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8. Psychopharmacology > Antipsychotics > Flashcards

Antipsychotics Flashcards

1
Q

name the first antipsychotic… when was it introduced

A

chlorpromazine –> 1955

*antipsychotics considered the single greatest advance in the treatment of mental disorders

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2
Q

names of the psychiatrists who introduced chlorpromazine as the first antipsychotic

A

pierre deniker

jean delay

*french

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3
Q

what dopaminergic pathway to antipsychotics target to treat the positive symptoms of schizophrenia

A

mesolimbic

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4
Q

list the 4 key dopaminergic pathways that antipsychotics affect

A

mesocortical

mesolimbic

nigrostriatal

tuberoinfundibular

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5
Q

what areas does the mesocortical pathway connect

A

prefrontal cortex

to the

ventral tegmental areas

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6
Q

what areas does the mesolimbic pathway connect

A

nucleus accumbens

to the

ventral tegmental area

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7
Q

what areas does the nigrostriatal pathway connect

A

substantia nigra

to the

basal ganglia (striatum)

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8
Q

what areas does the tuberoinfundibular pathway connect

A

hypothalamus–arcuate (infundibular) nucleus

to the

hypothalamus–median eminence

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9
Q

why do we care about the MESOCORTICAL pathway in schizophrenia

A

DECREASED dopamine leads to NEGATIVE SYMPTOMS

cognitive symptoms are also thought to be due to a HYPOACTIVE mesocortical pathway

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10
Q

why do we care about the MESOLIMBIC pathway in schizophrenia

A

INCREASED dopamine leading to POSITIVE symptoms

**same pathway for nicotie-reward

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11
Q

why do we care about the NIGROSTRIATAL pathway in schizophrenia

A

also gets blocked by antipsychotics leading to EPS and akathesia

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12
Q

why do we care about the TUBEROINFUNDIBULAR pathway in schizophrenia

A

the decrease of dopamine in this pathway (thru use of antipsychotics) can cause elevated PROLACTIN

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13
Q

what is the regular role of dopamine in the tuberoinfundibular pathway

A

to tonically inhibit prolactin release

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14
Q

where is the tuberoinfundibular pathway found

A

entirely in the hypothalamus

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15
Q

what is the physiologic action of the normal mesolimbic pathway

A

motivation

emotion

reward

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16
Q

what is the physiologic action of the normal mesocortical pathway

A

cognition and executive function (dorsolateral PFC)

emotion and affect (ventromedial PFC)

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17
Q

the nigrostriatal system contains what % of the brains dopamine

A

about 80%

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18
Q

what two structures make up the striatum

A

caudate and putamen

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19
Q

what is the physiologic action of the normal nigrostriatal pathway

A

motor planning

(dopaminergic neurons stimulate purposeful movement)

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20
Q

the therapeutic action of an antipsychotic occurs when what % of brain dopamine (D2) receptors are occupied

A

65-85%

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21
Q

what happens when more than 80% of D2 receptors are occupied

A

hyperprolactinemia

parkinsonism

*CAN happn

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22
Q

what factors influence the likelihood of a patient experiencing EPS (or other side effects)

A

% receptor occupancy + amount of time the antipsychotic remains bound to the receptor

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23
Q

does serum level of antipsychotics correlate to brain receptor occupancy?

A

no–> due to the blood brain barrier

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24
Q

name an antipsychotic that remains bound to D2 receptors for quite a long time?

name two antipsychotics that are bound to D2 receptors for only a very short time

A

haldol–> bound for about 38 min

clozapine, quetiapine–> bound for about 15 seconds (“kiss and run hypothesis”)

*suggested reason for why haldol has more EPS than clozapine and quetiapine

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25
Q

what does antipsychotic “potency” describe

A

affinity for dopamine receptor

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26
Q

what is the relationship between antipsychotic potency and anticholinergic action? why do we care?

