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MH701 Psychopharmacology > Pharmacogenetic Considerations for Psychiatric Drugs > Flashcards

Pharmacogenetic Considerations for Psychiatric Drugs Flashcards

1
Q

Generic
aripiprazole

A

BRAND
Abilify
Abilify Maintena

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2
Q

aripiprazole (Abilify, Abilify Maintena)

A

Biomarker - CYP2D6

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3
Q

aripiprazole (Abilify)
Dosage note

A

Poor metabolizers (PMs): initially reduce
dose to ½ the usual dose; adjust based on
clinical response.

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4
Q

aripiprazole (Abilify Maintena)
Dosage note

A

PMs: 300mg once monthly.

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5
Q

aripiprazole (Abilify)
administration note

A

Concomitant strong CYP3A4
inhibitors: reduce aripiprazole dose to ¼ the
usual dose.

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5
Q

Generic
atomoxetine

A

Brand
Strattera

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5
Q

aripiprazole (Abilify Maintena)
Admin note

A

Concomitant CYP3A4 inhibitors: 200mg once monthly. See
full labeling.

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6
Q

atomoxetine (Strattera)
Biomarker

A

CYP2D6

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7
Q

atomoxetine (Strattera)
Children & Adolescents (PMs greater than 70 kg) or concomitant strong CYP2D6 inhibitors in
adults

A

initially 40mg/day; titrate to usual target dose of 80mg/day after 4wks if needed.

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8
Q

atomoxetine (Strattera)
Children & Adolescents
PMs less than 70kg or concomitant strong CYP2D6 inhibitors:

A

initially 0.5mg/kg/day; titrate to usual target
dose of 1.2mg/kg/day after 4wks if needed.

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9
Q

Generic
carbamazepine

A

Brand
Tegretol

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10
Q

carbamazepine (Tegretol)
Biomarker

A

HLA-B*1502

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11
Q

carbamazepine (Tegretol)

A

Chinese ancestry: studies have found strong
association between HLA-B1502 and the risk
of developing SJS/TEN. Test for HLA-B1502 prior to initiation of Tegretol; should not be used if HLA-B*1502-positive.

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12
Q

carbamazepine (Tegretol)

A

Other antiepileptic drugs (phenytoin): limited evidence suggests that HLA-B1502 may be a risk factor for the development of SJS/
TEN. Consider avoiding use of other drugs associated with SJS/TEN in HLA-B1502-positive
patients, when alternative therapies are equally
acceptable.

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13
Q

Generic
citalopram

A

Brand
Celexa

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14
Q

citalopram (Celexa)
biomarker

A

CYP2C19, CYP2D6

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15
Q

citalopram (Celexa)

A

CYP2C19 PMs, concomitant cimetidine or
other CYP2C19 inhibitors, hepatic impairment, or >60yrs: max 20mg/day due to the
risk of QT prolongation.

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16
Q

citalopram (Celexa)

A

CYP2D6 PMs and EMs: levels not significantly different.

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17
Q

Generic
clobazam

A

Brand
Onfi

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18
Q

clobazam (Onfi)
biomarker

A

CYP2C19

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19
Q

clobazam (Onfi)

A

PMs: initially 5mg/day; titrate according to
weight but to ½ the usual dose, an additional
titration to max dose (20mg/day or 40mg/day,
depending on weight) may be started at Day 21

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20
Q

chlordiazepoxide/
amitriptyline
Biomarker

A

CYP2D6

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21
Q

chlordiazepoxide/
amitriptyline

A

PMs: normal metabolizers (NMs) may resemble PMs since certain drugs inhibit CYP2D6. Caution with concomitant SSRIs or when switching
from one class to the other. Sufficient time (at
least 5wks) must elapse before initiating TCAs
in patients being withdrawn from fluoxetine.
Concomitant CYP2D6 inhibitors: may need to
adjust dose of either drug; if withdrawn, may
need to increase TCA dose (monitor).

