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PHAR222 > L17 Antidepressants > Flashcards

L17 Antidepressants Flashcards

1
Q

emotional symptoms

A

low mood, negative thought; loss of motivation, indecisiveness; low self-esteem

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2
Q

imipramine

A

block noradrenaline and serotonin uptake → improve mood in depressed schizophrenics

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3
Q

Monoamine theory of depression

A

a functional deficit of noradrenaline and serotonin in certain brain regions
↑ noradrenaline and ↑ 5-HT are equally effective as antidepressants (individual variation)

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4
Q

Monoamine theory of depression issue/limits

A
  • pharmaco weeks not hours or minutes
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5
Q

BDNF (brain-derived neurotrophic factor)

A
  • CNS development and neuronal plasticity
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6
Q

Neuroplasticity BDNF path to CREB

A

Prepro-bdnf
↓
Pro-bdnf
↓
Mature BDNF
↓Bind to TrkB (tropomypsin rec kinase B)
CREB (cAMP response element
↓
Gene expression

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7
Q

Neuroplasticity of depression involves decrease

A

BDNF levels in hippocampus/prefrontal cortex

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8
Q

Activity of CREB

A

transcriptional activity of CREB
↓
Promotes BDNF expression
↓
Causes neurogenesis in the prefrontal cortex and hippocampus

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9
Q

What happens to CREB activity when there is increased stress an cortisol levels

A

Suppresses he transcription activity of CREB therefore imparing BDNF expression and neurogenesis

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10
Q

What does cortisol and stress do to the prefrontal cortex and hippocampus

A

Can cause apoptosis in neurons

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11
Q

selective serotonin reuptake inhibitor (SSRIs)

A

fluoxetine

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12
Q

tricyclic antidepressants (TCAs)

A

imipramine

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13
Q

monoamine oxidase inhibitors (MAOIs)

A
  • phenelzine
  • moclobemide
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14
Q

Which drug has a fast onset of antidepressant effects

A

Ketamine

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15
Q

fluoxetine simple

A
  • most prescribed antidepressants; first-line treatment
  • binds to serotonin transporter and blocks the reuptake of serotonin,
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16
Q

Blocking 5-HT reuptake by drugs (fluoxetine) causes

A

Elevated synaptic [5HT] but decreased release

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17
Q

somatodendritic 5-HT1A receptor desensitisation + ↑ synaptic [5-HT] postsynaptic

A

5-HT1 receptor → antidepressant effects

17
Q

Why does antidepressants take so long (Inhibit serotonin uptake)

A

Because desensitisation of receptors (5-HTa1) takes long

18
Q

What is fluoxetine metabolised by

A

CYP2D6

19
Q

What enzyme does fluoxetine inhibit

A

CYP2D6

20
Q

What is serotonin syndrome

A

If fluoxetine is taked with another increaser of serotonin but via a different method it will increase via both methods

21
Q

Fluoxetine Side effects

A
  • agitation and insomnia (5 HT2 receptor)
  • nausea (5-HT3 receptor)
  • sexual dysfunction
22
Q

Better adverse effect profile for Fluoxetine

A

lack of affinity for muscarinic acetylcholine receptors and histamine H1 receptors

23
Q

Mirtazapine on receptor

A

a2-adrenoceptors antagonist

24
Q

Mirtazapine as an antagonist

A
  • inhibit alpha-2 adrenoceptors (central presynaptic) and enhance NA and 5-HT release
  • Antagonist to 5-HT2 and 5-HT3 receptors
25
Q

Mirtazapine side effects

A
  • Histamine H1 antagonism - sedation
  • Increase appetite and weight gain
  • headaches
26
Q

Good alternative if adverse effects of SSRIs are problematic

A

Mirtazapine

27
Q

Tricyclic antidepressants function

A

bind serotonin and noradrenaline transporters and inhibit reuptake of 5-HT and noradrenaline → synaptic [5-HT] and [noradrenaline] ↑

28
Q

Name 1 Tricyclic antidepressants

A

imipramine

29
Q

imipramine half life and antagonism

A
  • long half-life - repeated dosing ↑ risk of adverse effects
  • muscarinic acetylcholine receptor antagonist - dry mouth, blurred vision
  • histamine H1 receptor antagonist - sedation
  • not to be combined with monoamine oxidase inhibitor
30
Q

imipramine metabolite from CYP2C19

A

desipramine (active)
both parent and this can be further metabolised by CYP2D6

31
Q

Monoamine oxidase inhibitor drugs

A
  • Phenelzine
  • Moclobemide
32
Q

Monoamine oxidase inhibitors

A

inhibit monoamine oxidase type A and/or type B ⟶ cytoplasmic concentrations of monoamines ↑ ⟶ rate of spontaneous leakage of monoamines ↑

33
Q

irreversible MAO-A and MAO-B inhibitor
non-selective, long acting

A

phenelzine* -

34
Q

reversible MAO-A inhibitor
Short acting

A

moclobemide

35
Q

Monoamine oxidase inhibitors effects

A
  • atropine-like effects - dry mouth, blurred vision
  • other drugs that ↑ serotonin levels
  • ‘cheese reaction’ (drug-food interaction)
36
Q

MAO inhibition + tyramine ingestine

A

Hypertension and headache by MAO would have metabolised Tyramine so it doesn’t go into circulation but MAO inhibited

37
Q

Ketamine

A

a non-competitive NMDA receptor antagonist

38
Q

Ketamine dose

A

one single subanaesthetic dose - rapid (within hours) and sustained (~24 hours), including in individuals with treatment-resistant depression
* BDNF release

39
Q

Ketamine spray

A

nasal spray of Spravato (esketamine, the S-enantiomer) in conjunction with an oral antidepressant for treatment-resistant depression

40
Q

Ketamine as a rapid acting antidepressant

A

–proposed mechanisms
* NMDA receptor inhibition
* on GABAergic interneurons (a)
* extrasynaptic (b)
* synaptic (c)
– BDNF translation or release ↑

PHAR222 (25 decks)

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