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RCPsych Paper A > PSYCHOPHARMACOLOGY > Flashcards

PSYCHOPHARMACOLOGY Flashcards

1
Q

full agonists

A
  • can take place on both ionotropic and metabotropic receptors
  • endogenous factors naturally act as full agonists (eg NTs, hormones)
  • some psychotropic drugs can also stimulate agonistic action, triggering a full signal transduction
  • in metabotropic receptors process takes place through second messengers
  • in ionotropic receptors, agonists can cause the ion channel to open as wide as possible and at the highest frequency
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2
Q

direct action of full agonist

A

binds to receptor, producting the sequence of events

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3
Q

indirect action of full agonist

A

assists in full agonistic action of endogenous ligands.

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4
Q

partial agonists

A

ionotropic and metabotropic
some intrinsic action that places them between competitive and full agonists
activity depends on density and expression of receptors, and efficiency of effector systems

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4
Q

antagonists

A

ionotropic and metabotropic

act by binding with receptor without triggers direct action or known signal transduction.
work by blocking the binding of natural NT agonists

can be competitive or non-competitive.
competitive is reversible

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5
Q

inverse agonists

A

ionotropic and metabotropic
bind to receptors but bring about opposite result
reduce signal transduction lower than receptors baseline

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6
Q

pharmacodynamics - up regulation

A

number of receptors on a cell increases as a response to an external message

increases the sensitivity of the cell to molecules

eg critical for the development of dependence on nicotine in smokers

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7
Q

pharmacodynamics - down regulation

A

number of receptors on a cell reduces as a response to an external message

decreases the sensitivity of the cell to molecules

eg tolerance in opioid use

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8
Q

affinity

A

the ability of a drug to bind to its relevant receptor tightly or not

thermodynamic forces determine affinity

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8
Q

sensitisation

A

increases of the pharmacological action of a drug following repeated exposure to it

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9
Q

potency

A

amount of drug needed to produce a desired effect
high potency = desired effect at lower concentrations

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10
Q

efficacy

A

‘intrinsic activity’
‘a proportionality factor denoting the amount of physiological response a given ligand imparts to a biological system for a given amount of receptor occupancy’

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11
Q

potency of a drug determined by… (3)

A

proportion of the drug reaching the receptor
affinity for the receptor
efficacy

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12
Q

GABA

A

major inhibitory NT in the brain
binds to GABAa and GABAb

eg benzos

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13
Q

Serotonin

A

involved in depression phenotypes
5-HT rec approx 15 subtypes
most are excitatory

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14
Q

dopamine

A

involved in salience and reinforcement
related to schizophrenia and parkinsons
can be excitatory or inhibitory
receptors D1-D5

D2 receptors responsible for EPSEs of antipsychotics

D3 and D4 receptors play a role in the negative sx of schizophrenia

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15
Q

glutamate

A

major excitatory NT involved in learning and memory

4 types of receptors:
NMDA, AMPA, kainite (all ionotropic)
mGluR (metabotropic)

eg memantine

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16
Q

acetylcholine

A

excitatory and inhibitory
CNS and PNS
related to cognition and memory

nicotinic rec and muscarinic rec
nicotinic are excitatory

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17
Q

norepinephrine

A

involved in attention and flight or flight

binds to adrenergic receptors

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18
Q

glycine

A

inhibitory
sensory and motor pathways

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18
Q

histamine

A

H1 and H2 rec mediated actions mainly excitatory
H3 actions inhibitory

sleep wake cycle, learning and memory

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19
Q

types of metabolisers (genetic)

A

poor metabolisers (no alleles)
intermediate metabolisers (one allele)
extensive metabolisers (two alleles)
ultra rapid metabolisers (three alleles)

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20
Q

4 core components of pharmacokinetics

A

absorption
distribution
metabolism
elimination

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21
Q

drug absorption

A

after administration, released from pharmaceutical formulation to enter the person’s blood stream

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22
Q

bioavailability

A

how much of the original drug enters the bloodstream unchanged

IV = 100%

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22
Q

drug distribution

A

the transfer of a drug from one point to another in the body

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23
Q

drug metabolism

A

the biotransformation of compounds into new compounds, in order that they are made more water-soluble and can be more easily excreted from the body

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24
Q

drug elimination and potential routes (8)

