Jetlax's CNS Pharmacology Cheat Sheet for the Philippines v5.0 - see bit.ly_CNSHandouts for Corrections-converted.pptx

“What does the psych- in psychopharmacology mean?
Soul. The pharmacology of the soul. You are a soul chemist.”
Dr. Sotiris Posporelis

CNS Pharmacology Cheat Sheet
v5.0
ThereisnoRPhwithout mentalhealth. quick legend:
Jarvin EnoshTan,RPh
October 10, 2020
TABLE OF CONTENTS
DISCLAIMER 5
PREFACE 6
ACKNOWLEDGEMENTS 7
MISCONCEPTIONS 8
PSYCHOTROPIC DRUG DISCOVERY PATHWAY: INFOGRAPHIC 9
ANTIDEPRESSANTS 10
I. SELECTIVE SEROTONIN REUPTAKE INHIBITORS(SSRIS)
II. SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS(SNRIS)
III. NORADRENERGIC AND SPECIFIC SEROTONERGIC ANTIDEPRESSANT(NASSA)
IV. MULTIMODAL ANTIDEPRESSANT
V. NOREPINEPHRINE-DOPAMINE REUPTAKE INHIBITOR
VI.TRICYCLIC ANTIDEPRESSANTS (TCAS)
ANTIDEPRESSANTS NOT AVAILABLELOCALLY
10
11
11
12
12
12
12
ANTIPSYCHOTICS 14
FIRST GENERATION ANTIPSYCHOTICS / D2 ANTAGONISTS
SECOND GENERATION ANTIPSYCHOTICS / D2-5HTANTAGONISTS
THIRD GENERATION ANTIPSYCHOTICS / D2 PARTIAL AGONISTS-5HTANTAGONISTS
ANTIPSYCHOTICS NOT AVAILABLELOCALLY
14
16
18
19
ANTICHOLINERGICS 19
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ANXIOLYTICS AND SEDATIVE-HYPNOTICS 20
STIMULANTS, WAKE-PROMOTING AGENTS, AND MEDICATIONS FOR ADHD 22
ANXIOLYTICS, SEDATIVE-HYPNOTICS, STIMULANTS, AND WAKE-PROMOTING AGENTS NOT AVAILABLE LOCALLY 23
“MOOD STABILIZERS” 24
DEMENTIA 26
PARKINSON’S DISEASE 27
OTHER ANTIEPILEPTICS 28
BARBITURATES / GABAERGIC
SODIUM CHANNEL BLOCKERS (VSSCBLOCKERS)
SYNAPTIC VESICLE SV2ABINDER
AMPA RECEPTOR ANTAGONIST
ANTIEPILEPTICS NOT AVAILABLELOCALLY
28
28
30
30
31
SUBSTANCE USE DISORDERS 34
MNEMONICS 35
BONUS SECTION: LAST-LINE AGENTS/ALTERNATIVES IN REFRACTORY CONDITIONS 37
REFERENCES 39
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Disclaimer
The writer of this cheat sheet does not have any financial or
other relationships with the manufacturer/s of any commercial
product/s discussed in this cheat sheet. While the writer of this
cheat sheet exercised due diligence to ensure the accuracy of
all information provided here along with the necessary cross-
checking in the Philippine context, this does not take away from
the responsibility of the intern or healthcare professional to
exercise their rational clinical judgment, or that of the student in
double-checking with other quality references. The writer cannot
accept responsibility for the use of this cheat sheet (past
versions, current version, and future versions) in actual practice.
All medications referenced in this document should be used only
as intended as per the relevant laws, ordinances, rules,
regulations, and other policies applicable and in accordance
with their respective package inserts or monographs. If you
have any concerns, comments, or feedback, please feel to let
the writer know at ! If you are a service user,
do not change your dosing or stop your medications and
consult your doctor or pharmacist for any concerns you may
have. Fair Use disclaimer and citations for art inspirations are in
the references section.
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Preface
I think this project has gone on long enough that it deserves an introduction of its own. This cheat sheet started out as an offshoot of a project I was
working on back in 2018. Version 1 came out around September 24, 2018 as a means to make learning CNS Pharmacology or Psychopharmacology
less threatening to health students (especially pharmacy students) and health professionals. This was also rooted in a frustration with the insufficiency
of currently adopted references in the national pharmacy curricula in accurately explaining medications for mental health in an organized manner, and
its consequent impact on the prevalence of misconceptions on psychotropic medications (see below). Eventually, this grew into a desire to capture
and engage students’ and health professionals’ interest in the rational use of psychopharmacologics. This handy reviewer of sorts has a summarized
mixture of CNS Pharmacology topics in neuropsychiatry and some practical pearls for psychiatric therapeutics covering medications used in ADHD,
anxiety disorders, bipolar disorder, body dysmorphic disorder, clinical depression, dementia, eating disorders, epilepsy, OCD, Parkinson’s disease,
PTSD, schizophrenia, substance use disorders, and sleep-wake disorders, with a focus on Philippine practice. Medications for analgesia and
anesthesia are beyond its scope as I don’t want to overreach on my knowledge and clinical experience.
Version 5.0 takes this cheat sheet to greater heights with a brand new piece of cover art to celebrate both World Mental Health Day 2020 and the
cheat sheet’s upgrade. This portrait aims to give the impression that psychopharmacology shouldn’t be something to be afraid of or be intimidated by,
but embraced with the same curiosity and fervor as we would other medication classes for the sake of Filipino mental health service users. This is
further supplemented by thirteen illustrations commissioned from a talented clinical pharmacy graduate which are scattered across this document,
each demonstrating highlights for various drugs, their effects, and their proper use.
An infographic was also created for those with an interest for the pharmaceutical sciences to better appreciate the history of psychotropic drug
discovery and development. As neuroscience-based nomenclature (NbN) has not yet been fully embraced, and popular class names still dominate
the discourse on psychotropic medications, standardization of the terminology in this infographic was challenging and a compromise was adopted
between these two naming systems. The first cited reference in the infographic was key to weaving the multiple intersecting threads of serendipity,
dogma-defiance, and rational drug design together into a working illustrated narrative of all that has been accomplished within the past few decades.
If you look closely, you will also spot hints of how the future pipeline may proceed through novel mechanisms of action or even through old classics
revisited once more.
As a bonus, eleven (11) links have been embedded across the entire document – nine (9) music videos and two (2) video clips. See if you can spot
all the blue hyperlinks! Check out my Youtube series as well for additional supplementary educational materials!
 bit.ly/AntipsychoticsPcolPH
 bit.ly/AntidepressantsPcolPH
 bit.ly/MoodStabilizersPcolPH
 bit.ly/AnxiolyticsPcolPH
I wish you all the best and remember the focus and center of why we study all of this: all for the mental health service users! #MoveforMH

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Acknowledgements
This still ongoing journey towards improving mental health education in the pharmacy profession has been long and undeniably tiring on occasion,
which is why it would be only appropriate to give credit and thank the many people who have been supportive and constructively critical all throughout.
Firstly, to my colorful, multidisciplinary set of mentors: sir Renz Christian Argao, Dr. Gia Sison, Dr. Raymond Naguit, Dr. Yolanda Robles, ma’am
Christine Ching Benosa, Dr. Dinah Nadera, and Ms. Trudi Hilton, thank you for indulging my constant questions, extending utmost patience, providing
opportunities for growth, and most of all, helping me learn the hard lessons beyond healthcare that invaluably inform my practice today. I would also
like to express gratitude to my seniors and peers (tbh there’s a big gray area/overlap with these terms) – Deeh Aninon Agaceta, Diana Orolfo, Frances
Ngo, Louie Legaspi, orgmates and team members in the Youth for Mental Health Coalition and RPh for Mental Health, and more who have helped
provide better perspectives on advocacy in the context of the local pharmacy profession.
This section wouldn’t be complete either without extending thanks to the wonderful psychiatric/mental health pharmacists from the College of
Psychiatric and Neurologic Pharmacists and the College of Mental Health Pharmacy who extended their technical assistance and encouragement
from across borders to support the move for mental health integration into Philippine pharmacy practice. A special dedication goes to the late Dr.
Michael Z. Wincor, a psychiatric pharmacist who partly inspired me to focus on sleep issues in youth mental health and for the unforgettable line: “A
dedicated pharmacist can do in 5 years what a residency-trained pharmacist can do in 2.”
Thanks as well to my seniors at my first ever formal job – Dr. Gina Castro, ma’am Danda Chua, ma’am Sandra Sy, sir Stan Cruz, ma’am Rhona
Ramos, Sharmaine Dela Cruz, **H, and more for further guiding me in refining my knowledge and skills in the academe (and everything else in
between!). A special shoutout goes to an unexpected friend, Ser Loisse Mortel, whose enthusiasm and fire in the pharmaceutical sciences and
education continues to serve as an inspiration to keep moving forward, as well as to Justin Samar (I miss our food dates ugh)! To my students, current
and former, who continue to defy expectations in the face of systemic failures and injustice, keep being stellar and always remember: it’s honor before
excellence!
Personal thanks to my parents who patiently supported me during the earlier (and costlier) stages of my mental health pharmacy education, and our
family therapist for helping make quarantine so much more peaceful for all of us. Eternal thanks to the support and memories throughout the years
with Joshua Chavez, Genmar Pasion, Vienne Pinlac, and James Tronco, and cheers to the lives ahead of us! Lastly, to AJ Elicaño and Lotad who
stayed with me during quarantine, you have my many thanks! – @Jetlax
Jarvin Enosh Tan, RPh
Postgraduate Certificate in Psychiatric Therapeutics (with distinction), Aston University
Technical Writer, Philippine National Formulary (8th edition)
Contributor, ASHP Therapeutic Position Statement on the Use of Antipsychotic Medications in the Treatment of Adults with Schizophrenia and
Schizoaffective Disorder

