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Mental Health > Antipsychotic Pharmacotherapy > Flashcards

Antipsychotic Pharmacotherapy Flashcards

1
Q

The 5 major receptor targets of AP’s are…

A

Dopamine (D2)
5HT2a
Muscarinic
Alpha-1
Histaminic-1

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2
Q

Majority of 1st generation AP’s primarily target these receptors:

A

Strong D2 receptor antagonism
“dirty” - mixed receptor affinity at alpha, muscarinic, and histamine receptors

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3
Q

Majority of 2nd generation AP’s primarily target these receptors:

A

D2 receptor antagonism
5HT2A/2C antagonism
“dirty” - mixed receptor affinity at alpha, muscarinic, histamine receptors

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4
Q

Majority of 3rd generation AP’s primarily target these receptors:

A

D2 receptor partial agonism
5HT2A antagonism
5HT1A/2C partial agonism

And additional receptor effects

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5
Q

1st generation AP’s are associated with higher rates of this AE…

A

Movement adverse effects

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6
Q

2nd generation AP’s are associated with higher rates of this AE…

A

Metabolic adverse effects

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7
Q

3rd generation AP’s are associated with higher rates of this AE…

A

Akathisia

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8
Q

Despite grouping of AP’s, they are…

A

Very different from each other; receptor profiles relate to tolerability and differences in metabolic pathways are important for drug interactions

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9
Q

Overall efficacy of AP’s is…

EXCEPT FOR??

A

Similar - except for clozapine

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10
Q

D2 antagonism’s therapeutic effect is…

A

The antipsychotic effect - improvement in positive symptoms

Blocking dopamine in the mesolimbic pathway

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11
Q

AE’s that may result from D2 antagonism includes…

A

EPS
Elevated prolactin: gynecomastia, amenorrhea, impotence, osteoporosis - sexual dysfunction
Worsening of negative symptoms

Nigrostriatal and tuberoinfundibular dopamine blockade

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12
Q

5HT therapeutic effect is…

Some are antagonistic, and some are agonistic…

A

2A/2C antagonism: antipsychotic effect (theoretically improve negative symptoms via increased dopamine release in mesocortical pathway)
1A agonism: anxiolytic

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13
Q

AE’s that may result from 5HT receptor interaction includes…

A

Sedation
Hypotension
Sexual dysfunction

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14
Q

Alpha1/2 antagonism therapeutic effects include…

A

None

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15
Q

AE’s associated with alpha1/2 receptors include…

A

Alpha1 - Sedation, hypotension, dizziness, reflex tachycardia, incontinence, drooling
Alpha2 - sexual dysfunction

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16
Q

Muscarinic antagonism therapeutic effects include…

A

None - perhaps potentiation of drugs that have anticholinergic properties

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17
Q

AE’s that result from muscarinic antagonism include…

Anticholinergic !

A

Dry mouth
Blurred vision
Constipation
Urinary retention
Confusion/memory disturbance

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18
Q

Histamine antagonism therapeutic effects include…

A

None - May potentiate effect of other CNS depressant drugs

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19
Q

AE’s that result from histamine antagonism include…

A

Sedation, drowsiness
Postural hypotension
Weight gain

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20
Q

High potency 1st generation AP’s have higher risk of ____ but weaker ____

A

Higher risk of movement disorders, but weaker anticholinergic effects

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21
Q

Common high potency 1st generation AP’s include…

A

Haloperidol
Flupenthixol
Fluphenazine
Perphenazine

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22
Q

Low potency 1st generation AP’s have lower risk of ____ but stronger ____

A

Lower risk of movement disorders, but stronger anticholinergic effects (highly sedating)

Metabolic effects are stronger due to stronger anticholinergic

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23
Q

Common low potency 1st generation AP’s include…

A

Chlorpromazine
Methotrimeprazine

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24
Q

2nd generation AP’s have lower risk of ____ but higher risk of ____

A

Lower risk of movement disorders, but higher risk of metabolic AE’s

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25
Q

Metabolic AE’s may include…

A

Lipid dysfunction
Development of diabetes or HTN
Obesity

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26
Q

Risperidone has high affinity for the following receptors:

