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Antipsychotics Flashcards

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
What is the difference between first and second generation antipsychotics?
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
26
How do second generation antipsychotics reduce the risk of extrapyrimidal side effects?
Blocking 5HT-2A receptors can reduce antipsychotic receptor occupancy from 80-60% within the nigrostriatal pathway, reducing the risk of EPSEs
27
What are the side effects of clozapine?
- Sedation (blocks histamine-H1 receptors) - Increased appetite (weight gain) (H1) - Neutropenia - Leucopenia - Agranulocytosis - Prothrombotic (increased risk of DVT/PE) - Severe constipation - Hypersalivation - Cardiomyopathy - Tachycardia
28
What is the risk if clozapine is abruptly stopped?
High risk of rebound psychosis within 2 weeks
29
Why should clozapine be started at a low dose and titrated slowly?
Due to the risk of cardiovascular instability
30
What is the protocol if clozapine is stopped for more than 48 hours?
It must be re-titrated
31
When is the highest risk of neutropenia/ leucopenia/ agranulocytosis with clozapine?
In the first 18 weeks
32
Where do patients have to be registered if they're taking clozapine?
With a national clozapine monitoring service Eg: - Zaponex treatment access system - Clozaril - Denzapine
33
How often is FBC monitored for patients on clozapine?
- Weekly - Then fortnightly - Then monthly after one year of treatment
34
What are the green, amber and red results of clozapine blood tests?
- Green - ok to continue - Amber - continue but increase FBC monitoring to twice weekly - Red - stop immediately
35
What are the symptoms of agranulocytosis?
- Ulcer development in mucous membranes - Susceptible to bacterial infections - Sepsis occurs to bacterial contamination
36
Which colour blood bottle is used for clozapine monitoring?
EDTA purple top
37
What are long acting injectable antipsychotics?
Antipsychotics given via a long acting IM injection rather than oral tablet (depots)
38
Which antipsychotics are available as depots?
- 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
How long do antipsychotics take to work?
- Sedative effects occur rapidly (minutes - hours) - Clear antipsychotic effects after 1-2 weeks, maximum benefit generally seen within 6 weeks
40
When is clozapine generally considered as an antipsychotic?
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
What is high dose antipsychotic treatment (HDAT)?
Total antipsychotic dose >100% BNF maximum dose Eg. 15mg olanzapine (75% BNF max) + 8mg risperidone (50% BNF max) = 125% of BNF limit
42
What risks is HDAT associated with?
Increased risk of: - Cardiovascular side effects - Metabolic syndrome - Neuroleptic malignant syndrome
43
Which routes of administration can be used for rapid tranquilisation medications?
PO or IM PRN (medications taken when needed) antipsychotics count towards total BNF max when determining HDAT
44
What are the most commonly used antipsychotics for rapid tranquilisation?
Olanzapine and haloperidol
45
What is needed before haloperidol administration?
Pre-treatment ECG, due to the risk of QTc prolongation
46
Which medication should not be given with olanzapine?
IM olanzapine should not be given within 1 hour of IM lorazepam due to the risk of respiratory depression
47
What is the maximum number of days in a row that IM olanzapine can be given?
No more than 3 days of IM olanzapine in a row due to post-injection syndrome
48
What is post injection syndrome?
Symptoms such as: - Confusion - Dizziness - Anxiety - Sedation - Extrapyrimidal symptoms Occurring within an hour of olanzapine injection
49
Which medication classes are used for rapid tranquilisation?
1st line: benzodiazepines (PO or IM lorazepam) 2nd line: Promethazine 3rd line: Antipsychotics
50
Which medication would be used in patients who have required multiple IM tranquilisation injections?
Accuphase (Zuclopenthixol Acetate) - 50-150mg IM - Dose can be repeated 48-72 hours - 400mg in 2 weeks maximum cumulative dose
51
Which hormone stimulates prolactin release?
Thyrotropin-releasing hormone (TRH)
52
What is a clinically significantly elevated prolactin?
>1,000mlU/L
53
Which antipsychotics commonly increase prolactin levels?
- Risperidone - Haloperidol
54
What are the symptoms of hyperprolactinaemia in women?
- Reduced libido - Amenorrhoea - Galactorrhoea - Osteoporosis - ?increased risk of breast cancer
55
What are the symptoms of hyperprolactinaemia in men?
- Reduced libido - Erectile dysfunction - Gynaecomastia - Galactorrhoea
56
What are the prolactin sparing antipsychotics?
- Quetiapine - Ziprasidone
57
What is the management of antipsychotic induced hyperprolactinaemia?
Switch to a prolactin sparing agent and add in aripiprazole (partial dopamine agonist)
58
What is the QT interval corrected for?