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MISCONCEPTIONS
1. ONLY A FEW psychotropic medications are scheduled on the dangerous drugs list
and require an S2 license. The ones that require an S2 license to prescribe will bear
NEED S2.
2. Naming conventions for psychotropic medication classes are chronologic, and only
imply what the drug was first discovered for. The full indication list may go beyond.
See antidepressant indications below as an example.
3. Psychotropic medications do not correct a chemical imbalance or neurotransmitter
deficiency. There is no such thing as a chemical imbalance or deficiency.
4. Antidepressants are not addicting but can still cause withdrawal especially when used
for a prolonged duration. All individual psychotropic medications that carry an
addiction risk are specified.
5. Antidepressants do not take 4-6 weeks to start working for depression. See below.
6. Antidepressants are not all sedating. The ones that are generally sedating are the
tricyclics and Mirtazapine. Paroxetine and Fluvoxamine are sedating, to an extent.
The rest can go either way.
7. Antidepressants’ black box warning on risk of suicidality is rare (~0.07%) and has
qualifications (see below). Suicidal ideation does not automatically proceed to
attempt, though it can be a risk.
8. Benzodiazepines: The Golden Concept (by Dr. Tyler Black @tylerblack32) – “These
are temporary medications. Always plan their stop when you plan their start. Whatever
treatment they need, the benzo is buying you a short time to arrange it. Prescribe
small [amounts].” See details below.
9. Benzodiazepines are not recommended for phobias & PTSD, and some guidelines
note they are contraindicated in these conditions due to the risk of worsening them.
These should generally be last-line considerations.
10.Quetiapine 25-50 mg is an inappropriate option if used exclusively for insomnia and
should not be considered unless all other options have been exhausted. There is
nothing Quetiapine can do at that dose that sedating antihistamines can’t (mood
stabilizing and antipsychotic effects occur at doses of 300 mg/day & 400-500 mg/day,
respectively). Moreso, Quetiapine’s metabolic syndrome is not proven to be dose-
dependent and is a risk factor for worse COVID-19 outcomes.
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PSYCHOTROPIC DRUG DISCOVERY PATHWAY: INFOGRAPHIC
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ANTIDEPRESSANTS
Medication Specific Information General (MOA, Side Effects, Interaction) Indications, Side Effect Management, & More
I. SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIs) Indications (depending on individual SSRI; SSRIs
generally preferred):
 Major Depressive Disorder (MDD)
 Generalized Anxiety Disorder (GAD)
 Panic Disorder (PD)
 Social Anxiety Disorder (SAD)
 Obsessive Compulsive Disorder (OCD)
 Post-traumatic Stress Disorder (PTSD)
 Binge Eating Disorder (BED)
o 2nd line for vasomotor symptoms ofmenopause
Side Effect Management (Tolerance develops
over time):
 N/V – take with food / move dose to bedtime
 Constipation – fiber
 Diarrhea – maintain hydration, ORS (if needed),
antispasmodic
 Insomnia/sedation – shift dosing to morning/
bedtime; sleep hygiene
 Headache, dizziness – take at night
Non-pharmacologic
 Psychotherapy (all indications); psychological
debriefing is not recommended for trauma
 Aerobic exercise (especially for MDD; Tx &
prevention)
 St. John’s wort (MDD; multiple drug interactions)
 Lavender oil (GAD)
 Progressive muscle relaxation (PMR) (phobias,
PD)
 Saffron (SSRI-induced sexual dysfunction)
1. Sertraline Additional MOA: Also weakly blocks dopamine
transporters (DAT) and σ1 receptors
Caution in urine drug screens as it may give a
false positive result for benzodiazepines; CNS-
activating side effects
Mechanism of Action (MOA)
MDD: Block serotonin (5-HT) transporters (SERT) 
↑5-HT  Delayed ↑brain-derived neurotrophic f
a
c
t
o
r
(BNDF); removes affective biases
(see Ketamine MOA for BDNF’s role in neuroplasticity)
Anxiety disorders: Block SERT  ↑5-HT
 a
d
a
p
t
i
v
e neuronal/receptor events in brain
circuits involved in fear (amygdala) and worry
(prefrontal cortex, striatum, thalamus)
Onset
 MDD: 1-2 weeks
 Anxiety and related disorders: 4 weeks
(up to 8-12 weeks, especially OCD)
Safe duration: 6-9 months (MDD), 12 months (GAD,
PD, SAD, OCD, PTSD)
Common SideEffects
 GIT: Decreased/increased appetite, nausea,
diarrhea, constipation, dry mouth
 CNS: Insomnia/sedation, agitation, tremors,
headache, dizziness, anxiety, nervousness, fatigue
 Others: Sexual dysfunction, sweating, bruising,
weight gain/loss, asthenia
Rare/Serious S/E
 Manic switch in bipolar disorder
 ↑risk of GI, peri-operative, uterine, cerebral bleeding
2. Fluoxetinea
Additional MOA: Also weak 5-HT2C antagonist
and NET blocker
Specific indication for bulimia nervosa and body
dysmorphic disorder
- Most studied antidepressant for children w/
MDD (≥9 yo)
CNS-activating side effects
Drug-Drug Interactions
Multiple CYP drug interactions, especially with
CYP2D6 substrates (ex: Tamoxifen)
Longest t1/2 (less likely for withdrawal)
Cipriani et al. (2018): on average less dropouts on
fluoxetine vs placebo but less efficacious vsother
antidepressants
3. Escitaloprama MOA: pure SERT blockade (racemic citalopram
is H1 blocker)
(R)
May prolong QT interval
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4. Paroxetine Additional MOA: Also slight M1 antagonist, NET
blocker, nitric oxide synthetase inhibitor (higher
incidence: sexual dysfunction)
- Anticholinergic side effects
- Potent CYP2D6 inhibition
- Shortest t1/2 (higher risk for withdrawal)
- Avoid in children, adolescents, adults≤24 y.o.
 Rare hyponatremia and SIADH, esp. in elderly and
dehydrated persons
 Rare post-SSRI sexual dysfunction (PSSD)
 Rare, increased suicidal ideation ≤24 years old
Withdrawal Symptoms aka brain zaps
 Affective – anxiety, irritability, sadness
 Gastrointestinal – nausea
 Neuromotor – ataxia
 Vasomotor – diaphoresis
 Neurosensory – electric shock sensation
 Other neurologic – increased dreaming, insomnia,
headache
Interactions
a. NSAIDs and aspirin may increase bleeding risk and
decrease SSRI efficacy
b.Anticoagulants, antiplatelets, and ω3 fatty acids
may increase bleeding risk
c. Serotonin syndrome (when combined with
serotonergic agents): ginseng, St. John’s wort,
Tryptophan, Dextromethorphan, methylene blue,
Linezolid, serotonergic drugs
d. Levothyroxine efficacy decreased
Tapering
Traditional tapering: x mg/day (usual references)
Proposed tapering: x% mg/day corresponding with
SERT occupancy (Horowitz et al., 2019)
Ashton manual: 1-2 weeks every dose reduction (e.g.
take dose once a day  every other day 
every
3rd
day)
5. Fluvoxamine Additional MOA: Also binds σ1 receptor – only
indicated for OCD
6. Dapoxetine Rapid absorption, onset, elimination: Indicated for
premature ejaculation; single dose prior to sexual
activity
N/A in Philippines
Trazodone (SARI), Vilazodine (SPARI), Doxepin
(TCA), Agomelatine (melatonergic), other TCAs,
MAOIs, Venlafaxine (SNRI), Mianserin (NaSSA),
Milnacipran (SNRI), Levomilnacipran (SNRI),
Esketamine (Glutamatergic),
II. SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIS) Brexanolone/Allopregnanolone (GABAergic)
1. Desvenlafaxine Venlafaxine’s active metabolite
Caution in urine drug screens as it may give a
false positive result for amphetamines
Financially toxic !!$$$$!!
MOA
Block SERT and NET
Side effects
 Increased BP (2 mmHg)
 Sweating
 Urinary retention (NE agonizes bladder α receptors)
2. Duloxetine Has M1 antagonism
SNRIs also used in neuropathic pain
Contraindication
 Uncontrolled angle-closure glaucoma
 Similar general interactions and side effects with
SSRIs
III. NORADRENERGIC AND SPECIFIC SEROTONERGIC ANTIDEPRESSANT (NaSSA)
Mirtazapine Antagonist at α2, H1, 5-HT2A, 5-HT2C, 5-HT3 receptors (noradrenergic and serotonergic antagonist);
does NOT block SERT
Side effects:
 Sedation
 Weight gain (worst), ↑cholesterol
 Less sexual dysfunction
 Possibly no clinical benefit as SSRI/SNRI adjunct (MIR Trial – Kessler et al., 2018)

ANTIDEPRESSANTS NOT AVAILABLE LOCALLY
AKA not-so-nice to know
SSRI: Citalopram Racemic version of Escitalopram
MOA: Also blocks H1 receptors
MOA: same as above
Side effects: QT prolongation
Indications: similar to Escitalopram; dose limitation in elderly
to reduce QT prolongation risk
SNRI:
Venlafaxine
Milnacipran
Levomilnacipran
Venlafaxine’s selectivity for DAT increases
with dose
SNRIs less tolerable; alternatives
MOA: same as above
Side effects: similar as above; manic switch &
withdrawal higher with Venlafaxine
Indications: same as above for SNRIs;
Venlafaxine MR studied for MDD, GAD, PD, PTSD, SAD,
binge-eating disorder
Venlafaxine in general: 2nd line, cataplexy (narcolepsy type 1)
NaSSA:
Mianserin
MOA: Same as Mirtazapine with added α1
antagonism
MOA: same as above with added property (see column
to the left)
SARIs:
Trazodone
Nefazodone
Serotonin Antagonist-Reuptake Inhibitors
MOA:
Trazodone: also blocks H1 receptors
Nefazodone: also blocks NET
MOA: Blocks SERT, α1 receptors,
5-HT2A (potently), 5-HT2C receptors
Side effects (notable):
Trazodone: Priapism – painful, persistent erection
Nefazodone: Hepatotoxic (less preferred)
Indications: MDD (trazodone is preferred), insomnia (only
trazodone, low doses only for selectivity of H1 receptors)
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IV. MULTIMODAL ANTIDEPRESSANT
Vortioxetine MOA
 Blocks SERT
5-HT1A agonist, 5-HT1B partial agonist, 5-HT1D and 5-HT7 antagonist
5-HT3 antagonist
Pro-cognitive effect in elderly and less sexual dysfunction; Financially toxic !!$$$$!!
V. NOREPINEPHRINE-DOPAMINE REUPTAKE INHIBITOR
Bupropion MOA: Blocks DAT and NET; does NOT block SERT
Additional indication: Smoking cessation
Contraindications: History of seizures, medical conditions increasing risk (traumatic brain injury/TBI,
anorexia, etc.)
Side effects: Hypertension and insomnia; less/minimal sexual dysfunction
Rare S/E: Seizures (substituted cathinone; risk goes up when exceeding maximum doses, if with risk
factors, and IR>SR/XL), SJS-TEN
VI. TRICYCLIC ANTIDEPRESSANTS (TCAs)
Amitriptyline
Clomipramine
Trimipramine
MOA: NET blocker, HAM antagonist, voltage-sensitive Na+
channel (VSSC) blocker; some also block SERT,5-HT2A,5-HT2C receptors
 Na+
channel blockade (cardiotoxicity)  lowers seizure threshold, sudden death, sudden arrythmias, tachycardia (esp. at higher doses)
 Antimuscarinic + NET blockade combo also enhances cardiotoxicity
Indications: 2nd
/3rd
line for MDD (DO NOT GIVE to those at risk of suicide; Amitriptyline most efficacious but very intolerable) AND:
2nd
line in GAD, PD, OCD, Body Dysmorphic Disorder, Cataplexy: Clomipramine (caution: abrupt discontinuation in cataplexy can cause status cataplecticus)
2nd
line in PTSD: Amitriptyline
Contraindications: Recovery from myocardial infarction (MI), CYP (esp. 2D6), QT prolonging drugs
Side Effects:
Common: HAM blockade (H1 – sedation, α1 – orthostatic hypotension, M1 – anticholinergic), serotonergic, blue/green urine discoloration (Amitriptyline)
Rare: Manic switch, suicidal thoughts and behavior, QT prolongation, hepatic failure, extrapyramidal symptoms (EPS), increased intraocular pressure (IOP)
Interactions: CYP; false positive in urine drug tests for amphetamines (Trimipramine) and frequent false negatives (Clomipramine)

