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pharmacology 3 > drugs for mood disorders > Flashcards

drugs for mood disorders Flashcards

1
Q

depression

A

most common type of the affective disorder - mood and actions are innappropriate to circumstances

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2
Q

unipolar depression

A

major depression - the mood changes in the same direction

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3
Q

bipolar disorder

A

(manic depression) - oscillates between depression and mania (excessive enthusiasm and self-confidence, impatience and aggression)

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4
Q

monoamine theory of depression

A

hypothesized based on clinical effects of drugs that cause or alleviate symptoms of depression and their known neurochemical effects of monoaminergic transmission

a functional deficit of noradrenaline and serotonin in certain brain regions

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5
Q

problem with the monoamine theory

A
  • doesnt differentiate between noradrenaline and serotonin as to which neurotransmitter plays a dominant role
    drugs affecting either are equally effective
  • antidepressatn drugs have immidate neurochemical effect, yet symptom relief is not seen for two weeks, belived that serotonin and noradrenlaine are mediating long term antidepressant effects
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6
Q

imipramine

A

block noradrenaline and serotonin uptake

depressed schitzophrenics show mood improvement

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7
Q

ipromiazid

A

monoamine oxidase inhibitor (MAOI)

improved mood of depressed people

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8
Q

reserpine

A

inhibit noradrenaline and serotonin storage

patients developed depression

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9
Q

time scale of neurotransmission

A

immediate effects due to release of transmitters and fast synaptic transmission

long term effects due to structural remodelling and degeneration/regeneration

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10
Q

brain-derived neurotrophic factor BDNF

A

a member of the neurotrophic factor family
CNS development and neuronal plasticity

binds to TrkB (tropomyosin receptor kinase B), which activates three signalling pathways
all three pathways converge on the transcription factor CREB (cAMP response element binding protein) to up-regulate gene expression

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11
Q

how is BDNF produced in the body

A

prepro-BDNF (a precursor protein) - cleaved into pro-BDNF - further cleaved into mature BDNF

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12
Q

CREB

A

(cAMP response element binding protein)

up-regulates gene expression

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13
Q

what does BDNF bind

A

binds to TrkB (tropomyosin receptor kinase B), which activates three signalling pathways
all three pathways converge on the transcription factor CREB

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14
Q

chronic elevated levels of cortisol inhibits the transcriptional activity of of

A

CREB

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15
Q

chornic elevated levels of corticol is caused by

A

stress

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16
Q

reduced transcriptional activity of CREB causes

A

reduced BDNF expression > apoptosis of prefrontal cortex and hippocampus

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17
Q

increased transcriptional activity of CREB promotes

A

BDNF expression (BDNF binds to TrkB) > neurogenesis of prefrontal cortex and hippocampus

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18
Q

neuroplasticity theory of depression

A

depression is as a result of extended decreased BDNF levels in the hippocampus/prefrontal cortex

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19
Q

2 theories of cause of depressioon

A
  • monoamine theory

- neuroplasticity theory

20
Q

evidence for neuroplasticity theory

A

in animal studies, chronic stress decreased BDNF expression in hippocampus
antidepressant treatment increased BDNF levels in hippocampus
BDNF infusion into hippocapmus produced antidepressant like effects

post mortem analysis in humans shows decreased hippocampal BDNF levels in suicide victims and depressed individuals

21
Q

selective serotonin reuptake inhibitors

A

bind to 5-HT transporter - block reuptake of 5-HT - elevate synaptic [5-HT], but
decrease release of 5-HT (due to negative feedback)

desensitisation of somatodendritic 5-HT1a receptor (weeks to develop) and increase in synaptic [5-HT]

22
Q

4 examples of SSRIs

A
  • fluoxetine (prozac)
  • paroxetine
  • sertraline
  • citalopram
23
Q

adverse effects associated with SSRIs

A

better side effect profile - due to no affinity for mAch receptors and histamine H1-receptors
safer than TCAs and MAOIs in overdose
5-HT2 receptor - agitation and insomnia
5-HT3 receptor - nausea
sexual dysfunction
‘serotonin syndrome’ if combined with MAOIs
CYP2D6-mediated drug-drug interactions - co-administration of fluoxetine with drugs that are metabolised by CYP2D6