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22
Q

Generic
clomipramine

A

Brand
Anafranil

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23
Q

clomipramine (Anafranil)
Biomaker

A

CYP2D6

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24
Q

clomipramine (Anafranil)
Interactions

A

PMs: normal metabolizers (NMs) may resemble PMs since certain drugs inhibit CYP2D6. Caution with concomitant SSRIs or when switching
from one class to the other. Sufficient time (at
least 5wks) must elapse before initiating TCAs
in patients being withdrawn from fluoxetine.
Concomitant CYP2D6 inhibitors: may need to
adjust dose of either drug; if withdrawn, may
need to increase TCA dose (monitor).

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25
Q

Generic
clozapine

A

Brand
Clozaril,
FazaClo

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26
Q

clozapine
(Clozaril, FazaClo)
Biomarker

A

CYP2D6

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27
Q

clozapine
(Clozaril, FazaClo)

A

PMs: may need to reduce dose. Increased clozapine levels possible since it’s completely
metabolized and then excreted.

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28
Q

Generic
desipramine

A

Brand
Norpramin

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29
Q

desipramine (Norpramin)
BioMarker

A

CYP2D6

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30
Q

desipramine (Norpramin)

A

PMs: normal metabolizers (NMs) may resemble PMs since certain drugs inhibit CYP2D6. Caution with concomitant SSRIs or when switching
from one class to the other. Sufficient time (at
least 5wks) must elapse before initiating TCAs
in patients being withdrawn from fluoxetine.
Concomitant CYP2D6 inhibitors: may need to
adjust dose of either drug; if withdrawn, may
need to increase TCA dose (monitor).

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31
Q

Generic
dextromethorphan/
quinidine

A

Brand
Nuedexta

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32
Q

dextromethorphan/
quinidine (Nuedexta)
Biomarker

A

CYP2D6

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33
Q

dextromethorphan/
quinidine (Nuedexta)

A

PMs: quinidine component does not contribute
to the effectiveness of Nuedexta in PMs but a
possible risk of significant toxicity is present.
Consider genotyping to determine PM status
prior to initiation.

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34
Q

Generic
doxepin

A

Brand
Silenor

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35
Q

doxepin (Silenor)
Biomarker

A

CYP2D6, CYP2C19

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36
Q

doxepin (Silenor)
Special populations

A

PMs: may have higher doxepin plasma levels
than NMs

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37
Q

Generic
fluoxetine

A

Brand
Prozac

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38
Q

fluoxetine (Prozac)
Biomarker

A

CPY2D6

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39
Q

fluoxetine (Prozac)

A

Concomitant drugs metabolized by
CYP2D6 or narrow therapeutic index: NMs may resemble PMs since fluoxetine is a CYP2D6
inhibitor. Initiate lowest effective dose if receiv-
ing fluoxetine or have taken it in previous 5wks.
If already taking drugs metabolized by CYP2D6
and fluoxetine is added afterwards, consider
decreasing dose of original drug.

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40
Q

Generic
fluoxetine/
olanzapine

A

Brand
Symbyax

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41
Q

fluoxetine/
olanzapine (Symbyax)
biomaker

A

CYP2D6

42
Q

fluoxetine/
olanzapine (Symbyax)

A

Concomitant drugs metabolized by
CYP2D6 or narrow therapeutic index: NMs may resemble PMs since fluoxetine is a CYP2D6
inhibitor. Initiate lowest effective dose if receiv-
ing fluoxetine or have taken it in previous 5wks.
If already taking drugs metabolized by CYP2D6
and fluoxetine is added afterwards, consider
decreasing dose of original drug.

43
Q

fluvoxamine
Biomarker

A

CYP2D6

44
Q

fluvoxamine

A

PMs: caution with fluvoxamine and other
concomitant drugs known to inhibit CYP2D6.

45
Q

Generic
galantamine

A

Brand
Razadyne

46
Q

galantamine (Razadyne)
Biomarker

A

CYP2D6

47
Q

galantamine (Razadyne)

A

PMs: similar pharmacokinetics parameters com-
pared to EMs. No dosage adjustment needed
in PMs since the dose is individually titrated to
tolerability.