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SPARI:
Vilazodone
Serotonin Partial Agonist-Reuptake Inhibitor
MOA: Blocks SERT, partial agonist at 5-HT1A receptors
Requires food (significant nausea without food), very slow dose titration
Indications: MDD
Melatonergic:
Agomelatine
MOA: MT1 and MT2 agonist, 5-HT2B and 5-HT2Cantagonist
Relatively better efficacy profile vs other antidepressants; more tolerable vs placebo
Use limited by hepatotoxicity concerns
Indications: MDD, GAD
NRI:
Reboxetine
MOA: Blocks NET
Relatively inferior efficacy and tolerability vs other antidepressants
Indications: MDD
RIMA:
Moclobemide
Reversible Inhibitor of Monoamine Oxidase-A (MAO-A)
MOA: reversible, selective MAO-A inhibition
Lower risk of tyramine-cheese reaction (hypertensive crisis) at therapeutic doses
Indications: MDD, PD, SAD
TCAs:
Doxepin, Nortriptyline,
Desipramine, Imipramine,
Lofepramine, Amoxapine
Lofepramine – least cardiotoxic of all TCAs
Nortriptyline – less anticholinergic
Doxepin – most selective agent for H1
receptors (only at 1-6 mg) in existence
Amoxapine – seizures at therapeutic doses
Doxepin – very sedating
Indications:
BED (2nd line) – Desipramine, Imipramine
Nocturnal enuresis (3rd line; vs 1st line: alarms and 2nd line:
desmopressin) – Imipramine
Insomnia – Doxepin (low-dose; 1-6 mg)
MAOIs:
Phenelzine
Isocarboxacid
Tranylcypromine
Selegiline
MOA (additional):
Tranylcypromine – blocks DAT& NET
Selegiline: tyramine diet restrictions not
needed for 6 mg/24 hour patch
Contraindications: Tranylcypromine – renal
impairment
MOA: Irreversible inhibition of MAO-A & MAO-B 
monoamines not broken down
(effect duration ~ time to make new MAO: 2-3 weeks)
Side Effects: manic switch (w/ bipolar), headache, GI
symptoms and weight gain, postural hypotension,
bradycardia, edema, sexual dysfunction, hypertensive
crisis
Contraindications: pheochromocytoma, heart
disease, hypertension, history of headache, hepatic
impairment
Interactions: Serotonergic agents (serotonin
syndrome; wait 4-5 half-lives of the agent before
starting MAOIs or 5 weeks after stopping Fluoxetine),
sympathomimetics (hypertensive crisis)
Indications
Phenelzine: MDD, PD, SAD
Side Effect Management:
Preventing hypertensive crisis* – avoid the ff:
 Aged foods (aged cheese, meats, sausages, etc.)
 Fermented foods (pickled food, atchara, spoiled food, tap or
non-pasteurized beer, yeast extract, soy sauce, tofu)
 Fava beans, other broad bean pods
*Hypertensive crisis: MAO-A in gut that breaks down tyramine
is inhibited  more tyramine absorption  displacement
of NE from storage vesicles  adrenergic agonism
Glutamatergic: Esketamine
CONTROLLED
S-isomer of Ketamine
Rapid, antidepressant and anti-suicidal effect
within 24 hours
Administration: Intranasal
MOA: Non-selective, non-competitive NMDA receptor
antagonist; exact mechanism for depression unclear
(effect of parent compound and S-norketamine
metabolite dependent on mTOR kinase but
independent of AMPA receptors)
Side Effects: Dizziness, nausea/ vomiting, sedation,
vertigo, hypertension, financial toxicity, ↓ feeling/
sensitivity (hypoesthesia), feeling drunk. anxiety,
Interactions: Minor substrate of CYP2B6, 2C19, 2C9, 3A4;
additive CNS depression from other CNS depressants; additive
toxicity from other serotonergic agents and NMDA antagonists
lethargy, sedation, dissociation, potential for addiction
GABAergic: Brexanolone/
Allopregnanolone
Endogenous neurosteroid derived from
progesterone for postpartum depression
IV infusion (60 min) in hospital setting
MOA: α1β2γ2, α4β3δ, and α6β3δ GABAA positive allosteric
modulator
Side Effects: Extreme sedation, financial toxicity
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ANTIPSYCHOTICS
FIRST GENERATION ANTIPSYCHOTICS / D2 ANTAGONISTS
1. Chlorpromazine
a, b, *
Specific Side Effects
 Urine discoloration (red to red-brown)
 More sedation, orthostatic
hypotension, and anticholinergic
effects (HAM blockade) and less EPS
(less potent D2 blockade)
 photosensitivity
Contraindications
 Impaired consciousness
 Pheochromocytoma
 Reye’s syndrome
Drug-drug interactions:
 Antacids may lower absorption
 Contraindicated: oral K+
salts; their
ulcerogenic effect is enhanced by
strong anticholinergics
 Levels may be increased by
antimalarials including quinine
Caution in urine drug screens: Urinary
chlorpromazine metabolites may give
false positive result for amphetamines;
may cause false positives in pregnancy
tests.
MOA: D2 blockade (mesolimbic), HAM blockade
Side Effects:
Common: Sedation, rash, urticaria
Anticholinergic side effects (H1, α1, M1)
 Dizziness, blurred vision, dry mouth, urinary
retention, constipation, tachycardia
Serious: Orthostatic hypotension, weight gain,
blood dyscrasias, ECG changes (prolonged QT
interval), photosensitivity, priapism
Extrapyramidal symptoms/EPS (nigrostriatal)
 Acute dystonia
 Pseudoparkinsonism
 Akathisia
 Tardive dyskinesia
Hyperprolactinemia (tuberoinfundibular)
 Oligomenorrhea, galactorrhea (women)
 Gynecomastia (men)
 Sexual dysfunction
Neuroleptic malignant syndrome (NMS):
muscular rigidity, hyperthermia, altered
consciousness, and autonomic dysfunction
Indications: 1st gen. antipsychotics less efficacious in bipolar disorder;
limited to schizophrenia, and Haloperidol for acute agitation;
Fluphenazine decanoate, Flupentixol decanoate, and Haloperidol
decanoate depot injections to improve adherence
Side Effect Maagement:
EPS – decrease dose/switch/add medication
 Acute dystonia – adjunctive anticholinergic (preferred), adjunctive
IM diphenhydramine
 Akathisia – adjunctive propranolol / BZD / mirtazapine /
anticholinergic (weak) / B6 / trazodone
 Pseudoparkinsonism – adjunctive anticholinergic or adjunctive
diphenhydramine
Tardive dyskinesia – adjunctive vit. B6 / branched-chain amino acids
(esp. male) / Levetiracetam / botox / deep brain stimulation (DBS)
Anticholinergic SEs
 Dry mouth – drink small amount of fluids frequently, switch oral
hygiene products, Sugar-free candy/gum, avoid desiccants (alcohol,
smoke, coffee), keep nasal passages open, humidifiers
 Excessive saliva – adjunctive oral Hyoscine, oral Benztropine, SL
Atropine
 Constipation – dietary fibers, exercise, inc. fluid intake, laxatives;
possibility of paralytic ileus
 Urinary incontinence – avoid high fluid intake in evening, ensure
complete voiding at bedtime
Other indications
 Hiccups (2nd line)
 Chemotherapy-induced N/V
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2. Fluphenazine
a, d, LAI
Specific Side Effects: Less sedation,
orthostatic hypotension, and
anticholinergic effects (HAM blockade),
more EPS (potent D2 blockade)
Neuroleptic induced deficit syndrome (NIDS):
secondary negative symptoms (mesolimbic
pathway D2 blockade)
Cardiovascular
 Orthostatic hypotension – stand up slowly from sitting/lying
position, ↑fluid intake (if not fluid-restricted), use supportive
stockings
 Tachycardia – low-dose peripheral β-blocker, reduce caffeine and
nicotine intake
 QTc prolongation – note concurrent meds with potential for QT
prolongation, document
Hyperprolactinemia
 Sexual dysfunction – evaluate prolactin, note pregnancy plans
 Osteoporosis risk – bone density screening
Neuroleptic Malignant Syndrome
 Supportive care: cool body; maintain hydration
 Manage complications – renal failure, aspiration, etc.
 Pharmacologic management:
 BZD
 Bromocriptine
 Dantrolene
 Amantadine
 ECT
 Avoid anticholinergics
Contraindications: hepatic disease
Drug-drug interactions
– Contraindicated: oral K+ salts; their
ulcerogenic effect is enhanced by strong
anticholinergics
Interactions:
 Increases effects of BP-lowering meds
 Lowers BP if combined with epinephrine
 CNS depressant effects stack with other
depressants
 Anticholinergics may decrease dissolution of
sublingual tablets (nitroglycerin, etc), increase
concentration of thiazide diuretics
 Increased hyperthermia risk w/ Topiramate
Contraindications: blood dyscrasias, bone
marrow suppression, comatose, subcortical brain
injury, hypersensitivity, Parkinson’s
3. Flupentixola(LAI)
anticholinergic effects (HAM blockade),
more EPS 9potent D2 blockade); though
more anticholinergic vs Fluphenazine or
Haloperidol
Only decanoate LAI is in PNF and
primary care formulary, but not FDA-
registered (tablets are registered)
4. Haloperidol
a, c, LAI
antichlinergic effects (HAM blockade),
more EPS 9potent D2 blockade)
Drug-drug Interactions:
 Increases effects of blood pressure
lowering medications.
 Lowers blood pressure if combined
with epinephrine
Other Indications: Tourette’s
May cause depressive switch in bipolar
disorder
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SECOND GENERATION ANTIPSYCHOTICS / D2-5HT ANTAGONISTS
1. RisperidoneLAI Specific Side Effects
Dose-dependent EPS; risk significantly increases
beyond 6 mg, where there is no additional clinical
benefit
Dose-dependent hyperprolactinemia
Metabolic syndrome (moderate risk)
Substrate of CYP2D6, 3A4
MOA
Positive symptoms: D2 antagonist
 Less EPS/hyperprolactinemia:
5-HT2A antagonist & 5-HT1A partial agonist
Mood/anxiolytic effects: 5-HT1A partial
agonist, 5-HT2C antagonism, 5-HT7
antagonism, α2 antagonism
 Multiple other receptor affinities
Onset: 1-2 weeks for mood; 4-6 weeks for full-
response for some
Side Effects
Common: Dizziness, insomnia/sedation, N/V,
headache, asthenia, dyspepsia, orthostatic
hypotension (occasionally during initial dosing),
anticholinergic effects
Rare/Serious:
 Metabolic syndrome
– Possibly due to combined H1 + 5-HT2C
antagonism, M3 antagonism on
pancreatic β-cells, and/or other
receptors
– Hypertension, ↑ weight, dyslipidemia,
hyperglycemia (within 6-8 weeks)
– Monitor metabolic parameters
(FBG, Hba1c, fasting lipids, BP, wt.)
 Schizophrenia spectrum disorders
– Clozapine used mainly for this indication only
due to safety concerns
 Acute agitation
 Bipolar disorder (see figure below)
 Adjunct to “treatment-resistant” depression
– Risperidone, Quetiapine XR, Aripiprazole,
Brexpiprazole
– Olanzapine (least preferred)
 Adjunct to anxiety and related disorders
– Quetiapine (also 2nd
line monotherapy): GAD
– Risperidone (preferred), Aripiprazole: OCD
 Chemotherapy-induced nausea and vomiting (CINV)
prophylaxis: Olanzapine
 LAST-LINE for psychosis in dementia
(EXCEPT Lewy body dementia; avoid):
– Risperidone (max. 1 mg twice daily)
2. PaliperidoneLAI Specific Side Effects
 Dose-dependent EPS
 Hyperprolactinemia
 Metabolic syndrome (moderate risk)
Only its LAI form is included in PNF;
oral dosage form is financially toxic !!$$$$!!
3. Amisulpride Specific Side Effects
 Hyperprolactinemia
 QT prolongation
Best avoid in renal failure
Useful in those with prominent negative symptoms
(but may not be clinically significant)
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4. Quetiapinea,b Specific SideEffects
 QT prolongation
 Very sedating
Decreased T3/T4
 Metabolic syndrome (moderate risk)
 Weight +1.6 kg
 BMI +0.7
 LDL +0.17 mmol/L
 Total cholesterol +0.31 mmol/L
 TG +0.32 mmol/L
DO NOT GIVE EXCLUSIVELY FOR INSOMNIA IF
OTHER OPTIONS AVAILABLE #QueHorror
 Increased risk of death, cerebrovascular
events in elderly with dementia
*Lamotrigine: for maintenance only
Side Effect Management (Tolerance develops over
time): same as above
Clozapine-induced constipation (gastric hypomotility/
CIGH)
 Lifestyle: exercise, dietary fiber, fluid intake
 Oral: Lactulose, Senna, Bisacodyl
 Rectal (severe): Glycerin suppositories, Sodium
Picosulfate enemas
Clozapine-induced sialorrhea
 Prop pillows up at night
 Reduce caffeine intake
Aripiprazole-induced akathisia/agitation: take with
chocolate (~4 bars) but consider service user’s
comorbidities (e.g. type 2 diabetes mellitus)
Metabolic syndrome: diet, aerobic exercise, sleep
management
A l l of the above on 2nd gen applicable to 3rd gen
Nonpharmacologic Interventions
 Schizophrenia
–Cognitive behavioral therapy for psychosis (CBTp)
– Cognitive remediation therapy (CRT) & compensation
– Social cognition therapy
– Music therapy
– Vocational rehabilitation
 Bipolar Disorder (during euthymia, only for dep.)
– Psychoeducation
– CBT
– Family-focused therapy (FFT)
– Interpersonal and social rhythm therapy (IPSRT)
– Peer support (should not encourage harmfulbehaviors,
i.e. nonadherence to meds, substance use)
 Extreme hyperglycemia associated with
ketoacidosis/hyperosmolar coma/death
 NMS
 Seizures
 Dysphagia
 Aspiration pneumonia
 Priapism
 Changes in body thermoregulation
 Blood dyscrasias (leukopenia, neutropenia,
agranulocytosis)
Discontinuation symptoms: Rebound
insomnia and anticholinergic effects
Contraindications: Parkinson’s disease
psychosis (possible efficacy for Clozapine, less
for Quetiapine)
A l l of the above on 2nd generation
antipsychotics applicable to 3rd
generation
antipsychotics, except MOA and details on
certain side effects
5. Olanzapine Specific SideEffects
 Strong sedation
 Metabolic syndrome (highest risk)  metabolic
parameter monitoring
 Weight +2.7 kg
 BMI +1.0
 LDL +0.20 mmol/L
 Cholesterol +0.40 mmol/L
 TG +0.46 mmol/L
Dose cut by up to 50% in smokers (CYP1A2
induction)
6. Clozapine Specific Side Effects
 Strong sedation
 Sialorrhea (Norclozapine = M3 agonist)
 Metabolic syndrome (highest risk)  me
t
a
b
o
l
i
c
parameter monitoring
 Weight +3.0 kg
 BMI +1.0
 FBG +1.05 mmol/L
 Cholesterol +0.56 mmol/L
 TG +0.98 mmol/L
Serious: Agranulocytosis (differentiate benign
ethnic neutropenia/BEN), myocarditis, orthostatic
hypotension, seizures,
constipation/fatal ileus*, aspiration pneumonia
(swallow reflex inhibition+sialorrhea)
Absolute Neutrophil Count (ANC) monitoring, when
possible, is advised, along with metabolic
parameters