A

can be excreted unaltered or in the form of metabolites

breast milk, faeces, urine, breath, tears, hair, saliva, sweat

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25
Q

first pass metabolism

A

intestinal and hepatic degradation or alteration of a drug or substance take by mouth after absorption, removing some of the active substance from the blood before it enters the general circulation

reduces bioavailability

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26
Q

factors affecting bioavailability (5)

A

formulation of the drug
with vs without food
interactions with food
interactions with other drugs
diseases affecting liver or GI tract

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27
Q

diazepam PO bioavailability

A

almost 100%

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28
Q

diazepam rectal bioavailability

A

around 90%

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29
Q

diazepam time to peak plasma levels oral administration

A

30-90 minutes

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30
Q

diazepam time to peak plasma level IM administration

A

30-60 min

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31
Q

half life

A

time taken to eliminate 50% of absorbed dose of a drug from plasma

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32
Q

drug clearance

A

the volume of plasma form which the drug is completely removed, or cleared, in a given time period

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33
Q

steady state

A

when the intake of a drug is at the same overall rate as its excretion or elimination, so there is no net change in the amount of drug in the persons system

usually 4-5x half life

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33
Q

dietary CYP450 inhibitors

A

grapefruit
soya
caffeine

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34
Q

first order kinetics

A

same fraction of a drug is eliminated per unit time, regardless of plasma levels of the drug

the actual amount of drug eliminated over a certain time period decreases proportionally with the amount of drug in the body

clearance of a drug is constant

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34
Q

zero order kinetics

A

the fraction of drug eliminated per unit time varies. the amount of drug eliminated for each time interval is constant, regardless of the amount o drug in the body

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35
Q

ssri longest half life

A

fluoxetine

least likely to experience withdrawal effects

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36
Q

ssri shortest half life

A

paroxetine

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37
Q

CVS changes with ageing

A

cardiac output slowly and steadily decreases

BP tends to increase

arteriosclerosis more prevalent

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38
Q

renal changes with ageing

A

renal size and function decrease with age
total number of glomeruli decreases
renally excreted drugs can have significantly higher half lives in elderly

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39
Q

respiratory system changes with ageing

A

vital capacity and other functional respiratory measurements eg FEV decrease

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40
Q

endocrine changes with ageing

A

peripheral insulin resistance worsens
diabetes
osteoporosis increasing issue
menopause an issue for women

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41
Q

GI and liver changes with ageing

A

atrophic gastritis more frequent
decreased intestinal motility
liver volumes decrease, but functional differences not always marked
hepatic half lives can be prolonged

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42
Q

skin changes with ageing

A

skin cell replacement slows
appearance, tone and elasticity change

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43
Q

MSK changes with ageing

A

degenerative joint disease
overall decrease in muscle mass

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44
Q

age - absorption

A

changes in gastric pH can lead to differences in absorption

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45
Q

age - distribution

A

typically fat levels increase with age, therefore lipophilic or lipid soluble drugs tend to be more widely distributed in older people than younger people

water soluble drugs tend to be less well distributed

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46
Q

age - metabolism

A

with reduced liver activity and perfusion, first pass metabolism can be reduced, leading to higher than expected levels of unchanged drugs when administered orally, or lower than expected levels of metabolites

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47
Q

age - excretion

A

reduction in renal function can lead to decreased clearance of drugs, and this can lead to higher serum levels and even toxicity in older patients

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48
Q

CYP450 poor metabolisers eg

A

asian population
african american populations

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49
Q

CYP450 ultrarapid metabolisers eg

A

middle eastern and north african populations

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50
Q

pregnancy - absorption

A

changes to rate of gastric emptying and pH during pregnancy
need to consider N+V in pregnancy

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51
Q

pregnancy - distribution

A

water content rises quite markedly, fat stores also rise
can lead to dilution and lower plasma levels of drugs

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52
Q

pregnancy - metabolism

A

some CPY450 enzymes inducted by hormone changes in pregnancy, others can be reduced by competitive inhibition

metabolism of drugs can be increased or decreased during pregnancy

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53
Q

pregnancy - excretion

A

increased blood flow during pregnancy, kidney clears out a lot more drug during pregnancy.

