Jetlax's CNS Pharmacology Cheat Sheet For The Philippines v5.0 - See Bit - Ly - cNSHandouts For Corrections

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

October 10, 2020
There is no RPh without mental health. quick legend:
CNS Pharmacology Cheat Sheet v5.0
Jarvin Enosh Tan, RPh
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) 10

II. SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIS) 11
III. NORADRENERGIC AND SPECIFIC SEROTONERGIC ANTIDEPRESSANT (NASSA) 11
IV. MULTIMODAL ANTIDEPRESSANT 12
V. NOREPINEPHRINE-DOPAMINE REUPTAKE INHIBITOR 12
VI. TRICYCLIC ANTIDEPRESSANTS (TCAS) 12
ANTIDEPRESSANTS NOT AVAILABLE LOCALLY 12
ANTIPSYCHOTICS 14
FIRST GENERATION ANTIPSYCHOTICS / D2 ANTAGONISTS 14

SECOND GENERATION ANTIPSYCHOTICS / D2-5HT ANTAGONISTS 16
THIRD GENERATION ANTIPSYCHOTICS / D2 PARTIAL AGONISTS-5HT ANTAGONISTS 18
ANTIPSYCHOTICS NOT AVAILABLE LOCALLY 19
ANTICHOLINERGICS 19
CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 3 of 43
October 10, 2020
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 28
SODIUM CHANNEL BLOCKERS (VSSC BLOCKERS) 28
SYNAPTIC VESICLE SV2A BINDER 30
AMPA RECEPTOR ANTAGONIST 30
ANTIEPILEPTICS NOT AVAILABLE LOCALLY 31
SUBSTANCE USE DISORDERS 34
MNEMONICS 35
BONUS SECTION: LAST-LINE AGENTS/ALTERNATIVES IN REFRACTORY CONDITIONS 37
REFERENCES 39

October 10, 2020
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.

October 10, 2020
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

October 10, 2020
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

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

October 10, 2020
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.

October 10, 2020
PSYCHOTROPIC DRUG DISCOVERY PATHWAY: INFOGRAPHIC

October 10, 2020
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
1. Sertraline Additional MOA: Also weakly blocks dopamine Mechanism of Action (MOA) generally preferred):
transporters (DAT) and σ1 receptors MDD: Block serotonin (5-HT) transporters (SERT) → • Major Depressive Disorder (MDD)
↑5-HT → Delayed ↑brain-derived neurotrophic factor • Generalized Anxiety Disorder (GAD)
Caution in urine drug screens as it may give a (BNDF); removes affective biases • Panic Disorder (PD)
false positive result for benzodiazepines; CNS- (see Ketamine MOA for BDNF’s role in neuroplasticity) • Social Anxiety Disorder (SAD)
activating side effects • Obsessive Compulsive Disorder (OCD)
Anxiety disorders: Block SERT → ↑5-HT → adaptive • Post-traumatic Stress Disorder (PTSD)
2. Fluoxetinea Additional MOA: Also weak 5-HT2C antagonist neuronal/receptor events in brain circuits involved in • Binge Eating Disorder (BED)
and NET blocker fear (amygdala) and worry (prefrontal cortex, striatum, o 2nd line for vasomotor symptoms of menopause
thalamus)
Specific indication for bulimia nervosa and body Side Effect Management (Tolerance develops
dysmorphic disorder Onset over time):
- Most studied antidepressant for children w/ • MDD: 1-2 weeks • N/V – take with food / move dose to bedtime
MDD (≥9 yo) • Anxiety and related disorders: 4 weeks • Constipation – fiber
(up to 8-12 weeks, especially OCD) • Diarrhea – maintain hydration, ORS (if needed),
CNS-activating side effects antispasmodic
Safe duration: 6-9 months (MDD), 12 months (GAD,
• Insomnia/sedation – shift dosing to morning/
Drug-Drug Interactions PD, SAD, OCD, PTSD)
bedtime; sleep hygiene
Multiple CYP drug interactions, especially with • Headache, dizziness – take at night
CYP2D6 substrates (ex: Tamoxifen) Common Side Effects
• GIT: Decreased/increased appetite, nausea,
Non-pharmacologic
Longest t1/2 (less likely for withdrawal) diarrhea, constipation, dry mouth
• Psychotherapy (all indications); psychological
Cipriani et al. (2018): on average less dropouts on • CNS: Insomnia/sedation, agitation, tremors,
debriefing is not recommended for trauma
fluoxetine vs placebo but less efficacious vs other headache, dizziness, anxiety, nervousness, fatigue
• Aerobic exercise (especially for MDD; Tx &
antidepressants • Others: Sexual dysfunction, sweating, bruising,
prevention)
3. Escitaloprama MOA: pure SERT blockade (racemic citalopram weight gain/loss, asthenia
• St. John’s wort (MDD; multiple drug interactions)
is H1 blocker)
Rare/Serious S/E • Lavender oil (GAD)
May prolong QT interval • Manic switch in bipolar disorder • Progressive muscle relaxation (PMR) (phobias,
(R) PD)
• ↑risk of GI, peri-operative, uterine, cerebral bleeding
• Saffron (SSRI-induced sexual dysfunction)

October 10, 2020
4. Paroxetine Additional MOA: Also slight M1 antagonist, NET • Rare hyponatremia and SIADH, esp. in elderly and Tapering
blocker, nitric oxide synthetase inhibitor dehydrated persons Traditional tapering: x mg/day (usual references)
(higher incidence: sexual dysfunction) • Rare post-SSRI sexual dysfunction (PSSD) Proposed tapering: x% mg/day corresponding with
• Rare, increased suicidal ideation ≤24 years old SERT occupancy (Horowitz et al., 2019)
- Anticholinergic side effects
- Potent CYP2D6 inhibition Withdrawal Symptoms aka brain zaps Ashton manual: 1-2 weeks every dose reduction (e.g.
- Shortest t1/2 (higher risk for withdrawal) • Affective – anxiety, irritability, sadness take dose once a day → every other day →every 3rd
- Avoid in children, adolescents, adults≤24 y.o. • Gastrointestinal – nausea day)
• Neuromotor – ataxia
5. Fluvoxamine Additional MOA: Also binds σ1 receptor – only • Vasomotor – diaphoresis
indicated for OCD • Neurosensory – electric shock sensation
• Other neurologic – increased dreaming, insomnia,
headache
Interactions
a. NSAIDs and aspirin may increase bleeding risk and
6. Dapoxetine Rapid absorption, onset, elimination: Indicated for
decrease SSRI efficacy
premature ejaculation; single dose prior to sexual
b. Anticoagulants, antiplatelets, and ω3 fatty acids
activity may increase bleeding risk
N/A in Philippines
c. Serotonin syndrome (when combined with
Trazodone (SARI), Vilazodine (SPARI), Doxepin
serotonergic agents): ginseng, St. John’s wort,
(TCA), Agomelatine (melatonergic), other TCAs,
Tryptophan, Dextromethorphan, methylene blue,
MAOIs, Venlafaxine (SNRI), Mianserin (NaSSA),
Linezolid, serotonergic drugs
Milnacipran (SNRI), Levomilnacipran (SNRI),
d. Levothyroxine efficacy decreased
Esketamine (Glutamatergic),
II. SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIS) Brexanolone/Allopregnanolone (GABAergic)
1. Desvenlafaxine Venlafaxine’s active metabolite MOA
Block SERT and NET
Caution in urine drug screens as it may give a
false positive result for amphetamines Side effects
• Increased BP (2 mmHg)
Financially toxic !!$$$$!! • Sweating
• Urinary retention (NE agonizes bladder α receptors)
2. Duloxetine Has M1 antagonism Contraindication
SNRIs also used in neuropathic pain • 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)