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Clozapine Interactions
Dose cut up to 50% in smokers (CYP1A2
induction); substrate of 2D6, 3A4, 2C19, 2C8/9, &
2A6
Others:
 Benefits in schizophrenia: near-zero EPS &
minimal TD risk, anti-suicidal, efficacious in
managing aggression & violent behavior
 Target serum concentration: 350 ng/mL
 Minimum duration: 6 months
THIRD GENERATION ANTIPSYCHOTICS / D2 PARTIAL AGONISTS-5HT ANTAGONISTS
1. AripiprazoleLAI
Specific Side Effects: Akathisia, compulsive
behaviors (gambling, spending, eating/sex, etc);
less risk of metabolic syndrome & QT prolongation
Also for Tourette’s and in; caution in urine drug
screens, may give false positive for phencyclidine
and amphetamines
LAI is non-PNF
MOA: partial D2 agonist, 5-HT2A antagonism, 5-
HT1A partial agonism
Multiple other receptor affinities
N/A in Philippines:
1st gen.: Cyamemazine, Loxapine, Mesoridazine,
Perphenazine, Pimozide, Pipothiazine, Sulpride,
Thioridazine, Thiothixene, Trifluoperazine, Zuclopenthixol
2nd gen.: Asenapine, Lurasidone, Ziprasidone, Iloperidone,
Olanzapine LAI
“3rd gen.”: Cariprazine, Lumateperone
2. Brexpiprazole Weight gain (~1.23-1.89 kg; dose dependent)
No glucose intolerance and lipid abnormalities in
clinical trials (will most likely be most $$$$)
MOA: partial agonist leaning towards
antagonist at D2 receptors, potent 5-HT2A
antagonist and potent 5-HT1A partial agonist;
also strong α1 antagonist
Multiple other receptor affinities
Antipsychotic Polypharmacy
*** Generally, guidelines, such as the WFSBP 2012 Guidelines, TMAP 2006 Guidelines, APA 2004 (and 2009 commentary) Guidelines, RANZCP 2016, and BAP2019 guidelines note that at minimum,
adequate monotherapy trial of Clozapine is undertaken, including considerations for smoking and CYP1A2 inducers, adherence, adequate serum clozapine levels >350 ng/mL, etc. Most data look at
Clozapine augmentation. At best, only small effect sizes were observed. On the downside, antipsychotic polypharmacy has been associated with an increased side effect burden, high-dose prescribing,
increased hospitalization rates and length of stay, higher treatment costs and increased mortality (Gallego et al., 2012). For better context and to consider the contrary argument, a recently published
review of systematic reviews of antipsychotic polypharmacy and metabolic syndrome noted conflicting evidence on association of antipsychotic polypharmacy, particularly Clozapine augmentation, with
metabolic syndrome and noted a trend in studies showing a possibly protective effect of Aripiprazole add-on against metabolic syndrome (Ijaz et al., 2018). It should also be noted that any benefit from
polypharmacy may simply be a result of an extended duration of treatment with the first antipsychotic.
With all this, it may be more prudent to err on the side of caution and recommend that apart from cross-titration of antipsychotics, antipsychotic polypharmacy be reserved, at the very minimum, after an
adequate trial of Clozapine and only as augmentation to Clozapine. Ensure informed consent.
Acute agitation: Prioritize de-escalation techniques (e.g. reassurance, respect, etc.) over pharmacologic interventions (e.g. rapid tranquilization/RT)
 Pre-RT: oral Haloperidol/Olanzapine/Quetiapine/Risperidone/Aripiprazole
 RT: IM Promethazine (N/A in PH, so likely oral Biperiden) PLUS IM Haloperidol (AVOID giving Haloperidol without an anticholinergic)
Insufficient evidence: high-dose prescribing

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ANTIPSYCHOTICS NOT AVAILABLE LOCALLY
Medication Specific information MOA, Side Effects, Interaction Indications, Side Effect Management, and More
1st Gen:
Cyamemazine
Loxapine
Mesoridazine
Perphenazine
Pimozide
Pipothiazine
Sulpride
Thioridazine
Thiothixene
Trifluoperazine
Zuclopenthixol
Sulpride – at low doses, D2 partial agonist
(leaning to antagonist) and D3-preferring
Zuclopenthixol – has depot LAI, may be more
efficacious at the cost of more ADRs
Loxapine – has 2nd gen properties
MOA: all D2 and HAM antagonism
Side Effects: Pimozide, Thioridazine – marked QT prolongation
Trifluoperazine, Perphenazine – hepatotoxic; contraindicated:
hepatic disease
*Class info relevant in Organic Medicinal Chemistry, not Pcol:
Phenothiazines:
 Aliphatic – Chlorpromazine
 Piperazine – Fluphenazine, Trifluoperazine, Perphenazine
Piperidine – Mesoridazine, Thioridazine
Butyrophenones – Haloperidol, Droperidol
Thioxanthines – Thiothixene, Flupenthixol, Zuclopentixol
Indications: Schizophrenia, tics (Pimozide)
2nd Gen:
Asenapine
Iloperidone
Lurasidone
Perospirone
Sertindole
Ziprasidone
Ziprasidone – take with 300-calorie meal Side Effects:
Asenapine – anaphylaxis, QT prolong.
Iloperidone – QT prolongation, rare priapism
Sertindole – marked QT prolongation, severe orthostatic
hypotension
Ziprasidone – marked QT prolongation
Indications: Schizophrenia, acute bipolar mania
(Ziprasidone), acute bipolar depression (Lurasidone), both
bipolar mania and depression (Asenapine)
3rd Gen:
Cariprazine
Lumateperone
Cariprazine – D2 partial agonism, weaker 5-
HT2A antagonism, more portent 5-HT1A partial
agonism, D3 selectivity at low doses
Lumateperone – 5-HT2A antagonism, D2
presynaptic partial agonism, D2 post synaptic
antagonism, and GluN2B modulation
MOA: Partial D2 agonists,etc.
Side Effects: lesser risk for metabolic syndrome
Indications: Schizophrenia, acute bipolar mania/mixed
(Cariprazine)
Others:
Pimavanserin
Tetrabenazine
MOA:
Pimavanserin: 5-HT2A inverse agonist
Tetrabenazine: VMAT2 inhibitor
Indications:
Pimavanserin: Parkinson’s disease psychosis
Tetrabenazine: Tardive dyskinesia
ANTICHOLINERGICS
Medication Information
Biperidena Indication: EPS (only dystonia and pseudoparkinsonism; generally not efficacious for akathisia), Parkinson’s (caution in elderly)
Side effects:
Common: sedation, confusion, memory disturbance (esp. in older adults), tachycardia, dry mouth, urinary retention and constipation, and other anticholinergic side effects
(opposite of D.U.M.B.B.E.L.S.S.)
Rare: angle-closure glaucoma, myasthenia gravis, gastrointestinal obstruction
Caution in patients with angle-closure glaucoma, mechanical stenoses in GI tract, paralytic ileus, megacolon, prostatic adenoma, prostatic hypertrophy, diseases predisposing
perilous tachycardia, arrythmias, cognitive/memory problems, excessive sedation, hallucinations, seizures; caution in the elderly
Administration: Morning if once daily (less likely to experience EPS in sleep)
Other anticholinergics for EPS (N/A locally): Benztropine, Trihexyphenidyl, Procyclidine
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ANXIOLYTICS AND SEDATIVE-HYPNOTICS
1. Benzodiazepines
NEED S2
 Alprazolam (t1/2 12-15 h)
- ↑ Concentration by Estrogen
products
 Bromazepam (t1/2 11-12 h)
 Clonazepam (t1/2 30-40 h)
- Absence seizures with Valproate
 Clorazepateb (decarboxylation to
Nordiazepam is rapid: t1/2 =40-50h)
 Diazepama (injection) (t1/2 20-80 h)
- Concentration and t1/2 ↑ by
omeprazole
 Lorazepam (t1/2 10-20 h)
- Preferred in hepatic impairment
- ↓ Clearance by Valproate &
Probenecid
- ↓ Concentration by Estrogen
products (glucuronidation)
- In the PNF but not FDA-
registered
MOA: GABAA positive allosteric modulator; GABA
effect is enhanced  Cl- enters cell, “supercharging”
neuron and making it less responsive to other
neurotransmitters
Ineffective and potentially harmful in PTSD and
phobias
Side Effects
Common: Sedation, anterograde amnesia, fatigue,
depression, dizziness, ataxia, slurred speech,
weakness, confusion, GI disturbances, paradoxical
hyperexcitability, nervousness
Rare: Hallucinations, mania, hypotension, grand mal
seizures, CNS depression, hypersalivation, dry mouth,
hepatic & renal dysfunction, blood dyscrasias, (BZDs
generally do NOT cause respiratory depression in
absence of comorbidities/drug interactions)
Indications
 Panic disorder and generalized anxiety disorder, acute use only
(general)
 Insomnia (acute use only; CBTi = 1st line)
 Acute alcohol withdrawal
 Catatonia (Lorazepam)
 Epilepsy (1st line in status epilepticus: IM Midazolam, IV
Lorazepam, IV Diazepam)
Antidote: Flumazenil (may precipitate seizures those with epilepsy)
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,
Benzodiazepines
NEED S2
 Midazolam (t1/2 4.8-6.4 h)
- IM administration non-inferiorto
IV Lorazepam for status
epilepticus in RAMPART trial
(possibly superior in terms of
administration route and lack of
need for significant temperature
control)
To minimize the risk of addiction and/or dependence From Behnoush et al., 2015:
use should be limited to not more than 4 weeks in
anxiety disorders & not more than 7 days for insomnia
Needs careful tapering to avoid seizure recurrence /
withdrawal symptoms
Withdrawal:
Stiffness Anxiety/insomnia
Weakness Nightmares
GI disturbance Depersonalization
Paresthesia ↓ Memory
Flu‐like symptoms ↓ Concentration
Visual disturbances Delusions, hallucinations
Convulsions Depression
Cognitive impairment
Interactions:
“Holy trinity” – opioid + benzodiazepine + skeletal
muscle relaxant (esp. Cyclobenzaprine);
avoid (CNS depression)
2. Gabapentin and
Pregabalin
MOA: binds α2δ subunits of voltage-sensitive Ca2+ channels (VSCC)
long-term: increased GABA transporter density & functional GABA transport
Side effects:
Common: Sedation, weight gain, peripheral edema
CNS: Dizziness, ataxia, fatigue, tremor, dysarthria, paresthesia, memory impairment,
coordination abnormal, impaired attention, confusion, euphoric mood, irritability GIT: Vomiting,
dry mouth, constipation, weight gain, increased appetite, flatulence
Etc.: Blurred vision, diplopia, libido decreased, erectile dysfunction
Rare: <12 y.o.: Hostility, emotional lability, hyperkinesia, thought disorder, weight gain; rare
activation of suicidal behavior/suicidality
Gabapentin: Anaphylaxis, angioedema, sudden unexplained deaths in epilepsy (unknown if due
to Gabapentin use)
Interactions:
 Absorption decreased by antacids, increased by naproxen, cimetidine
 Serum concentration decreased by Mg2+ salts and orlistat, and increased by Morphine and
Hydrocodone, and Cimetidine
 Breathing difficulties with CNS depressants (high risk in elderly, those with COPD)
Caution: Emerging addiction risk; Gabapentin aggravates absence seizures; renal excretion
Indications: GAD, postherpetic neuralgia and diabetic neuropathy,
restless leg syndrome (only for Gabapentin enacarbil ER), epilepsy
(focal seizures; adjunctive), intractable hiccups (Gabapentin)
Gabapentin also has evidence of efficacy in alcohol use disorder
3. Prazosin MOA: α1 antagonist in CNS (crosses BBB)
Note: α1 agonism causes the ff:
 Disrupts higher-order cognitive processing and induces primitive fear response
 Disrupts REM sleep
 Increases non-REM sleep
 Stimulates CRH release  more cortisol
Side effects: First-dose phenomenon
PTSD nightmares*
*Doxazosin available locally instead of Prazosin but less studied
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4. Hydroxyzinea
MOA: H1 receptor antagonist; Some action at muscarinic and 5-HT2 receptors; suppression of
some subcortical regions
Side Effects: Anticholinergic, sedation
Acute GAD
Not to be used >3 days for insomnia
5. Zolpidem
NEEDS2
MOA: NOT a BZD; positive allosteric
modulator of GABA receptors
(preference for GABAA) w/ α1 subunits
Indication: Not more than 7 days for
insomnia; Zolpidem CR not restricted
to short-term use, but only IR available
locally
Contraindications: Significant
obstructive sleep apnea syndrome
and acute and/or severe impairment
of respiratory function; myasthenia
gravis; severe hepatic impairment;
personal or family history of
sleepwalking
Common: Sedation, dizziness, ataxia, dose-
dependent amnesia, hyperexcitability, nervousness,
diarrhea, nausea, headache
Rare/serious: Hallucinations, angioedema, respiratory
depression,
Interactions:
Synergistic with CNS depressant
Sertraline, Ketoconazole – may increase zolpidem levels
Rifampicin – may decrease zolpidem levels
Notes:
**First line for insomnia is psychotherapy: CBTi (stimulus control, sleep
restriction, relaxation response)
**Melatonin is the only OTC with evidence for efficacy (Jetlag, phase-
delayed sleep)
**TAKE BEFORE BEDTIME and without food. Ensure possibility of
7-hour sleep time, minimum.
somnambulism, sleep-driving, sleep-eating, sleep-
sex, sleep-phone calls
STIMULANTS, WAKE-PROMOTING AGENTS, AND MEDICATIONS FOR ADHD
1. Methylphenidate
(Ritalin1, Concerta2)
NEED S2
MOA: Allosteric blocker for both NET and DAT
Indications: ADHD (1st line),
narcolepsy (excessive daytime sedation/EDS)
Contraindications: Extreme anxiety or agitation,
motor tics or Tourette’s syndrome or w/ family
history, glaucoma, cardiovascular disease,
hyperthyroidism and thyrotoxicosis,
gastrointestinal obstruction or severe GI narrowing
(specific for Concerta), history of substance use
disorders
Common:
CNS: Insomnia, headache, worsening of tics, nervousness,
irritability, overstimulation, tremor, dizziness,
GIT: Anorexia, nausea, abdominal pain, weight loss
Rare/serious: Priapism, dysphoria, psychotic episodes, especially
with parenteral misuse, seizures, rare neuroleptic malignant
syndrome, rare activation of hypomania, mania, or suicidal ideation
(controversial), cardiovascular adverse effects (palpitations,
tachycardia, hypertension, sudden death in patients with preexisting
cardiac structural abnormalities)
Antihypertensives (BP effects)
PPIs – increase methylphenidate absorption
Antidepressant, anticonvulsant, andwarfarin
– inhibits metabolism
May have synergistic effects with other
stimulants or NE/DA reuptake inhibitors
Bioequivalence does not equate to
clinical equivalence
In narcolepsy, taper to prevent rebound
hypersomnia
Risk of dependence, tolerance, and addiction

