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Drugs Flashcards

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1
Q

amitriptyline is what type of anti-depressant?

A

tricyclic

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2
Q

fluoxetine and citalopram are what types of anti-depressants?

A

SSRIs

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3
Q

reboxetine is what type of anti-depressant?

A

noradrenaline re-uptake inhibitor

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4
Q

venlafaxine is what type of anti-depressant?

A

serotonin noradrenaline re-uptake inhibitors

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5
Q

mirtazapine is what type of anti-depressant?

A

noradrenaline and specific serotonin antidepressant

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6
Q

how long should anti-depressants be trialled for before switching?

a) 1 week
b) 3 weeks
c) 6 weeks
d) 3 months

A

c) 6 weeks

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7
Q

should patients be weaned off their current anti-depressants to avoid withdrawal before commencing new meds?

a) yes
b) no

A

a) yes

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8
Q

how do tricyclic antidepressants work?

A

inhibit re-uptake of noradrenaline and serotonin from synaptic cleft
also block histamine, dopamine, a-adrenergic and muscarinic receptors

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9
Q

why should tricyclic antidepressants be used with caution in those with suicide?

A

easier to OD than SSRIs

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10
Q

are TCAs 1st or 2nd line for depression?

A

2nd

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11
Q

what is the major contraindication for TCAs in men?

A

prostatic hypertrophy

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12
Q

what is the major contraindication for TCAs in women?

A

pregnancy

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13
Q

what are the anticholinergic side effects of TCAs?

A 
hot as a hare
blind as a bat
dry as a bone
red as a beet
mad as a hatter
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14
Q

what are the H1 and H1 side effects of TCAs?

A

sedation

hypotension

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15
Q

what are the dopamine side effects of TCAs?

A

EPSEs
breast changes
sexual dysfunction

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16
Q

what are the cardiac side effects of TCAs?

A

prolonged QT, arrhythmia

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17
Q

why should TCAs not be used alongside class 1 and class 3 anti-arrhythmics?

A

prolong depolarisation and can increase risk of QT elongation

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18
Q

how are TCAs metabolised?

A

p450 inhibitors

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19
Q

how do SSRIs work?

A

inhibit neuronal re-uptake of serotonin from synaptic cleft

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20
Q

why do SSRIs have fewer side effects and are less dangerous in overdose?

A

don’t inhibit noradrenaline uptake

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21
Q

in what percentage of people are SSRIs effective?

a) 5-10%
b) 25-40%
c) 55-75%
d) 100%

A

c) 55-75%

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22
Q

are SSRIs 1st or 2nd line treatment for depression?

A

1st

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23
Q

what is the minimum time for a course of SSRIs?

a) 1 months
b) 3 months
c) 6 months
d) 1 year

A

c) 6 months

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24
Q

why are SSRIs contraindicated in epilepsy?

A

lower seizure threshold

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25
Q

why are SSRIs contraindicated in peptic ulcer disease?

A

risk of upper GI bleed

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26
Q

why are SSRIs used with caution in young people?

A

increased risk of aggression, DSH and suicidal behaviours

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27
Q

why should SSRIs be used with caution in those with renal/hepatic impairment?

A

metabolised by the liver

citalopram is best for these patients

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28
Q

why should SSRIs only be used if the benefit really outweighs the risk in pregnant women?

A

excreted at high levels in breast milk

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29
Q

what electrolyte imbalance are elderly women at risk of with SSRIs?

A

hyponatraemia

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30
Q

what cardiac abnormality is a particular risk with citalopram (SSRI)?

A

QT prolongation

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31
Q

how are SSRIs excreted?

A

liver P450 inhibitor

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32
Q

how do mono-amine oxidase inhibitors work?

A

inactive an enzyme which oxidises dopamine, serotonin and tyramine

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33
Q

when are MAOIs used nowadays?

A

rarely used, resistant or atypical depression

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34
Q

what are the dietary restrictions of MAOIs?

A

tyramine containing foods e.g. cheese, game, liver, broad beans, marmite, red wine

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35
Q

what is the emergency tyramine reaction that can occur with MAOIs?

A

hypertensive crisis leading to SAH

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36
Q

why is reboxetine (NARI) used in those with bipolar and epilepsy?

A

less likely to trigger mania or seizures

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37
Q

name 2 side effects of reboxetine

A

dry mouth
constipation
insomnia

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38
Q

when is venlafaxine (SNARI) indicated?