A

all low potency antipsychotics are also more anticholinergic (anti-muscarinic) –> this means low potency antipsychotics have “built in” benztropine

(as benztropine is also anticholinergic med)

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27
Q

list high potency antipsychotics

A

haloperidol

risperidone

flupenthixol

paliperidone

fluphenazine

pimozide

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28
Q

list medium potency antipsychotics

A

loxapine

olanzapine

zuclopenthixol

ziprasidone

perphenazine

aripiprazole

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29
Q

list low potency antipsychotics

A

chorpromazine

quetiapine

methotrimeprazine

clozapine

amisulpride

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30
Q

what is a schema to best understand the most prominent side effects associated with high vs low potency antipsychotics

A

high potency–> higher risk of EPS and hyperprolactinemia
(due to higher affinity for D2); relatively less sedating (lower affinity for H1 receptor)

low potency–> more anticholergic symptoms and more sedating + more constipation (due to more anticholinergic and H1 binding); relatively fewer EPS

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31
Q

how are MOST antipsychotics metabolized

A

by CYP 2D6 and 3A4

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32
Q

clozapine and olanzapine are also metabolized by which CYP enzyme? (in addition to 3A4 and 2D6)

A

1A2

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33
Q

which population has increased CYP metabolism of antipsychotic medications

A

mediterranean

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34
Q

when did SGAs begin to arise

A

1990s

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35
Q

name the trial that showed SGAs were no more effective that FGAs

A

CATIE trial

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36
Q

GENERALLY speaking, what is the difference between SGAs and FGAs

A

FGAs–> higher D2 receptor occupancy–> higher risk of causing EPS

SGAs–> lower D2 occupancy–> lower risk of EPS

*some considerations i.e risperidone which acts like an SGA at low doses but like an FGA at higher doses, due to its high potency

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37
Q

is the FGA/SGA distinction really useful?

A

not really–> distinction is more historical than black and white

more important to look at individual antipsychotics potency, receptor profile, and pharmacokinetics rather than if FGA/SGA

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38
Q

state whether the following is low, mid or high potency:

haloperidol

A

high

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39
Q

state whether the following is low, mid or high potency:

quetiapine

A

low

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40
Q

state whether the following is low, mid or high potency:

clozapine

A

low

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41
Q

state whether the following is low, mid or high potency:

aripiprazole

A

mid

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42
Q

state whether the following is low, mid or high potency:

zuclopenthizol

A

mid

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43
Q

state whether the following is low, mid or high potency:

paliperidone

A

high

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44
Q

state whether the following is low, mid or high potency:

risperidone

A

high

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45
Q

state whether the following is low, mid or high potency:

olanzapine

A

mid

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46
Q

state whether the following is low, mid or high potency:

loxapine

A

mid

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47
Q

state whether the following is low, mid or high potency:

methotrimeprazine

A

low

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48
Q

state whether the following is low, mid or high potency:

ziprasidone

A

mid

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49
Q

state whether the following is low, mid or high potency:

fluphenazine

A

high

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50
Q

state whether the following is low, mid or high potency:

amisulpride

A

low

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51
Q

list common FGAs

A

methotrimeprazine

haldol

chlorpromazine

loxapine

zuclopenthixol

flupentixol

perphenazine

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52
Q

list common SGAs

A

risperidone

paliperidone

aripiprazole

brexpiprazole

lurasidone

olanzapine

quetiapine

ziprasidone

clozapine

amisulpride

pimavanserine

asenapine

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53
Q

how quickly do most people begin responding to antipsychotics

A

within a week

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54
Q

which antipsychotic has the lowest rehospitalization rate

A

clozapine

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55
Q

how has understanding shifted recently in terms of recommended treatment length for those with first episode psychosis

A

compared to standard maintenance treatment regimen, dose reduction or supervised d/c of antipsychotic during early phases of first episode psychosis may lead to HIGHER RELAPSE rate INITIALLY but IMPROVED LONG TERM OUTCOMES