October 10, 2020
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 MOA: NET blocker, HAM antagonist, voltage-sensitive Na+ channel (VSSC) blocker; some also block SERT,5-HT2A,5-HT2C receptors
Clomipramine • Na+ channel blockade (cardiotoxicity) → lowers seizure threshold, sudden death, sudden arrythmias, tachycardia (esp. at higher doses)
Trimipramine • 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)
ANTIDEPRESSANTS NOT AVAILABLE LOCALLY

AKA not-so-nice to know
SSRI: Citalopram Racemic version of Escitalopram MOA: same as above Indications: similar to Escitalopram; dose limitation in elderly
to reduce QT prolongation risk
MOA: Also blocks H1 receptors Side effects: QT prolongation
SNRI: Venlafaxine’s selectivity for DAT increases MOA: same as above Indications: same as above for SNRIs;
Venlafaxine with dose Venlafaxine MR studied for MDD, GAD, PD, PTSD, SAD,
Milnacipran Side effects: similar as above; manic switch & binge-eating disorder
Levomilnacipran SNRIs less tolerable; alternatives withdrawal higher with Venlafaxine Venlafaxine in general: 2nd line, cataplexy (narcolepsy type 1)
NaSSA: MOA: Same as Mirtazapine with added α1 MOA: same as above with added property (see column
Mianserin antagonism to the left)
SARIs: Serotonin Antagonist-Reuptake Inhibitors MOA: Blocks SERT, α1 receptors, Indications: MDD (trazodone is preferred), insomnia (only
Trazodone 5-HT2A (potently), 5-HT2C receptors trazodone, low doses only for selectivity of H1 receptors)
Nefazodone MOA:
Trazodone: also blocks H1 receptors Side effects (notable):
Nefazodone: also blocks NET Trazodone: Priapism – painful, persistent erection
Nefazodone: Hepatotoxic (less preferred)
October 10, 2020
SPARI: Serotonin Partial Agonist-Reuptake Inhibitor Indications: MDD

Vilazodone MOA: Blocks SERT, partial agonist at 5-HT1A receptors
Requires food (significant nausea without food), very slow dose titration
Melatonergic: MOA: MT1 and MT2 agonist, 5-HT2B and 5-HT2C antagonist Indications: MDD, GAD
Agomelatine Relatively better efficacy profile vs other antidepressants; more tolerable vs placebo
Use limited by hepatotoxicity concerns
NRI: MOA: Blocks NET Indications: MDD
Reboxetine Relatively inferior efficacy and tolerability vs other antidepressants
RIMA: Reversible Inhibitor of Monoamine Oxidase-A (MAO-A) Indications: MDD, PD, SAD
Moclobemide MOA: reversible, selective MAO-A inhibition
Lower risk of tyramine-cheese reaction (hypertensive crisis) at therapeutic doses
TCAs: Lofepramine – least cardiotoxic of all TCAs Amoxapine – seizures at therapeutic doses Indications:
Doxepin, Nortriptyline, Nortriptyline – less anticholinergic Doxepin – very sedating BED (2nd line) – Desipramine, Imipramine
Desipramine, Imipramine, Doxepin – most selective agent for H1 Nocturnal enuresis (3rd line; vs 1st line: alarms and 2nd line:
Lofepramine, Amoxapine receptors (only at 1-6 mg) in existence desmopressin) – Imipramine
Insomnia – Doxepin (low-dose; 1-6 mg)
MAOIs: MOA (additional): MOA: Irreversible inhibition of MAO-A & MAO-B → Indications
Phenelzine Tranylcypromine – blocks DAT& NET monoamines not broken down Phenelzine: MDD, PD, SAD
Isocarboxacid (effect duration ~ time to make new MAO: 2-3 weeks)
Tranylcypromine Selegiline: tyramine diet restrictions not Side Effect Management:
Selegiline needed for 6 mg/24 hour patch Side Effects: manic switch (w/ bipolar), headache, GI Preventing hypertensive crisis* – avoid the ff:
symptoms and weight gain, postural hypotension, • Aged foods (aged cheese, meats, sausages, etc.)
Contraindications: Tranylcypromine – renal bradycardia, edema, sexual dysfunction, hypertensive • Fermented foods (pickled food, atchara, spoiled food, tap or
impairment crisis non-pasteurized beer, yeast extract, soy sauce, tofu)
• Fava beans, other broad bean pods
Contraindications: pheochromocytoma, heart
disease, hypertension, history of headache, hepatic *Hypertensive crisis: MAO-A in gut that breaks down tyramine
impairment is inhibited → more tyramine absorption → displacement of NE
from storage vesicles → adrenergic agonism
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)
Glutamatergic: Esketamine S-isomer of Ketamine MOA: Non-selective, non-competitive NMDA receptor Interactions: Minor substrate of CYP2B6, 2C19, 2C9, 3A4;
CONTROLLED Rapid, antidepressant and anti-suicidal effect antagonist; exact mechanism for depression unclear additive CNS depression from other CNS depressants; additive
within 24 hours (effect of parent compound and S-norketamine toxicity from other serotonergic agents and NMDA antagonists
metabolite dependent on mTOR kinase but
Administration: Intranasal independent of AMPA receptors)
Side Effects: Dizziness, nausea/ vomiting, sedation,

vertigo, hypertension, financial toxicity, ↓ feeling/
sensitivity (hypoesthesia), feeling drunk. anxiety,
lethargy, sedation, dissociation, potential for addiction
GABAergic: Brexanolone/ Endogenous neurosteroid derived from MOA: α1β2γ2, α4β3δ, and α6β3δ GABAA positive allosteric
Allopregnanolone progesterone for postpartum depression modulator
IV infusion (60 min) in hospital setting Side Effects: Extreme sedation, financial toxicity

October 10, 2020
ANTIPSYCHOTICS
FIRST GENERATION ANTIPSYCHOTICS / D2 ANTAGONISTS
1. Chlorpromazine Specific Side Effects MOA: D2 blockade (mesolimbic), HAM blockade Indications: 1st gen. antipsychotics less efficacious in bipolar disorder;
a, b, *
• Urine discoloration (red to red-brown) limited to schizophrenia, and Haloperidol for acute agitation;
• More sedation, orthostatic Side Effects: Fluphenazine decanoate, Flupentixol decanoate, and Haloperidol
hypotension, and anticholinergic Common: Sedation, rash, urticaria decanoate depot injections to improve adherence
effects (HAM blockade) and less EPS
(less potent D2 blockade) Anticholinergic side effects (H1, α1, M1) Side Effect Maagement:
• photosensitivity • Dizziness, blurred vision, dry mouth, urinary EPS – decrease dose/switch/add medication
retention, constipation, tachycardia • Acute dystonia – adjunctive anticholinergic (preferred), adjunctive
Contraindications IM diphenhydramine
• Impaired consciousness Serious: Orthostatic hypotension, weight gain, • Akathisia – adjunctive propranolol / BZD / mirtazapine /
• Pheochromocytoma blood dyscrasias, ECG changes (prolonged QT anticholinergic (weak) / B6 / trazodone
• Reye’s syndrome interval), photosensitivity, priapism • Pseudoparkinsonism – adjunctive anticholinergic or adjunctive
diphenhydramine
Drug-drug interactions: Extrapyramidal symptoms/EPS (nigrostriatal) • Tardive dyskinesia – adjunctive vit. B6 / branched-chain amino acids
• Antacids may lower absorption • Acute dystonia (esp. male) / Levetiracetam / botox / deep brain stimulation (DBS)
• Contraindicated: oral K+ salts; their • Pseudoparkinsonism
ulcerogenic effect is enhanced by • Akathisia Anticholinergic SEs
strong anticholinergics • Tardive dyskinesia • Dry mouth – drink small amount of fluids frequently, switch oral
• Levels may be increased by hygiene products, Sugar-free candy/gum, avoid desiccants (alcohol,
antimalarials including quinine Hyperprolactinemia (tuberoinfundibular) smoke, coffee), keep nasal passages open, humidifiers
• Oligomenorrhea, galactorrhea (women) • Excessive saliva – adjunctive oral Hyoscine, oral Benztropine, SL
Caution in urine drug screens: Urinary • Gynecomastia (men) Atropine
chlorpromazine metabolites may give • Sexual dysfunction • Constipation – dietary fibers, exercise, inc. fluid intake, laxatives;
false positive result for amphetamines; possibility of paralytic ileus
may cause false positives in pregnancy Neuroleptic malignant syndrome (NMS): • Urinary incontinence – avoid high fluid intake in evening, ensure
tests. muscular rigidity, hyperthermia, altered complete voiding at bedtime
consciousness, and autonomic dysfunction
Other indications
• Hiccups (2nd line)
• Chemotherapy-induced N/V