A

Dopamine, serotonin, and alpha-adrenergic receptors

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27
Q

Initial dosing of risperidone is…

A

1-2mg/day, once daily or BID

May start at 0.5mg for elderly or those with co-morbidities

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28
Q

Regular doses of risperidone are…

A

4-6mg/day

No higher; 1st generation features at over 8mg/day

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29
Q

Different formulations of risperidone include…

A

Oral solution
Oral tablets
Orally disintegrating tablets
Long acting injectable

Switching to injectable would require overlap with oral risperidone for 3 weeks

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30
Q

When considering 2nd generation AE’s, we can consider the AE’s related to receptors, such as…

Consider the 5 receptors and AE’s caused when affected

A

Alpha-blockade: Dizziness, sedation, orthostatic hypotension
Dopamine-blockade: Worsening of negative symptoms, EPS, prolactin
Muscarinic-blockade: Anticholinergic + metabolic effects
Histaminic-blockade: Anticholinergic + metabolic effects

Serotonin tries to help improve negative symptoms, but clinically has not seen much benefit - adds to sedation, hypotension, sexual dysfunction

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31
Q

Risperidone is unique in that it has low/no affinity for…

A

Low: alpha2, histamine
No affinity for muscarinic
No anticholinergic, lower rate of sedation

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32
Q

Aside from typical AP AE’s, unique AE’s with risperidone include…

A

Weight gain risk is lower vs. other 2nd gen AP’s
Increased risk of prolactin/sexual dysfunction and EPS vs. other 2nd gen AP’s
Headache, rhinitis, anxiety
QT Prolongation

NO anticholinergic, but may still be sedating from histamine action

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33
Q

Important drug interactions for risperidone include…

A

Pharmacodynamic interactions with other CNS depressants + QTc prolonging agents
3A4/2D6 interactions

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34
Q

Paliperidone is the primary active metabolite of…

A

Risperidone

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35
Q

Dosing forms of paliperidone includes…

A

Tablets
Long-acting injectable

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36
Q

Paliperidone AE’s and DI’s are quite similar to risperidone, but some are more pronounced than others, such as…

A

Less risk of orthostatic hypotension, weight gain
More risk of insomnia
Similar risk of prolactin/sexual dysfunction

Minimal risk of DI’s compared to risperidone

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37
Q

Olanzapine is often not initially used due to…

A

Metabolic AE’s - A LOT of histamine/muscarinic blockade

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38
Q

Initial dosing of olanzapine is usually…

A

5-10mg at bedtime

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39
Q

Usual dosing of olanzapine is…

A

10-20mg once daily

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40
Q

Dosing formulations of olanzapine includes…

A

Tablets
Orally disintegrating tablets
Short or long-acting injectable

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41
Q

Aside from typical AP AE’s, unique AE’s with olanzapine includes…

A

Weight gain - increased risk of T2DM and/or dyslipidemia compared to other 2nd gen AP’s
Dose-dependent risk of EPS, especially akathisia
QT Prolongation

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42
Q

Important DI’s with olanzapine includes…

A

Smoking - will lower olanzapine levels
1A2 inhibitors/inducers
Pharmacodynamic interactions with drugs of similar actions

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43
Q

2nd generation AP’s include the following drugs…

A

Risperidone, paliperidone
Olanzapine
Ziprasidone
Asenapine
Lurasidone
Clozapine

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44
Q

The 2 quetiapine formulations include…

A

XR (once daily)
IR (BID)

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45
Q

XR quetiapine for psychosis is dosed as follows…

A

1st day: 300mg HS
2nd day: 600mg HS
After day 2: up to 800mg HS

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46
Q

IR quetiapine for psychosis is dosed as follows…

A

25mg BID, increasing q4-7 days up to 400mg po BID

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47
Q

Lower doses of quetiapine are used for ____, because…

A

Insomnia, bipolar, depression, anxiety… Different doses have different affinities for different receptors

