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4th year psych > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Which is the only antidepressant recommended in <18y? why?

A

Fluoxetine

Because of increase in suicidal thoughts in the others

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2
Q

What are 4 classes of antidepressants?

A

SSRIs
SNRIs
MAOIs
TCAs

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3
Q

Which of the following is not an SSRI:

citalopram, duloxetine, sertraline, paroxetine

A

duloxetine is an SNRI

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4
Q

What does SNRI stand for

A

serotonin and noradrenaline reuptake inhibitor

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5
Q

SEs SSRI

A

GI bleed, sexual dysfunction, hyponatraemia, increase in suicidal ideation, QT prolongation

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6
Q

Any drug that increases the availability of serotonin can cause____?

A

serotonin syndrome

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7
Q

Symptoms of serotonin syndrome

A

confusion

delirium

shivering

sweating

BP changes

myoclonus

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8
Q

In which situations is serotonin syndrome likely to occur?

A

When initiating an antidepressant, increasing the dose, overdose, adding another AD or switching AD without allowing ‘washout period’ of the last one

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9
Q

How can you reduce the risk of GI bleed in SSRI

A

if elderly taking NSAID/aspirin give PPI

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10
Q

Which two SSRIs would be good for patients on a lot of medication?

A

Citalopram and sertraline have fewest interactions

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11
Q

How should a patient starting an antidepressant be monitored?

A

Review every 1-2w at the start (1w if <30 or suicide risk). Wait at least 4w before deciding it isn’t working. If partial response, keep waiting for another 2-4 more weeks. See them every 2-4w in the first 3m.

If <30 or suicide risk- see frequently until the risk is no longer clinically significant.

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12
Q

Name two SNRIs

A

venlafaxine, duloxetine

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13
Q

Which SNRI has different side effects to SSRIs?

A

Venlafaxine

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14
Q

What extra SEs does venlafaxine have?

A

BP changes, cardiotoxic in overdose

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15
Q

How long should you remain on an antidepressant for?

A

about 6m after symptom resolution

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16
Q

How are antidepressants metabolised

A

hepatic

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17
Q

Can any antidepressants cause withdrawal symptoms?

A

Yes

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18
Q

How should you come off antidepressants?

A

Taper over 2-4w

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19
Q

What is the action of Mirtazapine?

A

Blocks presynaptic alpha 2 receptors which normally inhibit neurotransmitters via negative feedback. This increases monoamine output

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20
Q

Side effects of mirtazipine

A

Dry mouth, drowsiness, wt gain

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21
Q

Dothiepin, imipramine and lofepramine are what type of antidepressant?

A

TCA

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22
Q

What type of antidepressant has the highest risk of overdose?

A

TCAs except lofepramine

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23
Q

Mechanism of TCAs

A

Block monoamine reuptake (each to different extents)

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24
Q

SEs TCAs

A

Anticholinergic, antiadrenergic, cardiac arrhythmias, seizures

hypotension, tachycardia, QTc prolongation

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25
Q

Which TCA has fewer side effects

A

Lofepramine, but rarely it causes hepatic toxicity

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26
Q

TCAs can be split into what two groups?

A

Sedating and non-sedating

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27
Q

Name some sedating TCA

A

amitriptyline, clomipramine, dosulepin, doxepin, mianserin, trazodone, trimipramine

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28
Q

Name some less sedating TCAs

A

Imipramine, lofepramine, nortriptyline.

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29
Q

Mechanism of MAOIs?

A

Inhibit breakdown of serotonin, and, to a lesser extent, noradrenaline.

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30
Q

Name two MAOIs

A

phenelzine, tranylcypromine

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31
Q

SEs MAOIs

A

Anticholinergic, antiadrenergic, tyramine reaction

Hypertensive crisis

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32
Q

What is a tyramine reaction (SE of MAOI)

A

HTN and throbbing headache if eat food with lots of tyramine- cheese and red wine. Occasionally fatal.

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33
Q

Treatment with _______ is associated with a higher risk of withdrawal effects compared with other antidepressants

A

Venlafaxine

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34
Q

What is the antidepressant general progression of treatment?

A
  1. SSRI
  2. Up dose
  3. Switch to different SSRI or alternate antidepressant
  4. Augment with antipsychotic/lithium etc
  5. Combination therapy: Venlafaxine & Mirtazapine, or Olanzapine & Fluoxetine
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35
Q

Antipsychotics are split into which two categories?

A

Typical and atypical

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36
Q

Are typical or atypical antipsychotics first line?

A

Atypical

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37
Q

Benefit of atypical antipsychotics?

A

Fewer SEs and may be slightly better at treating negative Sx schizophrenia

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38
Q

Which is the most effective antipsychotic? But what are its negatives?