October 10, 2020
2. Fluphenazine Specific Side Effects: Less sedation, Neuroleptic induced deficit syndrome (NIDS): Cardiovascular
a, d, LAI
orthostatic hypotension, and secondary negative symptoms (mesolimbic • Orthostatic hypotension – stand up slowly from sitting/lying
anticholinergic effects (HAM blockade), pathway D2 blockade) position, ↑fluid intake (if not fluid-restricted), use supportive
more EPS (potent D2 blockade) stockings
Interactions: • Tachycardia – low-dose peripheral β-blocker, reduce caffeine and
Contraindications: hepatic disease • Increases effects of BP-lowering meds nicotine intake
• Lowers BP if combined with epinephrine • QTc prolongation – note concurrent meds with potential for QT
Drug-drug interactions • CNS depressant effects stack with other prolongation, document
– Contraindicated: oral K+ salts; their depressants
ulcerogenic effect is enhanced by strong • Anticholinergics may decrease dissolution of Hyperprolactinemia
anticholinergics sublingual tablets (nitroglycerin, etc), increase • Sexual dysfunction – evaluate prolactin, note pregnancy plans
concentration of thiazide diuretics • Osteoporosis risk – bone density screening
• Increased hyperthermia risk w/ Topiramate
Neuroleptic Malignant Syndrome
a(LAI)
Contraindications: blood dyscrasias, bone • Supportive care: cool body; maintain hydration
3. Flupentixol Specific Side Effects: Less sedation, marrow suppression, comatose, subcortical brain • Manage complications – renal failure, aspiration, etc.
orthostatic hypotension, and injury, hypersensitivity, Parkinson’s • Pharmacologic management:
anticholinergic effects (HAM blockade),
• BZD
more EPS 9potent D2 blockade); though
• Bromocriptine
more anticholinergic vs Fluphenazine or
Haloperidol • Dantrolene
• Amantadine
Only decanoate LAI is in PNF and • ECT
primary care formulary, but not FDA- • Avoid anticholinergics
registered (tablets are registered)
4. Haloperidol Specific Side Effects: Less sedation,
a, c, LAI
orthostatic hypotension, and
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

October 10, 2020
SECOND GENERATION ANTIPSYCHOTICS / D2-5HT ANTAGONISTS

1. RisperidoneLAI Specific Side Effects MOA ✓ Schizophrenia spectrum disorders
Dose-dependent EPS; risk significantly increases • Positive symptoms: D2 antagonist – Clozapine used mainly for this indication only
beyond 6 mg, where there is no additional clinical • Less EPS/hyperprolactinemia: due to safety concerns
benefit 5-HT2A antagonist & 5-HT1A partial agonist ✓ Acute agitation
• Mood/anxiolytic effects: 5-HT1A partial ✓ Bipolar disorder (see figure below)
Dose-dependent hyperprolactinemia agonist, 5-HT2C antagonism, 5-HT7 ✓ Adjunct to “treatment-resistant” depression
antagonism, α2 antagonism – Risperidone, Quetiapine XR, Aripiprazole,
Metabolic syndrome (moderate risk) • Multiple other receptor affinities Brexpiprazole
Substrate of CYP2D6, 3A4 – Olanzapine (least preferred)
Onset: 1-2 weeks for mood; 4-6 weeks for full- ✓ Adjunct to anxiety and related disorders
LAI response for some – Quetiapine (also 2nd line monotherapy): GAD
2. Paliperidone Specific Side Effects – Risperidone (preferred), Aripiprazole: OCD
• Dose-dependent EPS ✓ Chemotherapy-induced nausea and vomiting (CINV)
Side Effects
• Hyperprolactinemia prophylaxis: Olanzapine
Common: Dizziness, insomnia/sedation, N/V,
• Metabolic syndrome (moderate risk) ✓ LAST-LINE for psychosis in dementia
headache, asthenia, dyspepsia, orthostatic
hypotension (occasionally during initial dosing), (EXCEPT Lewy body dementia; avoid):
Only its LAI form is included in PNF; – Risperidone (max. 1 mg twice daily)
anticholinergic effects
oral dosage form is financially toxic !!$$$$!!
Rare/Serious:
• Metabolic syndrome
3. Amisulpride Specific Side Effects – Possibly due to combined H1 + 5-HT2C
• Hyperprolactinemia antagonism, M3 antagonism on
pancreatic β-cells, and/or other
• QT prolongation
receptors
– Hypertension, ↑ weight, dyslipidemia,
Best avoid in renal failure
hyperglycemia (within 6-8 weeks)
– Monitor metabolic parameters
Useful in those with prominent negative symptoms
(FBG, Hba1c, fasting lipids, BP, wt.)
(but may not be clinically significant)

October 10, 2020
4. Quetiapinea,b Specific Side Effects • Increased risk of death, cerebrovascular