~50mg primarily histamine blockade
~300mg includes serotonin receptors

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48
Q

Aside from typical AP AE’s, unique AE’s with quetiapine at high doses include…

A

Increased risk of T2DM and dyslipidemia vs. other 2nd gen AP’s
May reduce thyroid hormone levels
QT Prolongation

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49
Q

Important DI’s with quetiapine include…

A

Pharmacodynamic interactions; CNS depressants, QTc prolonging agents
3A4 interactions

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50
Q

Ziprasidone is not often used due to…

A

The need for high food intake with it

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51
Q

Ziprasidone needs to be administered with ____, because…

A

WITH FOOD: >500 kcal to maximize absorption and therapeutic effect

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52
Q

Initial dosing of ziprasidone is…

A

40mg BID; 20mg BID for antipsychotic naive first episode psychosis patients

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53
Q

Ziprasidone-induced “activation” syndrome includes symptoms such as…

A

Anxiety, restlessness, insomnia, hypomanic-like symptoms

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54
Q

Ziprasidone-induced activation syndrome usually develops…

A

After treatment initiation and occur at the lower end of the dosage range

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55
Q

Ziprasidone-induced activation syndrome can be avoided by…

A

Rapidly titrating in the first week, up to 120-160 mg/day especially in bipolar disorder or agitated/irritable patients

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56
Q

Aside from typical AP AE’s, unique AE’s with ziprasidone include…

A

Less hyperglycemia/dyslipidema risk vs. other 2nd gen AP’s
Higher risk of QT prolongation
Dyspepsia, nausea, constipation

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57
Q

Important DI’s with ziprasidone include…

A

Pharmacodynamic interactions; CNS depressants, QTc prolongation
3A4 Inducers/inhibitors

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58
Q

Asenapine is EDS for bipolar but is not covered for us in schizophrenia because…

A

Superiority vs. placebo was not clearly demonstrated, therefore is not clinically used for schizophrenia

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59
Q

Dosing of asenapine is…

A

Initial 5mg BID, up to 10mg BID

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60
Q

Dosing formulation of asenapine is…

A

Sublingual tablets

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61
Q

Aside from typical AP AE’s, unique AE’s with asenapine includes…

A

Mouth numbness x 1hr post dose
Minimal effect on weight, glucose, lipids
Headache, dizziness
QT prolongation

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62
Q

Important DI’s with asenapine includes…

A

PD with CNS depressants, QTc prolonging agents

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63
Q

Luraisdone is not used often for schizophrenia in clinical practice, since…

A

Efficacy has only been established in studies up to 6 weeks

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64
Q

Lurasidone has a better AE profile than most 2nd gen AP’s, since…

A

Little to no metabolic concerns
Still some EPS, prolactin, sedation, QTc, -typical AP AE’s, but likely less concerning

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65
Q

Important DI’s with lurasidone includes…

A

PD interactions with CNS depressants and QTc prolonging agents
3A4 inhibitors + inducers

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66
Q

Dosing of lurasidone is…

A

40mg daily, titrated up to 120-160 mg daily

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67
Q

Lurasidone administration is unique like zipraidone in that…

A

Food is needed to increase bioavailability (350 kcal)

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68
Q

3rd generation AP’s include these three drugs…

A

Aripiprazole
Brexpiprazole
Cariprazine

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69
Q

3rd generation AP’s are unique in that they are dopamine ____

A

Partial agonists

70
Q

Dopamine partial agonists are unique in that they partially…

AKA Dopamine system stabilizer

A

Activate dopamine receptor output, and cause stabilizing balance between stimulation and blockade of dopamine receptors

High levels of dopamine = antagonist
Low levels of dopamine = agonist

71
Q

3rd generation AP’s have a lower risk of ____, but higher rates of ____

A

Lower risk of metabolic + movement AE’s, but higher rates of akathisia

Aripiprazole&raquo_space; Brexpiprazole

72
Q

Dosing of oral aripiprazole is…

A

10-15mg po once daily; max of 30mg/day

73
Q

Key factor for aripiprazole titration is that the half-life is ____, so we cannot increase dose faster than ______

A

Half-life is 75 hours; cannot increase dose faster than 2 weeks

74
Q

Dosing of long-acting aripiprazole is…

A

Long-acting injectable 400mg IM q4weeks

May reduce down to 300mg IM q4weeks when stable, or adverse effects

75
Q

When choosing to initiate depot aripiprazole, we need to continue oral dosing for..

