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Psychiatric Pharmacology > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

Important early evidence for Monoamine theory came from the observation that reserpine, which inhibits ___ and ____ storage, depressed mood.

A

NA (noradrenaline)

5-HT (serotonin)

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2
Q

Initially, the monoamine theory was formulated for ____, but the emphasis for Monoamine theory has since shifted towards _____.

A
  1. NA

2. 5-HT

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3
Q

Where is Monoamine oxidase (MAO) found in the human body?

A

Found in nearly all tissues, including nerve terminals, intestine, and liver.
Found intracellularly, mostly on the mitochondrial surface

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4
Q

There are 2 major forms of MAO.

Neurochemical _____ is mainly broken down by MAO-A.

A

5-HT

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5
Q

Which MAO form acts on NA and dopamine?

A

Both forms of MAO act on NA and dopamine and have equal selectivity.

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6
Q

MAO-B selective inhibitors (i.e. selegiline) are used in _________.

A

Parkinson’s disease

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7
Q

Which part of the synapse is MAO found at the synaptic junction?

A

Pre-synapse (intraceullarly)

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8
Q

Effect of MAO-inhibitors on monoamines?

A

Increased biological availability of monoamines.

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9
Q

Phenelzine is more/less/non selective for MAO-A vs MAO-B.

A

Non-selective

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10
Q

Phenelzine is more/less/non selective for MAO-A vs MAO-B.

A

Non-selective

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11
Q

What are the adverse effects of MAO inhibitors?

A
  1. Postural Hypotension

2. Restlessness and insomnia

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12
Q

MAOIs can cause Postural Hypotension via ________ caused by accumulation of dopamine in cervical (neck) ganglia, where it acts as an ______ transmitter.

A
  1. sympathetic block
  2. inhibitory

(heart can no longer pump faster in response to postural change = insufficient blood to brain)

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13
Q

MAOIs can cause restlessness and insomnia due to _____ stimulation.

A

CNS

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14
Q

Why should MAOIs not be combined with drugs that enhance serotoninergic function, such as Pethidine?

A

May lead to: Hyperexcitability, increased muscular tone, myoclonus (jerking, involuntary movements), loss of consciousness

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15
Q

What is the interaction in the ‘Cheese’ reaction and what is it caused by?

A

A Drug-Food interaction arising from consuming cheeses and concentrated yeast products (i.e. marmite) together with MAOIs

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16
Q

What are the consequences of a ‘Cheese reaction’?

A

Acute hypertension, giving severe throbbing headache, and occasionally intracranial haemorrhage

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17
Q

How can we try to prevent ‘cheese’ reaction?

A
  1. Avoid taking Cheese/conc. yeast food with MAOI

2. Use reversible MAO-A/B selective inhibitors (i.e. moclobemide)

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18
Q

‘Cheese’ reaction is _____ likely to occur with reversible, MAO-A/MAO-B selective(e.g. moclobemide) vs. irreversible, non-selective MAOIs

A

less

non selective = more enzymes blocked = worse reaction

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19
Q

What is the MOA of the cheese reaction?

A
  1. Amines such as tyramine (in cheese) accumulate when MAOs are inhibited.
  2. Tyramine is taken up into adrenergic terminals and competes with NA for vesicular compartment.
  3. Increased NA release into synapses. (sympathomimetic effect)
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20
Q

What is the MOA of the cheese reaction?

A
  1. Amines such as tyramine (in cheese) accumulate when MAOs are inhibited.
  2. Tyramine competes with NA for vesicular compartment.
  3. Increased NA release into synapses and a sympathomimetic effect.
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21
Q

_________ are TCAs that are non-selective for SERT/NET.

A

Imipramine, Amitriptyline, nortriptyline

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22
Q

________ is a TCA that is selective for NET.

A

Desipramine

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23
Q

Nortriptyline is a _______ TCA that has _______ compared to amitriptyline and imipramine which leads to _______________.

A
  1. 2nd gen TCA
  2. milder side effects
  3. improved compliance
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24
Q

Nortriptyline is a _______ TCA that has _______ compared to amitriptyline and imipramine and improved compliance.

A
  1. 2nd gen TCA

2. milder side effects

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25
Q

TCAs can lead to sedation due to ________ receptor antagonism. Tolerance to sedation can develop in ____ weeks

A
  1. H1 Histamine

2. 1-2wks

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26
Q

TCAs can lead to ______ due to α-adrenoceptor sympathetic block.

A

Postural Hypotension

27
Q

What are some adverse effects of TCAs?

A
  1. Sedation
  2. Postural hypotension
  3. Dry mouth, blurred vision, constipation
28
Q

TCAs are _______ bound and eliminated via _______ route.

A
  1. plasma protein

2. Hepatic

29
Q

SSRIs have greater ______ and fewer ______ when compared to TCAs.

A
  1. 5-HT reuptake selectivity

2. Fewer adverse effects

30
Q

Place in therapy for TCAs?

