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Psych Exam 1 > Antidepressants (Linger) - SRS > Flashcards

Antidepressants (Linger) - SRS Flashcards

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1
Q

What are the selective serotonin reuptake inhibitors?

7 with 6 bolds

A
  1. Citalopram (Celexa)
  2. Escitalopram (Lexapro)
  3. Fluoxetine (Prozac)
  4. Fluvoxamine*
  5. Paroxetine (Paxil)
  6. Sertraline (Zoloft)
  7. Vilazodone (Viibryd)
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2
Q

What are the selective serotonin-norepinephrine reuptake inhibitors?

5 with 2 bolds

A
  1. Desvenlafaxine (Pristiq)
  2. Duloxetine (Cymbalta)
  3. Levomilnacipran (Fetzima)
  4. Milnacipran (Savella)** (fibromyalgia only)
  5. Venlafaxine (Effexor)
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3
Q

What are the tricyclic antidepressants we need to know?

8 with 4 bolds

A
  1. Amitriptyline (Elavil)
  2. Clomipramine (Anafranil)*
  3. Desipramine (Norpramin)
  4. Doxepin (Sinequan)
  5. Imipramine (Tofranil)
  6. Nortriptyline (Pamelor)
  7. Protriptyline (Vivactil)
  8. Trimipramine (Surmontil)
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4
Q

What are the 5-HT2 Antagonists we need to know?

2 with one bold

A
  1. Nefazodone
  2. Trazodone (desyrel)
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5
Q

What are the Tetracyclic and Unicyclic Agents we need to know?

4 with 2 bolds

A
  1. Amoxipine
  2. Bupropion (Wellbutrin)
  3. Maprotiline
  4. Mirtazapine (Remeron)
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6
Q

What are the Monoamine Oxidase Inhibitors (MAOIs) used for antidepression?

4 with one bold

A
  1. Isocarboxazid (Marplan)
  2. Phenelzine (Nardil)
  3. Selegiline
  4. Tranylcypromine (Parnate)
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7
Q

What is the monoamine hypothesis of depression?

A
  1. Depression is caused by a decrease in biogenic amines (primarily NE and 5-HT, but also DA); excess biogenic amines results in mania and psychotic states
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8
Q

All currently available antidepressant drugs are classified as having their primary MOA on?

A

the metabolism, reuptake, or selective receptor antagonism of serotonin, norepinephrine, or both

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9
Q

What is the receptor hypothesis ofdepression?

A
  1. Antidepressants may take 1-4 weeks to produce any improvement and 6-8 weeks to achieve substantial benefit; yet the acute pharmacological effects of these drugs on neurotransmitter levels and subsequent receptor activation are immediate (minutes)
  2. This lag in onset of clinical efficacy implies that dynamic changes in neural circuits must occur before benefits can be realized; This probably involves regulation of receptor signaling, cellular sensitivity to signals, and trophic factor-induced changes in neuronal plasticity
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10
Q

What is the neurotrophic factor hypothesis of depression?

A

Several lines of evidence implicate brain-derived neurotrophic factor (BDNF), a critical growth factor involved with neurogenesis and neural plasticity, as a key modulator of mood and depression

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11
Q

What is the neuroendocrine hypothesis of depression based on?

A

A number of hormonal abnormalities are associated with depression including changes in the hypothalamic-pituitary-adrenal (HPA) axis, thryoid dysregulation, and sex steriod deficiencies (Katzung, p. 524-525)

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12
Q

Describe the pharmacodynamics of the SSRIs.

A

Allosterically inhibit the serotonin transporter (SERT) effectively increasing the concentration of serotonin in the synaptic cleft; about 80% of SERT activity is blocked at therapeutic doses

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13
Q

What do the SNRIs and TCAs have in common as far as pharmacodynamics?

A
  1. Both classes inhibit SERT and NET, the norepinephrine reuptake transporter, effectively increasing the concentration of both neurotransmitters in the synaptic cleft
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14
Q

Do most SNRIs have greater affinity for SERT or NET?

A

SERT

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15
Q

Apart from NET and SERT, what other receptors do TCAs also exhibit affinity for?

A
  1. Muscarinic
  2. H1
  3. alpha-adrenergic

(accounts for the many ADRs)

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16
Q

Describe the relative affinity of the SNRIs for the following receptor types as high, moderate, negligable.

  1. H1
  2. Muscarinic
  3. alpha-adrenergic
A

SNRIs have negligable affinity for all three of these receptor types and thus have more favorable ADR profiles than do the TCAs.

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17
Q

What is the MOA of trazodone and nefazodone?

A

5-HT2 Antagonists - post synaptic

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18
Q

It is counterintuitive how antagonism of a postsynaptic 5-HT receptor can enhance monoamine tone; nevertheless, both animal and human studies have shown that 5-HT2A receptor inhibition is associated with substantial antianxiety, antipsychotic, and antidepressant effects. What is another point of evidence that supports the use of these drugs?