76
Q

Aside from typical AP AE’s, unique AE’s with aripiprazole includes…

A

Akathisia
Some anxiety
Headache, GI complaints, insomnia
Minimal weight gain :)
Suicidal behaviour
QT prolongation

77
Q

DI’s with aripiprazole revolve around…

A

CYP 2D6 and 3A4

78
Q

Brexpiprazole is similar to aripiprazole in AE’s except for…

A

Less risk of akathisia

79
Q

Half-life of brexpiprazole is around…

80
Q

Target dosing of brexpiprazole for schizophrenia is…

A

2-4mg/day

If MDD add-on: 0.5-2mg daily

81
Q

Dosing of brexpiprazole for schizophrenia should be initiated at…

82
Q

Cariprazine is unique in that it targets…

A

D2 + D3 - partial agonist
5HT1A - partial agonist
5HT2A + 2B - antagonist

83
Q

D3 receptors are associated with…

A

Mood, cognition, addictive behaviours, and reward behaviours

84
Q

Partial agonism of the D3 receptor may help…

A

Improve negative symptoms + cognitive impairment of schizophrenia

85
Q

Important PK parameters with cariprazine involve…

A

Highly protein bound
Extensively metabolized by CYP3A4 - affected by inducers/inhibitors
Has active metabolites that extend half-life

86
Q

The downside with cariprazine is that trials did not…

A

Detect clinically meaningful responses for efficacy in improving negative symptoms compared to placebo
No direct comparative evidence vs. other antipsychotics

87
Q

To summarize evidence of cariprazine so far, it may be effective in schizophrenia for treatment of…

A

Acute exacerbations, and prevention of relapse after acute exacberations
Implications for negative symptoms of schizophrenia

MORE direct comparative evidence and research is needed

88
Q

1st generation AP’s have shown higher discontinuation rates due to…

A

Adverse effects (EPS)
Lack of treatment effect

89
Q

____ are the prefered agents for treatment of patients with early psychosis, due to ______

A

2nd generation AP’s, due to significant increased risk of EPS with 1st generation AP’s

90
Q

When selecting an AP, we should individualize to the patient based on factors such as…

A

Symptomatology
AE’s
DI’s
Cost
Convenience

91
Q

If oral AP’s are effective and tolerated, we could…

A
  1. Continue with oral therapy
  2. Switch to long-acting injectable depot
92
Q

Benefit of LAIA’s is…

A

Improved adherence; given q2-4 weeks

93
Q

LAIA’s can be considered if a patient…

A

Relapses due to non-adherence
Or if they simply prefer the injection

94
Q

Proven benefits of LAIA’s include…

A

Lower risk of relapse
Decreased hospitalization rates
Decreased patient/caregiver burden
Improved adherence

95
Q

Before starting a patient on LAIA, we need to…

A

Ensure tolerability, with oral formulation first
Double check how long to overlap with oral formulation

96
Q

The only 3rd generation AP that can be given depot is…

A

Aripiprazole

97
Q

Does aripiprazole require overlap from oral to depot formulation?

A

Yes, 2 weeks

98
Q

2nd gen AP’s that can be given as depot include…

A

Paliperidone
Risperidone

99
Q

Paliperidone is unique in that it has two depot formulations that differ by…

A

Time of administration. One is every 1 month, and another is every 3 months.

100
Q

Do 2nd gen AP require overlap from oral to depot?