A

For patients allergic to SSRIs

31
Q

SSRIs have low affinity for α-adrenoceptors, leading to ________

A

Lack of cardiovascular effects, safer in overdose

32
Q

SSRIs have low affinity for α-adrenoceptors, leading to ________

A

Lack of cardiovascular effects, safer in overdose

33
Q

SSRIs have Lack of effect at _________ receptors, leading to ________

A
  1. histamine

2. Reduced sedation

34
Q

SSRIs have Minimal anticholinergic side effects (e.g. dry mouth and constipation) due to __________

A

Low affinity for muscarinic cholinergic receptors

35
Q

What is the main advantage of SSRIs?

A

SSRIs are safer in overdose and less side effects lead to better compliance. (compared to TCAs)

36
Q

Adverse effects of TCAs lead to _______, which is seen at a lower frequency for SSRIs.

A

prescription of subtherapeutic doses.

37
Q

Adverse effects of SSRIs include: ________, _______ and _________

A

Nausea
Insomnia
Sexual dysfunction

38
Q

Nausea and vomiting (SSRIs) may be caused by __________________ when plasma levels of drug drop between doses.

A

Discontinuation/rebound symptoms of withdrawal (i.e. skipped dose)

39
Q

Which SSRI still has histamine receptor antagonism and can cause sedation?

A

Citalopram

40
Q

SSRIs can induce sexual dysfunction by increased stimulation of ________ and can be prevented by ___________, a _____ blocker.

A
  1. 5-HT2 receptors
  2. Cyproheptadine
  3. 5-HT2
41
Q

What is “Serotonin Syndrome” caused by?

A

Drug-drug interactions with other drugs increasing serotoninergic activity (e.g. MAOIs).

42
Q

Effects of “Serotonin Syndrome” includes _____, _____ and _______

A
  1. tremor
  2. hyperthermia
  3. cardiovascular collapse
43
Q

For patients using SSRIs, only ____ get remission (respond).

44
Q

Adverse effects of SSRIs are more pronounced when _____ and ______ the drug.

A
  1. initiating

2. discontinuing

45
Q

NARIs have ________ selectivity than TCAs.

A

Greater NA reuptake

46
Q

NARIs (i.e. Reboxetine) have approximately _______ fold selectivity for NA.

47
Q

NARIs have _______ adverse effects compared to TCAs and SSRIs

48
Q

Maprotiline, an earlier NARI, had TCA-like adverse effects due to _______ and ______ receptor effects and occasionally caused _______.

A
  1. α-adrenoceptor
  2. histamine
  3. seizures
49
Q

Reboxetine can lead to _______ and ______ due to its anti-cholinergic effects.

A
  1. Dry mouth

2. Constipation

50
Q

Reboxetine can lead to ________, likely due to increased noradrenergic effects in CNS.

51
Q

Reboxetine can lead to tachycardia, likely due to increased _______.

A

Increased availability of NA at sympathetic “fright, flight or fight” synapses.

52
Q

Adverse effects of Reboxetine?

A
  1. Dry mouth
  2. Constipation
  3. Insomnia
  4. Tachycardia
    Note: new drug, adverse effects not well described
53
Q

SNRIs have similar ______ reuptake inhibition profiles to non-selective TCAs.

A

dual 5-HT and NA

54
Q

The Issue of additional receptor antagonism is controversial in SNRIs because ______?

A

We are not sure what are the other receptors SNRIs are binding to

55
Q

3 SNRI examples in clinical use?

A
  1. Venlafaxine
  2. Desvenlafaxine(synthetic metabolite of venlafaxine)
  3. Duloxetine
56
Q

Venlafaxine has a different ________ compared to TCAs and _____ adverse effects than TCAs.

A
  1. structure

2. fewer

57
Q

Venlafaxine claims to work _____ than other antidepressants and work better in _____ patients

A
  1. slightly faster

2. treatment-resistant

58
Q

SNRIs have similar serotoninergic adverse effects similar to SSRIs, which include _______, _____, _______ and _______ when combined with other serotoninergic drugs and MAOIs.

A
  1. Nausea
  2. Insomnia
  3. Sexual dysfunction
  4. “Serotonin syndrome”
59
Q

Withdrawal effects of SNRIs may be ______________ than SSRIs and TCAs.

A

more common and stronger

60
Q

Mirtazapine is an _______ and specific ______ antidepressant (NaSSA).
Antagonist of _______ autoreceptors and ____ receptor, among others.

A
  1. norepinephrine
  2. serotonin
  3. adrenergic α2
  4. 5-HT2C
61
Q

Bupropion is an ______________ reuptake inhibitor (NDRI).

A

norepinephrine-dopamine

62
Q

Agomelatine is an agonist of _______ receptors (also has antagonism at _________), less TCA / SSRI-associated side-effects and also helps in ______.

A
  1. melatonin MT1 and MT2
  2. 5-HT2C receptors
  3. sleep disorders
63
Q

Argomelatine is hypothetically safer to combine with MAOIs/SSRIs due to ____________.

A

lower risk of serotonin syndrome (antagonism of 5-HT)

64
Q

Ketamine is a _____________ used as an anesthetic, currently evaluated for rapid-onset antidepressant effect.

A

glutamate NMDA receptor antagonist

Psychiatric Pharmacology (8 decks)

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