• QT prolongation events in elderly with dementia
• Very sedating • Extreme hyperglycemia associated with
• Decreased T3/T4 ketoacidosis/hyperosmolar coma/death
• Metabolic syndrome (moderate risk) • NMS
• Weight +1.6 kg • Seizures
• BMI +0.7 • Dysphagia
• LDL +0.17 mmol/L • Aspiration pneumonia
• Total cholesterol +0.31 mmol/L • Priapism
• TG +0.32 mmol/L • Changes in body thermoregulation
• Blood dyscrasias (leukopenia, neutropenia,
Substrate of CYP2D6, 3A4 agranulocytosis)
*Lamotrigine: for maintenance only
DO NOT GIVE EXCLUSIVELY FOR INSOMNIA IF Discontinuation symptoms: Rebound
OTHER OPTIONS AVAILABLE #QueHorror insomnia and anticholinergic effects
Side Effect Management (Tolerance develops over
time): same as above
5. Olanzapine Specific Side Effects Contraindications: Parkinson’s disease
Clozapine-induced constipation (gastric hypomotility/
• Strong sedation psychosis (possible efficacy for Clozapine, less
CIGH)
• Metabolic syndrome (highest risk) → metabolic for Quetiapine)
• Lifestyle: exercise, dietary fiber, fluid intake
parameter monitoring
→All of the above on 2nd generation • Oral: Lactulose, Senna, Bisacodyl
• Weight +2.7 kg
antipsychotics applicable to 3rd generation • Rectal (severe): Glycerin suppositories, Sodium
• BMI +1.0 Picosulfate enemas
• LDL +0.20 mmol/L antipsychotics, except MOA and details on
• Cholesterol +0.40 mmol/L certain side effects
Clozapine-induced sialorrhea
• TG +0.46 mmol/L • Prop pillows up at night
• Reduce caffeine intake
Dose cut by up to 50% in smokers (CYP1A2
induction) Aripiprazole-induced akathisia/agitation: take with
chocolate (~4 bars) but consider service user’s
6. Clozapine Specific Side Effects comorbidities (e.g. type 2 diabetes mellitus)
• Strong sedation
• Sialorrhea (Norclozapine = M3 agonist) Metabolic syndrome: diet, aerobic exercise, sleep
management
• Metabolic syndrome (highest risk) → metabolic →All of the above on 2nd gen applicable to 3rd gen
parameter monitoring
• Weight +3.0 kg Nonpharmacologic Interventions
• BMI +1.0 • Schizophrenia
• FBG +1.05 mmol/L – Cognitive behavioral therapy for psychosis (CBTp)
• Cholesterol +0.56 mmol/L – Cognitive remediation therapy (CRT) & compensation
• TG +0.98 mmol/L – Social cognition therapy
Serious: Agranulocytosis (differentiate benign – Music therapy
ethnic neutropenia/BEN), myocarditis, orthostatic – Vocational rehabilitation
hypotension, seizures, • Bipolar Disorder (during euthymia, only for dep.)
constipation/fatal ileus*, aspiration pneumonia – Psychoeducation
(swallow reflex inhibition+sialorrhea) – CBT
– Family-focused therapy (FFT)
Absolute Neutrophil Count (ANC) monitoring, when – Interpersonal and social rhythm therapy (IPSRT)
possible, is advised, along with metabolic – Peer support (should not encourage harmful behaviors,
parameters i.e. nonadherence to meds, substance use)
October 10, 2020
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 MOA: partial D2 agonist, 5-HT2A antagonism, 5- N/A in Philippines:
behaviors (gambling, spending, eating/sex, etc); HT1A partial agonism 1st gen.: Cyamemazine, Loxapine, Mesoridazine,
less risk of metabolic syndrome & QT prolongation Perphenazine, Pimozide, Pipothiazine, Sulpride,
Multiple other receptor affinities Thioridazine, Thiothixene, Trifluoperazine, Zuclopenthixol
Also for Tourette’s and in; caution in urine drug
screens, may give false positive for phencyclidine 2nd gen.: Asenapine, Lurasidone, Ziprasidone, Iloperidone,
and amphetamines Olanzapine LAI
LAI is non-PNF “3rd gen.”: Cariprazine, Lumateperone
2. Brexpiprazole Weight gain (~1.23-1.89 kg; dose dependent) MOA: partial agonist leaning towards
antagonist at D2 receptors, potent 5-HT2A
No glucose intolerance and lipid abnormalities in antagonist and potent 5-HT1A partial agonist;
clinical trials (will most likely be most $$$$) also strong α1 antagonist
Substrate of CYP2D6, 3A4 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
October 10, 2020
ANTIPSYCHOTICS NOT AVAILABLE LOCALLY

Medication Specific information MOA, Side Effects, Interaction Indications, Side Effect Management, and More
1st Gen: Sulpride – at low doses, D2 partial agonist MOA: all D2 and HAM antagonism Indications: Schizophrenia, tics (Pimozide)
Cyamemazine (leaning to antagonist) and D3-preferring Side Effects: Pimozide, Thioridazine – marked QT prolongation
Loxapine Trifluoperazine, Perphenazine – hepatotoxic; contraindicated:
Mesoridazine Zuclopenthixol – has depot LAI, may be more hepatic disease
Perphenazine efficacious at the cost of more ADRs
Pimozide *Class info relevant in Organic Medicinal Chemistry, not Pcol:
Pipothiazine Loxapine – has 2nd gen properties Phenothiazines:
Sulpride • Aliphatic – Chlorpromazine
Thioridazine • Piperazine – Fluphenazine, Trifluoperazine, Perphenazine
Thiothixene • Piperidine – Mesoridazine, Thioridazine
Trifluoperazine Butyrophenones – Haloperidol, Droperidol
Zuclopenthixol Thioxanthines – Thiothixene, Flupenthixol, Zuclopentixol
2nd Gen: Ziprasidone – take with 300-calorie meal Side Effects: Indications: Schizophrenia, acute bipolar mania
Asenapine Asenapine – anaphylaxis, QT prolong. (Ziprasidone), acute bipolar depression (Lurasidone), both
Iloperidone Iloperidone – QT prolongation, rare priapism bipolar mania and depression (Asenapine)
Lurasidone Sertindole – marked QT prolongation, severe orthostatic
Perospirone hypotension
Sertindole Ziprasidone – marked QT prolongation
Ziprasidone
3rd Gen: Cariprazine – D2 partial agonism, weaker 5- MOA: Partial D2 agonists, etc. Indications: Schizophrenia, acute bipolar mania/mixed
Cariprazine HT2A antagonism, more portent 5-HT1A partial Side Effects: lesser risk for metabolic syndrome (Cariprazine)
Lumateperone agonism, D3 selectivity at low doses
Lumateperone – 5-HT2A antagonism, D2

presynaptic partial agonism, D2 post synaptic
antagonism, and GluN2B modulation
Others: MOA: Indications:
Pimavanserin Pimavanserin: 5-HT2A inverse agonist Pimavanserin: Parkinson’s disease psychosis
Tetrabenazine Tetrabenazine: VMAT2 inhibitor 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

October 10, 2020
ANXIOLYTICS AND SEDATIVE-HYPNOTICS

1. Benzodiazepines • Alprazolam (t1/2 12-15 h) MOA: GABAA positive allosteric modulator; GABA Indications
NEED S2 - ↑ Concentration by Estrogen effect is enhanced → Cl- enters cell, “supercharging” ✓ Panic disorder and generalized anxiety disorder, acute use only
products neuron and making it less responsive to other (general)
• Bromazepam (t1/2 11-12 h) neurotransmitters ✓ Insomnia (acute use only; CBTi = 1st line)
• Clonazepam (t1/2 30-40 h) ✓ Acute alcohol withdrawal
- Absence seizures with Valproate Ineffective and potentially harmful in PTSD and ✓ Catatonia (Lorazepam)
• Clorazepateb (decarboxylation to phobias ✓ Epilepsy (1st line in status epilepticus: IM Midazolam, IV
Nordiazepam is rapid: t1/2 =40-50 h) Lorazepam, IV Diazepam)
• Diazepama (injection) (t1/2 20-80 h) Side Effects
- Concentration and t1/2 ↑ by Common: Sedation, anterograde amnesia, fatigue, Antidote: Flumazenil (may precipitate seizures those with epilepsy)
omeprazole depression, dizziness, ataxia, slurred speech,
• Lorazepam (t1/2 10-20 h) weakness, confusion, GI disturbances, paradoxical
- Preferred in hepatic impairment hyperexcitability, nervousness
- ↓ Clearance by Valproate &
Probenecid Rare: Hallucinations, mania, hypotension, grand mal
- ↓ Concentration by Estrogen seizures, CNS depression, hypersalivation, dry mouth,
products (glucuronidation) hepatic & renal dysfunction, blood dyscrasias, (BZDs
- In the PNF but not FDA- generally do NOT cause respiratory depression in
registered absence of comorbidities/drug interactions)

October 10, 2020
Benzodiazepines • Midazolam (t1/2 4.8-6.4 h) To minimize the risk of addiction and/or dependence, From Behnoush et al., 2015:
NEED S2 - IM administration non-inferior to use should be limited to not more than 4 weeks in
IV Lorazepam for status anxiety disorders & not more than 7 days for insomnia
epilepticus in RAMPART trial
(possibly superior in terms of Needs careful tapering to avoid seizure recurrence /
administration route and lack of withdrawal symptoms
need for significant temperature
control) 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 MOA: binds α2δ subunits of voltage-sensitive Ca2+ channels (VSCC) Indications: GAD, postherpetic neuralgia and diabetic neuropathy,
Pregabalin long-term: increased GABA transporter density & functional GABA transport restless leg syndrome (only for Gabapentin enacarbil ER), epilepsy
(focal seizures; adjunctive), intractable hiccups (Gabapentin)
Side effects:
Common: Sedation, weight gain, peripheral edema Gabapentin also has evidence of efficacy in alcohol use disorder
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
3. Prazosin MOA: α1 antagonist in CNS (crosses BBB) PTSD nightmares*
Note: α1 agonism causes the ff:
• Disrupts higher-order cognitive processing and induces primitive fear response *Doxazosin available locally instead of Prazosin but less studied
• Disrupts REM sleep
• Increases non-REM sleep
• Stimulates CRH release → more cortisol
Side effects: First-dose phenomenon

