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Psychopharmacology > Side effects > Flashcards

Side effects Flashcards

1
Q

What percent of patients exposed to typical antipsychotics develop acute dystonia?

A

10%

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2
Q

Dystonia is more likely when in treatment?

A

early stages of treatment
or after an increase in dose
can also occur on drug withdrawal.

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3
Q

Torticollis and oculogyric spasm are examples of what

A

dystonia

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4
Q

Drugs most associated with priapism?

A

Trazodone
Chlorpromazine
Thioridazine

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5
Q

Dystonias resulting from antipsychotic treatment are most common in which group

A

Young men

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6
Q

Which antipsychotics should be avoided in renal failure

A

sulpiride and amisulpride

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7
Q

Dystonia - time taken to develop?

A

Acute dystonia can develop within minutes or hours of starting antipsychotics

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8
Q

Prevalance of pseudo parkinsonism eg tremor?

A

Approximately 20%

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9
Q

Time taken for symptoms of psuedo parkinsonism eg tremor to develop?

A

Days to weeks after antipsychotic started or dose increased

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10
Q

Prevalance of akisthesia?

A

Approximately 25%

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11
Q

Prevelence of tardive dyskinesia?

A

5% of patients per year of antipsychotic exposure

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12
Q

Who is tardive dyskinesia most common in?

A
  • elderly women
  • those with affective illness
  • those who have had EPSE early on in treatment
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13
Q

Time taken for tardive dyskinesia to develop?

A

Months to years

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14
Q

Time taken for akisthesia to develop?

A

Hours to weeks

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15
Q

Treatment for dystonia or pseudo parkinsonism

A

Anticholinergic drugs (e.g. trihexyphenidyl, procyclidine, orphenadrine, benztropine. The antihistamine, diphenhydramine, is also used due to its anticholinergic properties)
Switching to alternative antipsychotic
Botulinum toxin in dystonia

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16
Q

Treatment for akisthesia?

A
  • Reduce the dose or Switching to alternative antipsychotic (quetiapine/ olanzapine)
  • Propranolol
  • Mirtazapine or mianserin (low dose)
  • Anticholinergic drugs ( (e.g. trihexyphenidyl, procyclidine, orphenadrine, benztropine)
  • Cyproheptadine
  • Benzodiazepine
  • Clonidine
17
Q

Treatment for tardive dyskinesia

A

Stop anticholinergic (if prescribed)
Reduce the dose
Switch to an atypical (clozapine and quetiapine have best evidence)
Tetrabenazine
Ginkgo biloba

18
Q

In addition to patients being on antiPs, when may you also see EPSEs?

A

also been reported in the use of SSRI’s and tricyclics (TCA).
Higher rates are also seen in patients with schizophrenia who have never received medication suggesting EPSE may be a feature of the illness itself
can also occur when antipsychotics are discontinued (withdrawal dystonia).

19
Q

EPSE’s are thought to be due to what action and where?

A

Antagonism of dopaminergic D2 receptors in the basal ganglia.
The cells of the basal ganglia are referred to as extra pyramidal as they are separate from the axons of the pyramidal cells that connect the cortex to the spinal cord.

20
Q

What is cervical muscles spasms, resulting in a twisted posturing of the neck.

A

torticollis

21
Q

What is contraction of the jaw musculature.

A

trismus/lockjaw

22
Q

What is the name for arched posturing of the head, trunk, and extremities.

A

Opisthotonus

23
Q

Dystonia leading to difficulty breathing?

A

Laryngeal dystonia

24
Q

Involuntary contraction of one or more of the extraocular muscles, which may result in a fixed gaze with diplopia?

A

Oculogyric crises

25
Q

Which antiP carries least risk of EPSEs?

A

clozapine

26
Q

Which antiP carries highest risk of EPSEs?

A

haloperidol

27
Q

Which is the most resistant EPSE to treat?

A

akisthesia

28
Q

What part of body is affected in tardive dyskinesia?

A

the face (3/4 of affected individuals) but also affects the limbs (1/2 of affected) and the trunk (1/4 of affected).

29
Q

When does TD tend to occur

A

when a person has been on neuroleptics for months to years. This time period can be as short as one month in the elderly.

30
Q

Where does TD occur in the body

A
31
Q

What is the most prominent hypothesis for TD?

A

post-synaptic dopamine (D2) receptor supersensitivity. This is thought to result from chronic blockade of receptors.

32
Q

Non modifiable risk factors for TD

A

Advancing age
Female sex
Ethnicity (White and African decent)
Longer illness duration
Intellectual disability and brain damage
Negative symptoms in schizophrenia
Mood disorders

33
Q

Modifiable risk factors for TD

A

Diabetes
Smoking
Alocohol and substance misuse
FGA vs SGA treatment
Higher antipsychotic dose
Anticholinergic co-treatment
Akathisia

34
Q

How do TD fluctuate

A

The movements fluctuate over time, increase with emotional arousal, decrease with relaxation and disappear with sleep.
They also decrease when affected muscles are used for voluntary tasks. Distracting tasks such as mental arithmetic also worsen the movements.

35
Q

Add on treatment options for TD?

A

Tetrabenazine VMAT-2* inhibitor - only licensed treatment for TD in UK
Vitamin E Evidence for slowing rate of TD
Amantadine Rarely used but apparently effective

36
Q

Most resistant EPSE

A

akisthesia

Psychopharmacology (19 decks)

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