A

Clozapine

Significant SEs- agranulocytosis- requires regular monitoring (weekly for 18w, then fortnightly for 1y then monthly).

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39
Q

When do you prescribe clozapine?

A

when two antipsychotics have failed

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40
Q

Mechanism of action antipsychotics?

A

Reduce dopamine transmission (D2/D3)

Atypicals- antagonise 5HT2a receptors

Typicals- anticholingergic, antiadrenergic and antihistaminergic.

Unknown why these treat psychosis

May involve ventral striatum

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41
Q

antipsychotics route?

A

Normally oral, can be IM short acting, occasionally IV.

Some (flupenthixol, fluphenazine and risperidone) can be depot injections every 1-4w which improves adherence.

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42
Q

Would you use antipsychotics for behavioural disturbance in elderly?

A

No, risk stroke and reduce glycaemic control. Only one you’d use is risperidone short term.

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43
Q

Indications for antipsychotics?

A

Schizo

Mania

Psycotic depression

Violent/agitated behaviour (haloperidol usually)

Tourette’s in lower doses

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44
Q

SEs typical antipsychotics

A

Antidopaminergic:

Movement: parkinsonism, akathisia, tardive dyskinesia, acute dystonic reactions (torticollis, increased tone, oculogyric crisis)

AND

Hyperprolactinaemia: galactorrhoea, breast cancer, amenorrhoea, sexual dysfunction

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45
Q

What is an oculogyric crisis?

A

Keep looking up involuntarily

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46
Q

What types of typical antipsychotics have slightly different SEs?

A

Phenothiazines- blood dyscrasias, retinal pigmentation, photosensitivity, cholestatic jaundice

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47
Q

What are the SEs of atypical antipsychotics?

A

Metabolic- wt gain, T2DM, dyslipidaemia

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48
Q

Which atypical antipsychotic has different profile of SEs?

A

Clozapine:

Nocturnal enuresis, constipation, salivation, BP changes, fever, nausea, seizures, agranulocytosis

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49
Q

What are the side effects of all antipsychotics?

A

C-CHANS

Cardiac (QT prolongation, arrhyth, 2x risk sudden cardiac death)

Anti-Cholinergic (dry mouth, urinary retention, constipation, confusion)

Anti-Histaminergic (sedation)

Anti-Adrenergic (postural hypotension)

Neuroleptic malignant syndrome

Change Seizure threshold

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50
Q

What is neuroleptic malignant syndrome?

A

Increased serum CK, hyperpyrexia, increased muscle tone, confusion, autonomic instability

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51
Q

How long should antipsychotics be continued?

A

1-2y after first episode, but 98% relapse after 2y so often continue for 5y. Many are non-adherent anyway

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52
Q

What advice should you give to patients if they decide to stop their antipsychotic?

A

Taper it over at least 3w as stopping suddenly doubles the risk of relapse

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53
Q

What monitoring should be done when starting antipsychotics? And how frequently after starting?

A

Prior and yearly:

  • ECG
  • BMI and waist circ
  • Bloods: FBC, U&E, lipid profile, HbA1c, glucose, LFTs, prolactin
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54
Q

Why can’t clozapine and carbemazepine be used together?

A

Both risk agranulocytosis

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55
Q

What is the risk with antipsychotics and metaclopramide?

A

Extra pyramidal SEs

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56
Q

Risk with (IV) erythromycin & quetiapine?

A

QT prolongation

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57
Q

What is the main mood stabiliser?

A

Lithium

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58
Q

Indications for lithium?

A

Prophylaxis in recurrent uni/bipolar affective disorder

Acutely in mania

Augmentation of ADs in resistant depression

Schizoaffective illness

Control aggression

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59
Q

Mechanism of lithium

A

Unclear

Interacts with all body systems that involve sodium, potassium, calcium and magnesium

probably affects neurotransmitters (serotonin, dopamine, noradrenaline, acetylcholine)

Interferes with cAMP linked receptors- action on kidney and thyroid

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60
Q

Route of lithium

A

Oral

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61
Q

Excretion of lithium

A

Renal

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62
Q

Contraindications for lithium

A

Thyroid disease

Renal disease

Cardiac disease

Addison’s disease

63
Q

Monitoring required for lithium?

A

Prior and 6 monthly: TFTs, eGFR and weight

Serum lithium- weekly at first and then 12 weekly

64
Q

When should serum lithium be monitored in relation to dose?

A

12h after last dose

65
Q

SEs of lithium at the therapeutic dose

A

Nausea

fine tremor

wt gain

oedema

polydipsia and polyuria

worse psoriasis and acne

Hypothyroid

66
Q

What is the therapeutic dose of lithium?

