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Antipsychotics Flashcards

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1
Q

What is psychosis?

A

A loss of touch with reality, typified by the presence of psychotic symptoms and generally associated with a loss of insight

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2
Q

What are the three main symptom domains of psychosis?

A
  • Positive symptoms
  • Negative symptoms
  • Disorganisation symptoms
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3
Q

What are the positive symptoms in psychosis?

A
  • Hallucinations
  • Delusions
  • Thought disorder
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4
Q

What are the negative symptoms in psychosis?

A
  • Alogia
  • Apathy
  • Avolition
  • Asocialty
  • Affective blunting
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5
Q

What are the disorganisation symptoms in psychosis?

A

Bizarre, chaotic and agitated behaviour

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6
Q

What regulates motivation and facilitates reinforcement and reward?

A

Release of dopamine from the ventral tegmental area, through the prefrontal cortex, amygdala and into the nucleus accumbens via the mesolimbic pathway

This regulates motivation and facilitates reinforcement and reward

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7
Q

What are psychotomimetic drugs?

A

Dopamine increasing drugs eg. cocaine, amphetamine

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8
Q

Which area is key for the negative and cognitive symptoms in schizophrenia?

A

The prefrontal cortex

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9
Q

Which areas are related to negative symptoms in schizophrenia?

A

Dopamine deficiency in the mesocortical circuit and ventromedial prefrontal cortex

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10
Q

Which areas are related to cognitive symptoms in schizophrenia?

A

Dopamine deficiency in the dorsolateral prefrontal cortex

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11
Q

Which areas are linked to aggressive and impulsive symptoms in schizophrenia?

A

The orbitofrontal cortex and its connections to the amygdala

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12
Q

What are the four dopamine pathways in the brain?

A
  • Mesolimbic (positive symptoms)
  • Mesocortical (negative symptoms)
  • Nigrostriatal (extrapyrimidal side effects)
  • Tuberoinfundibular (hyperprolactinaemia)
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13
Q

What does the mesolimbic pathway connect?

A

Dopaminergic cell bodies in the ventral tegmental area (reward, motivation, cognition and aversion) of the midbrain to the ventral striatum of the basal ganglia (limbic region - tracking the subjective value of stimuli, signalling the presence of/ expectation of reward and encoding errors and outcomes of predictions) in the forebrain

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14
Q

What does the mesocortical pathway connect?

A

Dopaminergic cell bodies in the VTA to the prefrontal cortex - involved in cognitive control, motivation and emotional response

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15
Q

What does the nigrostriatal pathway connect?

A

Projects from the dopaminergic cell bodies in the substantia nigra (midbrain) to axons terminating in the striatum/ basal ganglia - pathway controls motor movements and is part of the extrapyrimidal nervous system

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16
Q

What does hyperactivity in the nigrostriatal pathway lead to?

A

Hyperkinetic movement disorders such as chorea, dyskinesia and tics

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17
Q

Where does the tuberinfundibular pathway connect?

A

Projects from dopaminergic neurones in the hypothalamus to the anterior pituitary gland - normally these dopaminergic neurones inhibit the release of prolactin

(they become less active during the postpartum period to allow for lactation)

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18
Q

What are antipsychotics used for?

A
  • Treatment of psychosis
  • Mood stabilisation in BPAD
  • Antidepressant augmentation in depression, anxiety, OCD
  • Treatment of Gilles de la Tourette’s
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19
Q

How are antipsychotics classified?

A
  • Typical (first generation)
  • Atypical (second generation)
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20
Q

What are the typical antipsychotics?

A
  • Chlorpromazine (first to be synthesised)
  • Haloperidol
  • Zuclopenthixol (clopixol)
  • Flupentixol (depixol)
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21
Q

Which receptors do typical antipsychotics widely act on?

A

D2 dopamine receptors

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22
Q

What are the atypical antipsychotics?

A
  • Clozapine (first to be synthesised)
  • Olanzapine
  • Quetiapine
  • Risperidone
  • Paliperidone
  • Aripiprazole
  • Lurasidone
  • Cariprazine
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23
Q

Where do atypical antipsychotics act?