24
Q

serotonin syndrome

A

can occur if SSRIs are combined with MAOIs

25
Q

mirtazapine

A

antagonist at A2 adrenoceptors, 5-HT 2A/C, 5-HT3, and H1 receptors

26
Q

mirtazapine side effect profile

A

does not cause agitation and nsomnia at the 5-HT2 receptor (antagonist for 5HT2a/c)
does not cause nausea at the 5-HT3 receptor (antagonist)
lower tendency of sexual dysfunctions
also causes weight gain
no significant drug-drug interactions

27
Q

how does mirtazapine work

A

released noradrenaline activates a2-adrenoceptor - inhibits noradrenaline release (negative feedback)

mirtazapine is a a2- adrenoceptor antagonist

28
Q

mirtazapine is helpful when

A

alternative to SSRIs if SSRI- related side effects are problematic

29
Q

tricyclic antidepressants

A

competitive binding at 5-HT and noradrenaline transporters - inhibit reuptake of 5-HT and noradrenaline - enhance synaptic [5-HT] and [noradrenaline]

30
Q

adverse effects of TCAs

A

long acting - long half life
repeated dosing increases risk of adverse effects
antagonist at mAChR - dry mouth, blurred vision (atropine-like effects)
antagonist at H1-receptor - sedation
CYP2D6-mediated drug-drug interactions
should not be combined with MAOIs

31
Q

what should TCAs not be combined with

A

MAOIs

32
Q

MAOIs stand for

A

monoamine oxdase inhibitors

33
Q

MAOIs act by

A

inhibit MAO-a and/or MAO-b
increases cytoplasmic concentrations of monoamines
increase in spontaneous leakage of monoamines

34
Q

irreversible MAOIs

A

phenelzine
non selective - acts on MAO (a and b)
long acting

35
Q

reversible MAOI

A

moclobemide
short acting
reversible

36
Q

adverse effects of MAOIs

A

atropine like effects - dry mouth, nausea, insomnia

drug-drug interaction - other drugs that increase serotonin levels

37
Q

cheese reaction

A

MAOI interact with tyramine rich food eg. cheese, tofu
causes hypertensive crisis - increase in sympathetic cardiovascular activity
minimal for moclobemide

38
Q

why does tyramine react with MAOI

A

normally tyramine is metabolised by MAO in the small intestine and liver, preventing it from reaching the circulation

in the presence of MAOI this is reduced, meaning tyramine reaches the circulation where it is transported into the synaptic nerve terminal by the same transporter responsible for noradrenaline reuptake

it replaces noradrenaline stored in vessicles causing noradrenaline to be released into the cytoplasm and released into the synaptic cleft, increasing [noradrenaline] in the synapse, stimulating adrenergic receptors

39
Q

ketamine

A

a non-competative NMDA receptor antagonist

rapid antidepressant actions (hours), including in treatment resistant depression

40
Q

how is ketamine different

A

works to release BDNF that has already been synthesised

41
Q

how is ketamine used

A

as a nasal spray - must be used in conjuction with an oral antidepressant

42
Q

lithium

A

lithium carbonate - tablet

plasma concentration monitoring is crucial

43
Q

lithium plasma level

A

clinically effective 0.5-1 mmol
toxicity >1/5 mmol
lethal 3-5 mmol

44
Q

lithium clearance

A

renally cleared
monitoring - patients with renal impariment
use of drugs that effect renal functions - diuretics, NSAIDs

45
Q

adverse effects of lithium

A

nausea, vomiting, diarrhoea, weight gain

prolonged treatment can cause renal tubular damage

46
Q

prolonged treatment with lithium can cause

A

renal tubular damage

pharmacology 3 (8 decks)

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