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October 10, 2020
2. Atomoxetine MOA: Blocks NET
Indications: ADHD (2nd line)
Contraindications: Pheochromocytoma or w/
history, severe cardiovascular disorder that might
deteriorate with clinically important increases in HR
and BP, angle-closure glaucoma
Financially toxic !!$$$$!!
Common:
CNS: Fatigue (esp. in children), decreased appetite, ↑ HR (6–9
beats/min), ↑ BP (2–4 mm Hg), insomnia, dizziness, anxiety,
agitation, aggression, irritability
GIT: Dry mouth, constipation, N/V, abdominal pain, dyspepsia
Genitourinary and others: Urinary hesitancy, urinary retention (older
men), dysmenorrhea, sweating, sexual dysfunction
Rare/serious: Priapism, hypertension, orthostatic hypotension,
severe liver damage, manic switch, suicidal ideation activation
Metabolized by CYP2D6
3. Clonidinea MOA:
Initial: Postsynaptic α2A, α2B, α2C receptor agonism.
α2A agonism  increased signal in prefrontal c
o
r
t
e
x
& reduced CNS sympathetic outflow (CNS),
vasoconstriction (ANS)
Then: Binds CNS Imidazoline 1 (I1) receptors 
downstream catecholamine release  presynaptic
α2 receptors  autoreceptor activation, NT r
e
l
e
a
s
e
stopped (sedation in CNS, hypotension in ANS)
Indications: 2nd
line for ADHD, Tourette’s, smoking
cessation, and hypertension
Common:
CNS: Sedation, weakness, fatigue, sexual dysfunction, depression,
insomnia, withdrawal symptoms on abrupt cessation: nervousness,
agitation, headache, and tremor
CV: Orthostatic hypotension, tachycardia or bradycardia, rebound
hypertension on abrupt withdrawal  reinstitute drug and t
a
p
e
r
slowly
GIT: Dry mouth, N/V
Rare/serious: Sinus bradycardia, AV block
Beta blockers – risk of worse withdrawal
CNS depressants – additive effects
TCAs – reduced hypotensive effects of
Clonidine
Rate controllers (Digoxin, CCBs, Beta
Blockers) – bradycardia, AV block risk
ANXIOLYTICS, SEDATIVE-HYPNOTICS, STIMULANTS, AND WAKE-PROMOTING AGENTS NOT AVAILABLE LOCALLY
1. Other
benzodiazepines
Chlordiazepoxide (t1/2 = 6.6-13.4 hours), Clobazam (t1/2 = 36-42 hours), Lormetazepam, Nitrazepam, Oxazepam (t1/2 =
5.6-10.4 hours)
Flurazepam (t1/2 = 2-6 days), Quazepam (t1/2 = 2-5 days), Triazolam (t1/2 = 1-2 hours), Estazolam (t1/2 = 12-30 hours),
Temazepam (t1/2 = 4-20 hours)
Indications: Only Flurazepam, Quazepam,
Triazolam, Estazolam, Temazepam indicated
for short-term management of insomnia among
ALL benzodiazepines (even local ones)
2. BZRAs Zaleplon (t1/2 = 1-2 hours)
Zopiclone (t1/2 = 3.5-6.5hours)
Eszopiclone (t1/2 = 3.5-6.5 hours)
Indications: short-term management of
insomnia
3. Buspirone MOA: 5-HT1A partial agonism
Onset: 6 weeks
Side Effects:
Dizziness, headache, nervousness, sedation, excitement, nausea,
restlessness, rare cardiac symptoms
Indication: Acute GAD
CYP3A4 substrate
4. Melatonin
Agonists:
Ramelteon and
Tasimelteon
MOA: MT1 and MT2 receptor agonist
(for Tasimelteon, MT2>>MT1)
Ramelteon: Contraindicated w/
Fluvoxamine
Side Effects:
 Ramelteon: Sedation, fatigue, dizziness, rare angioedema & CNS
depression (serious)
 Tasimelteon: Headache, nightmares, increased ALT, upper respiratory
infection, urinary infection
Indication: Insomnia
5. DORA:
Suvorexant
Dual Orexin Receptor Antagonist
MOA: orexin 1 & 2 receptor antagonist
Side Effects: Sedation, headache, dizziness, abnormal dreams; rarely sleep
paralysis and hypnogogic, hypnopompic hallucinations
Indications: Insomnia
6. Other
amphetamines
Dexamphetamine
Lisdexamphetamine – prodrug of
d-amphetamine (linked to Lysine)
Risk of tolerance, dependence, and addiction; rebound cataplexy with
abrupt discontinuation
Indications: ADHD, narcolepsy
Lisdexamphetamine: 2nd line, binge-eating
disorder
CONTROLLED
7. Modafinil and
Armodafinil
MOA: Slight DAT blockade
Armodafinil more potent
Side Effects: Headache (dose-dependent), anxiety, nervousness, insomnia,
dry mouth, diarrhea, nausea, anorexia, pharyngitis, rhinitis, infection,
hypertension, palpitations, rare SJS/TEN, angioedema, hypersensitivity
Indications: Narcolepsy (reduce EDS)
Interaction: Reduce efficacy of contraceptives
CONTROLLED