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54
Q

concentration steady state

A

when rate of administration equals rate of elimination
usually 5-7 half lives
plasma concentrations remain constant

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55
Q

therapeutic window

A

between minimum effective and maximum safe plasma drug concentration range

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56
Q

factors affecting metabolism (8)

A

genetic polymorphisms
CYP450
ethnicity
enzyme induction/inhibition by other drugs
liver disease
smoking
diet
caffeine

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57
Q

examples of drugs that increase plasma clozapine concentration (inhibitors) (4)

A

theophylline
caffeine
cimetidine
fluoxetine

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58
Q

cigarette smoke mainly induces which hepatic cytochrome

A

1A2

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58
Q

examples of drugs that decrease plasma clozapine concentration (inducers) (4)

A

carbamazepine
smoking
st john’s wort
phenytoin

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59
Q

clozapine optimal plasma level

A

0.35-0.6 mg/L

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60
Q

maximum acceptable clozapine level

A

1

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61
Q

lithium excretion

A

at least 95% renally excreted

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62
Q

norclozapine

A

major clozapine metabolite
longer t1/2 than clozapine, so can accumulate
ratio important in determining compliance

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63
Q

optimum lithium plasma range

A

0.6-0.75 mmol/L
may be higher in treatment of acute mania

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64
Q

lithium drug interactions (5)

A

! drugs that alter sodium handling
NSAIDS
angiotensin II receptor antagonists
ACE inhibitors
thiazide diuretics

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65
Q

amitriptyline active metabolite

A

nortriptyline

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66
Q

imipramine active metabolite

A

desipramine

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66
Q

fluoxetine active metabolite

A

norfluoxetine

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67
Q

sertraline active metabolite

A

desmethylsertraline

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68
Q

venlafaxine active metabolite

A

desmethylvenlafaxine

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69
Q

who introduced insulin therapy for schizophrenia

A

sakel

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69
Q

who introduced convulsive therapy for schizophrenia using metrazol?

A

meduna

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69
Q

who developed ECT

A

cerletti and bini

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70
Q

who developed frontal leucotomy for schizophrenia and depression

A

moniz

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71
Q

who invented disulfiram

A

jacobsen and hald

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72
Q

who discovered lithiums antimanic effect

A

cade

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73
Q

who invented chlorpromazine

A

charpentier

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74
Q

who first used reserpine as an antipsychotic

A

kline

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75
Q

who found imipramine had antidepressant effect

A

kuhn

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75
Q

who invented haloperidol

A

janssen

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76
Q

who discovered fluoxetine

A

eli lilly and company

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76
Q

who first used chlorpromazine

A

delay and deniker

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76
Q

who invented chlordiazepoxide

A

sternbach

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77
Q

who first used imipramine TCA

A

kuhn

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78
Q

mechanism of ssri

A

increase levels of serotonin in synaptic cleft

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79
Q

common SSRIs

A

fluoxetine
paroxetine
citalopram
escitalopram
sertraline
fluvoxamine

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80
Q

examples of tertiary amines TCAs

A

imipramine
amitriptyline
clomipramine
dothiepin/dosulepin

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80
Q

common SSRI side effects

A

GI
dizziness
sexual dysfunction
hyponatraemia

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81
Q

how do TCAs work

A

increasing levels of serotonin and noradrenaline

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82
Q

examples of secondary amines TCAs

A

desipramine
amoxapine
nortriptyline
protryptiline

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83
Q

TCA side effects

A

hypotension
tachycardia
QTc prolongation

very toxic in overdose

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84
Q

how do MAOIs work

A

increase levels of serotonin, noradrenaline and dopamine

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85
Q

available reversible MAOI

A

moclobemide
reversible inhibitor of monoamine oxidase type A

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86
Q

3 irreversible MAOIs

A

phenelzine
isocarboxazid
tranylcypromine

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87
Q

SNRI examples

A

venlafaxine
milnacipran
duloxetine

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88
Q

NARI exmaples

A

reboxetine
atomoxetine

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89
Q

DARI example

A

buproprion

dopamine reuptake inhibitors

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90
Q

SARI

A

serotonin antagonist and reuptake inhibitors

trazodone

91
Q

NaSSA

A

noradrenergic and specific serotonergic antagonists

mirtazapine
mianserin

92
Q

how to typical / first gen antipsychotics work

A

antagonists at the postsynaptic dopamine receptors

93
Q

group 1 typical antipsychotics

A

chlorpromaxine
levomepromazine
promazine

pronounced sedative effects
moderate antimuscaric
moderate EPSEs

94
Q

group 2 typical antipsychotics

A

pericyazine
pipotiazine

moderate sedative effects
fewer EPSEs than groups 1 or 3

95
Q

group 3 typical antipsychotics

A

fluphenazine
prochlorperazine
perphenazine
trifluperazine

characterised by fewer sedative and antimuscarinic SEs than groups 1 and 2

96
Q

atypical antipsychotic examples (8)