48
Q

Generic
iloperidone

A

Brand
Fanapt

49
Q

iloperidone (Fanapt)
Biomarker

A

CYP2D6

50
Q

iloperidone (Fanapt)

A

PMs: higher exposure to iloperidone vs. EMs.
Reduce dose by ½. Lab tests are available to
identify CYP2D6 PMs.

51
Q

Generic
imipramine

A

Brand
Tofranil

52
Q

imipramine (Tofranil)
Biomarker

A

CYP2D6

53
Q

imipramine (Tofranil)

A

PMs: normal metabolizers (NMs) may resemble PMs since certain drugs inhibit CYP2D6. Caution with concomitant SSRIs or when switching
from one class to the other. Sufficient time (at
least 5wks) must elapse before initiating TCAs
in patients being withdrawn from fluoxetine.
Concomitant CYP2D6 inhibitors: may need to
adjust dose of either drug; if withdrawn, may
need to increase TCA dose (monitor).

54
Q

Generic
modafinil

A

Brand
Provigil

55
Q

modafinil (Provigil)
Biomarker

A

CYP2D6

56
Q

modafinil (Provigil)

A

PMs: metabolism by CYP2C19 may be substantially increased. Provigil may cause elevation in
tricyclic levels; may need to reduce dose of tricyclics.

57
Q

Generic
nortriptyline

A

Brand
Pamelor

58
Q

nortriptyline (Pamelor)
Biomarker

A

CYP2D6

59
Q

nortriptyline (Pamelor)

A

PMs: normal metabolizers (NMs) may resemble PMs since certain drugs inhibit CYP2D6. Caution with concomitant SSRIs or when switching
from one class to the other. Sufficient time (at
least 5wks) must elapse before initiating TCAs
in patients being withdrawn from fluoxetine.
Concomitant CYP2D6 inhibitors: may need to
adjust dose of either drug; if withdrawn, may
need to increase TCA dose (monitor).

60
Q

Generic
phenytoin

A

Brand
Dilantin

61
Q

phenytoin (Dilantin)
Biomarker

A

HLA-B*1502

62
Q

phenytoin (Dilantin)

A

Chinese ancestry: limited evidence suggests
that HLA-B1502 may be a risk factor for the
development of SJS/TEN. Consider avoiding
phenytoin as an alternative for carbamazepine
if HLA-B1502-positive. Use of HLA-B*1502
genotyping has important limitations and must
never substitute for appropriate clinical vigilance and patient management.

63
Q

perphenazine
Biomarker

A

CYP2D6

64
Q

perphenazine
(PMs)

A

PMs: metabolize perphenazine slower and
have higher concentrations vs. NMs or extensive
metabolizers (EMs).

65
Q

perphenazine
(elderly)

A

Elderly: PMs have higher plasma concentra-
tions of antipsychotics at usual doses, which
may correlate with the emergence of side
effects. Prospective phenotyping prior to initiation may identify those at risk for adverse events.

66
Q

Generic
pimozide

A

Brand
Orap

67
Q

pimozide (Orap)
Biomarker

A

CYP2D6

68
Q

pimozide (Orap)
Children

A

Children (>0.05mg/kg/day): perform
CYP2D6 genotyping. PMs: max 0.05mg/kg/day;
should not increase dose earlier than 14 days.

69
Q

pimozide (Orap)
Adult

A

Adults (doses >4mg/day): perform CYP2D6
genotyping. PMs: max 4mg/day; should not increase dose earlier than 14 days

70
Q

Generic
protriptyline

A

Brand
Vivactil

71
Q

protriptyline (Vivactil)
Biomarker

A

CYP2D6

72
Q

protriptyline (Vivactil)

A

PMs: normal metabolizers (NMs) may resemble PMs since certain drugs inhibit CYP2D6. Caution with concomitant SSRIs or when switching
from one class to the other. Sufficient time (at
least 5wks) must elapse before initiating TCAs
in patients being withdrawn from fluoxetine.
Concomitant CYP2D6 inhibitors: may need to
adjust dose of either drug; if withdrawn, may
need to increase TCA dose (monitor).