October 10, 2020
4. Hydroxyzinea MOA: H1 receptor antagonist; Some action at muscarinic and 5-HT2 receptors; suppression of Acute GAD
some subcortical regions Not to be used >3 days for insomnia
Side Effects: Anticholinergic, sedation

5. Zolpidem MOA: NOT a BZD; positive allosteric Common: Sedation, dizziness, ataxia, dose- Interactions:
NEED S2 modulator of GABA receptors dependent amnesia, hyperexcitability, nervousness, Synergistic with CNS depressant
(preference for GABAA) w/ α1 subunits diarrhea, nausea, headache Sertraline, Ketoconazole – may increase zolpidem levels
Rifampicin – may decrease zolpidem levels
Indication: Not more than 7 days for Rare/serious: Hallucinations, angioedema, respiratory
insomnia; Zolpidem CR not restricted depression,
to short-term use, but only IR available somnambulism, sleep-driving, sleep-eating, sleep- Notes:
locally sex, sleep-phone calls **First line for insomnia is psychotherapy: CBTi (stimulus control, sleep
restriction, relaxation response)
Contraindications: Significant
obstructive sleep apnea syndrome **Melatonin is the only OTC with evidence for efficacy (Jetlag, phase-
and acute and/or severe impairment delayed sleep)
of respiratory function; myasthenia
gravis; severe hepatic impairment; **TAKE BEFORE BEDTIME and without food. Ensure possibility of
personal or family history of 7-hour sleep time, minimum.
sleepwalking
STIMULANTS, WAKE-PROMOTING AGENTS, AND MEDICATIONS FOR ADHD

1. Methylphenidate MOA: Allosteric blocker for both NET and DAT Common: Antihypertensives (BP effects)
(Ritalin1, Concerta2) CNS: Insomnia, headache, worsening of tics, nervousness, PPIs – increase methylphenidate absorption
Indications: ADHD (1st line), irritability, overstimulation, tremor, dizziness, Antidepressant, anticonvulsant, and warfarin
NEED S2 narcolepsy (excessive daytime sedation/EDS) GIT: Anorexia, nausea, abdominal pain, weight loss – inhibits metabolism
May have synergistic effects with other
Contraindications: Extreme anxiety or agitation, Rare/serious: Priapism, dysphoria, psychotic episodes, especially stimulants or NE/DA reuptake inhibitors
motor tics or Tourette’s syndrome or w/ family with parenteral misuse, seizures, rare neuroleptic malignant
history, glaucoma, cardiovascular disease, syndrome, rare activation of hypomania, mania, or suicidal ideation Bioequivalence does not equate to
hyperthyroidism and thyrotoxicosis, (controversial), cardiovascular adverse effects (palpitations, clinical equivalence
gastrointestinal obstruction or severe GI narrowing tachycardia, hypertension, sudden death in patients with preexisting
(specific for Concerta), history of substance use cardiac structural abnormalities) In narcolepsy, taper to prevent rebound
disorders Risk of dependence, tolerance, and addiction hypersomnia
October 10, 2020
2. Atomoxetine MOA: Blocks NET Common: Metabolized by CYP2D6

CNS: Fatigue (esp. in children), decreased appetite, ↑ HR (6–9
Indications: ADHD (2nd line) beats/min), ↑ BP (2–4 mm Hg), insomnia, dizziness, anxiety,
agitation, aggression, irritability
Contraindications: Pheochromocytoma or w/ GIT: Dry mouth, constipation, N/V, abdominal pain, dyspepsia
history, severe cardiovascular disorder that might Genitourinary and others: Urinary hesitancy, urinary retention (older
deteriorate with clinically important increases in HR men), dysmenorrhea, sweating, sexual dysfunction
and BP, angle-closure glaucoma
Rare/serious: Priapism, hypertension, orthostatic hypotension,
Financially toxic !!$$$$!! severe liver damage, manic switch, suicidal ideation activation
3. Clonidinea MOA: Common: Beta blockers – risk of worse withdrawal
Initial: Postsynaptic α2A, α2B, α2C receptor agonism. CNS: Sedation, weakness, fatigue, sexual dysfunction, depression, CNS depressants – additive effects
α2A agonism → increased signal in prefrontal cortex insomnia, withdrawal symptoms on abrupt cessation: nervousness, TCAs – reduced hypotensive effects of
& reduced CNS sympathetic outflow (CNS), agitation, headache, and tremor Clonidine
vasoconstriction (ANS) CV: Orthostatic hypotension, tachycardia or bradycardia, rebound Rate controllers (Digoxin, CCBs, Beta
Then: Binds CNS Imidazoline 1 (I1) receptors → hypertension on abrupt withdrawal → reinstitute drug and taper Blockers) – bradycardia, AV block risk
downstream catecholamine release → presynaptic slowly
α2 receptors → autoreceptor activation, NT release GIT: Dry mouth, N/V
stopped (sedation in CNS, hypotension in ANS)
Rare/serious: Sinus bradycardia, AV block
Indications: 2nd line for ADHD, Tourette’s, smoking
cessation, and hypertension
ANXIOLYTICS, SEDATIVE-HYPNOTICS, STIMULANTS, AND WAKE-PROMOTING AGENTS NOT AVAILABLE LOCALLY

