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Psych clerkship > Anti-depressants > Flashcards

Anti-depressants Flashcards

1
Q

What anti-depressant should be avoided in epileptics?

A

Buproprion (wellbutrin) should be avoided in epileptics because it lowers the seizure threshold

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2
Q

What anti-depressants can cause fever, myoclonus, and mental status changes?

A

SSRIs and/or SNRIs can cause Serotonin Syndrome (fever, myoclonus, and mental status changes)

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3
Q

Which anti-depressant should be used to help patients gain weight?

A

Mirtazapine (Remeron)

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4
Q

Which anti-depressant causes constipation, urinary retention, and dry mouth?

A

TCAs (anti-cholinergic side effects)

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5
Q

Which class of anti-depressants can cause hypertensive crisis?

A

MAOIs

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6
Q

What anti-depressant causes pulmonary hypertension?

A

Paroxetine (Paxil-SSRI)

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7
Q

Which anti-depressants should be used for patients who don’t sleep well?

A

Mirtazapine (Remeron) or Trazodone (Olepto)

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8
Q

Which classes of anti-depressants can be used to also help with chronic pain?

A

TCAs or Atypical anti-depressants

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9
Q

Which anti-depressants has the fewest sexual side effects?

A

Buproprion (Wellbutrin)
Mirtazepine
Trazodone (priapism)
Nefazodone

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10
Q

Which anti-depressant is CONTRAindicated in eating disorders?

A
  • Buproprion => eating disorders as well as Wellbutrin both lower the seizure threshold
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11
Q

Which anti-depressant should not be given to suicidal patients?

A

TCAs => 1 week’s dosage of TCAs can be lethal

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12
Q

Which class of anti-depressants can help with migraines?

A

TCAs (amitriptylline)

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13
Q

What is the mechanism of action of SSRIs?

A

Selectively inhibits serotonin reuptake by serotonin reuptake transporter proteins at presynaptic neuron, causing an increase in synaptic serotonin levels
- NO anticholinergic, antihistamnic (sedation) or anti-α1 adrenergic effects

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14
Q

Why does it take weeks to months for SSRIs to take clinical effect?

A

Clinical effect usually takes weeks to few months due to time needed to down-regulate B1 adrenergic and serotonin receptors in CNS so mechanism goes beyond simply increasing synaptic serotonin levels

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15
Q

What explains the GI effects associated with SSRIs?

A

Serotonin receptors are located throughout the body (especially GI tract)

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16
Q

Why is fluoxetine not a good choice for patients with hepatic disease?

A

Fluoxetine has a long half life (2-4 days), which may allow its active metabolite to build up

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17
Q

SSRIs and MAOIs should be separated by 5 weeks or else they can cause?

A

Serotonin syndrome

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18
Q

Which SSRI is more likely to induce mania?

A

Fluoxetine

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19
Q

Which SSRI should be used in adolescents and pregnant women?

A

Fluoxetine

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20
Q

What is the advantage of the liquid formulation of fluoxetine?

A

Good for low dosages as well as weekly formulations

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21
Q

In addition to having the highest serotonin specificity, Citalopram (celexa) also has effects at which receptor?

A

Citalopram also has anti-histaminic effects.

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22
Q

What is the major precaution that should be taken with Citalopram (celexa)?

A

Dose dependent QT prolongation/Torsades

- do NOT exceed 40mg/day

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23
Q

What are the benefits of the stereoisomer Escitalopram (Lexapro), over citalopram?

A
  • More effective than Citalopram in acute response and remission, primarily in tx of GAD
  • Lower risk of QTc prolongation
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24
Q

What is the primary indication for fluvoxamine (luvox)?

A

OCD (very short half life)

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25
Q

What are the major side effects of fluvoxamine (luvox)?

A

GI distress, headaches, sedation, weakness

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26
Q

What is one advantage sertraline (zoloft) has over paroxetine (paxil)?

A

Less sedating

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27
Q

Maximum absorbency of Sertraline (zoloft) requires….?

A

Max absorption requires a full stomach

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28
Q

What is the major benefit of Paroxetine’s (paxil) short half life?

A

Short half life with no active metabolite means no build-up (good if hypomania develops)

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29
Q

What is the primary disadvantage of Paroxetine’s short half life?