A
  1. Deceased suicidal and otherwise depressed patients have had more 5-HT2A receptors than normal patients, suggesting that postsynaptic 5-HT2A overdensity is involved in the pathogenesis of depression.
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19
Q

Describe the MOA of bupropion.

Do it.

A

The mechanism of action is incompletely understood; a selective inhibitor of the dopamine transporter (DAT) and stimulates presynaptic release of NE and DA; virtually no direct effect on serotonin reuptake or receptors

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20
Q

What do the two main monoamine oxidases do?

A
  1. MAO-A: metabolism of serotonin, norepinephrine and tyramine
  2. MAO-B: metabolism of Dopamine and tyramine
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21
Q

What is selegiline used for at its low and high doses?

A

Low: MAO-B inhibitor used for parkinsons

High: MAO-A/B inhibitor used for refractory depression

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22
Q

What is the MOA of phenelzine and tranylcypromine?

A

non-selective MAOIs

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23
Q

Most antidepressants are good for both acute and long term managment of major depression. What are acute episodes?

What percent of episodes last 2 or more years?

A
  1. 6-14 months
  2. 20% last 2 years or more
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24
Q

What percent of patients achieve remission within a single trial of 8-12 weeks?

A

30-40%

25
Q

What percent of patients acheive remission by switching to another agent or via augmentation by addition of another drug?

A

70-80%

26
Q

Once an adequate response is achieved, how long is continuation therapy recommended for?

A

Minimum of 6-12 months to reduce the substantial risk of relapse

27
Q

What percent of patients who have a single episode of MDD will have at least one recurrance in their lifetime?

A

85%

28
Q

Patients should be considered for long-term maintenance (years) treatment in what cases?

A

2 or more serious MDD episodes in the previous 5 years or more than 3 episodes in a lifetime.

29
Q

What is the second most common use of antidepressants?

A

Anxiety disorders

30
Q

What anxiety disorders are the SSRI and SNRI drugs approved for?

A

All the major ones including:

  • PTSD
  • OCD
  • Social anxiety disorder
  • GAD
  • Panic disorder
31
Q

What are four drugs OCD is particularly treatable with?

A
  1. fluoxetine
  2. fluvoxamine
  3. paroxetine
  4. clomipramine
32
Q

In addition to depression and anxiety, what are 7 other uses for these drugs?

A
  1. Pain disorders
  2. premenstrual dysphoric disorder
  3. smoking cessation
  4. eating disorders
  5. insomnia
  6. headaches
  7. pruritis
33
Q

Which classes are most useful for the treatment of pain disorders?

A

TCAs and SNRIs

34
Q

Treating for 2 weeks out of the month during the luteal phase may be as effective as continuous treatment for premenstrual dysphoric disorder. What two drugs are particularly good for this?

A

fluoxetine

sertraline

35
Q

What antidepressant is noted to have an impact on smoking cessation?

A

Bupropion

  • reduces the mood swings
  • reduces the weight gain d/t nicotine withdrawal
36
Q

Antidepressants are better for treating which eating disorder?

A

Bulemia, but no anorexia

37
Q

Which antidepressants are notably used for insomnia?

A

amitriptyline

trazodone

38
Q

What antidepressants are used for headaches?

A

TCAs (SSRIs shown to be no more useful than placebo)

39
Q

What are the most commonly prescribed first line agents for MDD and anxiety?

A

SSRIs

40
Q

In what patients is bupropion a good option?

What is it not good for treating?

A

Those who cannot tolerate the:

  1. sexual dysfunction
  2. weight gain
  3. sedation

That come with other antidepressants.

Not good for anxiety

41
Q

TCA and MAOI are relegated to 2nd or third line use. Why?

When are they nonetheless good options?

A
  1. Potentially lethal overdose
  2. titration needed for therapeutic dose
  3. serious DDIs
  4. numerous ADRs

Nonetheless good for refractory depression.

42
Q

5-HT2 antagonists are commonly prescribed for what disorders?

A

None. On the occasions it is used its for MDD or anxiety though.

43
Q

What do all antidepressants carry a warning against?

In what patient group does this matter?

A
  1. All antidepressants carry a warning of increased suicidality (suicidal ideation and gestures, but not completion) in patients under age 25; there is no increased risk or reduced risk in those over age 25
44
Q

Name as many ADRs of SSRI drugs as you are able.

7ish

A
  1. minor sedation
  2. anti-muscarinic effects
  3. diminished sexual function, loss of libido, delayed orgasm, diminished arousal (these last the entire duration of the therapy)
  4. headaches
  5. insomnia
  6. weight gain
  7. discontinuation syndrome
45
Q

What are some SSRI DDIs to be aware of?

A

Serotonin syndrome with MAOIs

46
Q

ADRs of SNRIs?