A

treatment resistant depression

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39
Q

how can venlafaxine affect blood pressure?

A

hypertension

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40
Q

which two classes of antidepressant cannot be augmented together?

A

TCAs and SSRIs

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41
Q

true or false:
if patients are started early in their degree progression on anti-psychotic medication, their response is better
a) true
b) false

A

a) true

42
Q

the tranquillising effects of anti-psychotics start to take effect in:

a) minutes
b) hours
c) days
d) weeks/months

A

b) hours

43
Q

the side effects of anti-psychotics start to take effect in

a) minutes
b) hours
c) days
d) weeks/months

A

c) days

44
Q

the anti-psychotic effects of anti-psychotics start to take effect in

a) minutes
b) hours
c) days
d) weeks/months

A

d) weeks/months

45
Q

what is the minimum time period that anti-psychotics should be taken for?

A

6 months

46
Q

what is the preferred total period of time that anti-psychotics should be taken for?

a) 6 months
b) 1 year
c) 18 months
d) 2 years

A

d) 2 years

47
Q

haloperidol, chlorpromazine, fluphenazine, flupenthixol are all examples of what generation of antipsychotics?

A

first (typical)

48
Q

how do anti-psychotics work?

A

dopamine receptor antagonists

49
Q

why do atypical anti-psychotics take time to work?

a) body has to ‘adjust’
b) poor adherance by patients
c) effective only when 60% of receptors blocked

A

c) effective only when 60% of receptors blocked

50
Q

what ‘line’ treatment are typical (first-gen) anti-psychotics?

A

second

51
Q

except for orally, how can anti-psychotics be administered?

A

depot injection

52
Q

fill in the blanks
1st generation anti-psychotics have more ____________ side-effects, 2nd generation anti-psychotics have more _________ side-effects
metabolic/neurological

A

1st gen = neurological

2nd gen = metabolic

53
Q

dystonia, akathisia, parkinsonism and tardive dyskinesia are all features of which group of side effects associated with 1st gen anti-psychotics?

A

extra pyramidal side effects (EPSEs)

54
Q

which cardiac side effect is common with 1st gen anti-psychotics (ESPECIALLY HALOPERIDOL)

A

prolonged QT

55
Q

what are anti-cholinergic side effects of 1st gen anti-psychotics?

A 
blind as a bat
hot as a hare
mad as a hatter
red as a beet
dry as a bone
56
Q

what are the anti-histaminergic side effects of 1st gen anti-psychotics?

A

weight gain

sedation

57
Q

what are the anti-adrenergic side effects of 1st gen anti-psychotics?

A

postural hypotension

tachycardia

58
Q

what are the serotoninergic side effects of 1st gen anti-psychotics?

A

hyperglycaemia, DMII, weight gain (appetite increase), anxiety, insomnia

59
Q

what are the effects of hyperprolactinaemia in 1st gen anti-psychotics?

A

galactorrhoea, amenorrhoea
weight gain
osteoporosis
reduced libido

60
Q

risperidone, olanzapine, aripiprazole, amisulpride, ziprasidone, palliperidone and clozapine are all examples of what generation of anti-psychotic?

A

second (atypical)

61
Q

why do second gen anti-psychotics have less EPSEs than 1st-gen?

A

higher therapeutic index

62
Q

clozapine works well with D2 AND D4 receptors. what situation is it used for?

A

treatment resistant psychosis (last resort)

63
Q

what ‘line’ treatment are atypical (2nd-gen) anti-psychotics?

A

first

64
Q

name 4 metabolic side effects of 2nd-gen anti-psychotics

A 
hyperglycaemia
weight gain
dyslipidemia
insulin resistance
drowsiness
65
Q

name a sexual side effect of 2nd-gen anti-psychotics

A

low libido

66
Q

agranulocytosis, hyper-salivation and lower seizure threshold are side effects of which 2nd-gen anti-psychotic?

A

clozapine

67
Q

in what psychiatric disorder are anti-convulsants often used?

A

bipolar

68
Q

what alternative therapy is indicated in treatment resistant or pharmacology-contraindicated mania or depression?

A

ECT

69
Q

how does lithium work?

