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Neuropharmacology > Drugs for Depression > Flashcards

Drugs for Depression Flashcards

1
Q

What is the lifetime incidence of major clinical depression?

A

1 in 6 (17%)

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2
Q

What are the emotional symptoms of depression?

A
  • misery, apathy, pessimism
  • low self-esteem
  • indecisiveness, loss of motivation
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3
Q

What are non-emotional symptoms of depression?

A
  • retardation of thought and action
  • loss of libido
  • sleep disturbance and loss of appetite
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4
Q

What are the 2 major types of depression?

A

unipolar and bipolar

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5
Q

What are the 2 types of unipolar depression?

A
  • reactive (75%) - non-familial, associated with life events and accompanied by symptoms of anxiety and agitation
  • endogenous (25%) - familial and not directly related to external stress
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6
Q

Describe bipolar depression

A

strongly familial with some genetic similarities to susceptibility to schizophrenia

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7
Q

What is the main cause of depression?

A

deficits in monoamine neurotransmitters serotonin (5-HT) and noradrenaline

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8
Q

Where is monoamine oxidase found?

A

intracellularly on the mitochondrial surface of nearly all tissues

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9
Q

What are the 2 forms of monoamine oxidase?

A

MAO-A and B

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10
Q

What does MAO-A do?

A

regulate both the free and intraneuronal concentration and the releasable stores of 5-HT and noradrenaline

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11
Q

What does MAO-B do?

A

regulate both the free intraneuronal concentration and the releasable stores of dopamine

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12
Q

How do MAOIs work?

A

by increasing the biological availability of monoamines

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13
Q

What is the mechanism of action of inhibition of MAO-A?

A
  1. initial inhibition reduces breakdown of monoamines then enhances the release of neurotransmitters into the synapse
  2. elevated levels of noradrenaline and 5-HT bind to their receptors and intensify their neural activity
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14
Q

What is the mechanism of action of inhibition of MAO-B?

A
  1. inhibition decreases breakdown of dopamine and increases its release into the synapse
  2. increased levels of dopamine bind to receptors and intensify the effect
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15
Q

What are adverse effects of MOAIs?

A

the cheese reaction

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16
Q

What is the cheese reaction?

A

an interaction of the MAOI with tyramine that can lead to accumulation and a sympathomimetic effect

17
Q

What are symptoms of the cheese reaction?

A
  • severe headache
  • nausea and vomiting
  • sweating
  • rapid heartbeat (tachycardia)
  • acute hypertension
18
Q

How can the cheese reaction cause acute hypertension?

A

tyramine is taken up into adrenergic terminals and initiates release of noradrenaline and subsequent stimulation of cardiovascular sympathetic NS activity

19
Q

What are the 3 key MAOIs?

A
  • irreversible non-selective MAOI e.g. phenelzine
  • reversible MAO-A selective MAOI e.g. moclobemide
  • irreversible MAO-B selective MAOI e.g. selegiline
20
Q

How do TCAs work?

A

by blocking the uptake of 5-HT and noradrenaline which increases their concentration in the synapse and intensifies their neuronal effects

21
Q

What is the source of TCA adverse effects?

A

binding to histamine and muscarinic ACh receptors

22
Q

What are adverse effects of TCAs?

A
  • sedation due to H1 histamine receptor antagonism
  • postural hypotension due to α-adrenoreceptor sympathetic block
  • dry mouth, blurred vision, constipation due to muscarinic receptor antagonism
  • risk of drug induced cardiac dysrhythmias due to block of hERG potassium channel
23
Q

What are the 2 key TCAs?

A
  • non-selective e.g. amitriptyline
  • selective for noradrenaline e.g. desipramine TCAs
24
Q

What are SSRIs?

A

selective serotonin reuptake inhibitors

25
Q

What is the most widely prescribed antidepressant?

A

fluoxetine

26
Q

What are the 2 main SSRIs?

A
  • fluoxetine (~50-fold selectivity for 5-HT)
  • citalopram (~1000-fold selectivity for 5-HT)
27
Q

How do SSRIs work?

A

by restoring the levels of 5-HT in the synaptic cleft by binding at the 5-HT reuptake transporter

28
Q

How do SSRIs have less adverse effects than TCAs?

A
  • low affinity for α-adrenoreceptors → lack of cardiovascular effects so safer in overdose
  • lack of effect at histamine receptors → reduced sedation
  • low affinity for muscarinic cholinergic receptors → minimal anticholinergic side effects e.g. dry mouth and constipation
29
Q

What are adverse effects of SSRIs?

A
  • 2/3 of patients get remission
  • nausea
  • sexual dysfunction (delayed ejaculation in men and delayed or blocked orgasm in women)
  • serotonin syndrome
30
Q

What is serotonin syndrome?

A

severe reaction resulting from drug-drug interactions with other drugs that increase serotoninergic activity e.g. MAOIs (symptoms include tremor, hyperthermia and cardiovascular collapse)

31
Q

What are NARIs?

A

antidepressants that have have a greater noradrenaline reuptake than TCAs; they have ~1000x higher selectivity for noradrenaline than 5-HT

32
Q

How do NARIs work?

A

by restoring the levels of noradrenaline in the synaptic cleft by binding at the reuptake transporter

33
Q

What are adverse effects of NARIs?

A
  • dry mouth and constipation due to anticholinergic effects
  • insomnia due to increased noradrenergic activity in the CNS
  • tachycardia due to increased availability of noradrenaline at sympathetic synapses
34
Q

What are SNRIs similar to?

A

non-selective TCAs since they have similar dual 5-HT and noradrenaline reuptake inhibition profiles

35
Q

What is the only clinical SNRI?

A

venlafaxine

36
Q

What are advantages of SNRIs?

A
  • different structure to and fewer adverse effects than TCA
  • claimed to work slightly faster than other antidepressants
  • claimed to work better in treatment-resistant patients
37
Q

How do SNRIs work?

A

by restoring the levels of 5-HT and noradrenaline in the synaptic cleft by binding at their reuptake transporters

38
Q

What are adverse effects of SNRIs?

A
  • nausea
  • insomnia
  • sexual dysfunction
  • serotonin syndrome
  • withdrawal effects that are more common and stronger than for SSRIs and TCAs

Neuropharmacology (12 decks)

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