A

Less affinity for dopamine, more on serotonin and 5-HT2A

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24
Q

Which atypical antipsychotics work as partial agonists?

A
  • Aripiprazole
  • Cariprazine
  • Luradisone

A partial agonist works as an antagonist in the presence of a full native agonist

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25
Q

What is the difference between first and second generation antipsychotics?

A

Second generation:
- Lower risk of extrapyrimidal side effects
- Antagonists of 5HT-2A serotonin receptors which has downstream effects to increase the dopamine within the nigrostriatal dopamine pathway

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26
Q

How do second generation antipsychotics reduce the risk of extrapyrimidal side effects?

A

Blocking 5HT-2A receptors can reduce antipsychotic receptor occupancy from 80-60% within the nigrostriatal pathway, reducing the risk of EPSEs

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27
Q

What are the side effects of clozapine?

A
  • Sedation (blocks histamine-H1 receptors)
  • Increased appetite (weight gain) (H1)
  • Neutropenia
  • Leucopenia
  • Agranulocytosis
  • Prothrombotic (increased risk of DVT/PE)
  • Severe constipation
  • Hypersalivation
  • Cardiomyopathy
  • Tachycardia
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28
Q

What is the risk if clozapine is abruptly stopped?

A

High risk of rebound psychosis within 2 weeks

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29
Q

Why should clozapine be started at a low dose and titrated slowly?

A

Due to the risk of cardiovascular instability

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30
Q

What is the protocol if clozapine is stopped for more than 48 hours?

A

It must be re-titrated

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31
Q

When is the highest risk of neutropenia/ leucopenia/ agranulocytosis with clozapine?

A

In the first 18 weeks

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32
Q

Where do patients have to be registered if they’re taking clozapine?

A

With a national clozapine monitoring service
Eg:
- Zaponex treatment access system
- Clozaril
- Denzapine

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33
Q

How often is FBC monitored for patients on clozapine?

A
  • Weekly
  • Then fortnightly
  • Then monthly after one year of treatment
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34
Q

What are the green, amber and red results of clozapine blood tests?

A
  • Green - ok to continue
  • Amber - continue but increase FBC monitoring to twice weekly
  • Red - stop immediately
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35
Q

What are the symptoms of agranulocytosis?

A
  • Ulcer development in mucous membranes
  • Susceptible to bacterial infections
  • Sepsis occurs to bacterial contamination
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36
Q

Which colour blood bottle is used for clozapine monitoring?

A

EDTA purple top

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37
Q

What are long acting injectable antipsychotics?

A

Antipsychotics given via a long acting IM injection rather than oral tablet (depots)

38
Q

Which antipsychotics are available as depots?

A
  • Zuclopenthixol (every 1-4 weeks)
  • Flupentixol (every 1-4 weeks)
  • Haloperidol (every 1-4 weeks)
  • Olanzapine (every 2-4 weeks)
  • Paliperidone (risperidone metabolite) (every 4 weeks, 3 months)
  • Aripiprazole (every 4 weeks)
39
Q

How long do antipsychotics take to work?

A
  • Sedative effects occur rapidly (minutes - hours)
  • Clear antipsychotic effects after 1-2 weeks, maximum benefit generally seen within 6 weeks
40
Q

When is clozapine generally considered as an antipsychotic?

A

In schizophrenia when two antipsychotics have been tried (and at least one is atypical) for at least 6 weeks, it can be labelled as treatment resistant and treated with clozapine

41
Q

What is high dose antipsychotic treatment (HDAT)?

A

Total antipsychotic dose >100% BNF maximum dose

Eg. 15mg olanzapine (75% BNF max) + 8mg risperidone (50% BNF max) = 125% of BNF limit

42
Q

What risks is HDAT associated with?

A

Increased risk of:
- Cardiovascular side effects
- Metabolic syndrome
- Neuroleptic malignant syndrome

43
Q

Which routes of administration can be used for rapid tranquilisation medications?

A

PO or IM

PRN (medications taken when needed) antipsychotics count towards total BNF max when determining HDAT

44
Q

What are the most commonly used antipsychotics for rapid tranquilisation?