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8. Sodium Oxybate
CONTROLLED
MOA: GHB receptor binder, GABAB
receptor partial agonist
Administration: Avoid taking with food
2 hours before dose; avoid activity until
6 hours after 2nd dose
Side Effects: Headache, dizziness, sedation, nausea, vomiting, enuresis,
respiratory depression, neuropsychiatric events, confusion and wandering at
night; caution on sodium content
Risk of tolerance, dependence, and addiction
Indication: Narcolepsy with cataplexy in
children and adults (EDS, cataplexy, sleep
paralysis, hypnagogic and hynopompic
hallucinations)
Onset: 1-2 months (max. effect: 3 months)
9. Pitolisant MOA: H3 receptor antagonist/inverse
agonist
Side Effects: Dose-dependent QT prolongation Indication: Narcolepsy with/without cataplexy
(EDS only)
Contraindication: Pregnancy
10. Solriamfetol
CONTROLLED
MOA: blocks NET and DAT
Administration: Take on empty
stomach and avoid food 30 min. after
dose; take 9 hours before bedtime
Side Effects: Headache, nausea, and decreased appetite; small dose-
dependent increases in BP and heart rate; uncommon insomnia
Indications: Narcolepsy (EDS) and obstructive
sleep apnea
“MOOD STABILIZERS”
Medication MOA, Indications, And C/Is Side Effects Interactions
1. Lithiumb MOA:
 Cellular: GSK-3 inhibition?
Growth factor neuroprotection and ↓ apoptosis
Decreased oxidative stress
Secondary messenger systems?
Inositol monophosphatase inhibition (more
inositol, less IP3)
Protein kinase C inhibition via GSK-3 inhibition:
reparative neuronal plasticity
Modulation of Ca2+ disturbances (↓ apoptosis)
↑cAMP-induced CREB gene transcription
 Neurotransmission?
 ↓excitatory Glu neurotransmission
 ↓DA release, GSK-3 inhibition via
D2 antagonism
 Higher-order biological systems?
 Circadian rhythm resynchronization via
modulation of clock genes
 HPA axis modulation via protein kinase C
inhibition (corticotrophin expression regulated)
 Ankyrin 3 (Ank3) modulation  regulates s
t
r
e
s
s
reactivity via corticosterone regulation
 Neurocircuitry and neurocognition?
Indications: Bipolar disorder (+reduces suicide;
1st line unless side effects can’t be monitored), 2nd
line adjunct for MDD
Contraindications: Severe cardiac or renal
disease, dehydration or sodium depletion
Side Effects
Common:
 CNS: Ataxia, dysarthria, delirium, tremor, memory problems
 GIT: diarrhea, nausea, weight gain
 Derma: acne, rash, alopecia (check Cu/Zn levels)
 Blood: leukocytosis
Rare/serious:
 Renal: Polyuria, polydipsia (nephrogenic diabetes insipidus)
 Thyroid: Euthyroid goiter/hypothyroid goiter
 CV: AV block, arrhythmias, ECG changes
 CNS: Pseudomotor cerebri, seizures
 Toxicity: Seizures, delirium, coma, and death
Increase lithium levels: ACEIs (maybe ARBs),
CCBs, Methyldopa, Carbamazepine, Thiazide
diuretics, Metronidazole, NSAIDs, Phenytoin,
Topiramate, Tetracycline
Decrease lithium levels:
Alkalizing agents, Calcitonin, Calcium/ sodium
polystyrene sulfonate, Carbonic anhydrase
inhibitors, Loop diuretics, Mannitol, NaCl (and
dehydration), Caffeine, Urea
Minimizing variations in Lithium levels:
 Keep daily coffee/tea and water consumption
consistent
 Ensure adequate hydration during fevers or
exercise
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2. Divalproex/
Valproic Acid
MOA: Hypotheses include
1. Reduced excessive neurotransmission by ↓flow
of ions through Na+
channels, T-type Ca2+
currents
2.↑GABA action via ↑release (GABAB),
↑synthesis (↑glutamic acid decarboxylase),
↓reuptake & ↓metabolism (↓GABA-T)
3. Downstream actions on
complex signal transduction cascades (e.g.
GSK-3 inhibition, phosphokinase C,
myristolated alanine-rich C kinase substrate
blockade) and activating various signals that
promote neuroprotection & long-term plasticity
(e.g. extracellular signal- regulated kinase,
cytoprotective protein B-cell
lymphoma/leukemia-2 gene, GAP43)
Unknown whether these explain mood-stabilizing
action, anticonvulsant action, anti-migraine action,
and/or side effects
Indications: Epilepsy (focal, GTC, myoclonic;
absence as alternative to ethosuximide but w/
attentional dysfunction; 1st line juvenile myoclonic
epilepsy/Janz syndrome and myoclonic/atonic
epilepsy or Doose syndrome; 2nd line status
epilepticus), mania & acute bipolar depression,
migraine prophylaxis
Contraindications: Urea cycle disorder, serious
liver disease, pancreatitis, thrombocytopenia
Side effects:
Common:
 CNS: Sedation, tremor, dizziness, ataxia, asthenia,
headache
 GIT: Abdominal pain, N/V, diarrhea, reduced appetite,
constipation, dyspepsia, weight gain
Unusual/controversial:
alopecia (unusual; check Cu/Zn levels), polycystic ovaries
(controversial), hyperandrogenism and hyperinsulinemia and
lipid dysregulation (controversial), decreased bone mineral
density (anticonvulsants and serotonin modulators in general)
Rare/Serious:
Hepatotoxicity, liver failure, pancreatitis. thrombocytopenia,
leukopenia, drowsiness, confusion (valproate-induced
hyperammonemic encephalopathy, a sign of toxicity)
*Antidote for valproate-induced hepatotoxicity and
hyperammonemic encephalopathy: L-carnitine
Interactions:
– Carbapenem: ↓ Valproate levels
– Lamotrigine: may ↓ Valproate concentrations
Sodium Valproate, Valproic Acid, and
Divalproex are NOT equivalent
STRICTLY AVOID in women and girls of
childbearing potential. The only exception is if
and only if there are no other options.
mitochondrial disorders due to mutations in
mitochondrial DNA polymerase-gamma (POLG),
pregnancy
3. Lamotrigine MOA: Blocks Na+ channels and increases brain
GABA (epilepsy); blocks L-, N-, P-type Ca2+
channels (decreases Glu release), weak 5-HT3
receptor and dihydrofolate reductase inhibitor
Indications: Focal seizures, GTC, absence
seizures (<Valproate);
only for bipolar depression
Side Effects:
Common: Dizziness, diplopia, insomnia, ataxia
Interactions: Dose adjustments needed for
inducers (carbamazepine, phenytoin,
phenobarbital, primidone,
rifampicin, lopinavir/ritonavir) and inhibitors
(valproate, UGT inhibitor)
Caution in urine drug screens as Lamotrigine may
cause a false positive result for phencyclidine and
synthetic cannabinoids
Serious: SJS/TEN: Titrate dose
VERY SLOWLY to prevent &
strictly adhere to very slow
titration recommendations;
avoid vitamin B complex and
new food/meds/cosmetics/
deodorants/detergents/fabric
softeners/sunburn; can
worsen/ppt myoclonic seizures
Drug reaction w/ eosinophilia &
systemic symptoms (DRESS)
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4. Carbamazepine
a, b
MOA:
 Interaction with Na+
channels at alpha-pore
forming subunit
 Adenosine 1 (A1) receptor antagonist 
upregulation of A1 receptors
 Decreases release of presynaptic Asp & Glu
 Blocks Ca2+ influx through NMDA receptor &
decreases Ca2+ serum concentrations
Indications: Focal and focal-to-bilateral seizures,
trigeminal neuralgia, 1st
line for benign occipital
epilepsies (for acute bipolar mania only, NOT
bipolar depression)
Contraindications: HLA*B1502 allele, bone
marrow suppression, hepatic porphyria
Side effects:
Common: Sedation, confusion, dizziness, ataxia, double
vision, nausea, diarrhea, benign leukopenia
Serious: SJS-TEN (avoid with paracetamol), DRESS,
hepatotoxicity, cardiac conduction delay,
bone marrow suppression (agranulocytosis and aplastic
anemia), hyponatremia and SIADH
HLA*B1502 screening required for first-time takers to prevent
SJS-TEN
Can aggravate absence seizures
Interactions:
Multiple psychotropics, including anticonvulsants,
antidepressants, & antipsychotics due to induction
of multiple CYP enzymes; may cause failure of
hormonal contraceptives
Additive myelosuppression with Clozapine
DEMENTIA
Medication MOA, Indications, C/Is Side Effects and Administration Interactions
1. Donepezil MOA: Reversible central & peripheral
acetylcholinesterase inhibitor
Useful for dementia with Lewy bodies
Side Effects:
Common:
N/V, diarrhea, appetite loss, increased gastric acid
secretion, dyspepsia (take with food), weight loss,
headache, dizziness, fatigue, depression, asthenia,
insomnia (if so, take Donepezil in morning)
Rare: seizures, syncope
Administration:
Donepezil: at bedtime with food
Rivastigmine and Galantamine: with food
**Rivastigmine: retitrate if stopped >3 days to avoid
vomiting with esophageal rupture
Can theoretically reduce Levodopa efficacy
Susceptible to CYP2D6, 3A4 interactions
2. Rivastigmine MOA: Pseudoirreversible (self-reverses over hours)
acetylcholinesterase (cortex & hippocampus) &
butylcholinesterase (glia) inhibitor
Also indicated for Parkinson’s disease dementia, useful
for dementia with Lewy bodies
Smoking can reduce clearance
No CYP interactions
3. Galantamine
(N/A locally)
MOA: Reversible, competitive central
acetylcholinesterase PAM at nicotinic receptors
Not recommended in severe renal, hepatic impairment
Susceptible to CYP2D6, 3A4 interactions
4. Memantine MOA: Low-affinity uncompetitive NMDAR antagonist;
adjunctive only
Dizziness, headache, hallucinations, insomnia,
constipation; rare seizures
- Urinary alkalizer (pH8): memantine clearance reduced by 80%
- Plasma levels increased by: Cimetidine, Ranitidine,
Procainamide, Quinidine, Quinine, Nicotine, Trimethoprim
- May enhance effects of: L-DOPA, DA agents, Selegiline,
anticholinergics
- May reduce effects of barbiturates, antipsychotics
- CNS toxicity: Amantadine, Ketamine, DXM
- HCTZ – Memantine may possibly reduce serum concentrations
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5. Ginkgo biloba
EGb 761
Publication bias, low quality studies, inconsistent and unreliable findings
*Tacrine no longer used due to poorer tolerability and hepatotoxictiy
Prevention and management of superimposed delirium:
 Treat/manage underlying cause (diseases, toxicity, medications, etc.)  Ask assistance from family members or carers person is familiar with
 Have a clock and calendar at the bedside to assist in orientation.  Keep room lighting low, especially at night.
 Ensure room has a window with a secured view.  Keep noise minimal and provide earplugs in the evening.
 Limit the number of staff changes to minimize confusion.  Checking if person requires any visual or hearing aids and make sure they are worn
 Limit visitors.  Assess for pain and provide Paracetamol and other interventions as needed.
 Constantly, patiently reassurance and repeatedly explain on sources of confusion  Assess for dehydration and/or constipation and provide fiber and fluids as needed.
PARKINSON’S DISEASE
1. Levodopa +
Carbidopa/
Benserazide
MOA: Aromatic amino acid (dihydroxyphenylalanine)
and precursor to DA passes through BBB, taken up by
DAergic neurons and converted into DA. Carbidopa and
Benserazide are peripheral dopamine decarboxylase
inhibitors
Acute: N/V, anorexia, orthostatic hypotension, arrhythmias
Long-term: Wearing-off and on-off phenomenon, dyskinesias
(choreiform, dystonic, involuntary), somnolence, vivid dreams,
confusion, hallucinations, agitation
Administration: Without food (1 h before, 2 h after meals)
Orthostatic hypotension with
antihypertensives, Selegiline
Low protein diets increase absorption by
50%, and high protein diets reduce
absorption
2. Entacapone MOA: Selective, reversible
catechol-o-methyltransferase inhibitor
Contraindications: Severe biliary disorder
Diarrhea (delayed 4-12 week onset), dyspnea, weakness,
brown-orange urine
May increase levodopa SEs – dyskinesias, nausea, orthostatic
hypotension, hallucinations, sleep attacks
Rare: Rhabdomyolysis
**Tolcapone: hepatotoxic (TOxic to Liver)
Administration: taken with Levodopa
Drugs that interfere w/ biliary excretion,
glucuronidation will increase effect:
Probenecid, Cholestyramine, Erythromycin,
Ampicillin, Rifampicin, Chloramphenicol
Drugs metabolized by COMT: E, NE, DA,
Dobutamine, CH3-DOPA, Apomorphine,
Isoproterenol
3. Pramipexolea,
Ropinirolea,b,
Rotigotine (patch)
4. Piribedil
MOA: Post-synaptic D2 agonist in caudate-putamen
Piribedil: D2/D3 agonist, α2 antagonist
Indications: Parkinson’s and restless leg syndrome
(RLS) (Pramipexole efficacy in PD depression)
N/V, low extremity edema, somnolence, lightheadedness,
postural hypotension, hallucinations, delusional behavior,
compulsive behavior (eating, sex, gambling, shopping)
Manic switch: high risk – Pramipexole, low risk – Ropinirole
Parkinson-hyperpyrexia syndrome (withdrawal)
Pramipexole – drugs inhibiting/competing w/
cationic tubular secretion: Verapamil,
Quinine, Probenecid, Ranitidine, Diltiazem,
Triamterene
Ropirinole – CYP1A2 modulators
5. Apomorphine(SQ)
(N/A locally)
MOA: Partial D2 agonist N/V, drowsiness, dizziness, postural hypotension,
hallucinations, edema, injection site reactions
Indication: Off-episode rescue
Contraindication: 5-HT3 antagonists (profound
hypotension)
6. Ergot D2 agonists Bromocriptine, Pergolide, Cabergoline: rarely used due to risk of pleural, retroperitoneal, and pericardial fibrosis
Pergolide, Cabergoline: 5-HT2B agonists  valvular heart disease
(low-dose Cabergoline used 1st line in hyperprolactinemia when surgery isn’t an option; Bromocriptine is an alternative)
7. Selegiline
(only tablet
available)
MOA: Irreversible, selective MAO-B inhibition at
dose<10mg/day
Indication: Adjunct for Parkinson’s (oral), MDD (patch)
Contraindications: Serotonin syndrome-inducing
agents, very high-tyramine foods (>150 mg/day)
Elevated ALT, nausea, headache, orthostatic hypotension,
musculoskeletal injuries, non-life-threatening arrhythmias
Hypertensive crisis with tyramine-rich food
and other MAOIs (less restrictions on diet
<10 mg); serotonin syndrome with
serotonergics
(NOTE: Linezolid and methylene blue also
have MAOI properties)

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8. Rasagiline
(N/A locally)
MOA: Irreversible and selective MAO-B inhibition when
Rasagiline<1 mg/day
Indication: Monotherapy, adjunct for idiopathic
Parkinson’s
Contraindications: Serotonin syndrome-inducing
agents, very high-tyramine foods (>150 mg/day)
Monotherapy – Flu syndrome, hallucination, depression,
arthralgia, dyspepsia, somnolence, psychotic-like behavior,
impulse control behaviors
Adjunct to Levodopa – Dyskinesia, dry mouth, vomiting,
anorexia, constipation, weight loss, postural hypotension,
accidental injury, abdominal pain, abnormal dreams, arthralgia,
tenosynovitis, nausea, headache
Hypertensive crisis with tyramine-rich food
and other MAOIs (less restrictions on diet <1
mg); serotonin syndrome with serotonergics
(NOTE: Linezolid and methylene blue also
have MAOI properties)
CYP1A2 modulators
9. Amantadinea
MOA: Induces release/decreases reuptake of DA;
upregulation of D2 receptors (in vivo); antimuscarinic;
non-competitive NMDA antagonist
Indication: Parkinson’s, EPS, influenza A prophylaxis/
treatment
Contraindications: Seizures, severe renal impairment,
gastric ulceration, untreated angle closure glaucoma
Nausea, dizziness, insomnia, blurred vision, depression,
anxiety, psychosis (high doses), confusion, livedo reticularis,
anticholinergic, nervousness, headache
Exacerbation of seizure disorder, rare suicidal ideation (even
without history)
Abrupt discontinuation: NMS (rare)
Impairing renal clearance of amantadine:
Quinidine, thiazides, triamterene,
cotrimoxazole
OTHER ANTIEPILEPTICS
All: Supplement with Folic Acid before, during pregnancy
General side effects: N/V, sedation, dizziness, headache; refrain from switching formulations (stick to 1 accessible, affordable formulation from the beginning)
BARBITURATES / GABAergic
1. Phenobarbitala
NEEDS S2
MOA: Raising seizure thresholds or altering
seizure patterns (unknown mechanism),possibly
thru enhancing GABAA receptor activity.
Depresses Glu excitability; alters Na+, Ca2+, and
K+
channel conductance; and affects
polysynaptic midbrain reticular formation
Indications: Focal and tonic-clonic seizures,
myoclonic seizures, neonatal seizures; 1st
line
for neonatal seizures
Contraindications: porphyria; dyspnea /airway
obstruction; marked hepatic impairment/hepatic
encephalopathy; intraarterial administration;
history of sedative/hypnotic addiction; nephritic
service users/patients
Common:
 CNS: Sedation, ataxia, vertigo, cognitive dysfunction (worst),
depression, nystagmus, irritability, emotional disturbances
 GI: N/V
 CV: Hypotension
 Derma: Rash, uncommon SJS-TEN
Rare/serious: Megaloblastic anemia, rare agranulocytosis, DRESS,
respiratory/CNS depression; risk of tolerance, dependence, and
addiction
*Cheap unit cost offset by expenses needed to locate and pay for
physician with S2 license
**DO NOT USE FOR INSOMNIA
CYP inducer
Interacts with CYP2C9, 2C19 modulators
Ethosuximide, acetazolamide, antacids – lower
phenobarbital levels
SODIUM CHANNEL BLOCKERS (VSSC BLOCKERS)
1. Phenytoin
a, b(tablets, capsules)
MOA: Reduces hyperexcitability on Na+
channels. It also modulates T-type Ca2+
channels, but not in the thalamus; diminishes
synaptic transmission, limits fluctuation of
neuronal ionic gradients via Na-K ATPase, and
inhibits calcium-calmodulin protein
phosphorylation
Indications: Focal and tonic-clonic seizures, 2nd
line status epilepticus***
Common:
 CNS: Nystagmus, ataxia, dysarthria, insomnia, nervousness,
motor twitching, tremor, dizziness, impaired memory
 Derma: Rash, hirsutism, coarsening of facial features, gingival
hyperplasia
 Respiratory: pneumonia, sinusitis, rhinitis, asthma
 Sensory: tinnitus, diplopia, eye pain, taste loss
 Etc: lymph node hyperplasia, chest pain, edema, soft tissue injury
(IV)
CYP inducer
Interacts w/
CYP2C9, 2C19,
3A4 modulators
Can displace
warfarin (protein
binding) 
bleeding

