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Psychiatry > Pharmacology of ADs and Mood Stabilisers > Flashcards

Pharmacology of ADs and Mood Stabilisers Flashcards

1
Q

why are psychiatric drugs often different from other drugs?

A

need to pass the BBB

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2
Q

which type of drugs diffuse across the BBB best?

A

hydrophobic/lipophilic

BBB is fatty

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3
Q

7 uses of antidepressants?

A 
mod-severe depression
dysthymia
generalised anxiety disorder
panic disorder, OCD, PTSD
premenstrual dysphoric disorder
bulimia
neuropathic pain
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4
Q

3 groups of antidepressants?

A

monoamine oxidase inhibitors
monoamine reuptake inhibitors
atypical drugs (post-synaptic receptor effects)

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5
Q

types of monoamine reuptake inhibitors?

A

tricyclics
other non-selective reuptake inhibitors
selective serotonin reuptake inhibitors
noradrenaline reuptake inhibitors

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6
Q

examples of monoamines?

A

noradrenaline
dopamine
5-HT

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7
Q

describe the monoamine hypothesis?

A

depression is due to a lack of monoamine transmitters (mainly serotonin and noradrenaline)
therefore any drug which depletes stores of monoamines can cause low mood
- not strictly true, depression is multifactorial not directly related to monoamines only

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8
Q

what does serotonin affect?

A

mood
sleep
behaviour
sensory perception

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9
Q

where does analgesia affect?

A

caudal raphe

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10
Q

describe the serotonin pathway?

A

trptophan >* 5-OH tryptophan >* 5HT > leaves presynaptic terminal and acts on postsynaptic 5HT receptor > 5HT reuptaken and metabolised to 5-HIAA by MAO enzyme

*tryptophan hydroxylase, then L-AA decarboxylase involved in these steps

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11
Q

where is the source of noradrenaline neurones?

A

locus caeruleus

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12
Q

what does noradrenaline affect?

A

arousal

emotion

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13
Q

pathway at noradrenergic synapse?

A

tyrosine >* DOPA >* DA >* NA > leaves presynaptic terminal and acts on postsynaptic alpha/beta receptor > reuptakes and metabolised to MHPG by MAO enzyme

  • = tyrosine hydroxylase
  • = L-AA decarboxylase
  • = DA beta-hydroxylase
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14
Q

how do MAO inhibitors work?

A

inhibit monoamine oxidase enzyme which breaks down neurotransmitter into metabolites
therefore more neurotransmitter is available and reuptake is inhibited

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15
Q

types of MOA inhibitors?

A

irreversible (phenelzine) or reversible (moclobemide) inhibitors of MOA-A and B

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16
Q

side effects of MOA inhibitors?

A

cheese reaction (tyramine reaction)/hypertensive crisis
potentiates effects of other drugs by decreasing their metabolism (e.g barbiturates)
insomnia
postural hypotension
peripheral oedema

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17
Q

tricyclic side effects?

A

anti-cholinergic effects

  • dry mouth
  • urinary retention
  • etc
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18
Q

tricyclic side effects?

A

anti-cholinergic effects

  • dry mouth
  • urinary retention
  • blurred vision
  • sedation
  • weight gain
  • cardiotoxic (tachycardia etc - so avoid in cardio disease)
  • etc
19
Q

SSRI side effect?

A 
nausea
headache
sweating/vivid dreams
worsened anxiety
sexual dysfunction
hyponatraemia (mainly in elderly)
transient increase in self harm/suicidal ideation in <25 years
20
Q

how do tricyclic antidepressants work?

A

block noradrenaline transporter so less makes it back to the presynaptic neurone to be reuptaken

21
Q

example of tricyclic?

A

imipramine
dosulepin
amitriptyline
lofepramine

22
Q

how do SSRIs work?

A

inhibit the reuptake of serotonin

23
Q

examples of SSRIs?

A

fluoxetine
citalopram/escitalopram
sertraline
paroxetine

24
Q

what are SNRIs and how do they work?

A

type of monoamine reuptake inhibitors
AKA dual reuptake inhibitors
block the reuptake of monoamines into presynaptic terminals

25
Q

2 examples SNRIs?

A

venlafaxine

duloxetine

26
Q

side effects of SNRIs?

A

similar to SSRIs

27
Q

non-selective antidepressants?

A

amitriptyline
imipramine
clopiramine

28
Q

5-HT selective antidepressants?

A 
venlafaxine
paroxetine
sertraline
fluoxetine 
citalopram
29
Q

examples of atypical antidepressant?

A

mirtazapine
- blocks mixed receptors
bupropion
- dopamine uptake inhibitor

30
Q

side effects of mirtazapine?

A

weight gain and sedation

31
Q

aims of acute bipolar treatment?

A

reduce mood in mania

raise mood in depression

32
Q

long term bipolar treatment?

A

stabilise mood and prevent recurrence of mania and depression

33
Q

signs of toxic lithium levels?

A 
vomiting
diarrhoea
ataxia/course tremor
drowsiness
convulsions
coma
34
Q

lithium side effects?

A 
hypothyroid
nausea
polyuria
tremor
dry mouth/strange taste
long term reduced renal function
nephrogenic diabetes insipidus 
weight gain
35
Q

lithium mode of action?

A

blocks phosphatidylinositol pathway (2nd messager system) or inhibits glycogen synthase kinase

36
Q

how is lithium metabolised?

A

it isn’t

  • no elements are metabolised
  • excreted in urine as lithium
37
Q

how are lithium levels affected by dehydration and why?

A

lithium levels increase

sodium and lithium ions are indistinguishable to renal tubules

38
Q

which mood stabiliser avoided in pregnancy?

A

valproic acid (mainly - same effects as sodium valproate)

39
Q

how can anticonvulsants help stabilise mood?

A

unclear

can block overactive pathways

40
Q

side effects of anticonvulsants?

A

valproate and carbamazepine - drowsiness, ataxia, cardio effects, induces liver enzymes
valproate - teratogenic
lamotrigine - small steven Johnson syndrome risk

41
Q

4 examples of antipsychotics?

A

quetiapine
aripiprazole
olanzapine
lurasidone

42
Q

how do antipsychotics work as mood stabilisers?

A

dopamine antagonists + 5HT antagonists

43
Q

side effects of antipsychotics?

A

sedation
weight gain
metabolic syndrome
aripiprazole = extra-pyramidal side effects

Psychiatry (36 decks)

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