A

Paliperidone does not. Risperidone does, for 3 weeks

101
Q

1st gen AP in depot formulations include ____, however…

A

Flupenthixol, haloperidol, and zuclopenthixol. These should not be used unless all other options are exhausted

102
Q

General monitoring guidelines for all AP’s include…

A

Vitals
Behaviours
AE’s - CNS changes, anticholinergic, EPS, hyperprolactin
CBC, LFT’s, ECG if cardiac risk factors or QT prolonging drugs

Will depend on the agent chosen

103
Q

Cloazpine has most distincitve activity for these receptors…

A

D4
5-HT2A
Alpha-1
Muscarinic

104
Q

Common AE’s with clozapine include…

THINK OF THE RECEPTORS

A

Anticholinergic (Constipation, blurred vision, drowsiness, dizziness)
Metabolic (weight gain, increased cholesterol, BG)
Alpha-1 (tachycardia, orthostatic hypotension, dizziness, drooling)

105
Q

Serious AE’s with clozapine include…

A

Agranulocytosis
Myocarditis/cardiomyopathy
Severe constipation
Seizures
Neuroleptic malignant syndrome

106
Q

Clozapine-induced agranulocytosis is…

A

A dangerously low neutrophil count - highly increases infection risk

107
Q

Clozapine-induced myocarditis is…

A

Inflammation of the heart muscle - allergic reaction

High mortality rate

108
Q

Severe constipation caused by clozapine can lead to…

A

Adynamic ileus

High mortality rate; monitor bowel functioning

Peristalsis stops in the GI tract, can rupture

109
Q

Agranulocyotis with clozapine is most likely to occur in…

Timeframe

A

The first 6 months of treatment

110
Q

Myocarditis with clozapine is most likely to occur in…

Timeframe

A

The first 4-8 weeks of treatment

111
Q

Cardiomyopathy with clozapine is most likely to occur in…

A

Months to years of treatment

112
Q

The difference between myocarditis and cardiomyopathy is…

A

Myocarditis = allergic-like reaction causing inflammation
Cardiomyopathy = Disease of heart muscle, making it harder to pump blood

113
Q

Clinical presentation of myocarditis and cardiomyopathy are similar when beginning, and this may include…

A

Orthostatic blood pressure changes
Fatigue, decreased exercise tolerance
Chest pain, discomfort, palpitations with increased heart rate
SOB
Peripheral edema
Fever

114
Q

Lab markers that can indicate cardiomyopathy or myocarditis include…

A

CRP - non-specific for inflammation
Troponin - protein in heart muscle (that typically should not be in the blood)

115
Q

Monitoring for agranulocytosis with clozapine requires specific blood tests, which is…

A

The absolute neutrophil count - need to order CBC with differential, vs. just a CBC

116
Q

Clozapine can ONLY be used and dispensed if…

A

Patient is actively registered with a clozapine registry, and hematological monitoring can be guaranteed

Remember CBC with diff - neutrophils

117
Q

How often does blood work need to be done for clozapine monitoring?

A

Weekly for first 6 months
Then once every 2 weeks if green light maintained and clinically stable
Then once every 4 weeks if green light for another 6 months

118
Q

If a patient stops clozapine, do they still need to monitor their neutrophil counts?

A

Yes, for 4 weeks after stopping

119
Q

Clozapine dosing needs to be re-titrated if missed for longer than…

120
Q

If clozapine therapy is disrupted for more than ____, blood testing needs to be done…

How frequently?

A

3+ days; blood testing resumed weekly for an additional 6 weeks

121
Q

“Green” neutrophil count with clozapine monitoring is above…

A

2.0 x 10^9/L

122
Q

“Yellow” neutrophil count with clozapine monitoring is…

How often do we test if yellow?

A

In range of 1.5-2.0 x 10^9/L

Test at least twice weekly until ANC stabilizes or increases

Can continue to dispense in meantime

123
Q

“Red” neutrophil count with clozapine monitoring is…

What do we do next?