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Phenytoin
a, b(tablets, capsules)
Contraindications: sinus bradycardia, second
or third degree AV block, Adams-Stokes
syndrome
Onset: 4 weeks
Prodrug: Fosphenytoin (N/A locally)
Rare/serious: Hypotension, cardiac conduction abnormalities ***Due to equal efficacy w/ Valproate and
Levetiracetam in ESSET trial as adjunct in
benzodiazepine-refractory status epilepticus,
Fosphenytoin is less preferred for this indication
as it has more contraindications as compared to
Levetiracetam
(rapid administration), hyperglycemia, rare diabetes insipidus, blood
dyscrasias, rare allergic rash (SJS, lupus erythematosus syndrome,
radiation-induced erythema multiforme, DRESS), rare lymphoma/
multiple myeloma, toxic hepatitis and liver damage, cerebellar atrophy
(long-term, high doses), purple glove syndrome (IV)
Fetal hydantoin syndrome: cleft lift/palate, microcephaly, mild
intellectual disability
Possibly carcinogenic to humans (IARC Group 2B), use gloves
2. Oxcarbazepine
tablets: a, b
MOA: Blocks Na+ channels via interaction at a
specific site of the alpha pore-forming subunit;
inhibits Glu release
Indication: Focal seizures (RCTs generally
negative for mood-stabilizing properties)
Onset: 2 weeks
No efficacy for bipolar disorder; May worsen
some generalized seizures
Common:
 CNS: Sedation (dose-dept), dizziness (dose-dept), headache,
ataxia (dose-dept), nystagmus, abnormal gait, confusion,
nervousness, fatigue
 GI: Nausea (dose-dependent), vomiting, abdominal pain,
dyspepsia
 Etc: Diplopia (dose-dependent), vertigo, abnormal vision, rash
Rare/serious: Hyponatremia, DRESS
CYP2C19 inhibitor
Mild CYP3A4 inducer (less interactions vsCBZ)
3. Topiramateb
MOA: Blocks Na+ channels, blocks NMDA-Glu
receptors, potentiates GABA activity (on non-
BZD GABAA site),
inhibits carbonic anhydrase
Indication: Epilepsy (focal, GTC, LGS),
migraine prophylaxis,
binge eating disorder (decrease binging and
weight loss
carbonic anhydrase inhibition)
Onset: 2-4 weeks
Common:
 CNS: Paresthesias, sedation, asthenia, dizziness, ataxia,
nervousness, nystagmus, tremor, headache
 GI: Nausea, ↓appetite, weight loss, dry mouth
 Etc: Blurred or double vision, mood problems, confusion,
psychomotor retardation, language and speech problems, fatigue,
taste perversion, upper respiratory tract infection, difficulty with
concentration & memory, hyperthermia,
nephrolithiasis (stay hydrated, ↓dietary Na+
& glucose/fructose,
↑dietary K+
& Ca2+
)
Rare/serious: Metabolic acidosis, secondary angle-closure
glaucoma, oligohidrosis & hyperthermia (more common in children),
sudden unexplained deaths in epilepsy (unknown if related to
topiramate use)
- Increase Topiramate clearance:
Carbamazepine, Phenytoin, and Valproate
- Topiramate increases clearance of Valproate,
Phenytoin, Metformin (may reduce topiramate
clearance)
- Increased risk of kidney stones with other
carbonic anhydrase inhibitors
- Reduce contraceptive efficacy
4. Zonisamide
a, b
MOA: Modulates Na+
channels by unknown
mechanism, modulates T-type Ca2+ channels,
facilitates DA and 5-HT release, inhibits carbonic
anhydrase
Indication: Epilepsy (focal, GTC, myoclonic),
binge eating disorder (decrease binging and
weight loss 
c a r b o n i c anhydraseinhibition)
Onset: 2-4 weeks
Common:
 CNS: Sedation, depression, agitation, difficulty concentrating,
irritability, psychomotor slowing, dizziness, ataxia, headache
 GI: N/V, anorexia, abdominal pain, dry mouth, taste perversion,
dyspepsia, weight loss
 Etc: Elevated serum creatinine and blood urea nitrogen, kidney
stones (stay hydrated, ↓dietary Na+ & glucose/fructose, ↑dietary K+
& Ca2+)
Rare/serious: Serious rash (SJS-TEN, DRESS; sulfonamide),
oligohidrosis & hyperthermia (pediatric patients), blood dyscrasias
(aplastic anemia; agranulocytosis), sudden hepatic necrosis, sudden
unexplained deaths*
- Susceptible to CYP3A4 modulators
- (theoretical) + carbonic anhydrase inhibitors
 kidney stones (mostly calcium phosphate)
*Unknown if sudden deaths related to
Zonisamide use

5. Rufinamideb
MOA: Na+ channel blocker (prolongs inactive
state), etc
Indications: Focal seizure, LGS adjunct (≥4 y.o.)
Contraindications: Familial short QT syndrome;
galactose intolerance, Lapp lactose deficiency, or
glucose– galactose malabsorption
Onset: 4 weeks
Common:
 CNS: Sedation, fatigue, coordination abnormalities, anorexia,
headache, dizziness, tremor
 GI: N/V
 Respiratory: nasopharyngitis, influenza
 CV: QT shortening
Rare/serious: Blood dyscrasias (leukopenia), multi-organ
hypersensitivity syndrome (fever, hematuria, abnormal LFTs,
lymphadenopathy, rash), suicidal ideation
Administration: Take with food (↑absorption)
Weak CYP2E1 inhibitor, weak CYP3A4 inducer
Lowers Carbamazepine, Lamotrigine, oral
contraceptive levels; increases Phenobarbital,
Phenytoin, and Valproate levels
Levels increased by Valproate
6. Lacosamidec
MOA: Enhances slow inactivation of Na+
channels; binds collapsing response mediator
protein 2 (CRMP2)
Indication: Focal seizures
Contraindications: Conduction problems or
severe cardiac disease (myocardial ischemia,
heart failure)
Onset: 4 weeks
Common:
 CNS: Dizziness, ataxia, diplopia, vertigo, abnormal coordination,
ataxia
 GI: N/V, increased LFTs (0.7%)
Rare/serious: Rare hepatitis and neutropenia, rare PR prolongation
and 1st-degree AV block, behavioral/mood effects and suicidal
ideation, multi-organ hypersensitivity syndrome
Has addiction potential
Theoretical pharmacokinetic interactions may
not yet shown to be clinically significant
Enhanced CNS side effects with Phenytoin,
Carbamazepine, Oxcarbazepine, Phenytoin
Increased risk for hyperammonemic
encephalopathy with Valproate
Others: Carbamazepine, Lamotrigine; Valproate (alternative to Ethosuximide, which is N/A locally, for absence seizures)
SYNAPTIC VESICLE SV2A BINDER
Levetiracetam MOA: Binds synaptic vesicle SV2A; Opposes
negative modulators of GABA- & Gly-gated
currents, partially inhibits N-type Ca2+ currents
Indication: 2nd
line status epilepticus; focal
seizures, GTC, myoclonic seizure
Contraindication: Fructose intolerance
Onset: 2 weeks
Common: Sedation, dizziness, asthenia, ataxia, decrease in RBCs
and Hgb, upper respiratory tract infection
Rare/serious: SJS-TEN, Neuropsychiatric Sx
Antiepileptic with *lowest*, if not 0%, risk of teratogenicity
None significant
AMPA RECEPTOR ANTAGONIST
Perampanel MOA: Noncompetitive AMPA glutamate receptor
antagonist
Indications: Adjunctive for focal, focal-to-
bilateral seizures, GTC seizures
Contraindication: Lactose intolerance
Common: Dizziness, somnolence, weight gain, fatigue, irritability
falls, nausea, ataxia, balance disorder,
Susceptible to CYP3A4/5 modulators;
Topiramate decreases Perampanel
concentrations; additive CNS depressant effect
>12 mg decreases efficacy of Levonorgestrel-
containing hormonal contraceptives
hostility/aggressive behavior (10-20%) w/in 6 weeks, other
neuropsychiatric Sx
Rare/serious: Has addiction potential
Broad spectrum (focal and generalized onset)*:
Brivaracetam
Clobazam
Felbamate
Lamotrigine
Levetiracetam
Perampanel
Narrow spectrum (focal)*:
Carbamazepine
Cenobamate
Eslicarbazepine
Ethosuximide (absence)
Gabapentin, Pregabalin
Lacosamide
N/A in Philippines:
Brivaracetam
Clobazam
Eslicarbazepine
Ethosuximide
Felbamate
Paraldehyde
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October 10, 2020

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Phenobarbital (except absence)
Rufinamide
Topiramate
Valproate
Zonisamide
*Lists vary with reference
Oxcarbazepine
Phenytoin
Primidone
Stiripentol
Tiagabine
Vigabatrin
Primidone
Sulthiamine
Stiripentol
Tiagabine
Vigabatrin
Cannabidiol (LGS/DS)
Note for all antiepileptics on the warning on increased suicidal ideation/behavior
Caley et al. (2018) review of descriptive data for bipolar disorder:
Suicide attempt frequencies arranged by treatment group: no treatment > Carbamazepine > Valproate > Lithium
Suicide death rates were, in order of frequency: no treatment > Valproate > Lithium > Carbamazepine.
For valproate, the risk of suicide attempts and suicide death appeared higher than lithium, but lower than no treatment
Caution in data interpretation: (1) an inconsistency in the studied outcomes; (2) a lack of detail with respect to the diagnosed type of BD; (3) an estimated 1.5:1 ratio of female-to-male subjectsstudied;
(4) a lack of detail with respect to suicidality risk factors; (5) very little monitoring of mood stabilizer treatment adherence; and (6) variability in how treatment exposure was measured.
ANTIEPILEPTICS NOT AVAILABLE LOCALLY
Medications MOA and Indications Side Effects and Administration Interactions
1. Brivaracetam MOA: SV2A binder (high-affinity), partial agonistat Na+ channels
Indication: Adjunct in focal seizures for people ≥16 years old
Side Effects: Sedation, dizziness, fatigue, N/V, psychiatric
events, rare bronchospasm and rare angioedema
Interactions: May ↑ Carbamazepine,
Phenytoin levels (no added benefit if
added to Levetiracetam)
2. Cenobamate MOA: Na+ channel blocker, modulates GABAA receptors
Indication: Adjunct, refractory focal seizures
Contraindication: Familial short QT syndrome
Not recommended in end-stage renal disease, severe hepatic
impairment
Side Effects: Dose-dependent somnolence, dizziness,
headache, fatigue, diplopia, suicidal ideation, QT shortening
Rare: Drug reaction with eosinophilia and systemic symptoms
(DRESS)
Interactions: ↑ Clobazam, Phenytoin,
Phenobarbital, , and CYP2C19
substrate levels,
Decrease Carbamazepine,
Lamotrigine, and CYP2B6 and CYP3A
substrate levels
3. Clobazam MOA: 1,4-benzodiazepine (same receptors as bound by BZDs,
different binding)
Indication: Adjunct in LGS for people ≥2 years
Side Effects: Sedation, somnolence, constipation, pyrexia,
drooling, paradoxical stimulation, withdrawal symptoms,
SJS/TEN
Contraindicated in significant renal/hepatic impairment, sleep
apnea, myasthenia gravis
Interactions: Inhibits CYP2D6 and
2C9, and UGT1A4, 1A6, and 2B4;
induces CYP3A4; substrate of
CYP2B6, 2C19, 3A4, and P-
glycoprotein
4. Eslicarbazepine
Acetate
MOA: Prodrug to S-licarbazepine  fast VSSC blocker, i
n
h
i
b
i
t
repetitive firing & decrease propagation of synaptic impulses,
↑ K+
conductance & modulation of high-voltage Ca2=
channels
Indication: Monotherapy, adjunct for focal seizures
Side Effects: Similar to Oxcarbazepine Interactions: Inhibitor of CYP2C19,
inducer of CYP3A4, substrate of
UGT2B4
5. Ethosuximide MOA: T-type Ca2+ channel blocker
Indication: Absence seizures, 1st line
Side Effects: Blood dyscrasias, drug-induced lupus,
dermatologic reactions, hiccups, other common GI and CNS
side effects
Interactions: Substrate of CYP3A,
2E, 2B/C
6. Retigabine/
Ezogabine
MOA: K+ channel opener
Indications: adjunct, focal seizures
Side Effects: Retinal abnormalities progressing to vision loss,
urinary retention, skin discoloration, QT prolongation,
neuropsychiatric events
WITHDRAWN FROM WORLDWIDE
MARKET
7. Felbamate MOA: Fast Na+ channel blocker, T-type Ca2+ channel blocker,
Glu receptor blocker, increased GABA
Indications: Monotherapy, adjunct to focal seizures; adjunct for
LGS in kids
Side Effects: Aplastic anemia, hepatic failure, other common
CNS and GI side effects
Interactions: ↑ Phenytoin & Valproate
levels, decrease Carbamazepine
levels; inhibits CYP2C19