A

risperidone
paliperidone
olanzapine
amisulpride
clozapine
quetiapine
aripiprazole
ziprasidone

97
Q

does clozapine undergo first pass metabolism

A

yes

98
Q

clozapine receptor action

A

high affinity for 5-HT receptors
antagonist at adrenergic, cholinergic and histaminergic receptors
occupies D2 receptor sites in a less tight bonding

99
Q

clozapine common side effects

A

hypersalivatio
drowsiness
orthostatic hypotension
hypertension
weight gain
hyperthermia

100
Q

serious clozapine side effects

A

constipation
agranulocytosis
myocarditis
NMS
seizures

101
Q

rate of agranulocytosis in clozapine patients

A

1-2%
more common in first 18 weeks, but can occur at any time

102
Q

constipation treatment in clozapine

A

bulk forming laxative as monotherapy or in combination with stimulant laxatives

103
Q

clozapine bloods

A

FBC weekly for first 18 weeks
fortnightly 18-52 weeks
then if stable, every 4 weeks
monitoring continued for 4 weeks after stopping clozapine

104
Q

lithium common side effects

A

metallic taste
GI side effects
weight gain
polyuria and polydipsia
interstitial nephropathy
benign T-wave changes and sinus node dysfunction
alopecia
acne
worsening of psoriasis
leukocytosis
hyperthyroidism
hypothyroidism
hyperparathyroidism
hypercalcaemia
parathyroid adenoma
physiological tremor if used long term

105
Q

teratogenic effects of lithium

A

Ebstein’s anomaly - prolapse of the tricuspid valve into the right ventricle
1:1000
contraindicated in breastfeeding

106
Q

how does carbamazepine work

A

stabilising sodium channels
narrow therapeutic window
evidenced in treating rapid cycling

107
Q

carbamazepine side effects

A

dizziness
drowsiness
cardiac conduction deficits
rash

neural tube defect in 0.1-1% of the population

108
Q

sodium valproate mechanism

A

GABA agonist

109
Q

sodium valproate side effects

A

nausea
lethargy
weight gain
alopecia (with curly regrowth)
thrombocytopenia
leucopenia
tremor
sedation
hyponatraemia due to SIADH
PCOS

110
Q

topiramate side effects

A

1.5% develop renal caluli (10x placebo)

used in refractory or rapid cycling bipolar

111
Q

phenytoin side effects

A

sedation
ataxia
diplopia
acne
gingival overgrowth
hirsuitism
osteomalacia
hematotoxicity

112
Q

lithium and pregnancy

A

high red USS and echo at 6 and 18 weeks
intensive monitoring and lithium levels in third trimester

serum levels 4 weekly up to 36w then weekly
also level taken within 24 hours after birth

113
Q

carbamazepine and pregnancy

A

should be avoided during pregnancy
lower risk than valproate
lower risk of neural tube defects compared to depakote
prophylactic vit K should be administered after delivery if used

114
Q

valproate and pregnancy

A

avoid
highest risk of teratogenicity

115
Q

benzo mechanism

A

GABA agonists
potentiate GABA inhibitory effect on CNS by increasing number and frequency of chloride channels opened

116
Q

lipid solubility of benzos, poor to good

A

temazepam
lorazepam
diazepam
flurazepam
midazolam

taylor lautner didnt find me

117
Q

benzos to use in hepatic impairment

A

temazepam
oxazepam
Lorazepam

Tired old liver

118
Q

common benzo side effects

A

drowsiness
ataxia
impaired new learning
anterograde amnesia

119
Q

benzo withdrawal effects

A

anxiety
irritability
dizziness
depersonalisation/derealisation
increased sensory perception
abnormal perception