Heart rate - Typically using the Bazett's formula - <440ms in males, <470ms in females
59
What is QT prolongation a risk factor for?
Developing cardiac arrhythmias - Polymorphic ventricular tachycardia (Torsade de Pointes) - Risk increases significantly in QTc intervals >500ms
60
Which medications increase the risk of QTc prolongation?
- Citalopram - Venlafaxine - Clarithromycin - Fluconazole - Most antipsychotics
61
Which antipsychotics are most likely to increase QTc prolongation?
High risk: - HDAT - Haloperidol Moderate risk: - Chlorpromazine - Quetiapine - Amisulpride
62
What is neuroleptic malignant syndrome?
- A complication of antipsychotic treatment - Disorder of thermoregulation and neuromotor control
63
What are the risk factors for neuroleptic malignant syndrome?
- High dose typicals - Rapid dose changes - Male gender - Younger age
64
What are the signs and symptoms of neuroleptic malignant syndrome?
- Muscle rigidity - Hyperthermia - Hyporeflexia - Diaphoresis - Autonomic dysregulation - Altered consciousness
65
What's the difference in presentation between neuroleptic malignant syndrome and serotonin syndrome?
Serotonin syndrome leads to hyperreflexia whereas neuroleptic malignant syndrome leads to hyporeflexia Otherwise, they present clinically very similar
66
What are the investigations for neuroleptic malignant syndrome?
- Raised creatine kinase - Leucocytosis - Deranged liver function - Deranged renal function (secondary to rhabdomyolysis from raised CK)
67
What's the management of neuroleptic malignant syndrome?
- Stop causative antipsychotic - Transfer to hospital/ ITU - Support care and fluids - Benzodiazepines (muscle relaxant) - Bromocriptine (dopamine agonist) and Dantrolene (muscle relaxant)
68
Which four abnormalities are observed with extra-pyramidal side effects?
- Parkinsonism - Dystonia - Tardive dyskinesia - Akathisia
69
What does extra-pyramidal side effects refer to?
Movement abnormalities mediated by movement pathways outside of the medullary pyramids (eg. basal ganglia, cerebellum and motor cortex not the corticospinal tract)
70
What causes extra-pyramidal side effects?
Dopamind blocked within the nigrostriatal dopamine pathway
71
What are the symptoms of (psuedo)parkinsonism?
- Stooped posture - Shuffling gait - Rigidity - Bradykinesia - Tremors at rest (pill-rolling)
72
What are the symptoms of acute dystonia?
- Facial grimacing - Involuntary upward eye movement - Muscle spasms of the tongue, face, neck and back (causing the trunk to arch forward) - Laryngeal spasms
73
What are the symptoms of akathisia?
- Restless - Trouble standing still - Paces the floor - Feet in constant motion, rocking back and forth
74
What are the symptoms of tardive dyskinesia?
- 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
What is the difference between parkinsonism and parkinson's disease?
Parkinsonism is generally bilateral, whereas parkinson's disease is typically asymmetrical
76
What scan can be used to determine whether someone has parkinson's disease or drug induced parkinsonism?
Dopamine transporter scan (DAT)
77
What is the management of drug induced parkinsonism?
Switch medicaiton, add in a regular antimuscarinic (procyclidine 5mg)
78
How long after treatment does tardive dyskinesia develop?
Months or years of treatment Chronic blockade of D2 receptors in the basal ganglia causes them to become hypersensitive
79
What is the management of tardive dyskinesia?
- Stop causative agent - Consider tetrabenazine 25mg
80
What is the mechanism of tetrabenazine?
Inhibits vesicular monoamine transporter 2 leading to depletion of dopamine and other monoamines in the CNS
81
How long after commencing treatment does dystonia come on?
Acutely, within hours of starting antipsychotics
82
What is an oculogyric crisis?
Dystonia where the eyes roll upwards
83
What is torticollis?
Dystonia where the head and neck twist to one side
84
What is laryngeal dystonia?
Dystonia of the larynx that can compromise the airway and be life threatening
85
What is the management for dystonia?
Anticholinergics (eg. procyclidine 5-10mg PO or IM)
86
What is akathisia?
A sense of internal restlessness where the patient feels compelled to move, rock, fidget or pace around
87
How long after starting treatment does akathisia occur?
Within days - weeks of starting or increasing an antipsychotic
88
What is the management of akathisia?
Change medication to: - Diphenhydramine (sedating antihistamine) - Propranolol - Low dose benzodiazepines
89
What is metabolic syndrome?
Antipsychotics, particularly acting on H1 receptors, can cause weight gain, dyslipidaemia and insulin insensitivity
90
What's the management for metabolic syndrome?
- Monitor weight, BP, lipids and HbA1C - Treat complications - Promote healthy eating and exercise
91
Why should SSRI and NSAIDs not be prescribed together?
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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