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8. GABAergic:
Tiagabine
Vigabatrin
MOA:
Tiagabine – increased GABA, possibly through blockade of
GABA transporter (GAT)
Vigabatrin – inhibits GABA transaminase
Indications:
Tiagabine – adjunct, focal seizures with or without secondary
generalization
Vigabatrin – monotherapy, infantile spasms, particularly
those with tuberous sclerosis (infants and children 1 month
to 2 years), adjunct for children≥16 and adults for refractory,
complex focal seizures
Side Effects:
Tiagabine – Dermatologic reactions, CNS depression, other
CNS side effects (may trigger seizures when used in people
without seizures)
Vigabatrin – Vision loss, anemia, neurotoxicity, peripheral
neuropathy, other CNS side effects
Interactions: Tiagabine highly
protein-bound and substrate of
CYP3A4
9. Primidone MOA: Metabolized to Phenobarbital, PEMA (phenylethyl
malonamide)
Indications: Monotherapy, adjunct for focal & generalized
seizures
Side Effects: Similar to Phenobarbital Interactions: Similar to Phenobarbital
10. Stiripentol MOA: May enhance GABA transmission via weak partial
agonism/ PAM ala barbiturate, CYP inhibition
Indication: Adjunct to Clobazam and Valproate for Dravet
syndrome
Side Effects:
Common:
CNS: Anorexia, sedation/insomnia, ataxia, hypotonia and
dystonia, hyperkinesias; paradoxical aggressiveness, irritability,
insomnia, behavior disorders, hyperexcitability
GI: Appetite loss, N/V
Life-threatening/Dangerous: Cutaneous photosensitivity,
rash, and urticaria
Interactions: Inhibits CYP enzymes
(contributes to efficacy by boosting
levels of other antiepileptics) –
Carbamazepine, Clobazam,
Ethosuximide, Phenobarbital,
Phenytoin, Primidone, Valproate
11. ACTH/
Corticotropin
MOA: Possibly through CRH suppression
Indication: 1st line for West syndrome
Contraindications: Serious bacterial or viral infection (TB,
varicella, cytomegalovirus), idiopathic hypertrophic
cardiomyopathy, osteoporosis, uncontrolled hypertension,
sensitivity to proteins of porcine origin, live or live-attenuated
vaccines
Side Effects:
Common: Irritability (sometimes severe), Cushingoid features,
hypertension, hyperglycemia, glycosuria, electrolyte
imbalances
Rare: Brain atrophy, peptic ulcer, subaortic hypertrophic
cardiomyopathy, usually reversible within 6 months of
discontinuation, cataracts, glaucoma, worsening seizures
Life-threatening/dangerous:
Immuno: Sepsis, immunosuppression, impaired function of
polymorphonuclear leukocytes, pneumonia (esp Pneumocystis)
Others: Fracture, congestive heart failure
12. Cannabidiol MOA: CB1 receptor negative allosteric modulator; might block
fatty acid amide hydroxylase (FAAH), 5-HT1A agonist, transient
receptor potential vanilloid type 1 (TRPV1) agonist, blocks
adenosine inactivation
Indication: LGS, DS; possible benefit for multiple sclerosis and
as adjunct for positive symptoms of schizophrenia
Side Effects:
CNS: Somnolence/insomnia, fatigue, convulsion, rare manic
switch
CV: Increased HR and BP
GI: Diarrhea, LFT elevation
Others: Increased risk of infection
Interactions: Inhibits CYP2C19,
substrate of CYP2C19 and CYP3A4;
effects may be enhanced or reduced
by opioid antagonists

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RPh
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13. Paraldehyde MOA: ???
Indication: Intractable/super-refractory status epilepticus
Side Effects:
Common (oral use):
GI: N/V, abdominal pain; unpleasant breath
CNS: Drowsiness, lethargy
Derma: Rash, unusual sweating, skin and eye irritant, yellow
skin (and eye) discoloration (long-term use)
Others: Muscle cramps
Rare: Impaired coordination, ataxia, aggravation of colitis
(rectal), worsening of gastric ulcer (oral)
Life- threatening/Dangerous:
IV (discouraged): Pulmonary edema, hemorrhage, cardiac
dilatation, cardiovascular shock, paraldehyde droplet emboli
(>5% IV infusion)
Prolonged use: Hepatitis, nephrosis
Partly degraded paraldehyde: deaths from corrosive poisoning
and metabolic acidosis
Interactions: Additive effect with CNS
depressants, Disulfiram may increase
toxicity
14. Sulthiame MOA: Blocks Na+ channel & Glu release; inhibits carbonic
anhydrase in glial cells  increases CO2  acidification of
extracellular space  reduction in inward currents
associated with NMDA receptors, depression of intrinsic
neuronal excitability
Indication: Benign focal epilepsies with centrotemporal spikes /
benign rolandic epilepsy, West syndrome
Side Effects:
Common:
CNS: Paresthesias (extremities, face), dizziness, headache,
diplopia
CV: Stenocardia, tachycardia
GI: Appetite loss, weight loss
Respiratory: Tachypnea, hyperpnea, dyspnea
Life- threatening/Dangerous:
Rare: Renal failure, serious rash w/ SJS/TEN or polyneuritis,
Renal: Nephrolithiasis, metabolic acidosis, electrolyte
disturbances
CNS: Increased seizure activity
Case (1): Progressive weakness of limbs, slurred speech,
increasing drowsiness, hypersalivation  coma
Interactions: Metabolic acidosis with
carbonic anhydrase inhibitors,
Topiramate, Zonisamide, ketogenic
diet; ↑ clearance with Carbamazepine
and Primidone; ↑ plasma levels of
Lamotrigine, Phenobarbital, and
Phenytoin; reduced absorption with
antacids containing Mg2+ Trisilicate,
Bismuth Oxycarbonate, and MgO
Rare (not dangerous): Anxiety, hallucinations, joint pain,
myesthetic phenomena

v5.0
Jarvin EnoshTan,RPh
October 10, 2020
SUBSTANCE USE DISORDERS
Medications MOA, Indications, Contraindications Side Effects and Administration Interactions
1. Buprenorphine
NEEDS S2
MOA: μ-opioid receptor partial agonist – relieves withdrawal
in absence of agonist (understimulated receptors), may
precipitate withdrawal in presence of agonist; κ-opioid
receptor antagonist
Indication: Maintenance for opioid use
disorder/dependence, moderate-to-severe pain
Contraindication: Person should be in mild withdrawal
prior to initiation in opioid use disorder; opioid-naïve
Common: Headache, constipation, nausea,
orthostatic hypotension;
Sublingual: Oral hypoesthesia, glossodynia
Rare/serious: Respiratory depression,
hepatotoxicity
*Unfortunately, locally available dosage form is
transdermal patch (dosage forms indicated for
opioid use disorder: sublingual tablet with Naloxone,
implant)
Substrate of CYP3A4
CNS Depressants – Additive CNS depression
2. Naltrexone
(tablet imported, but
not locally FDA-
registered)
MOA: μ-opioid receptor antagonist
-
Indication: Opioid use disorder/ dependence treatment
(oral/injection) and relapse prevention (injection); alcohol
use disorder/dependence (oral/injection), cholestatic
pruritis
Contraindication: Current opioid use, opioid dependence,
acute opioid withdrawal, naloxone challenge failure or
confirmed positive urine drug test, acute hepatitis or liver
failure; hypersensitivity to polylactidecoglyco-lide (PLG),
carboxymethylcellulose, other injection components
Common: N/V, decreased appetite, dizziness,
dysphoria, anxiety, injection site reactions (pain,
tenderness, pruritis, induration, swelling, erythema,
or bruising)
Rare: Eosinophilic pneumonia, hepatic injury,
severe injection site reactions
*Ensure person is opioid-free for 7-10 days before
initiating
Beyond opioid antagonism, no significant
interactions (liver metabolism by dihydrodiol
dehydrogenase; Acamprosate interaction not
significant)
3. Nicotine (pastilles) Indication: Tobacco use disorder/ dependence Common: GI (N/V/D, abdominal pain), headache,
local irritation (if topical)
Varenicline – increased ADRs
4. Varenicline MOA: α4β2-nicotinic receptor (NN) partial agonist
Indication: Tobacco use disorder/ dependence
Superior to Nicotine but financially toxic !!$$$$!!
Common: Dose-dependent nausea, vomiting,
constipation, flatulence, insomnia, headache,
abnormal dreams
Alcohol – decreased tolerance
N/A in the Philippines:
Alcohol Use Disorder
Acamprosate (taurine metabolite) – blocks mGluR2 and mGluR5 receptors
Disulfiram – irreversible aldehyde dehydrogenase inhibitor  formaldehyde accumulates (causes vomiting when taken with alcohol; classical conditioning)

Contraindicated in psychosis: higher doses block dopamine beta-hydroxylase
Opioid Use Disorder (Methadone and Buprenorphine found superior to Naltrexone)
Methadone – μ receptor agonist, NMDA receptor antagonist, monoaminergic reuptake transporter blocker (prolongs QT interval)
Buprenorphine/Naloxone (SL Tablet) – naloxone prevents diversion to parenteral use (naloxone blocks opioid effects of buprenorphine, but will not be absorbed if taken appropriately as sublingual tablet
Naloxone – opioid intoxication antidote (life-saving)
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RPh
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v5.0
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October 10, 2020
Upcoming:
 Psilocybin (phase II: MDD)
 Sarcosine / N-methylglycine, Sodium benzoate (phase II, schizophrenia adjuncts)
 Roluperidone, Evenamide, SEP-363856 (phase III, schizophrenia)
 MDMA (phase III, MDMA-assisted PTSD psychotherapy)
 Centanafadine (phase III, ADHD)
Legend:
Yellow highlight: DOH Medicines Access Program for Mental Health (MAP-MH) and EML2017
Bold name: EML 2017 only
aProtect from light.
bProtect from moisture
cDo not freeze ampule
dKeep vial in carton until ready for use
LAILong-acting injectable formulation available locally
Storage information collated only for drugs available locally from drugs.com. For drugs available locally without a superscript, this means room temperature storage within the permissible excursions.
Always cross-check storage information with the package insert as formulations listed on the website may vary compared to those available locally.
MNEMONICS
1. Drugs that prolong QT interval
 ‘E s(c)i prof na QT, ma-pride sa 1st queso halo-halo. Nakakasuka. May amag. PI
 Escitalopram, Ciprofloxacin (FQs), Macrolides, Amisulpride, Quetiapine (include all 2nd gen na rin, but NOT 3rd gen), Haloperidol (1st gen APs), 5-HT3 antagonists (except Palonosetron),
fungal azoles, HIV Protease Inhibitors
2. Mood stabilizers
 Lamotrigine
o Pag walang BIDEt, nakaka-“”depress””, kaya magla-LAMOn  LAMOtrigine is for BIpolar DEpression
o LamoTENgine – SJS-TEN
o LamoTRIGINe – after you TRI GIN, you pee a lot  false positive UDS for phencyclidine, synthetic cannabinoids
 Carbamazepine
o CAR BA to? HaLA oo, kasi mabilis. Mga 1502 mph  CARBAmazepine is used for bipolar mania; HLA-B*1502 allele linked to SJS-TEN in Han Chinese
o CarBaMAZepine – Bone Marrow Zuppression (Suppression), ZIADH (SIADH)
o Ethel Booba takes Phen-Phen and Refuses Greasy CARB Shakes  CYP Inducer
 Valproic acid
o Branched chain carboxylic acid – for both bipolar mania and depression
o Carbonyl group resembles baby’s spinal cord coming out (spina bifida): NEVER GIVE THIS TO PREGNANT WOMEN OR WOMEN OF CHILDBEARING POTENTIAL
3. D2/D2-5HT blockers (“Antipsychotics”)
 Risk of metabolic syndrome:CoQ10
o Clozapine ~ Olanzapine > Quetiapine, Paliperidone (write 10 as P), Risperidone
o Not on the list: A (Aripiprazole, Amisulpride: minimal risk)
 Fluphenazine, Flupentixol
o FLU shots last a while – most-often used long-acting injectables in the community (others: Haloperidol, Risperidone, Paliperidone, Aripiprazole)
 Notable properties per individual drug
o Risperidone – RICEperidone
 Excitement for RICE leads to motor side effects (dose-dependent EPS)
 Excess RICE leads to more fat in the breasts  hyperprolactinemia  RisperiDONE with this sh*t
o Amisulpride – PRIDE
 Lost pride due to gynecomastia  hyperprolactinemia
Sheet
Jarvin Enosh Tan,
RPh
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