*study has been criticized though

other studies have suggests that up to 40% of those with first episode psychosis may achieve good outcomes with either low or no doses of antipsychotics

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56
Q

what remains the most evidenced based practice for those with first episode schizophrenia

A

for the majority of patients, relapse rates are greater than 80% with med-discontinuation after several years

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57
Q

which medications have the lowest rates of relapse in schizophrenia

A

clozapine and LAIs

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58
Q

how does treatment with an LAI change risk of rehospitalization risk compared to those treated with oral equivalents

A

for those on LAIs, risk is 20-30% of those on oral equivalents

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59
Q

should you switch FGA LAI to SGA LAI if the patient is doing well on FGA LAI?

A

no–> this switch (assuming they are doing well on FGA LAI) puts them at higher risk of treatment discontinuation and weight gain

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60
Q

is treatment with multiple antipsychotic agents generally recommended?

what combo of meds recently suggested superiority over monotherapy?

A

generally, NOT recommended–> generally does not improve clinical response, should try and keep to/switch to monotherapy

*one cohort study recently showed superiority of CLOZAPINE + ARIPIPRAZOLE vs clozapine alone

61
Q

list FGA LAIs available

A

haloperidol decanoate

fluphenazine decanoate

flupenthixol decanoate

zuclopenthixol decanoate

62
Q

dose of haloperidol decanoate IM

A

50-200mg IM q3-4 weeks

63
Q

dose of zuclopenthixol decanoate IM

A

200-500mg IM q1-4 weeks

64
Q

list SGA LAIs available

A

aripiprazole monohydrate–> abilify maintenna

aripiprazole lauroxil–> aristada

olanzapine pamoate–> zyprexa

paliperidone palmitate (multiple formulations)–> invega sustenna, xeplion, invega trinza

risperidone microspheres–> risperidone consta

65
Q

formulations of aripiprazole monohydrate (maintenna) available

A

300mg, 400mg

admin qmonthly

66
Q

what is a consideration when starting abilify maintenna

A

requires 2 weeks of oral dosing (“oral bridging”) with oral abilify

67
Q

formulations avail. of paliperidone palmitate (invega sustenna)

A

39 mg, 78mg, 117mg, 156 mg, 234 mg (prefilled syringes)

admin qmonthly

*oral supplementation not necessary

68
Q

formulations avail. of risperidone consta

A

12.5mg, 25mg, 37.5mg, 50mg

69
Q

what is a consideration when starting risperidone consta

A

requires period of 3 week overlap with oral risperidone

70
Q

how do you switch antipsychotics

A

no difference in clinical outcome if maintain on old antipsychotic while introducing the new one, vs stopping the old one and introducing the new one immediately

71
Q

for those on antipsychotics, when should you monitor:

electrolytes

A

initiation

as clinically indicated thereafter

72
Q

for those on antipsychotics, when should you monitor:

fasting plasma glucose

A

initiation

1 mo if clinically indicated

3 months after initiation

annually thereafter

73
Q

for those on antipsychotics, when should you monitor:

HbA1C

A

initiation

at 3 months

annually thereafter

74
Q

for those on antipsychotics, when should you monitor:

lipid panel

A

initiation

1 mo if clinically indicated

3 months after initiation

annually thereafter

75
Q

for those on antipsychotics, when should you monitor:

BMI

A

at initiation

at 1 month, 3 months, then annually

76
Q

for those on antipsychotics, when should you monitor:

BP

A

initiation

1 mo if clinically indicated

3 months after initiation

annually thereafter

77
Q

for those on antipsychotics, when should you monitor:

EPS exam

A

at initiation, 1 mo, 3 mo, and annually thereafter

78
Q

for those on antipsychotics, when should you monitor:

endocrine function history (gynecomastia, galactorrhea, libido)