120
Q

benzo reversal

A

flumazenil

121
Q

benzo half lives - chlordiazepoxide

A

5-30 hours

122
Q

benzo half lives - lorazepam

A

10-20 hours

123
Q

benzo half lives - temazepam

A

8-22 hours

124
Q

benzo half lives - nitrazepam

A

15-38 hours

125
Q

benzo half lives - diazepam

A

20-100 hours

126
Q

zolpidem half life

A

2 hours

127
Q

zopiclone half life

A

5-6 hours

128
Q

zaleplon half life

A

2 hours

129
Q

chemical make up of clozapine

A

dibenzodiazepine

130
Q

active placebo

A

drug that produces noticeable effects, but none for the condition for which it is being given

131
Q

nocebo effect

A

when patient experience adverse effects when treated with a placebo

132
Q

placebo - natural remission theory

A

proposes that the improvement that occurs in a placebo group is by chance nadwould have happened anyway

133
Q

placebo - psychological factors

A

patients expectations when given the placebo are very important

134
Q

placebo - classical conditioning

A

patients who have got better in the past with an active treatment may be habituated to expect improvement by any subsequent treatment, even if it is a placebo

135
Q

factors that affect medication adherence

A

cognitive deficits
substance misuse
clinician access
side effects
high frequency of doses
homelessness
poor family support
lack of insight
chronic illness
polypharmacy

136
Q

4 categories considered before taking medication in the health belief model

A

benefits
costs
susceptibility
secondary benefits of medication and adherence

137
Q

cognitive approaches to improving adherence (4)

A

behaviour modification intervention
motivational interviewing
compliance theory
psychoeducation

138
Q

placebo rates in depression

A

up to 60%

139
Q

principles of rational prescribing (10)

A

1 clear reasons for prescribing
2 awareness of pts medication history
3 consider other factors that might influence the prescription
4 take into account the patients ideas concerns expectations
5 choose effective, save and cost effective medications
6 adhere to national guidelines and local formularies
7 legible writing of prescriptions
8 monitor for benefits and adverse effects
9 communicate and document prescribing decisions
10 prescribe within the limitations of your knowledge, skills and experience

140
Q

Type A adverse drug reactions

A

augmented / dose related reactions

  • predictable from the known drug properties
  • related to dose
  • mostly reversible by stopping/decreasing dose

eg oversedation, EPSEs

141
Q

Type B adverse drug reactions

A

bizarre or idiosyncratic/immunological reactions
cannot be predicted from drugs known properties, and not dose dependent

  • immunological eg SJS
  • other idiosyncratic reactions eg agranulocytosis with clozapine
142
Q

hyperprolactinaemia pathway

A

tuberoinfundibular

143
Q

increased negative symptoms pathway

A

mesocortical

144
Q

reduced positive symptoms pathway

A

mesolimbic pathway

145
Q

antipsychotics with highest risk of metabolic ADRs

A

olanzapine
clozapine

146
Q

antipsychotics with lowest risk metabolic ADRs

A

aripiprazole
amisulpride
haloperidol
sulpride

147
Q

Type c adverse drug reactions

A

chronic eg diabetes secondary to second gen antipsychotics

148
Q

Type D adverse drug reactions

A

delayed
eg tardive dyskinesia secondary to antipsychotics

149
Q

type E adverse drug reactions

A

end of use
eg SSRI discontinuation symptoms

150
Q

type F adverse drug reactions

A

failure of therapy
eg SSRIs that dont treat depression

151
Q

factors influencing likelihood and nature of ADRs (7)

A

drug pharmacology
dose and therapeutic window
route of administration
route of metabolism and elimination
interactions with other pharmacology
patient factors including variance in pharmacokinetics
excipients in different generic forms of the drug

152
Q

patient factors influencing ADRs (7)

A

age
weight
gender
pregnancy
cormorbid illness and physical functioning
genetic factors including ethnicity
use of other drugs including alcohol and smoking

153
Q

managing type A ADRs (6)

A
  1. stop the drug
  2. reduce the dose
  3. switch to drug less likely to cause the effect
  4. treat the symptoms
  5. change timing to help tolerability of the ADR
  6. may be appropriate to continue and monitor the ADR
154
Q

