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YEAR 3 PSYCH > Pharmacology > Flashcards

Pharmacology Flashcards

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1
Q

what is the monoamine hypothesis

A

depression results from a functional deficit of monoamine transmitters in particular serotonin (5HT) and noradrenaline

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2
Q

what does serotonin influence

A 
mood 
sleep 
feeding
behaviour
sensory perception
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3
Q

what is the post-synaptic serotonin receptor

A

5-HT

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4
Q

what is the post-synaptic noradrenaline receptor

A

a1

b

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5
Q

serotonin is synthesised in the presynaptic neurone from what

A

tryptophan

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6
Q

noradrenaline is synthesised in the presynaptic neurone from what

A

tyrosine

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7
Q

when serotonin and noradrenaline are reuptaken into the presynaptic neurone what breaks them down

A

Monoamine oxidase

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8
Q

give an example of a reversible MAOI

A

moclobemide

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9
Q

give an example of an irreversible MAOI

A

phenelzine

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10
Q

what is a major side effect of MAOIs

A

cheese reaction

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11
Q

what is a cheese reaction

A

hypertensive crisis caused by a build up of tyramine

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12
Q

how does a hypertensive/cheese reaction occur

A

MAOIs block MAO-A in the gut and liver which breaks down dietary tyramine. The build up of tyramine causes NA release which makes BP skyrocket

or by interaction with other drugs that potentiate amine transmission e.g. other antidepressants (SSRI, TCA), pseudoephedrine

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13
Q

what foods should be avoided when taking MAOI

A

foods that have been aged or fermented
red wine
cheese
soy

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14
Q

what other issues arise with MAOI

A

potentiate the effects of other drugs

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15
Q

what are some side effects of MAOI

A

insomnia, postural hypotension, peripheral oedema, dizziness

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16
Q

what drugs can MAOIs potentiate the action of

A

TCAs, barbiturates, morphine, ethanol, pseudoephedrine

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17
Q

how do TCAs work

A

block the reuptake of noradrenaline and serotonin into presynaptic terminals by blocking their transporters

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18
Q

what additional actions do TCAs have and what does this lead to

A

also block dopamine, histamine and muscarinic Ach receptors leading to lots of side effects

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19
Q

give 6 examples of tricyclics

A 
imipramine
amitriptyline
clomipramine
doxepin
dosulepin
lofepramine
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20
Q

what are some side effects of tricyclics

A

cardiovascular
anticholinergic
weight gain and sedation

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21
Q

TCAs are ____ in overdose

A

cardiotoxic in overdose

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22
Q

what are the anticholinergic side effects of TCAs

A 
blurred vision
dry mouth
constipation
urinary retention
sexual dysfunction
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23
Q

what are some cardiovascular effects of TCAs

A

postural hypotension
tachycardia
arrhythmias - QT prolongation

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24
Q

give 5 examples of SSRIs

A 
fluoxetine
sertraline
citalopram
escitalopram
paroxetine
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25
Q

how do SSRIs work

A

selectively block the reuptake of serotonin (5HT) from the synaptic cleft

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26
Q

what are some things to be careful of when using SSRIs in the elderly

A

hyponatraemia and falls

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27
Q

what are some things to be careful of when using SSRIs in young people

A

transient increase in suicidality in first few weeks

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28
Q

what are some side effects of SSRIs

A 
increased anxiety, sweating
vivid dreams, insomnia
head ache 
sexual dysfunction
GI upset
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29
Q

what kind of GI symptoms do you get with SSRIs

A

nausea
abdominal pain
constipation
increased risk of GI bleed

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30
Q

when does the nausea with SSRIs usually settle

A

2 weeks

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31
Q

SSRIs are ____ in overdose

A

safe

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32
Q

what should be done when stopping an SSRI and why

A

taper dose as assoc. with withdrawal

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33
Q

some SSRIs can alter drug levels - how?

A

inhibit CP450 enzyme

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34
Q

how do SNRIs work

A

block the reuptake of noradrenaline and 5HT into the pre-synaptic terminals

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35
Q

give 2 examples of SNRIs

A

venlafaxine

duloxetine

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36
Q

what is another time when duloxetine is used

A

stress incontinence

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37
Q

what are the side effects of SNRIs

A

GI upset similar to SSRIs

cardiovascular

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38
Q

what cardiovascular side effects do you get with SNRIs

A

hypertension
palpitations
dizziness

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39
Q

why are SNRIs preferred to TCAs

A

lack major receptor blocking properties of TCAs so more limited range of SEs

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40
Q

how does mirtazapine work

A

blocks a2, 5HT2 and 5HT3 presynaptic receptors

- noradrenaline, serotonin and histamine

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41
Q

why is mirtazapine beneficial when given with an SSRI

A

blocks serotonergic side effects

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42
Q

what are some side effects of mirtazapine

A

sedation and weight gain

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43
Q

how does bupropion work

A

dopamine uptake inhibitor

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44
Q

how does trazadone work

A

potent serotonin and noradrenaline receptor antagonist

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45
Q

what is the main side effect of trazadone

A

sedation

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46
Q

when should patients be reviewed after starting antidepressant

A

2 weeks

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47
Q

how long should treatment be continued before switching drug

A

should have treatment for 4 weeks (6 in elderly)