A

Olanzapine and haloperidol

45
Q

What is needed before haloperidol administration?

A

Pre-treatment ECG, due to the risk of QTc prolongation

46
Q

Which medication should not be given with olanzapine?

A

IM olanzapine should not be given within 1 hour of IM lorazepam due to the risk of respiratory depression

47
Q

What is the maximum number of days in a row that IM olanzapine can be given?

A

No more than 3 days of IM olanzapine in a row due to post-injection syndrome

48
Q

What is post injection syndrome?

A

Symptoms such as:
- Confusion
- Dizziness
- Anxiety
- Sedation
- Extrapyrimidal symptoms

Occurring within an hour of olanzapine injection

49
Q

Which medication classes are used for rapid tranquilisation?

A

1st line: benzodiazepines (PO or IM lorazepam)
2nd line: Promethazine
3rd line: Antipsychotics

50
Q

Which medication would be used in patients who have required multiple IM tranquilisation injections?

A

Accuphase (Zuclopenthixol Acetate)
- 50-150mg IM
- Dose can be repeated 48-72 hours
- 400mg in 2 weeks maximum cumulative dose

51
Q

Which hormone stimulates prolactin release?

A

Thyrotropin-releasing hormone (TRH)

52
Q

What is a clinically significantly elevated prolactin?

A

> 1,000mlU/L

53
Q

Which antipsychotics commonly increase prolactin levels?

A
  • Risperidone
  • Haloperidol
54
Q

What are the symptoms of hyperprolactinaemia in women?

A
  • Reduced libido
  • Amenorrhoea
  • Galactorrhoea
  • Osteoporosis
  • ?increased risk of breast cancer
55
Q

What are the symptoms of hyperprolactinaemia in men?

A
  • Reduced libido
  • Erectile dysfunction
  • Gynaecomastia
  • Galactorrhoea
56
Q

What are the prolactin sparing antipsychotics?

A
  • Quetiapine
  • Ziprasidone
57
Q

What is the management of antipsychotic induced hyperprolactinaemia?

A

Switch to a prolactin sparing agent and add in aripiprazole (partial dopamine agonist)

58
Q

What is the QT interval corrected for?

A

Heart rate
- Typically using the Bazett’s formula
- <440ms in males, <470ms in females

59
Q

What is QT prolongation a risk factor for?

A

Developing cardiac arrhythmias
- Polymorphic ventricular tachycardia (Torsade de Pointes)
- Risk increases significantly in QTc intervals >500ms

60
Q

Which medications increase the risk of QTc prolongation?

A
  • Citalopram
  • Venlafaxine
  • Clarithromycin
  • Fluconazole
  • Most antipsychotics
61
Q

Which antipsychotics are most likely to increase QTc prolongation?

A

High risk:
- HDAT
- Haloperidol

Moderate risk:
- Chlorpromazine
- Quetiapine
- Amisulpride

62
Q

What is neuroleptic malignant syndrome?

A
  • A complication of antipsychotic treatment
  • Disorder of thermoregulation and neuromotor control
63
Q

What are the risk factors for neuroleptic malignant syndrome?

A
  • High dose typicals
  • Rapid dose changes
  • Male gender
  • Younger age
64
Q

What are the signs and symptoms of neuroleptic malignant syndrome?

A
  • Muscle rigidity
  • Hyperthermia
  • Hyporeflexia
  • Diaphoresis
  • Autonomic dysregulation
  • Altered consciousness
65
Q

What’s the difference in presentation between neuroleptic malignant syndrome and serotonin syndrome?

A

Serotonin syndrome leads to hyperreflexia whereas neuroleptic malignant syndrome leads to hyporeflexia

Otherwise, they present clinically very similar

66
Q

What are the investigations for neuroleptic malignant syndrome?

A
  • Raised creatine kinase
  • Leucocytosis
  • Deranged liver function
  • Deranged renal function (secondary to rhabdomyolysis from raised CK)
67
Q

What’s the management of neuroleptic malignant syndrome?

