little benefit (~placebo) in patients with mild unipolar depression.

72
Q

Treatment outcomes (of antidepressants) are defined as “___” and “___” based on the degree of improvement from baseline on a clinician adminstered ___ ___ __

A

Response, remission, depression rating scale

73
Q

Define therapeutic “response”

A

Improvement ≥ 50% but less than the threshold for remission

74
Q

Define therapeutic “remission”

A

Score ≤ a specific cutoff that defines the normal range

75
Q

Continuation treatment - administered ___(duration) longer after resolution of the major depressive episode to preserve ___ and prevent relapse

A

4-9 months, remission

76
Q

Maintenance therapy - ___(duration) for patients with severe unipolar depression @ high risk of relapse

A

1-3 years or indefinitely

77
Q

T/F: The efficacy of antidepressants is generally equal across & within classes

78
Q

Boxed warning for all antidepressants

A

Suicidal ideation & behavior (esp. during initial treatment period & in children & adolescents)

79
Q

List the 3 strategies and associated drugs used to elevate synaptic monoamine NT levels (SSRIs, SNRIs, TCAs, MAOIs, mirtazepine)

A
  1. Block NT reuptake - SSRI, SNRI, TCA
  2. Block NT degradation - MAOI
  3. Increase NT release - mirtazepine
80
Q

MOA of SSRIs (fluoxetine)

A

Selective inhibition of 5-HT reuptake by SERT

81
Q

SERT vs. NET relative affinity - fluoxetine

A

SERT&raquo_space;>NET (300X)

82
Q

What “off target” effects do SSRIs have that influence the side effects that these drugs cause? (A1, a2, H1, M, etc.)

A

Little to no action of alpha, H1, or muscarinic receptors; stimulates multiple 5-HT receptor subtypes

83
Q

3 disadvantages of using SSRIs over TCAs or MAOIs (adverse effect related)

A

Greater frequency of sexual dysfunction, GI complaints, insomnia

84
Q

3 advantages of using SSRIs over TCAs or MAOIs

A

Milder side effects/less lethal overdose, less sedation, less likely to worsen CVD

85
Q

Uses: major depressive disorder
anxiety
Bulimia nervosa, binge eating, premenstrual dysphoric disorder

A

Fluoxetine (SSRI)

86
Q

When treating major depressive disorder with fluoxetine (or another SSRI), what would you expect to occur initially? (2)

A

Little to no improvement, side effect

87
Q

When treating major depressive disorder with fluoxetine (or another SSRI), what would you expect to occur in 3-8 weeks? (3)

A

Therapeutic effects, tolerance to most side effects, sexual dysfunction begins

88
Q 
When treating major depressive disorder with fluoxetine (or another SSRI), when would you expect efficacy to wear off?
A. Never - can be treated indefinitely
B. 6 months (42 weeks)
C. > 3 years
D. > 18 months
89
Q 
When using fluoxetine (or any SSRI), serotonin syndrome is a concern. Which subtype is responsible for serotonin syndrome?
A. 5-HT3
B. 5-HT2
C. 5-HT1a/2a
D. 5-HT5/7
90
Q

When using fluoxetine (or any SSRI), a patient is especially at risk for serotonin syndrome when given with what other drug class?

A

MAOIs (phenelzine, selegiline)

Pharmacology II Exam 1 (9 decks)

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