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48
Q

following remission how long should an antidepressant be continued

A

6 months

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49
Q

how long should patients be treated for GAD

A

12 months

50
Q

Patients with a history of recurrent depression should receive maintenance treatment for _____

A

at least 2 years

51
Q

what should be considered in all patients who develop drowsiness, confusion, or convulsions while taking an antidepressant

A

hyponatraemia

52
Q

what is 1st line in the treatment of depression

A

SSRI

53
Q

if the SSRI doesn’t work what should you consider

A

dose increase
swap drug
combine drug
or augment

54
Q

what drug could you combine the SSRI with

A

mirtazapine

55
Q

what can be used to augment the SSRI

A

antipsychotic or lithium

56
Q

what could be considered in severe refractory depression

A

ECT

57
Q

what are absolute contraindications to ECT

A

recent MI (3 months)
recent CVA
intracranial mass lesion
phaeochromocytoma

58
Q

what are relative contraindications to ECT

A 
angina
CHF
severe pulmonary disease
severe osteoporosis
pregnancy
59
Q

if a patient with capacity is detained under the MHA and is refusing ECT can you give it anyway

A

no

60
Q

what are some side effects of ECT

A 
headache
memory problems
muscle aches 
confusion
nausea
61
Q

when is lithium used

A

LT treatment of bipolar to stabilise mood and prevent recurrence of both depression and mania

62
Q

lithium is normally given as

A

lithium carbonate

63
Q

how does lithium work

A

blocks phosphatidylinositol pathway

inhibits glycogen synthase kinase 3B

64
Q

when are lithium levels checked

A

12 hours post dose

levels checked weekly until stable then 3 monthly

65
Q

over what level is lithium toxic

A

> 1.5 mmol/L

66
Q

what are some side effects of lithium

A 
metallic taste in mouth 
polydipsia, polyuria
tremor
hypothyroidism
LT reduced renal function / nephrogenic DI
weight gain
67
Q

what does lithium toxicity look like

A

D+V, course tremor, ataxia, myoclonus, drowsiness, coma

convulsions, confusion, seizures, restlessness, electrolyte disturbance, renal failure, arrhythmia (QTP) , death

68
Q

what drug should lithium not be given with and why

A

NSAID –> renal impairment

69
Q

what is the treatment of lithium toxicity

A

stop lithium

gastric lavage or dialysis depending on severity

70
Q

is lithium safe in pregnancy

A

not in first trimester - teratogenic

71
Q

name 3 anticonvulsants sometimes used in LT treatment of bipolar

A

valproic acid
lamotrigine
carbamazepine

72
Q

what can valproate cause if given during pregnancy

A

neural tube defects

73
Q

how does valproate work

A

inhibits enzymes that block GABA

74
Q

what are some side effects of valproate and carbamazepine

A

drowsiness
ataxia
cardiovascular effects
induces liver enzymes

75
Q

what is there a very small risk of when taking lamotrigine

A

stevens johnson syndrome

76
Q

what is the first line treatment in acute bipolar mania

A

antipsychotic

olanzapine, quetiapine, risperidone

77
Q

what is the first line treatment in acute bipolar depression

A

antipsychotic + antidepressant

quetiapine, olanzapine) (fluoxetine

78
Q

how do antipsychotics work

A

dopamine D2 receptor antagonists blocking dopaminergic transmission in the mesolimbic pathways

79
Q

are typical or atypical antipsychotics associated with EPSEs

A

typical

80
Q

give 2 examples of typical antipsychotics

A

haloperidol

chlorpromazine

81
Q

what EPSEs can typical antipsychotics cause

A

parkinsonism
Acute dystonia
Akathasia
Tardive Dyskinesia

82
Q

what is parkinsonism

A

bradykinesia + resting tremor + rigidity

83
Q

what is acute dystonia

A

sustained muscle contraction usually in eyes, jaw, neck

occurs within a few hours of starting treatment

84
Q

what is an important feature of acute dystonia

A

oculogyric crisis

85
Q

what is an oculogyric crisis

A

restlessness, agitation and involuntary upward deviation of the eyes

86
Q

what is akathasia

A

severe restlessness, constant need to wander

87
Q

what is tardive dyskinesia

A

occurs with LT use, late onset of choreoathetoid movements (abnormal, involuntary)
- chewing, facial grimaces, blinking, lip smacking, pouting of jaw