1. Other Chlordiazepoxide (t1/2 = 6.6-13.4 hours), Clobazam (t1/2 = 36-42 hours), Lormetazepam, Nitrazepam, Oxazepam Indications: Only Flurazepam, Quazepam,
benzodiazepines (t1/2 = 5.6-10.4 hours) Triazolam, Estazolam, Temazepam indicated
Flurazepam (t1/2 = 2-6 days), Quazepam (t1/2 = 2-5 days), Triazolam (t1/2 = 1-2 hours), Estazolam (t1/2 = 12-30 hours), for short-term management of insomnia among
Temazepam (t1/2 = 4-20 hours) ALL benzodiazepines (even local ones)
2. BZRAs Zaleplon (t1/2 = 1-2 hours) Indications: short-term management of
Zopiclone (t1/2 = 3.5-6.5 hours) insomnia
Eszopiclone (t1/2 = 3.5-6.5 hours)
3. Buspirone MOA: 5-HT1A partial agonism Side Effects: Indication: Acute GAD
Dizziness, headache, nervousness, sedation, excitement, nausea,
Onset: 6 weeks restlessness, rare cardiac symptoms CYP3A4 substrate
4. Melatonin MOA: MT1 and MT2 receptor agonist Side Effects: Indication: Insomnia
Agonists: (for Tasimelteon, MT2>>MT1) • Ramelteon: Sedation, fatigue, dizziness, rare angioedema & CNS
Ramelteon and depression (serious)
Tasimelteon Ramelteon: Contraindicated w/ • Tasimelteon: Headache, nightmares, increased ALT, upper respiratory
Fluvoxamine infection, urinary infection
5. DORA: Dual Orexin Receptor Antagonist Side Effects: Sedation, headache, dizziness, abnormal dreams; rarely sleep Indications: Insomnia
Suvorexant MOA: orexin 1 & 2 receptor antagonist paralysis and hypnogogic, hypnopompic hallucinations
6. Other Dexamphetamine Risk of tolerance, dependence, and addiction; rebound cataplexy with Indications: ADHD, narcolepsy
amphetamines Lisdexamphetamine – prodrug of abrupt discontinuation Lisdexamphetamine: 2nd line, binge-eating
CONTROLLED d-amphetamine (linked to Lysine) disorder
7. Modafinil and MOA: Slight DAT blockade Side Effects: Headache (dose-dependent), anxiety, nervousness, insomnia, Indications: Narcolepsy (reduce EDS)
Armodafinil dry mouth, diarrhea, nausea, anorexia, pharyngitis, rhinitis, infection,
CONTROLLED Armodafinil more potent hypertension, palpitations, rare SJS/TEN, angioedema, hypersensitivity Interaction: Reduce efficacy of contraceptives
October 10, 2020
8. Sodium Oxybate MOA: GHB receptor binder, GABAB Side Effects: Headache, dizziness, sedation, nausea, vomiting, enuresis, Indication: Narcolepsy with cataplexy in
CONTROLLED receptor partial agonist respiratory depression, neuropsychiatric events, confusion and wandering at children and adults (EDS, cataplexy, sleep
night; caution on sodium content paralysis, hypnagogic and hynopompic
Administration: Avoid taking with food hallucinations)
2 hours before dose; avoid activity until Risk of tolerance, dependence, and addiction
6 hours after 2nd dose Onset: 1-2 months (max. effect: 3 months)
9. Pitolisant MOA: H3 receptor antagonist/inverse Side Effects: Dose-dependent QT prolongation Indication: Narcolepsy with/without cataplexy
agonist (EDS only)
Contraindication: Pregnancy
10. Solriamfetol MOA: blocks NET and DAT Side Effects: Headache, nausea, and decreased appetite; small dose- Indications: Narcolepsy (EDS) and obstructive
CONTROLLED dependent increases in BP and heart rate; uncommon insomnia sleep apnea
Administration: Take on empty
stomach and avoid food 30 min. after
dose; take 9 hours before bedtime
“MOOD STABILIZERS”
Medication MOA, Indications, And C/Is Side Effects Interactions
1. Lithiumb MOA: Side Effects Increase lithium levels: ACEIs (maybe ARBs),
• Cellular: GSK-3 inhibition? Common: CCBs, Methyldopa, Carbamazepine, Thiazide
•Growth factor neuroprotection and ↓ apoptosis • CNS: Ataxia, dysarthria, delirium, tremor, memory problems diuretics, Metronidazole, NSAIDs, Phenytoin,
•Decreased oxidative stress • GIT: diarrhea, nausea, weight gain Topiramate, Tetracycline
•Secondary messenger systems? • Derma: acne, rash, alopecia (check Cu/Zn levels)
•Inositol monophosphatase inhibition (more • Blood: leukocytosis Decrease lithium levels:
inositol, less IP3) Alkalizing agents, Calcitonin, Calcium/ sodium
•Protein kinase C inhibition via GSK-3 inhibition: Rare/serious: polystyrene sulfonate, Carbonic anhydrase
reparative neuronal plasticity • Renal: Polyuria, polydipsia (nephrogenic diabetes insipidus) inhibitors, Loop diuretics, Mannitol, NaCl (and
•Modulation of Ca2+ disturbances (↓ apoptosis) • Thyroid: Euthyroid goiter/hypothyroid goiter dehydration), Caffeine, Urea
•↑cAMP-induced CREB gene transcription • CV: AV block, arrhythmias, ECG changes
Minimizing variations in Lithium levels:
• Neurotransmission? • CNS: Pseudomotor cerebri, seizures
• Keep daily coffee/tea and water consumption
• ↓excitatory Glu neurotransmission • Toxicity: Seizures, delirium, coma, and death
consistent
• ↓DA release, GSK-3 inhibition via
• Ensure adequate hydration during fevers or
D2 antagonism
exercise
• 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 stress
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

October 10, 2020
2. Divalproex/ MOA: Hypotheses include Side effects: Interactions:

Valproic Acid 1. Reduced excessive neurotransmission by ↓flow Common: – Carbapenem: ↓ Valproate levels
of ions through Na+ channels, T-type Ca2+ • CNS: Sedation, tremor, dizziness, ataxia, asthenia, – Lamotrigine: may ↓ Valproate concentrations
currents headache
2. ↑GABA action via ↑release (GABAB), • GIT: Abdominal pain, N/V, diarrhea, reduced appetite, Sodium Valproate, Valproic Acid, and
↑synthesis (↑glutamic acid decarboxylase), constipation, dyspepsia, weight gain Divalproex are NOT equivalent
↓reuptake & ↓metabolism (↓GABA-T)
3. Downstream actions on complex signal Unusual/controversial:
transduction cascades (e.g. GSK-3 inhibition, alopecia (unusual; check Cu/Zn levels), polycystic ovaries
phosphokinase C, myristolated alanine-rich C (controversial), hyperandrogenism and hyperinsulinemia and
kinase substrate blockade) and activating lipid dysregulation (controversial), decreased bone mineral
various signals that promote neuroprotection & density (anticonvulsants and serotonin modulators in general)
long-term plasticity (e.g. extracellular signal-
regulated kinase, cytoprotective protein B-cell
lymphoma/leukemia-2 gene, GAP43) Rare/Serious:
Hepatotoxicity, liver failure, pancreatitis. thrombocytopenia,
Unknown whether these explain mood-stabilizing leukopenia, drowsiness, confusion (valproate-induced
action, anticonvulsant action, anti-migraine action, hyperammonemic encephalopathy, a sign of toxicity)
and/or side effects
*Antidote for valproate-induced hepatotoxicity and
Indications: Epilepsy (focal, GTC, myoclonic; hyperammonemic encephalopathy: L-carnitine
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 STRICTLY AVOID in women and girls of
liver disease, pancreatitis, thrombocytopenia childbearing potential. The only exception is if
mitochondrial disorders due to mutations in and only if there are no other options.
mitochondrial DNA polymerase-gamma (POLG),
pregnancy
3. Lamotrigine MOA: Blocks Na+ channels and increases brain Side Effects: Interactions: Dose adjustments needed for
GABA (epilepsy); blocks L-, N-, P-type Ca2+ Common: Dizziness, diplopia, insomnia, ataxia inducers (carbamazepine, phenytoin,
channels (decreases Glu release), weak 5-HT3 Serious: SJS/TEN: Titrate dose phenobarbital, primidone, rifampicin,
receptor and dihydrofolate reductase inhibitor VERY SLOWLY to prevent & lopinavir/ritonavir) and inhibitors (valproate, UGT
strictly adhere to very slow inhibitor)
Indications: Focal seizures, GTC, absence titration recommendations;
seizures (<Valproate); avoid vitamin B complex and Caution in urine drug screens as Lamotrigine may
only for bipolar depression new food/meds/cosmetics/ cause a false positive result for phencyclidine and
deodorants/detergents/fabric synthetic cannabinoids
softeners/sunburn; can
worsen/ppt myoclonic seizures
Drug reaction w/ eosinophilia &

systemic symptoms (DRESS)