A

0.4-1mmol/L (serum)

67
Q

Symptoms of lithium toxicity

A

D&V

coarse tremor

slurred speech

ataxia

drowsy and confused

convulsions and coma

68
Q

What is the treatment for lithium toxicity?

A

Stop the lithium and fluids

69
Q

What could precipitate lithium toxicity?

A

Dehydration and diuretics

70
Q

What does lithium interact with?

A

NSAIDs

Calcium Channel Bs

some abx

71
Q

What are 3 other mood stabilisers?

A

Sodium valproate

Carbemazepine

Lamotrigine

72
Q

What is lamotrigine especially good at as a mood stabiliser?

A

Preventing depressive episodes

73
Q

SEs sodium valproate?

A

GI, weight gain, hair loss with curly regrowth, dose related tremor, thrombocytopenia

74
Q

SEs lamotrigine

A

skin incl SJS

aseptic meningitis

dizziness

diplopia

leucopenia

insomnia

nausesa

75
Q

Which mood stabilisers should be avoided in pregnancy?

A

Lithium

Lamotrigine

Valproate

76
Q

Are different brands of lithium bioequivalent?

A

No, should know which brand they are on

77
Q

Does lithium need to be tapered to stop?

78
Q

SSRI + lithium could lead to what?

79
Q

What type of diuretic should be used with lithium?

80
Q

What can NSAIDs do to lithium levels in blood?

81
Q

Mechanism Valproate?

82
Q

What is a caution in carbemazepine?

A

Hepatic enzyme inducer

83
Q

SEs carbemazepine?

A

agranulocytosis, hyponatraemia.

84
Q 
Nitrazepam
Flurazepam
Diazepam
Alprazolam
Clobazam
Chlordiazepoxide

These are short or long acting benzos?

85
Q

Lorazepam
Loprazolam
Lormetazepam
Temazepam

Short or long acting benzos?

86
Q

What do benzos do?

A

anxiolytic

sleep inducing

anticonvulsant

muscle relaxant

87
Q

Indications of benzos?

A

Insomnia

GAD (short term and not for phobias or panic disorders)

Alcohol withdrawal

Control violent behaviour

2nd line for refractory epilepsy

88
Q

Route of benzos?

A

Usually oral

Sometimes IM, IV, rectal

89
Q

What is it important to consider when giving benzos?

A

Exclude underlying conditions and consider behavioural alternative treatment

90
Q

Mechanism of benzos

A

Potentiate the inhibitory effects of GABA (Decreases neuronal excitability)

91
Q

What are some other anxiolytics other than benzos?

A

Zopiclone and related

Antihistamines

Buspirone

92
Q

SEs benzodiazepines?

A

Drowsy

Ataxia (falls risk)

Amnesia

Dependence

Disinhibition (may lead to aggression)

Potentiates alcohol and other sedatives- may be a dangerous combo

93
Q

Signs of benzo OD?

A

Resp depression

Drowsy

Dysarthria

Ataxia

94
Q

Treatment for benzo OD

A

Flumazenil

but caution in mixed OD or benzo-dependent pts

95
Q

What is a risk with anything but short term benzo?

96
Q

Withdrawal Sx benzos?

A

Anxiety

Shakiness

Abdo cramps

Perceptual disturbances

Persecutory delusions

Seizures

97
Q

Why might you get increased dreaming when stopping benzos?

A

They inhibit REM sleep

98
Q

How long can weaning off iatrogenic benzo dependence take?

A

months- years

99
Q

What does zopiclone do?

A

Hypnotic but without the anti-convulsant or muscle relaxing properties

100
Q

Can zopiclone cause dependency?

101
Q

What is Buspirone? Including mechanism.

A

Anxiolytic used short term for anxiety. 5HT1a partial agonsit

102
Q

What are the two dementia drugs?

A

Acetylcholinesterase inhibitors

Memantine

103
Q

Name the three AChE inhibitors

A

Donepezil

Rivastigmine

Galantamine

104
Q

First line for mild-mod alzheimers?

105
Q

First line for mild-mod Lewy body? What if this isn’t tolerated?

A

Donezepil or Rivastigmine first line, if not then galantamine

106
Q

Severe lewy body treatment?

A

donezepil or rivastigmine, if not tolerated then memantine

107
Q

Should you give AChEi or memantine in fronto temporal dementia?

108
Q

Donezepil mechanism

A

Reversible inhibitor of AChE

109
Q

Donezepil cautions in?

A

asthma/copd

some cardiac

peptic ulcer

110
Q

Donezepil SEs

A

Mood/behavioural changes

muscle cramps

hallucinations

syncope

Urinary incontinence

Appetite decrease

sleep probs

111
Q

AChEi doses should start ____

A

low and increase

112
Q

Galantamine mechanism?