A

at initiation, 3 mo, then annually

79
Q

for those on antipsychotics, when should you monitor:

prolactin

A

if clinically indicated

80
Q

for those on antipsychotics, when should you monitor:

ECG (Qtc monitoring)

A

at initiation if clinically indicated

at 3 mo if on multiple QTc prolonging meds

annual if clinically indicated (could also reasonably just do it annually)

81
Q

for those on antipsychotics, when should you monitor:

smoking history

A

initiation, 3 mo, annually thereafter

82
Q

what are the “main” side effects of antipsychotics

A

EPS

sexual side effects

anticholinergic SEs (i.e sedation)

cardiovascular SEs

83
Q

what causes the EPS and sexual side effects associated with antipsychotics

A

potent dopamine receptor blockade

84
Q

what causes the anticholinergic side effects like sedation with antipsychotics

A

histaminergic and muscarinic receptor blockade

85
Q

what causes the cardiovascular side effects of antipsychotics

A

anticholinergic effects and adrenergic blockade

86
Q

who introduced the concept of Neuroleptic Induced Dopamine Supersensitivity Psychosis (DSP)

A

psychiatrist Guy Chouinard in 1980

87
Q

what is the hypothesis behind DSP

A

chronic antipsychotic use leads to the upregulation of dopamine (D2) receptors in the BASAL GANGLIA –>

tardive dyskinesias + tolerance of increasing doses of antipsychotic –>

rebound psychosis could occur with reduction or discontinuation of the antipsychotic (separate from underlying illness)

88
Q

why is the idea of DPS controversial?

A

could be iatrogenic

89
Q

list side effects associated with antipsychotics

A
  1. metabolic syndrome
  2. constipation
  3. sedation
  4. hyperprolactinemia
  5. amenorrhea
  6. sexual dysfunction
  7. hypotension
  8. tachycardia
  9. QTc prolongation
  10. SIADH + hyponatremia
  11. sialorrhea
90
Q

first line management for constipation due to antipsychotic use?

A

use of an osmotic agent–> PEG and/or stimulant laxative such as Senna

*patients on clozapine should have regular bowel monitoring

91
Q

what determines the degree of sedation associated with an antipsychotic

A

affinity of the antipsychotic for the H1 receptor

*generally, low potency antipsychotics are more sedating than higher potency and atypicals are more sedating than typicals

92
Q

rank the following four antipsychotics from most to least sedating (by H1 receptor affinity):
quetiapine
olanzapine
risperidone
clozapine

A

most:
clozapine
olanzapine
quetiapine
risperidone
least

93
Q

how do you manage sedation due to antipsychotics

A

reduce dose or consider a switch to higher potency antipsychotic

94
Q

how might you manage amenorrhea in those on antipsychotics

A

(hyperprolactinemia can result in amenorrhea)

METFORMIN can restore menstruation in obese women with amenorrhea by restoring sex hormone levels and decreasing insulin resistance

95
Q

what causes the sexual dysfunction associated with antipsychotics

A

dopamine blockade and hyperprolactinemia

96
Q

management of sexual dysfunction associated with antipsychotics

A

sildenafil can be considered

97
Q

what causes the hypotension associated with antipsychotics

A

thought to be caused by anticholinergic effects and/or alpha-1 adrenorececptor blockade

98
Q

management of hypotension associated with antipsychotics

A

consider adjusting dose

increasing hydration

change to less anticholinergic agent (ie switch from low to high potency)

99
Q

how do antipsychotics increase the risk of QTc prolongation/ventricular arrthymias