88
Q

when antipsychotics are used in the elderly there is an increased risk of what

A

stroke

thromboembolism

89
Q

what is the main advantage of atypical antipsychotics

A

no EPSEs

90
Q

what drug can be used to manage EPSEs with typical antipsychotics

A

procyclidine, prochlorperazine

91
Q

what are some side effects of antipsychotics in general

A 
anticholinergic 
sedation, weight gain, increased appetite
raised prolactin
neuroleptic malignant syndrome
prolonged QT interval
92
Q

prolonged QT interval occurs particularly with what antipsychotics

A

haloperidol

93
Q

atypicals more than typicals can do what

A

reduce seizure threshold

94
Q

raised prolactin can lead to what

A 
galactorrhoea 
impaired glucose tolerance
sexual dysfunction
amenorrhoea
infertility
95
Q

why do you get raised prolactin from antipsychotics

A

dopamine negatively feeds back on prolactin release so its blockade results in raised prolactin

96
Q

what is neuroleptic malignant syndrome

A

seen with all antipsychotics but particularly typicals

  • hyperthermia
  • muscle rigidity and bradykinesia
  • altered mental state
  • autonomic dysfunction
97
Q

what autonomic dysfunction is seen with neuroleptic malignant syndrome

A

tachycardia, tachypnoea, dilated pupils, sweating

98
Q

what antipsychotics should be 1st line in schizophrenia

A

atypical

99
Q

what are the side effects of atypical antipsychotics

A 
weight gain, drowsiness, increased appetitie
T2DM, metabolic syndrome
hyperprolactinaemia
increased risk seizures
sexual dysfunction
100
Q

name 6 atypical antipsychotics

A 
clozapine
olanzapine
quetiapine
risperidone
amisulpride
aripiprazole
101
Q

true/false

EPSEs can be seen at higher doses of some atypical antipsychotics

A

true

102
Q

what 2 atypical antipsychotics have the most significant weight gain

A

clozapine

olanzapine (risk of dyslipidaemia and obesity)

103
Q

which atypical antipsychotic is particularly good for raised prolactin

A

aripiprazole

104
Q

with clozapine there is a risk of what

A

agranulocytosis

105
Q

when should you do a FBC for someone on clozapine

A 
weekly for 1st 6 months
fortnightly for next 6 months 
every 4 weeks thereafter 
1 month after stopping
sore throat
106
Q

what should be taken before starting clozapine

A

ECG and FBC

107
Q

why is an ECG needed before starting clozapine

A

risk of myocarditis

108
Q

how can you treat hypersalivation caused by clozapine

A

hyocine hydrobromide

109
Q

when should clozapine be used

A

schizophrenia that is not controlled despite use of 2 antipsychotics

110
Q

what should someone that smokes on clozapine be told

A

smoking reduces levels so suddenly stopping smoking can make levels dramatically increase

111
Q

what are the 3 parts to CBT

A

NATs
dysfunctional assumptions
core belief/schema

112
Q

what is the usual course of ECT

A

twice a week for 3 to 6 weeks (6 to 12 sessions in total)

113
Q

metabolic syndrome occurs more with atypicals/typicals

A

atypicals - 5HT2C receptors

114
Q

antagonism of what causes sedation

A

H1 receptors (histamine)

115
Q

histamine blockade also leads to what

A

increased appetite

116
Q

____ blockade can reduce nausea and vomiting

A

histamine

117
Q

a-adrenergic blockade can cause what

A

hypotension and interruption of baroreflex response –> dizziness, lightheadedness, fainting when going from sitting to standing

118
Q

what antipsychotic would you recommend to a woman on LT lithium who wants to have a child

A

olanzapine - doesnt pass across placenta or into breast milk

119
Q

what causes serotonin syndrome

A

Consumption of excessive amounts or multiple drugs that increase amount of serotonin

120
Q

what are the s/s of serotonin syndrome

A

Cognitive: headache, anxiety, agitiation, hallucination, confusions, coma.
Autonomic: shivering, sweating, hyperthermia, tachycardia, dilated pupils, nausea and diarrhoea.
Somatic: myoclonus (twitching), tremor, rigidity, hyper reflexia

YEAR 3 PSYCH (14 decks)

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