A
  1. SNRIs have the serotonergic side effects exhibited by SSRIs but also have noradrenergic side effects including insomnia, anxiety, and agitation
  2. Elevated blood pressure and heart rate are sometimes an issue, although not problematic in most patients
  3. Venlafaxine may increase the risk of bleeding via an antiplatelet aggregation effect; this agent is also more frequently associated with cardiac toxicity in overdose relative to other SNRIs or SSRIs
  4. Discontinuation syndrome like that seen with SSRIs
47
Q

ADRs of TCAs?

A
  1. Anticholinergic effects including drowsiness, dry mouth, constipation, urinary retention, blurred vision, and confusion
  2. Orthostatic hypotension due to α-adrenergic receptor blockade, especially in the elderly
  3. Weight gain and sedation due to H1 histamine receptor antagonism
  4. Cardiotoxicity, arrhythmias and heart block; Convulsions; hepatic dysfunction; Hyponatremia, which may lead to confusion in the elderly
  5. Hematological abnormalities (e.g., leucopenia, thrombocytopenia and agranulocytosis)
  6. Sexual side effects similar to those seen with SSRIs
  7. Imipramine and amitriptyline exhibit marked antimuscarinic and cardiac side effects
  8. Discontinuation syndrome like that seen with SSRIs
48
Q

ADRs of 5-HT2 Antagonists?

A
  1. Most common adverse effects are sedation and gastrointestinal disturbances
  2. Sexual side effects are uncommon
  3. Orthostatic hypotension due to α-adrenergic receptor blockade
  4. Nefazodone carries a black box warning for hepatotoxicity and potentially lethal hepatic failure; it is still available generically but rarely prescribed
49
Q

ADRs of bupropion and mirtazapine?

A
  1. Bupropion has CNS activating properties, it is occasionally associated with agitation, insomnia, and anorexia
50
Q

ADRs of MAOIs?

A
  1. Orthostatic hypotension and weight gain
  2. Highest rates of sexual side effects of all the antidepressants; anorgasmia is common
  3. May cause dangerous interactions with certain tyramine-containing foods and with serotonergic drugs (see “Drug Interactions” below)
  4. Sudden discontinuation syndrome manifested in delirium-like presentation with psychosis, excitement, and confusion
51
Q

In what cases are SSRIs CI?

A
  1. Contraindications: SSRIs should be discontinued or avoided in patients displaying active manic symptoms; paroxetine is contraindicated in pregnant patients
52
Q

What are some CIs for TCAs?

A
  1. Contraindications: ​
  • Arrhythmias,
  • recent myocardial infarction,
  • liver disease,
  • glaucoma,
  • mania
53
Q

What are the most toxic of the antidepressants?

A

TCAs, particularly amitriptyline. When taken in OD, leads to arrhythmias, altered mental status and seizures.

54
Q

Other than TCAs, what other antidepressant is particularly dangerous for OD?

A

MAOIs - produce potentially lethal autonomic instability with:

  • hyperadrenergic symptoms
  • psychotic symptoms
  • confusion
  • delirium
  • fever
  • seizures
55
Q

​Serotonin Syndrome is a Life-threatening pharmacodynamic interaction of MAOIs with serotonergic agents including SSRIs, SNRIs, most TCAs, and some analgesics and is thought to be caused by overstimulation of 5-HT receptors in the central gray nuclei and the medulla.

What are the symptoms?

A
  1. Symptoms range from mild to lethal:
    1. Cognitive: delirium, agitation, coma
    2. Autonomic: hypertension, tachycardia, hyperthermia, diaphoreses
    3. Somatic: myoclonus, hyperreflexia, tremor
56
Q

When switching to an MAOI, what must be done prior to initiation of new therapy?

A
  1. When a patient is switched from an SSRI (or other serotonergic agent) to an MAOI (or vice versa), the current therapy should be discontinued for at least 2 weeks (6 weeks for fluoxetine due to longer half-life) prior to initiation of the new therapy
57
Q

What is the treatment for serotonin syndrome?

A
  1. Treatment: withdraw the offending drug, sedation with benzodiazepines, paralysis, intubation, and ventilation; consider 5-HT2 block with cyproheptadine or chlorpromazine
58
Q

What is the tyramine effect?

A
  1. Tyramine is a naturally occurring monoamine compound that acts as a catecholamine releasing agent
  2. In foods, it is often produced by decarboxylation of tyrosine during fermentation or decay
  3. Foods containing considerable amounts of tyramine include foods that are pickled, aged, smoked, marinated, or meats that are potentially spoiled; chocolate; alcoholic beverages; and fermented foods, such as most cheeses, etc.
  4. Tyramine is normally metabolized by MAO; when large amounts of tyramine are ingested and MAOIs reduce metabolism, hypertensive crisis can occur – tyramine induces NE release from peripheral nerve terminals and subsequent dramatic (and potentially fatal) rise in heart rate and blood pressure
59
Q
A

Psych Exam 1 (6 decks)

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