A

Below 1.5 x 10^9/L

Immedaitely withhold and discontinue if confirmed. Monitor for signs of infection

124
Q

Clozapine is non-rechallengable in regards to agranulocytosis, whihch means…

A

Patient must stop and cannot ever restart therapy if they were in “red” neutrophil count

Still requires the weekly CBC x 4 weeks when stopped

125
Q

The amount of clozapine dispensed must align with…

A

The frequency of clozapine bloodwork

q2weekly blood work can only have 2 weeks of clozapine dispensed from the pharmacy

126
Q

Initial dosing and titration of clozapine is usually…

A

12.5-25mg/day PO; increase by 12.5-25mg on 2nd day, then 25-50mg daily PO depending on tolerance

Minimize risk of orthostatic hypotension and sedation

127
Q

Usual dosing of clozapine is ____, and can go up to…

A

300-600mg PO/day after 2 weeks - max of 900mg PO/day

OD, BID, or TID

128
Q

An important drug interaction with clozapine is…

A

SMOKING - induces 1A2, reducing levels
Also consider anything that may affect CYP 1A2

129
Q

Clozapine in relation to suicide risk has shown…

A

A reduction in risk of suicide in schizophrenia/schizoaffective patients

NNT = 13

130
Q

Extrapyramidal system differs from pyramidal system mainly by…

A

Pyramidal = Voluntary movement
Extrapyramidal = Involuntary movement

131
Q

Acute extrapyramidal effects usually onset within ____ days, and are mostly due to…

A

Within 30 days; mostly due to dopamine (D2) blockade

132
Q

Treatment of acute EPS is usually with…

A

Antiparkinsonian drugs - centrally acting anticholinergics (cross BBB, block excitatory muscarinic pathways, restore dopamine/ACh balance disrupted by AP’s)

133
Q

Treating acute EPS symptoms is important to prevent…

A

Tardive symptoms

134
Q

Tardive symptoms onset is usually after…

A

Months/years of treatment, especially if drug dose is decreased or discontinued; and tend to persist for years or decades

Can may become permanent even with removal of AP; precise pathophysiology remains unclear

135
Q

FDA-approved drugs for treating tardive dyskinesia includes…

A

Valbenazine
Deutetrabenazine

DOESN’T actually treat TD, just lowers AE’s. Also isn’t available in Canada yet; therefore PREVENTION IS KEY

136
Q

Important factors to consider with TD prevention include…

All related to AP’s, and dose

A

Early recognition + discontinuation of offending AP (not always an option)
Dose reduction/use of lowest effective dose (weigh against risk of relapse)
SLOW tapers with AP to avoid withdrawal emergent symptoms
Switch to atypical AP’s

137
Q

Acute EPS effects may include…

A

Dystonia
Akathisia
Pseudoparkinsonism
Pisa syndrome, rabbit syndrome

138
Q

Physical symptoms of acute dystonia includes…

A

Torsions and spasms of muscle groups - mostly affecting the muscles of the head and neck
Painful and spasmodic

139
Q

Psychological symptoms that can occur with acute dystonias include…

A

Anxiety, fear, panic
Dysphoria
Repetitive meaningless thoughts

140
Q

Time of onset for acute dystonia in relation to AP treatment is usually…

A

Within 24-48 hours of the 1st dose; 90% occur within 1st week of treatment

141
Q

Acute dystonia can be life-threatening because…

A

Dystonia relating to laryngeal/pharyngeal pathways may stop swallowing/breathing reflexes

142
Q

With acute dystonia, oculogyria may be present, which is…

A

Sustained upward and lateral deviation of the eyes

143
Q

Treatment options for acute dystonia includes…

A

1st line: IM benztropine
IM diphenhydramine, sublingual lorazepam

144
Q

Physical symptoms of akathisia include…

A

Motor restlessness (fidgeting, pacing, rocking, inability to be still)
Respiratory - dyspnea or breathing discomfort

145
Q

Psychological symptoms of akathisia include…

A

Restlessness, intense urges to move
Irritability, agitation, violent outbursts
Feeling uncomfrotable, “antsy”
Can contribute to suicide and violence

146
Q

Proposed risk factors for developing acute akathisia include…

A

High potency 1st gen AP’s, and 3rd gen AP’s
Anxiety, mood disorders
Stimulant usage; caffeine

147
Q

Time of onset of acute akathisia in relation to AP treatment is…

A

Hours-days; 90% occur within first 6 weeks of treatment and may continue throughout entire treatment