October 10, 2020
4. Carbamazepine MOA: Side effects: Interactions:

a, b
• Interaction with Na+ channels at alpha-pore Common: Sedation, confusion, dizziness, ataxia, double Multiple psychotropics, including anticonvulsants,
forming subunit vision, nausea, diarrhea, benign leukopenia antidepressants, & antipsychotics due to induction
• Adenosine 1 (A1) receptor antagonist → of multiple CYP enzymes; may cause failure of
Serious: SJS-TEN (avoid with paracetamol), DRESS, hormonal contraceptives
upregulation of A1 receptors
hepatotoxicity, cardiac conduction delay,
• Decreases release of presynaptic Asp & Glu bone marrow suppression (agranulocytosis and aplastic
• Blocks Ca2+ influx through NMDA receptor & anemia), hyponatremia and SIADH
decreases Ca2+ serum concentrations
HLA*B1502 screening required for first-time takers to prevent
Indications: Focal and focal-to-bilateral seizures, SJS-TEN
trigeminal neuralgia, 1st line for benign occipital
epilepsies (for acute bipolar mania only, NOT Can aggravate absence seizures
bipolar depression)
Contraindications: HLA*B1502 allele, bone

marrow suppression, hepatic porphyria
Additive myelosuppression with Clozapine
DEMENTIA
Medication MOA, Indications, C/Is Side Effects and Administration Interactions
1. Donepezil MOA: Reversible central & peripheral Side Effects: Can theoretically reduce Levodopa efficacy
acetylcholinesterase inhibitor Common: Susceptible to CYP2D6, 3A4 interactions
N/V, diarrhea, appetite loss, increased gastric acid
Useful for dementia with Lewy bodies secretion, dyspepsia (take with food), weight loss,
2. Rivastigmine MOA: Pseudoirreversible (self-reverses over hours) headache, dizziness, fatigue, depression, asthenia, Smoking can reduce clearance
acetylcholinesterase (cortex & hippocampus) & insomnia (if so, take Donepezil in morning) No CYP interactions
butylcholinesterase (glia) inhibitor Rare: seizures, syncope
Also indicated for Parkinson’s disease dementia, useful Administration:

for dementia with Lewy bodies Donepezil: at bedtime with food
3. Galantamine MOA: Reversible, competitive central Rivastigmine and Galantamine: with food Susceptible to CYP2D6, 3A4 interactions
(N/A locally) acetylcholinesterase PAM at nicotinic receptors
**Rivastigmine: retitrate if stopped >3 days to avoid
Not recommended in severe renal, hepatic impairment vomiting with esophageal rupture
4. Memantine MOA: Low-affinity uncompetitive NMDAR antagonist; Dizziness, headache, hallucinations, insomnia, - Urinary alkalizer (pH8): memantine clearance reduced by 80%
adjunctive only constipation; rare seizures - 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
October 10, 2020
5. Ginkgo biloba Publication bias, low quality studies, inconsistent and unreliable findings
EGb 761
*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 + MOA: Aromatic amino acid (dihydroxyphenylalanine) Acute: N/V, anorexia, orthostatic hypotension, arrhythmias Orthostatic hypotension with
Carbidopa/ and precursor to DA passes through BBB, taken up by Long-term: Wearing-off and on-off phenomenon, dyskinesias antihypertensives, Selegiline
Benserazide DAergic neurons and converted into DA. Carbidopa and (choreiform, dystonic, involuntary), somnolence, vivid dreams,
Benserazide are peripheral dopamine decarboxylase confusion, hallucinations, agitation Low protein diets increase absorption by
inhibitors 50%, and high protein diets reduce
Administration: Without food (1 h before, 2 h after meals) absorption
2. Entacapone MOA: Selective, reversible Diarrhea (delayed 4-12 week onset), dyspnea, weakness, Drugs that interfere w/ biliary excretion,
catechol-o-methyltransferase inhibitor brown-orange urine glucuronidation will increase effect:
Probenecid, Cholestyramine, Erythromycin,
Contraindications: Severe biliary disorder May increase levodopa SEs – dyskinesias, nausea, orthostatic Ampicillin, Rifampicin, Chloramphenicol
hypotension, hallucinations, sleep attacks
Drugs metabolized by COMT: E, NE, DA,
Rare: Rhabdomyolysis Dobutamine, CH3-DOPA, Apomorphine,
**Tolcapone: hepatotoxic (TOxic to Liver) Isoproterenol
Administration: taken with Levodopa
3. Pramipexolea, MOA: Post-synaptic D2 agonist in caudate-putamen N/V, low extremity edema, somnolence, lightheadedness, Pramipexole – drugs inhibiting/competing w/
Ropinirolea,b, Piribedil: D2/D3 agonist, α2 antagonist postural hypotension, hallucinations, delusional behavior, cationic tubular secretion: Verapamil,
Rotigotine (patch) compulsive behavior (eating, sex, gambling, shopping) Quinine, Probenecid, Ranitidine, Diltiazem,
Indications: Parkinson’s and restless leg syndrome Triamterene
4. Piribedil (RLS) (Pramipexole efficacy in PD depression) Manic switch: high risk – Pramipexole, low risk – Ropinirole
Parkinson-hyperpyrexia syndrome (withdrawal) Ropirinole – CYP1A2 modulators
5. Apomorphine (SQ) MOA: Partial D2 agonist N/V, drowsiness, dizziness, postural hypotension,
(N/A locally) 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 MOA: Irreversible, selective MAO-B inhibition at Elevated ALT, nausea, headache, orthostatic hypotension, Hypertensive crisis with tyramine-rich food
(only tablet dose<10mg/day musculoskeletal injuries, non-life-threatening arrhythmias and other MAOIs (less restrictions on diet
available) <10 mg); serotonin syndrome with
Indication: Adjunct for Parkinson’s (oral), MDD (patch) serotonergics
Contraindications: Serotonin syndrome-inducing (NOTE: Linezolid and methylene blue also
agents, very high-tyramine foods (>150 mg/day) have MAOI properties)

October 10, 2020
8. Rasagiline MOA: Irreversible and selective MAO-B inhibition when Monotherapy – Flu syndrome, hallucination, depression, Hypertensive crisis with tyramine-rich food
(N/A locally) Rasagiline<1 mg/day arthralgia, dyspepsia, somnolence, psychotic-like behavior, and other MAOIs (less restrictions on diet <1
impulse control behaviors mg); serotonin syndrome with serotonergics
Indication: Monotherapy, adjunct for idiopathic
Parkinson’s Adjunct to Levodopa – Dyskinesia, dry mouth, vomiting, (NOTE: Linezolid and methylene blue also
anorexia, constipation, weight loss, postural hypotension, have MAOI properties)
Contraindications: Serotonin syndrome-inducing accidental injury, abdominal pain, abnormal dreams, arthralgia,
agents, very high-tyramine foods (>150 mg/day) tenosynovitis, nausea, headache CYP1A2 modulators
9. Amantadinea MOA: Induces release/decreases reuptake of DA; Nausea, dizziness, insomnia, blurred vision, depression, Impairing renal clearance of amantadine:
upregulation of D2 receptors (in vivo); antimuscarinic; anxiety, psychosis (high doses), confusion, livedo reticularis, Quinidine, thiazides, triamterene,
non-competitive NMDA antagonist anticholinergic, nervousness, headache cotrimoxazole
Indication: Parkinson’s, EPS, influenza A prophylaxis/ Exacerbation of seizure disorder, rare suicidal ideation (even
treatment without history)
Contraindications: Seizures, severe renal impairment,
gastric ulceration, untreated angle closure glaucoma Abrupt discontinuation: NMS (rare)
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 MOA: Raising seizure thresholds or altering Common: CYP inducer
NEEDS S2 seizure patterns (unknown mechanism), possibly • CNS: Sedation, ataxia, vertigo, cognitive dysfunction (worst), Interacts with CYP2C9, 2C19 modulators
thru enhancing GABAA receptor activity. depression, nystagmus, irritability, emotional disturbances Ethosuximide, acetazolamide, antacids – lower
Depresses Glu excitability; alters Na+, Ca2+, and • GI: N/V phenobarbital levels
K+ channel conductance; and affects • CV: Hypotension
polysynaptic midbrain reticular formation • Derma: Rash, uncommon SJS-TEN
Indications: Focal and tonic-clonic seizures, Rare/serious: Megaloblastic anemia, rare agranulocytosis, DRESS,
myoclonic seizures, neonatal seizures; respiratory/CNS depression; risk of tolerance, dependence, and
1st line for neonatal seizures addiction
Contraindications: porphyria; dyspnea /airway *Cheap unit cost offset by expenses needed to locate and pay for
obstruction; marked hepatic impairment/hepatic physician with S2 license
encephalopathy; intraarterial administration;
history of sedative/hypnotic addiction; nephritic **DO NOT USE FOR INSOMNIA
service users/patients
SODIUM CHANNEL BLOCKERS (VSSC BLOCKERS)
1. Phenytoin MOA: Reduces hyperexcitability on Na+ Common: CYP inducer
a, b(tablets, capsules)
channels. It also modulates T-type Ca2+ • CNS: Nystagmus, ataxia, dysarthria, insomnia, nervousness, Interacts w/
channels, but not in the thalamus; diminishes motor twitching, tremor, dizziness, impaired memory CYP2C9, 2C19,
synaptic transmission, limits fluctuation of • Derma: Rash, hirsutism, coarsening of facial features, gingival 3A4 modulators
neuronal ionic gradients via Na-K ATPase, and hyperplasia
inhibits calcium-calmodulin protein • Respiratory: pneumonia, sinusitis, rhinitis, asthma Can displace
phosphorylation • Sensory: tinnitus, diplopia, eye pain, taste loss warfarin (protein
• Etc: lymph node hyperplasia, chest pain, edema, soft tissue injury binding) →
nd
Indications: Focal and tonic-clonic seizures, 2 (IV) bleeding
line status epilepticus***