A

Significant withdrawal symptoms with missed doses or abrupt d/c of drug
- slow taper over 3-4 weeks recommended

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30
Q

Which antidepressant causes the most weight gain?

A

Paroxetine (Paxil)

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31
Q

What anticholinergic effects are associated with paroxetine (paxil)?

A

Constipation, dry mouth – mild anticholinergic effects due to weak muscarinic receptor antagonist activity

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32
Q

Which antidepressant has the longest half life and is therefore best for patients who may miss doses?

A

Fluoxetine

33
Q

What are the withdrawal symptoms of paroxetine and fluvoxamine (due to short half life)?

A

Withdrawal symptoms: anxiety, irritability, dizziness, insomnia, nausea, dysphoria

34
Q

What are the major side effects of SSRIs?

A
  • Initially: N/V, diarrhea, HA, agitation/irritability
  • Not resolving with time: decreased sex drive and impaired sexual function (anorgasmia, erectile dysfunction, decreased libido, menstrual irregularity seen up to 30-40% of pt’s on SSRIs)
  • Some reports of hyperprolocatinemia
  • Increased anxiety (esp. fluoxetine), rash, apathy, insomnia, sedation, sweating/night sweats, nightmares, tremor, dry mouth and weight gain (esp. paroxetine), bruising
35
Q

What are the black box warnings of SSRIs?

A

1) Increased suicidal ideation in individuals

36
Q

Which substances/drugs have serotonin activity?

A 
SSRIs
MAOIs
SNRIs
TCAs
Meperidine (metabolite has serotonergic effects), Sumatriptan
St John’s Wort
MDMA (ecstasy)
LSD
OTC cold remedies
37
Q

What are the signs of serotonin syndrome?

A 
Abdominal pain
Diarrhea
Tremor
Sweating
Restlessness
Fever
Hyperreflexia
Tachycadia

HTN&raquo_space; disorientation, muscle rigidity, myoclonus, fever&raquo_space; coma, shock, seizures&raquo_space; death

38
Q

How do SSRIs affect other drugs?

A

SSRI levels usually not altered by other drugs but can potentially increase levels (inhibit metabolism) of certain drugs

39
Q

What medications are helpful in treating the symptom clusters associated with PTSD (reexperiencing, avoidance, hyperarousal)?

A

SSRI => Sertraline, paroxetine
SNRIs
(TCAs and MAOIs may also be effective)

40
Q

What medications are first line in dysthymic disorder?

A
  • SSRIs
  • SNRIs
  • Bupropion
    (and don’t forget that CBT co-therapy works better than both alone!)
41
Q

What medication should be used to treat bulimia?

A

SSRIs (fluoxetine and sertraline)

42
Q

Name the 6 atypical antidepressants?

A

1) Venlafaxine
2) Duloxetine
3) Bupropion
4) Mirtazipine
5) Trazodone
6) Nefazodone

43
Q

What is the mechanism of action of bupropion?

A

NE and Dopamine reuptake inhibitor – “NDRI”

44
Q

What is the mechanism of action of Mirtazapine (remeron)?

A
  • Complex serotonin receptor antagonism
  • α2 adrenergic receptor antagonism
  • Histaminergic H1receptor antagonism
45
Q

SNRIs are useful in what chronic condition (non-psych)?

A

SNRIs (venlafaxine/effexor and duloxetine/cymbalta) shown effective in chronic neuropathic pain due to NE component at higher doses

46
Q

What atypical anti-depressant can be used in nicotine/tobacco addiction cessation?

47
Q

What type of activity does Venlafaxine/Effexor have at higher doses?

A

Higher dose, more NE activity

48
Q

What are the advantages of Venlafaxine’s short half life?

A

Short half life and fast renal clearance avoids build-up (good for geriatric populations)

49
Q

What are the disadvantages of Venlafaxine’s short half life?

A

Can cause a bad discontinuation syndrome – slow taper recommended after 2 weeks of administration

50
Q

What are the major side effect concerns of Venlafaxine?

A
  • Significant nausea
  • Can induce mania
  • Can cause 10-15mmHg dose dependent increase in blood pressure
51
Q

In what way is duloxetine/cymbalta better than venlafaxine?