D2 antagonism related ADRs

A

hyperprolactinaemia
EPSEs
negative sx eg apathy, flat affect

155
Q

EPSE pathway

A

nigrostriatal

156
Q

antipsychotics with highest risk sedation as ADR

A

quetiapine
olanzapine
clozapine
chlorpromazine
zuclopenthixol

157
Q

antipsychotics with lowest risk sedation as ADR

A

amisulpride
aripiprazole
risperidone
paliperidone
sulpride

158
Q

antipsychotics highest risk long QT

A

haloperidol
chlorpromazine
quetiapine

159
Q

antipsychotics lowest risk long QT

A

aripiprazole

160
Q

antipsychotics highest risk parkinsonian symptoms

A

haloperidol
trifluoperazine

161
Q

antipsychotics lowest risk parkinsonian symptoms

A

aripiprazole
olanzapine
quetiapine
clozapine

162
Q

antipsychotics highest risk akathisia

A

aripiprazole
haloperidol
trifluoperazine

163
Q

antipsychotics lowest risk akathisia

A

quetiapine
clozapine

164
Q

antipsychotics highest risk dystonia

A

haloperidol
trifluoperazine

165
Q

antipsychotics lowest risk dystonia

A

aripiprazole
olanzapine
quetiapine
clozapine

166
Q

antipsychotics highest risk tardive dyskinesia

A

FGAs

167
Q

antipsychotics lowest risk tardive dyskinesia

A

clozapine
quetiapine
olanzapine

168
Q

antipsychotics highest risk hyperprolactinaemia

A

risperidone
paliperidone
FGAs

169
Q

antipsychotics lowest risk hyperprolactinaemia

A

aripiprazole
quetiapine
clozapine

170
Q

antipsychotics highest risk postural hypotension

A

chlorpromazine
clozapine

171
Q

antipsychotics lowest risk postural hypotension

A

amisulpride
sulpride
aripiprazole

172
Q

antipsychotics highest risk sexual dysfunction

A

risperidone
paliperidone
FGAs

173
Q

antipsychotics lowest risk sexual dysfunction

A

aripiprazole
quetiapine
clozapine

174
Q

antipsychotics highest risk anticholinergic ADRs

A

clozapine
flupentixol
zuclopentixol
quetiapine

175
Q

antipsychotics lowest risk anticholinergic ADRs

A

amisulpride
aripiprazole
sulpride

176
Q

NICE recommended antipsychotic monitoring

A

metabolic: activity, diet, weight, waist, BM, HbA1c, lipids
CVS: HR, BP, ECG
prolactin
movement disorder assessment

177
Q

agranulocytosis

A

severe reduction in production of granulocytes (WBCs)

178
Q

risk of agranulocytosis with cloapine

A

0.8%

179
Q

neutropenia

A

reduction in production of neutrophils

180
Q

risk of neutropenia with clozapine

A

2.7%

181
Q

lithium common ADRs (9)

A

nausea, diarrhoea
fine tremor
polyuria and polydipsia
ankle oedema
reduced eGFR
hypothyroidism
worsening psoriasis and acne
metallic taste
weight gain

182
Q

semisodium valproate common ADRs (7)

A

diarrhoea
gastric irritation
nausea
thrombocytopenia
hyperammonemia
transient hair loss with curly regrowth
weight gain

183
Q

carbamazepine common ADRs (10)

A

nausea and vomiting
ataxia
blurred vision
dizziness
drowsiness and fatigue
hyponatraemia
oedema
allergic skin reactions
dermatitis
dry mouth

184
Q

lamotrigine common ADRs (14)

A

dairrhoea
nausea
vomiting
blurred vision
dizziness
drowsiness
aggression headache
insomnia
nystagmus
tremor
arthralgia
back pain
rash
dry mouth

185
Q

symptoms of lithium toxicity

A

anorexia, nausea, diarrhoea
course tremor
muscle weakness and twitching
ataxia
drowsiness, disorientation
coma
seizures

186
Q

thiazide diuretic effect lithium. examples of these

A

metolazone
hydrochlorothiazide
chlorthalidone
indapamide
chlorothiazide
methylclothiazide

187
Q

5-HT1A types of ADRs

A

antidepressant action

188
Q

5-HT2 receptor ADR types

A

sexual dysfunction
vivid dreams

189
Q

5-HT3 receptor ADR types

A

nausea
increased intestinal motility

190
Q

5-HT4 receptor ADR types

A

positive chronotropic effects (arrhythmia)
increased intestinal motility

191
Q

5-HT6 receptor ADR types

A

possible role in memory function

192
Q

5-HT7 receptor ADR types

A

possible role in insomnia

193
Q

mirtazapine more likley and less likely SEs

A

more likely: sedation
less likely: sexual dysfunction, nausea, anorexia

194
Q

allosteric modulator

A

cause a change in a receptor that alters how responsive it is when an agonist binds