148
Q

Treatment options for acute akathisia include…

A

Reduce dose (slow taper) or change AP
Trial of benzodiazepines, non-selective beta-blocker, or mirtazapine

149
Q

Physical symptoms of acute pseudoparkinsonism include…

A

Tremor
Cogwheel rigidity
Bradykinesia

150
Q

Presentation of bradykinesia may include…

A

Mask-like facial expression
Diminished/absent arm swing
Shuffling gait; slowness of movement
Stooped posture

151
Q

Psychological symptoms of pseudoparkinsonism include…

A

Slowed thinking
Fatigue
Cognitive impairment, drowsiness

152
Q

Time of onset of pseudoparkinsonism in relation to AP treatment is…

A

Acute - 90% occur within first 6 weeks of treatment and may continue through entire treatment

153
Q

Treatment options for pseudoparkinsonism include…

A

Dose reduction, or changing AP
Antiparkinsonian drugs - anticholinergics (benztropine, diqphenhydramine, procyclidine, trihexyphenidyl)

154
Q

Pisa syndrome is when the patient is…

A

Leaning to one side

155
Q

Onset of pisa syndrome can be…

A

Either acute or tardive; usually ignored by patients

156
Q

Rabbit syndrome is defined by…

A

Fine tremor of the lower lip

157
Q

Onset of rabbit syndrome is usually…

A

After months of therapy; often ignored by patients

158
Q

Treatment of pisa and rabbit syndrome is with…

A

Antiparkinsonian drugs - benztropine, procyclidine, trihexyphenidyl

159
Q

Physical symptoms of tardive dyskinesia may include…

A

Involuntary, abnormal movement of the face, lips, jaw, tongue, eyelids, limbs, trunk, neck, or respiratory system

Can co-exist with parkinsonism and akathesia

160
Q

Psychological symptoms of tardive dyskinesia may include…

A

Cognitive impairment
Distress (talking, eating, swallowing)
Embarassment/anxiety

161
Q

Onset of tardive dyskinesia is usually…

A

After 3 or more months of therapy in adults; earlier in elderly

162
Q

Some proposed risk factors for tardive dyskinesia include…

A

40+, female
History of severe EPS early in treatment
Chronic usage of AP’s (1st gen > others), or high doses of dopamine agonists
Presence of mood component or cognitive impairment
Diabetes
Alcohol/drug abuse

163
Q

Tardive dyskinesia symptoms may be persistent + permanent, but discontinuation of AP early ____

A

Increases chance of remission

Spontaneous remission in 14-24% after 5 years

164
Q

Are there any approved options for treating tardive dyskinesia?

A

No - valbenazine and deutetrabenazine are not available in Canada
May possibly switch to 2nd gen or 3rd gen AP, or try options such as clonzaepam, tetrabenazine, levetiracetam…

165
Q

A good way to measure severity of tardive dyskinesia is using this scale…

A

AIMS - Abnormal Involuntary Movement Scale

166
Q

A good way to measure severity of akathisia is using this scale…

A

BARS - Barnes Akathisia Rating Scale

167
Q

Proposed risk factors for acute dystonia may include…

Contains both modifable risk factors and uncontrollable risk factors

A

Young male, AP naive, high potency FGA
Rapid dose increases
Prior dystonic reaction
Dehydration
Recent cocaine usage
Hypocalcemia, hyperthyroidism

168
Q

Tardive dystonia and akathisia are similar to acute presentations, except…

A

THey are persistent and may be permanent even with removal of the AP

169
Q

Neuroleptic Malignant Syndrome (NMS) is a type of ____ that is…

A

EPS that is acute and life-threatening, which can occur with any AP at any dose

VERY rare, idiosyncratic

170
Q

Physical manifestations of NMS include…

A

Severe muscle rigidity, fever, altered mental status, autonomic instability, elevated WBC and creatine kinase

171
Q

When can NMS occur with AP usage?

A

Anytime - often early in treatment

172
Q

Treatment for NMS mainly revolves around…

A

Stopping AP immediately, and providing supportive care
Bromocriptine may be used (D2 receptor agonist), dantrolene for malignant hyperthermia

Mental Health (11 decks)

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