73
Q

Generic
risperidone

A

Brand
Risperdal

74
Q

risperidone (Risperdal)
Biomarker

A

CYP2D6

75
Q

risperidone (Risperdal)

A

EMs and PMs have similar pharmacokinet-
ics even though EMs convert risperidone to
9-hydroxyrisperidone quicker than PMs.
Risperidone EMs half-life: 3hrs.
Risperidone PMs half-life: 20hrs.
Overall mean half-life: 20hrs.

76
Q

Generic
tetrabenazine

A

Brand
Xenazine

77
Q

tetrabenazine (Xenazine)
Biomarker

A

CYP2D6

78
Q

tetrabenazine (Xenazine)

A

> 50mg/day: perform CYP2D6 genotyping to
determine PM or EM status prior to initiation.
Individualize dose based on PM or EM status.
EMs or intermediate metabolizers (IMs): max 37.5mg/dose or 100mg/day.
PMs: max 25mg/dose or 50mg/day.

79
Q

Generic
trimipramine

A

Brand

80
Q

trimipramine (Surmontil)
Biomarker

A

CYP2D6

80
Q

trimipramine (Surmontil)

A

PMs: normal metabolizers (NMs) may resemble PMs since certain drugs inhibit CYP2D6. Caution with concomitant SSRIs or when switching
from one class to the other. Sufficient time (at
least 5wks) must elapse before initiating TCAs
in patients being withdrawn from fluoxetine.
Concomitant CYP2D6 inhibitors: may need to
adjust dose of either drug; if withdrawn, may
need to increase TCA dose (monitor).

81
Q

thioridazine
Biomarker

A

CYP2D6

82
Q

Psychopharmacology is the study of

A

how drugs interact with specific target sites in the nervous system to induce changes in mood, thinking, or behavior

are interested in a wide variety of drug classes that produce psychological side effects, such as antidepressants, stimulants, antipsychotics, hallucinogens, benzodiazepines, opiates, and hypnotics.

83
Q

Pharmacodynamics - Potency

A

Potency is an index of the concentration required for a given effect - usually the EC50. It is not the same as effect.

Drugs that are highly potent require only small doses (concentrations) to achieve their effects.

High potency is often considered desirable because less drug (in molar terms) is available to cause adverse effects.

84
Q

Pharmacodynamics - Efficacy

A

Efficacy is the desired effect (e.g. analgesia). Some drugs (e.g. morphine) have greater analgesic effect than others (e.g. paracetamol).

85
Q

Pharmacodynamics - Therapeutic Index

A

The therapeutic index represents the relationship between concentrations causing adverse effects and concentrations causing desired effects.

Drugs with a high or large therapeutic index are desirable in practice

86
Q

World Health Organization’s Six-Step Model of Rational Prescribing

A

Step 1: Define the patient’s problem.
Step 2: Specify the therapeutic objective.
Step 3: Choose the treatment.
Step 4: Start the treatment.
Step 5: Educate the patient.
Step 6: Monitor effectiveness.

87
Q

Brain Function & Deficits -
Cerebral Cortex (Frontal Lobes)

Functions

A

Functions:
– Consciousness (How we know what we are doing in our
environment)
– How we initiate activity in response to our environment
– Judgments we make about what occurs in our daily
activities
– Controls our emotional response
– Controls our expressive language
– Assigns meaning to the words we choose
– Involves word associations
– Memory for habits and motor activities

88
Q

Brain Functions & Deficits
Cerebral Cortex (Frontal Lobes)

Observed problems

A

Observed Problems:
– Loss of simple movement of various body parts (Paralysis)
– Inability to plan a sequence of complex movements needed to complete multi-stepped tasks, such as making coffee (Sequencing)
– Loss of spontaneity in interacting with others. Loss of flexibility in thinking
– Persistence of a single thought (Perseveration)
– Inability to focus on task (Attending)
– Mood changes (Emotionally Labile)
– Changes in social behavior. Changes in personality
– Difficulty with problem solving
– Inability to express language (Broca’s Aphasia)

89
Q

Brain Function & Deficits
Parietal Lobes
* Functions

A

Functions
–Location for visual attention
–Location for touch perception
–Goal-directed voluntary movements
–Manipulation of objects
–Integration of different senses that allows for
understanding a single concept