A

blockade of potassium channels and prolongation of QTc

100
Q

is hyponatremia common with antipsychotic use

A

no, its rare

101
Q

how are antipsychotics thought to cause hyponatremia

A

increase AVP release despite normal plasma osmolality–> SIADH–> hyponatremia

102
Q

why do we care about hyponatremia in psychiatry

A

can cause neuropsychiatric symptoms

acute onset hyponatremia can cause delirium and acute behavioural changes

diagnosis of SIADH may be delayed for psychiatric patients

103
Q

what are the four general etiologies of hyponatremia

A
  1. too much water in (water intox)
  2. too little water going out (too much ADH–> SIADH–> can be due to psych meds like antipsychotics)
  3. too little sodium in (“tea and toasters”)
  4. too much sodium going out (multiple causes like diuretics or diarrhea)
104
Q

symptoms of hyponatremia

A

nausea
vomiting
anorexia
disorientation
headache
fatigue
weakness
irritability
lethargy
confusion
muscle cramps

105
Q

what is first line treatment of SAIDH

A

fluid restriction

106
Q

what other type of psych med in particular is known to have SIADH as a potential side effect

A

antidepressants (especially in elderly)

107
Q

what does the QT interval represent

A

the length of cardiac repolarization (i,e time for ventricles to contract and relax)

108
Q

why do we care about the QT interval being long

A

causes heterogeneity in electrical phasing in different ventricular structures of the heart–>

can cause events like ventricular extrasystole and torsades

109
Q

what affects the risk of QT prolongation of a particular med

A

likely dose related

110
Q

is QTc “enough” to determine cardiac risk from QT prolonging medications?

A

its a good general indicator but can be imprecise for determining risk of torsades

best to combine QTc with T wave morphology to better predict risk (i.e involve cardio)–> some people with QTc above recommended limits can still take meds that alter cardiac repolarization without developing torsades

111
Q

under what limit is QTc generally considered normal, and no referral to cardio is recommended (unless other risk factors) when considering starting a QTc prolonging med like antipsychotics

A

under 440ms for men

under 470ms for women

112
Q

at what QTc might you consider reducing dose of QTc prolonging med, or switching to drug of lower effect? would you refer to cardio?

A

440-500ms for men

470-500ms for women

consider referral to cardio

once make changes to med, repeat ECG

113
Q

at what QTc do we really sit up and take notice and refer to cardio

A

above 500ms for both men and women

*repeat the ECG

*stop suspected QT-prolonging agents and switch to drug with less QT effects

*refer to cardio

114
Q

under what conditions would you refer to cardio when starting antipsychotics, even if QT normal

A

if abnormal T wave morphology

115
Q

above what limit is QTc considered “prolonged”

A

above 470ms for men

above 480ms for women

116
Q

list risk factors for QTc prolongation

A
  1. female gender
  2. use of meds primarily metabolized by CYP 3A4 (greater risk for drug-drug interactions)
  3. older age (above 65)
  4. eating disorders
  5. heart disease
  6. electrolyte disturbances (hypokalemia, hypomagnesemia)
  7. renal impairment
117
Q

indicate whether the following antipsychotic is felt to have no effect, low effect, moderate effect or high effect on QTc interval:

loxapine

A

low

118
Q

indicate whether the following antipsychotic is felt to have no effect, low effect, moderate effect or high effect on QTc interval:

brexpiprazole

A

no effect

119
Q

indicate whether the following antipsychotic is felt to have no effect, low effect, moderate effect or high effect on QTc interval:

risperidone

A

moderate to high

120
Q

indicate whether the following antipsychotic is felt to have no effect, low effect, moderate effect or high effect on QTc interval:

paliperidone

A

low

121
Q

indicate whether the following antipsychotic is felt to have no effect, low effect, moderate effect or high effect on QTc interval:

lurasidone

A

no effect

122
Q

indicate whether the following antipsychotic is felt to have no effect, low effect, moderate effect or high effect on QTc interval:

haloperidol

A

moderate

123
Q

indicate whether the following antipsychotic is felt to have no effect, low effect, moderate effect or high effect on QTc interval:

olanzapine

A

moderate

124
Q

indicate whether the following antipsychotic is felt to have no effect, low effect, moderate effect or high effect on QTc interval:

clozapine

A

low

125
Q

indicate whether the following antipsychotic is felt to have no effect, low effect, moderate effect or high effect on QTc interval:

aripiprazole

A

low

126
Q

indicate whether the following antipsychotic is felt to have no effect, low effect, moderate effect or high effect on QTc interval:

quetiapine

A

moderate

127
Q

indicate whether the following antipsychotic is felt to have no effect, low effect, moderate effect or high effect on QTc interval:

asenapine

A

low

128
Q

indicate whether the following antipsychotic is felt to have no effect, low effect, moderate effect or high effect on QTc interval:

amisulpride

A

moderate

129
Q

what medication used to treat OUD has high effect on QTc? (ie tends to prolong Qtc)

A

methadone

130
Q

what illicit substance is also a QTc prolonging agent

A

cocaine

131
Q

if patient is on antipsychotic and QTc is getting prolonged, what antipsychotic might you switch to instead?

A

aripiprazole or lurasidone

132
Q

what should you do if your patients ECG comes back with QTc above 500ms

A

order Mg and K+ levels

if these levels are LOW, replace and redo ECG

*try to keep K+ above 4 and Mg above 1.0 if you’re worried about QTc prolongation

133
Q

how do antipsychotics affect seizure threshold

A

lower it

134
Q

which typical antipsychotic has the highest risk of inducing seizures

A

chorpromazine

135
Q

which typical antipsychotics have a lower risk of seizures

A

haldol

pimozide
trifluoperazine
fluphenazine

136
Q

which atypical antipsychotic is most commonly associated with seizures

A

clozapine

137
Q

which atypical antipsychotic has the lowest risk of inducing seizures

A

risperidone

138
Q

why must antipsychotics be used only carefully in the elderly

A

ALL antipsychotic agents are associated with increased risk of MORTALITY in the elderly

–> also increased incidence of cerebrovascular events

139
Q

how might you adapt use of antipsychotics for use in elderly

A

make sure benefits outweigh risks

use lower doses

slower titration schedule

periodic reassessment for need for med

140
Q

must you alter Rx for antipsychotics in those with renal impairement

A

all FGAs can be used with caution without dose adjustment

SGAs must be titrated carefully

141
Q

must you alter Rx for antipsychotics in those with hepatic impairement

A

no dose adjustment needed for FGAs but recommend initiation at lowest dose

SOME antipsychotics should be avoided in those with hepatic impairment

142
Q

which FOUR antipsychotics should be avoided in those with hepatic impairement

A

asenapine

lurasidone

paliperidone

risperidone

143
Q

name the only two antipsychotics that are FDA risk category B (safe for use in pregnancy, but limited human data available) for use in pregnancy

I.e the two “safest” antipsychotics for use in pregnancy according to the FDA

A

lurasidone

clozapine

144
Q

are antipsychotics excreted in breast milk

A

all are either proven or presumed to be excreted in breast milk

145
Q

apart from lurasidone and clozapine, are any other antipsychotics considered safe in pregnancy according to the FDA

A

no–> all others are considered “category C–> not safe for use in pregnancy, use only if benefits outweigh the risks”

146
Q

do antipsychotics change brain structure

A

controversial

in 2020–> first study showing OLANZAPINE changes brain structure (showed 1.2% loss in cortical volume over 36 weeks olanzapine exposure, which is 2x yearly loss of cortical thickness in older adults) –> findings have been challenged

147
Q

is there a difference in all cause mortality between those on oral, injection or placebo antipsychotics in those with schizophrenia?

A

no difference

148
Q

what effect do antipsychotics seem to have on mortality?

in what population is this different?

A

antipsychotic use, particularly clozapine, seems to lead to LOWER mortality

**population based studies show risk of increased all cause mortality in NON ELDERLY patients with DEPRESSION who are treated with SGA augmentation

8. Psychopharmacology (21 decks)

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