A

Less blood pressure increase (also indicated for depression and neuropathic pain)

52
Q

What are the dose dependent actions of mirtazapine/remeron?

A
  • Sedation & weight gain at lower dose hence given qhs (antihistaminic).
  • At doses 30 mg and above, it can become activating (NE effect) and require change of administration time to qam
53
Q

What metabolic concerns are associated with mirtazapine?

A
  • increase in cholesterol and triglycerides in some patients
54
Q

What anti-depressant is also a second line treatment for ADHD?

55
Q

Unlike other antidepressants, which drug is NOT also indicated for anxiety?

A

Bupropion => can actually cause/worsen anxiety, agitation, and insomnia

56
Q

What is the mechanism of action of trazodone?

A
  • Serotonin 5HT2a receptor antagonist and 5HT2c receptor agonist
  • α1 adrenergic receptor antagonism
57
Q

What are the major side effects of trazodone?

A

Sedation, weight gain, low blood pressure (due to α1 receptor antagonism)

58
Q

What is the most common use for trazodone?

A

Off label=> insomnia

59
Q

What is the mechanism of action of TCAs?

A
  • Blocks reuptake of NE and Serotonin at presynaptic neuron (similar to SNRIs)
  • Antagonists of histamine, muscarinic (anti-cholinergic) and α1-adrenergic receptors in differing ratios
60
Q

What are the tertiary TCAs?

A

Imipramine, Amitriptyline, Doxepin, Clomipramine

61
Q

What are tertiary TCAs metabolized to?

A

Tertiary TCA’s get broken down to secondary TCAs, which has less sedating and anticholinergic side effects.

62
Q

What side effects are associated with TCAs?

A

Anticholinergic SE => dry mouth, constipation, blurred vision and urinary retention, cardiac arrhythmias and conduction changes
α1-antiadrenergic => Orthostatic hypotension
Antihistaminc => Sedation and weight gain

63
Q

What are the 3 Cs (toxicities) of TCAs and what are they attributed to?

A

Coma
Convulsions
Cardiotoxic => QRS and QTc prolongation

  • Due to lipophilic and protein binding properties
64
Q

Why are TCAs contraindicated for bipolar patients?

A

Pt’s with undiagnosed bipolar d/o may be pushed into mania or rapid cycling

65
Q

Why should TCAs generally not be used with low potency typical anti-psychotics?

A

Additive anticholinergic toxicity & hypotension

66
Q

What TCA is used to treat OCD?

A

Clomipramine

67
Q

What TCA is activating/used for ADHD?

A

Desipramine

68
Q

What TCA is used for insomnia?

69
Q

What TCA is used for bed wetting (enuresis)?

A

Imipramine

70
Q

What TCA is used for chronic pain?

A

Nortriptyline

71
Q

What class of antidepressant requires a baseline EKG?

A

TCA => due to QT prolongation/torsades

72
Q

What is the mechanism of action of MAOIs?

A

Bind irreversibly to monoamine oxidase => thereby preventing inactivation and degradation of biogenic amines (norepinephrine, dopamine, and serotonin) leading to increased synaptic levels of monoamines (dopamine, norepinephrine, epinephrine, serotonin)

73
Q

What are the major side effects of MAOIs?

A
  • Orthostatic hypotension
  • Weight gain
  • Dry mouth
  • Sedation
  • Sexual dysfunction
  • Sleep disturbance
  • HTN Crisis
  • Serotonin syndrome
74
Q

What drug class is particularly good for treating atypical depression?

75
Q

Name some sympathomimetic stimulants.

A

OTC cold remedies, amphetamines, pseudoephedrine

76
Q

What are tyramine containing foods?

A

aged cheeses, chocolate, soybeans, dry sausage, caffeine, alcohol, wine, pickles

77
Q

MAOIs combined with what sorts of substances can cause hypertensive crisis?

A

Tyramine containing foods or sympathomimetic stimulants

78
Q

MAOIs combined with what other drug classes can lead to serotonin syndrome?

A
  • SSRIs
  • SNRIs
  • TCAs
79
Q

What are the major MAOIs?

A 
MAO
Takes => Tranylcypromine
Pride => Phenylzine
In => Isocarboxazid
Shanghai => Selegiline (parkinson's tx)

Psych clerkship (13 decks)

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