90
Q

Brain Function & Deficits
Parietal Lobes
* Observed Problems

A

Observed Problems
– Inability to attend to more than one object at a time
– Inability to name an object (Anomia)
– Inability to locate the words for writing (Agraphia)
– Problems with reading (Alexia)
– Difficulty with drawing objects
– Difficulty in distinguishing left from right
– Difficulty with doing mathematics (Dyscalculia)
– Lack of awareness of certain body parts and/or surrounding space (Apraxia) that leads to difficulties in self-care. Inability to focus visual attention
– Difficulties with eye and hand coordination

91
Q

Brain Functions & Deficits
Occipital Lobes
* Functions

A

Vision

92
Q

Brain Functions & Deficits
Occipital Lobes
* Observed Problems

A

Observed Problems
– Defects in vision (Visual Field Cuts)
– Difficulty with locating objects in the environment
– Difficulty with identifying colors (Color Agnosia)
– Production of hallucinations Visual illusions - inaccurately seeing objects
– Word blindness - inability to recognize words
– Difficulty in recognizing drawn objects
– Inability to recognize the movement of an object (Movement Agnosia)
– Difficulties with reading and writing

93
Q

Brain Functions & Deficits
Temporal Lobes
* Functions

A

Functions
–Hearing ability
–Memory acquisition
–Some visual perceptions
–Categorization of objects

94
Q

Brain Functions & Deficits
Temporal Lobes
* Observed Problems

A

Observed Problems
– Difficulty in recognizing faces (Prosopagnosia)
– Difficulty in understanding spoken words (Wernicke’s Aphasia)
– Disturbance with selective attention to what we see and hear
– Difficulty with identification of, and verbalization about objects
– Short-term memory loss. Interference with long-term memory
Increased or decreased interest in sexual behavior
– Inability to categorize objects (Categorization)
– Right lobe damage can cause persistent talking
– Increased aggressive behavior

95
Q

Brain Functions & Deficits
Brain Stem
* Functions

A

Functions
–Breathing Heart Rate Swallowing Reflexes to seeing
and hearing (Startle Response)
–Controls sweating, blood pressure, digestion,
temperature (Autonomic Nervous System)
–Affects level of alertness
–Ability to sleep
–Sense of balance (Vestibular Function)

96
Q

Brain Functions & Deficits
Brain Stem
* Observed Problems

A

Observed Problems
–Decreased vital capacity in breathing, important for speech
–Swallowing food and water (Dysphagia)
–Difficulty with organization/perception of the environment
–Problems with balance and movement
–Dizziness and nausea (Vertigo)
–Sleeping difficulties (Insomnia, sleep apnea)

97
Q

Brain Functions & Deficits
Cerebellum
* Functions

A

Functions
– Coordination of voluntary movement Balance and equilibrium
– Some memory for reflex motor acts

98
Q

Brain Functions & Deficits
Cerebellum
* Observed Problems

A

Observed Problems
– Loss of ability to coordinate fine movements
– Loss of ability to walk
– Inability to reach out and grab objects
– Tremors. Dizziness (Vertigo)
– Slurred Speech (Scanning Speech)
– Inability to make rapid movements

99
Q

Thalamus

A

– “central switching station” – relays incoming sensory information (except olfactory) to the brain

100
Q

Hypothalamus

A

– controls the autonomic nervous system (maintains the body’s homeostasis)

101
Q

Limbic System

A

– Emotional expression, particularly the emotional component of behavior, memory, and motivation

102
Q

Amygdala

A

– Attaches emotional significance to information and mediates both defensive and aggressive behavior

103
Q

Hippocampus

A

– involved more in memory, and the transfer of information from short-term to long-term memory

104
Q

Glutamate –

A

– Glutamate is the major excitatory neurotransmitter in the brain.
– It is required for learning and memory.
– Low levels can lead to fatigue and poor brain activity.
– Increased levels of glutamate can cause death to the neurons (nerve cells) in the brain. Dysfunction in glutamate levels are involved in many neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s, Huntington’s, and Tourette’s. High levels also contribute to Depression, OCD, and Autism.

MH701 Psychopharmacology (7 decks)

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