195
Q

reversal of opioids

A

naloxone
naltrexone

196
Q

what does disulfiram do

A

inhibits acetaldehyde dehydrogenase which breaks down acetaldehyde - unpleasant reaction

197
Q

dementia drug lease likely to cause nausea/vomiting/diarrhoea

A

memantine

198
Q

dementia drug most likely to cause constipation

A

memantine

199
Q

dementia drug least likely to cause anorexia

A

memantine

200
Q

antidementia drugs most likely to cause agitation

A

rivastigmine, donepezil

201
Q

benzo reversal agent

A

flumazenil

202
Q

4 types of drug interaction

A

pharmaceutical - one substance interacts with another BEFORE administration

pharmacokinetic - one substance alters the bioavailability of another

pharmacodynamic - one substance alters the effect of another, leading to additive or opposing effects

behavioural - one substance alters a persons behaviour to enhance or reduce compliance to another substance

203
Q

mechanism different between serotonin syndrome and NMS

A

serotonin syndrome - excess serotonergic excitation

NMS - too little dopaminergic neurotransmission

204
Q

serotonin syndrome symptoms

A

hypertonia
tremor
myoclonus
hyperreflexia
delirium
tachycardia
HTN

205
Q

NMS symptoms

A

muscle rigidity
tremor
hyporeflexia
ataxia
delirium
tachycardia
hyperthermia

206
Q

green clozapine result

A

continue clozapine prescription

207
Q

amber clozapine result

A

blood monitoring should increase to twice weekly until a green result is achieved

208
Q

red clozapine result

A
  • stop clozapine immediately
  • daily blood monitoring required
  • monitor patient for signs of infection
  • patient may require hospital admission
209
Q

clozapine tachycardia management

A

beta blockers eg atenolol are first line after myocarditis is excluded

should be started after patient has been on cloz for few months as tolerance may develop and tachycardia may resolve

consider cardiology referral if tachycardia persists of if there are concerning features

210
Q

managing hypertension in clozapine

A

slow titration
antihypertensives eg ACE inhibitors and beta blockers

211
Q

managing hypotension in clozapine

A

tolerance tends to develop over 4-6 weeks
stand slowly etc
increase dietary salt and fluid intake
is persists, fludrocortisone may be used - but risk of CCF so gradual dose reduction

212
Q

myocarditis symptoms

A

chest pain
palpitations
breathlessness
fatigue

213
Q

myocarditis physical examination

A

fever
arrhythmia
tachycardia
signs of acute heart failure

214
Q

myocarditis investigations

A

CRP and trop elevated
ECG - diffused TWI and saddle ST segments

215
Q

myocarditis monitoring

A

baseline - trop, CRG, echo
weekly - CRG, trop
every other day for 28 days - HR, BP, temp, RR

216
Q

myocarditis management

A

suspected: continue clozapine, daily trop and CRP, monitor for signs of illness

top 2 times normal limit or CRP >100: stop clozapine immediately, echo, refer to cardiology

217
Q

management of clozapine hypersalivation

A

optimising dose and timing, consider split dose
watch and wait if tolerable

meds:
hyoscine hydrobromide
pirenzepine
amisulpride, sulpride, glycopyrrolate, propantheline

218
Q

why does clozapine cause nausea

A

anticholinergic effects leading to delayed gastric emptying
hypersalivation, increased appetite and effects on the hypothalamus may also contribute to nausea
especially problematic in first 6 weeks, often improves

if intolerable - antiemetics

219
Q

clozapine constipation non pharmacological management

A

dietary fibre increase
adequate hydration
exercise

220
Q

clozapine constipation laxatives

A

stimulants eg senna
can add other classes if stimulants alone ineffective

221
Q

pharmacological options for clozapine weight gain

A

metformin
aripiprazole
topiramate

222
Q

pharmacological options for dyslipidaemia in clozapine

A

statins
if only triglycerides raised - fish oils, fibrates

223
Q

clozapine hepatic effects

A

elevated LFTs in up to 50% of patients
most cases clinically insignificant and resolve by 13 weeks
however, cases of hepatitis and liver failure are reported

