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PR3136 > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

MoA of agomelatine

A

Agonist of melatonin MT1 and MT2 receptors (antagonism at 5-HT2c receptors)

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2
Q

MoA of TCAs

A

Blocks transporters such that monoamines do not undergo reuptake. This allows for more of the monoamines to stay within the synapse.

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3
Q

Adverse effects of MAOIs

A

postural hypotension (accumulation of dopamine)
restlessness and insomnia (CNS stimulation)
serotonin syndrome

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4
Q

Drug interactions of MAOIs

A

Cheese effect
tyramine accumulation
serotonin syndrome with serotonin and NA reuptake inhibitors

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5
Q

Symptoms of depression:

A 
Misery, apathy, pessimism 
Low self esteem 
Indecisiveness, loss of motivation 
retardation of thought and action 
loss of libido 
Sleep disturbances and loss of appetite
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6
Q

What is the monoamine theory:

A

Deficits in monoamine neurotransmitters cause depression

- from the observation of reserpine which inhibits NA and serotonin storage

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7
Q

MoA of MAOIs:

A

Increase biological availability of monoamines

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8
Q

Example of MAOIs:

A

Phenelzine

Moclobemide

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9
Q

Drug interactions involved with MAOIs

A

Other drugs enhancing serotoninergic function

Cheeses and concentrated yeast products

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10
Q

Describe Monoamine Theory

A
  • Theory about the cause of depression. It explains that depression is caused by deficits in monoamine neurotransmitters (NE and 5-HT)
  • Observed from Reserpine which inhibits NE and 5-HT storage
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11
Q

Limitations of monoamine theory

A
  1. Inconsistent results
  2. Alone is inadequate to explain pharmacological actions in depression
  3. Originally formulated for NE but shifted later to 5-HT
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12
Q

Main enzyme which breaks down 5-HT and NA respectively

A

5-HT: MAO-A

NA: Both MAO-A and MAO-B

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13
Q

What class of drug is Phenelzine under? Describe its MoA and selectivity

A
  • MAOI
  • Non-selective
  • Irreversible MAO inhibitor preventing breakdown of 5-HT and NA
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14
Q

AE of MAOIs and their causes

A
  1. Postural hypotension (by dopamine accumulation in cervical ganglia)
  2. Restlessness and insomnia due to CNS stimulation by NA (sympathetic stimulation)
  3. Hyperexcitability, increased muscular tone, myoclonus, lose consciousness
    (due to enhancing serotoningeric function when combined with other drugs)
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15
Q

Type of food that interacts with MAOIs and hence limits the use of MAOIs

A

Concentrated yeast products (e.g. marmite) and cheese (acute hypertension)

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16
Q

Describe the Drug-food interaction with tyramine and MAOI

A
  • MAO both breaks down ingested tyramine in intestines/liver, and also NA/Dopamine
  • When MAOI taken, tyramine not broken down, accumulates
  • Accumluated tyramine displaces NA out of vesicles in nerve terminals, cause increased NA release into synapse (hence tyramine is sympathomimetic)
  • Due to MAOI, released NA is not broken down
  • Causes excessive sympathetic stimulation
  • Resultant effect: acute hypertension, headache, intracranial haemorrhage (hypertensive crisis)
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17
Q

Why is the tyramine effect less likely to occur with moclobemide compared to Phenelzine

A

Moclobemide is a reversible MAO-A selective MAOI:

  1. MAO-B is not selectively inhibited, and can breakdown excess NA
  2. High concentrations of tyramine can displace moclobemide from MAO-A and be metabolised
18
Q

Name three TCAs which are non-selective for SERT/NET

A
  1. Imipramine
  2. Amitriptyline
  3. Nortriptyline
19
Q

Name a TCA selective for NET

A

Desipramine

20
Q

MoA of TCAs

A

Inhibits 5-HT and NA reuptake transporters (SET and NET)

21
Q

Benefits of Nortriptyline over the other TCAs

A

A second generation TCA.

Milder side-effects leading to increased compliance

22
Q

Three AEs of TCAs

A
  1. Sedation due to H1 antagonism
  2. Postural hypotension due to alpha-adrenoceptor sympathetic block
  3. M receptor antagonism (e.g. dry mouth, blurred vision, constipation)
23
Q

Two reasons why TCA can potentially participate in drug-drug interactions

A
  1. Plasma protein bound (interfere with other drugs, can displace them)
  2. Hepatic metabolism for elimination
24
Q

Why is sedation caused by TCA not a main concern in using it?

A

Tolerance can be developed in 1-2 weeks

25
Q

SSRI have better SE profile than TCAs due to

A

Better selectivity for 5-HT reuptake transporter than TCAs

26
Q

Three advantages of SSRIs over TCAs

A
  1. Less AE
    - Low affinity for a-adrenoceptors = less Cardio SE, safer in overdose
    - Lack effect at H receptors = reduced sedation
    - Low affinity for M receptors = less anticholinergic SE
  2. Better tolerance
  3. Safer in overdose
27
Q

Adverse effects of SSRIs and possible reason(s) for the AE

A
  1. Nausea
  2. Insomnia
  3. Sexual dysfunction
  • 1 & 2 due to rebound sx when plasma levels of drug drop between doses
  • 3 due to 5HT2 receptor stimulation
28
Q

What SSRI has some histamine receptor antagonism which leads to sedation?

A

Citalopram

29
Q

What drug can be given to prevent SSRI-induced sexual dysfunction?

A

Cyproheptadine

30
Q

What are the effects of serotonin syndrome, and what is it caused by?

A

Effects: Tremor, Hyperthermia, Cardiovascular collapse

Cause: DDI with other drugs increasing serotoninergic activity such as MAOIs

31
Q

SSRIs are first line therapy for depression. However, what are its imperfections?

A
  1. Only 2/3 get remission
  2. AE at the start
  3. Discontinuation can be a problem in some
32
Q

Examples of SSRIs

A
  • Fluoxetine (most commonly used)

- Citalopram

33
Q

Examples of NARIs

A
  • Reboxetine

- Maprotiline

34
Q

AE of reboxetine

A
  1. Anticholinergic effects (e.g. dry mouth, constipation)
  2. Insomnia (due to increased NA activity in CNS)
  3. Tachycardia (due to increased NA)
35
Q

Examples of SNRIs

A
  • Venlafaxine
  • Desvenlafaxine (synthetic metabolite of venlafaxine)
  • Duloxetine
36
Q

Advantages of Venlafaxine (SNRIs) over TCAs

A
  1. Less AE due to different structure
  2. Claimed: faster onset
  3. Claimed: better in treatment-resistant patients
37
Q

AE of SNRIs

A
  1. Nausea
  2. Insomnia
  3. Sexual Dysfunciton
    (similar to SSRIs)
38
Q

MoA of Mirtazapine

A
  • NaSSA (NA and specific serotonin antidepressant)

- Antagonist of a2-adrenergic receptors and 5-HT2c + others

39
Q

MoA of Bupropion

A
  • NA-dopamine reuptake inhibitor (NDRI)

- Shows that dopamine might be a player in depression

40
Q

Advantages of Agomelatine in treating depression

A
  1. Less risk of Serotonin syndrome as it does not target 5-HT
  2. Can help with insomnia
41
Q

MoA of Ketamine. What is it currently evaluated for?

A
  • Glutamate NMDA receptor antagonist

- Currently evaluated for rapid-onset antidepressant effect

PR3136 (18 decks)

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