A

mode unclear, affects the CNS

70
Q

what drug is indicated to prevent relapse in bipolar?

a) lithium
b) midazolam
c) citalopram
d) oxytocin

A

a) lithium

71
Q

at what blood concentration is lithium toxic?

a) 0.1mmol/L
b) 1.5mmol/L
c) 15mmol/L
d) 50mmol/L

A

b) 1.5mmol/L

72
Q

why should lithium only be prescribed if intended use is consistent around 3 years?

A

poor compliance or quick finishing could lead to rebound mania

73
Q

why does plasma lithium have to be measured after every dose for 5-7 days when the course is started?

A

to avoid toxicity which is v dangerous

74
Q

which of these is NOT a short term side effect of lithium

a) fine tremor and muscle weakness
b) GI disturbances
c) hypotension
d) polyuria & polydipsia
e) metallic taste in mouth

A

c) hypotension

75
Q

which of these is NOT a long term side effect of lithium?

a) weight gain
b) oedema
c) goitre (hypothyroidism & hyperparathyroidism)
d) muscle wasting
e) irreversible renal damage
f) T wave flattened on ECG

A

d) muscle wasting

76
Q

why is lithium contra-indicated in pregnancy and advised against during breastfeeding?

a) einstein abnormality
b) albert abnormality
c) napoleon abnormality
d) epstein abnormality

A

d) epstein abnormaloty - downwards displacement of tricuspid valve to right ventricle - tricuspid regurg and stenosis

77
Q

nystagmus, coarse tremor, dysarthria and ataxia are all symptoms of what adverse reaction to lithium therapy?

A

toxicity

78
Q

how do you manage lithium toxicity?

a) lithiite antidote
b) saline or haemodialysis
c) anti-convulsants
d) morphine

A

b) saline or haemodialysis

79
Q

how does lithium interact with diuretics (especially thiazides)?

A

sodium depletion which increases lithium leading to toxicity

80
Q

why shouldn’t lithium and carbamazepine be used together?

A

neurotoxicity - use valproate instead

81
Q

which blood pressure medications should not be prescribed with lithium?

A

ace-inhibitors

82
Q

how is lithium excreted?

A

unchanged by kidneys, half life related to kidney function

83
Q

how do BZDPs work?

A

GABA receptor agonist - increase its effect

84
Q

alprazolam and lorazepam have a ____ potency and a _____ half life

A

high

short

85
Q

clonazepam has a ____ potency and a ____ half life

A

high

long

86
Q

oxazepam and temazepam have a ___ potency and a _____ half life

A

low

short

87
Q

chlordiazepoxide has a ____ potency and a _____ half life

A

low
long
used to treat alcohol withdrawal

88
Q

why are BZDPs only given as a short course when possible?

A

risk of dependence

89
Q

which of these is NOT a symptom of BZDP withdrawal?

a) anxiety
b) irritability
c) incontinence
d) tremor
e) insomnia
f) altered perception

A

c) incontinence

90
Q

what is the antidote for BZDP overdose?

A

flumezanil

91
Q

which of these is NOT an example of a hypnotic to induce sleep?

a) donepezil
b) barbiturates
c) zolpidem
d) zopiclone
e) chlormethiazine/promethiazine

A

a) donepezil

92
Q

donepezil, rivastigmine, galantamine and tacrine are examples of what type of drug used in dementia?

A

cholinesterase inhibitors

93
Q

cholinesterase inhibitors improve cognitive and behavioural performance

a) temporarily
b) permanently

A

a) temporarily - maximum effect only lasts 9-12 months

94
Q

what body system most commonly experiences side effects of cholinesterase inhibitors

A

GI

95
Q

how many people respond well to cholinesterase inhibitors?

A

1/3 respond
1/3 won’t
1/3 unknown

96
Q

how does mementine (NMDA receptor antagonist) work in dementia?

A

protects neurones against neurotoxicity

97
Q

which anti-psychotic is liscenced for use in dementia?

A

risperidone

98
Q

which form of dementia should anti-psychotics never be prescribed in?

A

lewy body

99
Q

why should levodopa and carbidopa be prescribed together in parkinson’s disease?

A

levodopa = DOPA decarboxylase which activates all dopamine receptors including peripheral ones (N&V), carbidopa reduces peripheral side effects - DOPA decarboxylase inhibitor which cannot cross blood brain barrier

100
Q

what drug can be given in parkinson’s if the patient is unable to tolerate oral medication?

A

rivistigmine patch

PSYCH (3 decks)

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