224
Q

in context of hepatic effects, clozapine should be discontinued if… (3)

A

LFT raised more than 3 times upper normal
bilirubin is raised
hepatitis or jaundice develops

225
Q

management of clozapine sedation

A

usually improves over few months
start low and go slow
reduce/stop other sedating medications
gradually reduce to minimal effective dose
asymmetric dose splitting - largest dose in the evening
aripiprazole can help if other methods fail

226
Q

rate of seizures in clozapine

A

5% of those on doses >600mg develop seizures
EEG frequently abnormal, even in absence of seizures
effect is dose related
myoclonic jerks can indicated increased seizure risk

227
Q

prevention of clozapine seizures

A

monitor blood levels
use minimum effective dose
consider prophylactic anticonvulsants if plasma levels >0.5 or doses >600mg

228
Q

following clozapine seizure

A

withhold clozapine for 24 hours
check plasma levels
restart at dose 25-50% lower
add an anticonvulsant

229
Q

anticonvulsant choice in clozapine

A

sodium valproate - useful if mood stabilising effect also desirable

lamotrigine - also augments antipsychotic effect of clozapine but can exacerbate myoclonic jerks

topiramate - less commonly used, may aid weight loss

AVOID carbamazepine and phenytoin - impact on clozapine metabolism, increasing clearance and reducing levels. may also be increased risk of agranulocytosis.

230
Q

benign transient pyrexia clozapine

A

reasonably common in first 3 weeks of treatment
around 1:20 patients
can be managed by simple measures eg paracetamol

however, investigate in case of more serious cause eg myocarditis, agranulocytosis, NMS

231
Q

clozapine management of fever >37.5 degrees

A

urgent FBC, trop and CK
physical examination
consider echo, CXR, urinalysis, blood cultures
slow titration

232
Q

clozapine management of fever >38.5 degrees

A

same as fever >37.5 but also WITHHOLD CLOZAPINE

233
Q

clozapine eneuresis

A

1:5 may suffer eneuresis
under reported - need to ask specifically
may be persistent

234
Q

clozapine enuresis non pharmacological management

A

limit evening fluid intake and void before bed
avoid diuretic substances eg caffeine, alcohol
try waking to void at night - enuresis alarms

235
Q

clozapine enuresis pharmacological management

A

minimal effective clozapine dose
asymmetric dose splitting, smaller evening dose

desmopressin
anticholinergics eg oxybutinin, solfenacin, trihexiphenidyl
alpha 1 agonists eg ephedrine
amitriptyline

236
Q

OCD symptoms with clozapine

A

up to 10% of patients
can be delayed or insidious onset
frequently under reported
can be transient ~3 weeks, but may persist in some cases
could be relieved by higher doses at night

237
Q

management of OCD symptoms with clozapine

A

lowest effective cloz dose
CBT tried before pharm rx

antidepressants:
SSRIs
clomipramine
caution as antidepressants can elevate clozapine, esp fluvoxamine

sulpride/amisulpride
aripiprazole

238
Q

parotid swelling in clozapine

A

occasionally reported
sometimes spontaneously resolved, sometimes persists

management:
cessation of clozapine
minimal effective dose
combination of benzatropine and terazosin

239
Q

withdrawal of clozapine

A

should be done gradually over at least 1-2 weeks to avoid withdrawal effects including
- rebound psychosis
- cholinergic rebound

if needs to be stopped suddenly (eg myocarditis, agranulocytosis) - closely monitor and support symptomatically including benzos if needed

240
Q

cardiovascular adverse effects of clozapine

A

tachycardia - very common
hypertension - common
hypotension - common
myocarditis - very rare
cardiomyopathy - very rare

241
Q

GI adverse effects of clozapine

A

sialorrhoea - very common
nausea - very common
constipation - common

242
Q

metabolic adverse effects of clozapine

A

dyslipidaemia - very common
weight gain - very common
impaired glucose tolerance - very common

243
Q

CNS adverse effects of clozapine

A

sedation - very common
seizures - common
myoclonic jerks - common

244
Q

haematological adverse effects of clozapine

A

neutropenia - common
agranulocytosis - uncommon

245
Q

other adverse effects of clozapine

A

urinary incontinence - very common
fever - very common
OCD symptoms - common

RCPsych Paper A (3 decks)

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