A
  • Stop causative antipsychotic
  • Transfer to hospital/ ITU
  • Support care and fluids
  • Benzodiazepines (muscle relaxant)
  • Bromocriptine (dopamine agonist) and Dantrolene (muscle relaxant)
68
Q

Which four abnormalities are observed with extra-pyramidal side effects?

A
  • Parkinsonism
  • Dystonia
  • Tardive dyskinesia
  • Akathisia
69
Q

What does extra-pyramidal side effects refer to?

A

Movement abnormalities mediated by movement pathways outside of the medullary pyramids (eg. basal ganglia, cerebellum and motor cortex not the corticospinal tract)

70
Q

What causes extra-pyramidal side effects?

A

Dopamind blocked within the nigrostriatal dopamine pathway

71
Q

What are the symptoms of (psuedo)parkinsonism?

A
  • Stooped posture
  • Shuffling gait
  • Rigidity
  • Bradykinesia
  • Tremors at rest (pill-rolling)
72
Q

What are the symptoms of acute dystonia?

A
  • Facial grimacing
  • Involuntary upward eye movement
  • Muscle spasms of the tongue, face, neck and back (causing the trunk to arch forward)
  • Laryngeal spasms
73
Q

What are the symptoms of akathisia?

A
  • Restless
  • Trouble standing still
  • Paces the floor
  • Feet in constant motion, rocking back and forth
74
Q

What are the symptoms of tardive dyskinesia?

A
  • Protrusion and rolling of the tongue
  • Sucking and smacking movements of the lips
  • Chewing motion
  • Facial dyskinesia
  • Involuntary movements of the body and extremities
75
Q

What is the difference between parkinsonism and parkinson’s disease?

A

Parkinsonism is generally bilateral, whereas parkinson’s disease is typically asymmetrical

76
Q

What scan can be used to determine whether someone has parkinson’s disease or drug induced parkinsonism?

A

Dopamine transporter scan (DAT)

77
Q

What is the management of drug induced parkinsonism?

A

Switch medicaiton, add in a regular antimuscarinic (procyclidine 5mg)

78
Q

How long after treatment does tardive dyskinesia develop?

A

Months or years of treatment

Chronic blockade of D2 receptors in the basal ganglia causes them to become hypersensitive

79
Q

What is the management of tardive dyskinesia?

A
  • Stop causative agent
  • Consider tetrabenazine 25mg
80
Q

What is the mechanism of tetrabenazine?

A

Inhibits vesicular monoamine transporter 2 leading to depletion of dopamine and other monoamines in the CNS

81
Q

How long after commencing treatment does dystonia come on?

A

Acutely, within hours of starting antipsychotics

82
Q

What is an oculogyric crisis?

A

Dystonia where the eyes roll upwards

83
Q

What is torticollis?

A

Dystonia where the head and neck twist to one side

84
Q

What is laryngeal dystonia?

A

Dystonia of the larynx that can compromise the airway and be life threatening

85
Q

What is the management for dystonia?

A

Anticholinergics (eg. procyclidine 5-10mg PO or IM)

86
Q

What is akathisia?

A

A sense of internal restlessness where the patient feels compelled to move, rock, fidget or pace around

87
Q

How long after starting treatment does akathisia occur?

A

Within days - weeks of starting or increasing an antipsychotic

88
Q

What is the management of akathisia?

A

Change medication to:
- Diphenhydramine (sedating antihistamine)
- Propranolol
- Low dose benzodiazepines

89
Q

What is metabolic syndrome?

A

Antipsychotics, particularly acting on H1 receptors, can cause weight gain, dyslipidaemia and insulin insensitivity

90
Q

What’s the management for metabolic syndrome?

A
  • Monitor weight, BP, lipids and HbA1C
  • Treat complications
  • Promote healthy eating and exercise
91
Q

Why should SSRI and NSAIDs not be prescribed together?

A

SSRIs potentially deplete platelet serotonin, resulting in reduced clot formation and therefore increase the bleeding risk - particularly GI bleeds, when prescribed with NSAIDs

If the two must be prescribed, a PPI should also be prescribed

Psych (13 decks)

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