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PR3153 > Depression - Treatment > Flashcards

Depression - Treatment Flashcards

1
Q

How do the MAOIs result in therapeutic effects?

A

Inhibit monoamine oxidase to increase biological availability of monoamines – counteract deficits in monoamine neurotransmitters

  • MAO-A: noradrenaline, dopamine, 5-HT (Serotonin)
  • MAO-B: noradrenaline and dopamine only

(moclobemide - reversible antagonism)

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2
Q

What are the adverse effects of MAOIs

A
  • Postural hypotension – likely due to sympathetic block produced by accumulation of dopamine in the cervical (neck) ganglia, where it acts as an inhibitory transmitter
  • Restlessness and insomnia – due to CNS stimulation
  • Should not be combined with other drugs enhancing serotonergic function (e.g. pethidine) – can result in hyperexcitability, inc muscle tone, myoclonus (jerking, involuntary movements), loss of consciousness
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3
Q

How does the interaction between MAOIs and cheese work?

A
  • Amines (e.g. tyramine) in foods are usually broken down by MAO in the intestines and liver
  • Inhibition of MAO allows them to exert sympathomimetic effect – tyramine gets taken into adrenergic terminals , competes w NA for vesicular compartment, ↑NA release to synapses
  • Less likely with reversible MAO-A selective MAOIs (e.g. moclobemide)
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4
Q

What is the MOA of the TCAs?

A

Blocks reuptake of NA and 5-HT

Non-selective for Serotonin and Norepinephrine Transporters: Imipramine, Amitriptyline, Nortriptyline

Selective for Norepinephrine Transporter: Desipramine

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5
Q

What are the adverse effects of the TCAs?

A

Sedation – due to H1 histamine receptor antagonism
* Tolerance to sedation can develop in 1-2 weeks

Postural Hypotension – due to α-adrenoreceptor sympathetic block

Dry mouth, blurred vision, constipation – due to muscarinic receptor antagonism

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6
Q

What are the advantages of SSRIs?

A
  • Low affinity for α-adrenoreceptors – lack of CV effects, safer in overdose
  • Lack of effect at histamine receptors – reduced sedation
  • Low affinity for muscarinic cholinergic receptors – minimal anticholinergic SE
  • Due to less side effects, able to prescribe more adequate doses (compared to TCAs that are frequently used at subtherapeutic doses due to intolerability of adverse effects)
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7
Q

What is the MOA of SSRIs?

A

Selectively blocks reuptake of 5-HT

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8
Q

What are the adverse effects of SSRIs?

A

→ Nausea
→ Insomnia
→ Sexual dysfunction
→ Citalopram still has some histamine receptor antagonism leading to sedation
→ Serotonin Syndrome – DDI with other drugs increasing serotoninergic activity
(Tremor, Hyperthermia, Cardiovascular collapse)

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9
Q

What is the MOA of SNRIs?

A

Blocks reuptake of NA and 5-HT

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10
Q

What are the adverse effects of SNRIs?

A

→ Serotoninergic adverse effects similar to SSRIs: nausea, insomnia, sexual dysfunction
→ Serotonin syndrome when combined with other serotoninergic drugs
→ Withdrawal effects may be more common and stronger than for SSRIs and TCAs

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11
Q

What is the MOA of mirtazapine?

A

→ Norepinephrine and specific serotonin antidepressant
→ Antagonist of adrenergic α2 autoreceptors and 5-HT2C receptors, among others

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12
Q

What is the MOA of bupropion?

A

Blocks reuptake of NA and DA

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13
Q

What is the MOA of agomelatine?

A

MT-1, MT-2 agonist
5-HT2C antagonist
↑DA and NA

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14
Q

What is the MOA of ketamine?

A

Glutamate NMDA agonist used as anaesthetic, currently evaluated for rapid onset antidepressant effect

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15
Q

What is the MOA of vortioxetine?

A

Multimodal serotonergic antidepressant – novel class
* Agonist activity at 5-HT1A receptor
* Partial agonist activity at the 5-HT1B receptor
* Antagonism at 5-HT1D, 5-HT7, and 5-HT3 receptors

Additional receptor affinities may ↑release of serotonin and release other neurotransmitters

May be efficacious in patients resistant to other antidepressants

May also have pro-cognitive effects

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16
Q

How long is an adequate trial of acute phase treatment?

A

4-8 weeks, max 12 weeks

17
Q

How long does it take for treatment response to show up?

A
  • Physical Sx may improve in 1-2 weeks – eg sleep, appetite
  • Mood Sx may take longer time to improve eg 4-8 weeks
18
Q

How long should continuation phase treatment last?

A

1st episode of uncomplicated MDD – continue for at least another 4-9 months after acute phase Tx

19
Q

What are the strategies to manage partial/lack of response?

A
  • Switch antidepressant
  • Augmentation

Treatment-Resistant Depression – no response to ≥2 adequate trials of antidepressants: ECT, combination therapy

20
Q

How can antidepressants be switched?

A

→ If cross-titration – watch for serotonin syndrome if combining serotonergic agents
→ If direct switch, one SSRI can be stopped totally and the next serotonergic agent initiated
→ If switching from a serotonergic antidepressant used daily for the past 2 months to a non-serotonergic agent (eg SSRI/SNRI to bupropion), gradual cross-tapering over several weeks can reduce risk of Antidepressant Discontinuation Syndrome (by half tab Q1-2 weeks)
→ Moclobemide to another antidepressant: 24h washout
→ Another antidepressant to moclobemide: at least 1 week (5 weeks if stopping fluoxetine)

21
Q

What are the symptoms of Antidepressant Discontinuation Syndrome?

A

FINISH
Flu-like symptoms – lethargy, fatigue, headache, achiness, sweating
Insomnia – w vivid dreams or nightmares
Nausea – sometimes vomiting
Imbalance – dizziness, vertigo, light-headedness
Sensory disturbances – “burning”, “tingling”, “electric-like” sensations
Hyperarousal – anxiety, irritability, agitation, aggression, mania, jerkiness

22
Q

How long does Antidepressant Discontinuation Syndrome last for?

A

3-7 days

23
Q

How is Antidepressant Discontinuation Syndrome managed?

A

Typically resolves over 1-2 weeks w/o Tx
(Pt may feel some discomfort, but unlikely to be life threatening)

24
Q

What are the considerations in pregnancy?

A

consider nortriptyline in late pregnancy

25
Q

What are the considerations for breastfeeding?

A

can consider sertraline or mirtazapine

26
Q

What are the considerations for post-partum depression?

A

brexanolone (positive allosteric modulator of GABA)

27
Q

What are the preferred agents for bipolar depression?

A

lithium, lamotrigine, lurasidone, quetiapine etc

28
Q

What are the considerations for renal impairment?

A

may consider vortioxetine

29
Q

What are the considerations for hepatic impairment?

A

Avoid agomelatine. If mild-moderate, can consider vortioxetine

PR3153 (16 decks)

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