A

Reversible inhibitor of AChE with some nicotinic receptor agonist properties

113
Q

Galantamine is available in which two forms?

A

Modified and immediate release

114
Q

Galantamine cautions?

A

GI obstruciton or surgery

Urinary outflow obstructin or bladder surgery

Some HD

COPD/severe asthma

seizures

115
Q

SEs galantamine

A

Skin reactions- SJS

decreased appetite

arrhyth

Mood changes

hallucinations

HTN

muscle spasms

Tremor

116
Q

Galantamine and renal disease?

A

Avoid if eGFR <9mL/min

117
Q

Rivastigmine mechanism

A

Reversible non-competitive inhibitor of AChE

118
Q

Rivastigmine routes available

A

PO or transdermal

119
Q

Rivastigmine cautions

A

GI ulcers

Bladder outflow obstruction

Hx asthma/copd

Sick sinus synd

Seizures

120
Q

What is the risk with transdermal rivastigmine?

A

Leave the old patches on and have fatal OD

121
Q

SEs rivastigmine

A

Appetite decrease

Mood changes

Hyperhidrosis

Hypersalivation

HTN

Movement disorders

Skin reactions

Urinary incontinence

PO: hallucinations, parkinsonism, sleep disorder, gait change

TD: gastric ulcer

122
Q

What should you monitor when the pt is on rivastigmine

A

body weight

123
Q

Instructions for transdermal administration of rivastigmine

A

Clean, dry, non-hairy, non-irritated skin on back, upper arm or chest. Remove after 24h. Avoid same site for 14 days.

124
Q

Which AChEi for dementia in a patient who needs modified release?

A

Galantamine

125
Q

Which AChEi for dementia in a patient who can’t tolerate oral medication?

A

Rivastigmine transdermal

126
Q

Which AChEi for dementia in a patient with history of bladder outflow obstruction?

127
Q

Memantine action (and how does this help dementia)

A

Glutamate receptor antagonist. Glutamate is the major excitatory neurotransmitter in CNS. Inhibiting its action prevents cell damage.

128
Q

What is a glutamate receptor antagonist also known as?

A

NMDA receptor antagonist

129
Q

Memantine caution?

A

Epilepsy and avoid if eGFR <5mL/min

130
Q

SEs memantine

A

dizziness

headaches

constipation

confusion

worse balance

131
Q

St Johns wort is a complementary medicine used in what?

A

Depression (mild-mod)

Anxiety

SAD

Sleep disorders

132
Q

Is there evidence for St Johns wort in severe depression

133
Q

What is the problem with St John’s wort (2)

A

Interactions

May trigger mania in bipolar

134
Q

What is given for parkinsonian SEs of APs?

A

Procyclidine (or other antimuscarinics)

135
Q

Can you give procyclidine in tardive dyskinesia?

A

No it worsens it

136
Q

What does tardive dyskinesia look like?

A

TD causes stiff, jerky movements of your face and body that you can’t control. You might blink your eyes, stick out your tongue, or wave your arms without meaning to do so.

Smacking lips

Flapping arms

Blinking

137
Q

What is akathisia?

A

Feeling of inner restlessness. V unpleasant.

138
Q

Tardive dyskinesia treatment

A

Worrying as may be irreversible on withdrawing therapy and treatment is usually ineffective. Treat ASAP

Swap or stop the AP

139
Q

Akathisia treatment

A

Benzos, propanolol

140
Q

Neurotransmitter in depression, anxiety, ADHD, migraine, OCD

141
Q

Neurotransmitter in alzheimers

A

Acetylcholine

142
Q

Neurotransmitter in Schiz and parkinsons

A

Dopamine (increased in schiz and decreased in park)

143
Q

Neurotransmitter in Epileptic seizures and alcohol withdr

144
Q

GABA is brain on or off?

145
Q

What neurotransmitter is brain ‘on’

146
Q

Neurotransmitter in depression decreased (not serotonin)

A

Noradrenaline

147
Q

Neurotransmitter in migraine, stroke, autism

148
Q

What is the action of monoamine neurotransmitters on the nervous system?

A

–> second messengers–> increased transcription factors –> increased BDNF –> increase neuroplasticity and neurogenesis in hippocampus

149
Q

What decreases rate of transcription factors (and hence BDNF and neuroplasticity and genesis)?

150
Q

Neurotransmitter in caffeine

151
Q

Neurotransmitter in hunger

A

Cholecystokinin

152
Q

Neurotransmitter in pain and appetite regulation, co-ordination and learning

A

Endocannabinoids

153
Q

Neurotransmitters in tobacco

A

Acetylcholine and dopamine

4th year psych (15 decks)

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