October 10, 2020
Phenytoin Contraindications: sinus bradycardia, second Rare/serious: Hypotension, cardiac conduction abnormalities ***Due to equal efficacy w/ Valproate and
a, b(tablets, capsules)
or third degree AV block, Adams-Stokes (rapid administration), hyperglycemia, rare diabetes insipidus, blood Levetiracetam in ESSET trial as adjunct in
syndrome dyscrasias, rare allergic rash (SJS, lupus erythematosus syndrome, benzodiazepine-refractory status epilepticus,
radiation-induced erythema multiforme, DRESS), rare lymphoma/ Fosphenytoin is less preferred for this indication
Onset: 4 weeks multiple myeloma, toxic hepatitis and liver damage, cerebellar atrophy as it has more contraindications as compared to
(long-term, high doses), purple glove syndrome (IV) Levetiracetam
Prodrug: Fosphenytoin (N/A locally)
Fetal hydantoin syndrome: cleft lift/palate, microcephaly, mild
intellectual disability
Possibly carcinogenic to humans (IARC Group 2B), use gloves

2. Oxcarbazepine MOA: Blocks Na+ channels via interaction at a Common: CYP2C19 inhibitor
tablets: a, b
specific site of the alpha pore-forming subunit; • CNS: Sedation (dose-dept), dizziness (dose-dept), headache, Mild CYP3A4 inducer (less interactions vs CBZ)
inhibits Glu release ataxia (dose-dept), nystagmus, abnormal gait, confusion,
nervousness, fatigue
Indication: Focal seizures (RCTs generally • GI: Nausea (dose-dependent), vomiting, abdominal pain,
negative for mood-stabilizing properties) dyspepsia
• Etc: Diplopia (dose-dependent), vertigo, abnormal vision, rash
Onset: 2 weeks
No efficacy for bipolar disorder; May worsen Rare/serious: Hyponatremia, DRESS
some generalized seizures
3. Topiramateb MOA: Blocks Na+ channels, blocks NMDA-Glu Common: - Increase Topiramate clearance:
receptors, potentiates GABA activity (on non- • CNS: Paresthesias, sedation, asthenia, dizziness, ataxia, Carbamazepine, Phenytoin, and Valproate
BZD GABAA site), nervousness, nystagmus, tremor, headache
inhibits carbonic anhydrase • GI: Nausea, ↓appetite, weight loss, dry mouth - Topiramate increases clearance of Valproate,
• Etc: Blurred or double vision, mood problems, confusion, Phenytoin, Metformin (may reduce topiramate
Indication: Epilepsy (focal, GTC, LGS), psychomotor retardation, language and speech problems, fatigue, clearance)
migraine prophylaxis, taste perversion, upper respiratory tract infection, difficulty with
binge eating disorder (decrease binging and concentration & memory, hyperthermia, - Increased risk of kidney stones with other
weight loss→carbonic anhydrase inhibition) nephrolithiasis (stay hydrated, ↓dietary Na+ & glucose/fructose, carbonic anhydrase inhibitors
↑dietary K+ & Ca2+)
Onset: 2-4 weeks - Reduce contraceptive efficacy
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)
4. Zonisamide MOA: Modulates Na+ channels by unknown Common: - Susceptible to CYP3A4 modulators
a, b
mechanism, modulates T-type Ca2+ channels, • CNS: Sedation, depression, agitation, difficulty concentrating,
facilitates DA and 5-HT release, inhibits carbonic irritability, psychomotor slowing, dizziness, ataxia, headache - (theoretical) + carbonic anhydrase inhibitors
anhydrase • GI: N/V, anorexia, abdominal pain, dry mouth, taste perversion, → kidney stones (mostly calcium phosphate)
dyspepsia, weight loss
Indication: Epilepsy (focal, GTC, myoclonic), • Etc: Elevated serum creatinine and blood urea nitrogen, kidney
binge eating disorder (decrease binging and stones (stay hydrated, ↓dietary Na+ & glucose/fructose, ↑dietary K+
weight loss →carbonic anhydrase inhibition) & Ca2+)
Onset: 2-4 weeks Rare/serious: Serious rash (SJS-TEN, DRESS; sulfonamide), *Unknown if sudden deaths related to
oligohidrosis & hyperthermia (pediatric patients), blood dyscrasias Zonisamide use
(aplastic anemia; agranulocytosis), sudden hepatic necrosis, sudden
unexplained deaths*

October 10, 2020
5. Rufinamideb MOA: Na+ channel blocker (prolongs inactive Common: Weak CYP2E1 inhibitor, weak CYP3A4 inducer
state), etc • CNS: Sedation, fatigue, coordination abnormalities, anorexia,
headache, dizziness, tremor Lowers Carbamazepine, Lamotrigine, oral
Indications: Focal seizure, LGS adjunct (≥4 y.o.) • GI: N/V contraceptive levels; increases Phenobarbital,
• Respiratory: nasopharyngitis, influenza Phenytoin, and Valproate levels
Contraindications: Familial short QT syndrome; • CV: QT shortening
galactose intolerance, Lapp lactose deficiency, or Levels increased by Valproate
glucose– galactose malabsorption Rare/serious: Blood dyscrasias (leukopenia), multi-organ
hypersensitivity syndrome (fever, hematuria, abnormal LFTs,
Onset: 4 weeks lymphadenopathy, rash), suicidal ideation
Administration: Take with food (↑absorption)

6. Lacosamidec MOA: Enhances slow inactivation of Na+ Common: Theoretical pharmacokinetic interactions may
channels; binds collapsing response mediator • CNS: Dizziness, ataxia, diplopia, vertigo, abnormal coordination, not yet shown to be clinically significant
protein 2 (CRMP2) ataxia
• GI: N/V, increased LFTs (0.7%) Enhanced CNS side effects with Phenytoin,
Indication: Focal seizures Carbamazepine, Oxcarbazepine, Phenytoin
Rare/serious: Rare hepatitis and neutropenia, rare PR prolongation
Contraindications: Conduction problems or and 1st-degree AV block, behavioral/mood effects and suicidal Increased risk for hyperammonemic
severe cardiac disease (myocardial ischemia, ideation, multi-organ hypersensitivity syndrome encephalopathy with Valproate
heart failure)
Has addiction potential
Onset: 4 weeks
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 Common: Sedation, dizziness, asthenia, ataxia, decrease in RBCs None significant
negative modulators of GABA- & Gly-gated and Hgb, upper respiratory tract infection
currents, partially inhibits N-type Ca2+ currents
Rare/serious: SJS-TEN, Neuropsychiatric Sx
Indication: 2nd line status epilepticus; focal Antiepileptic with *lowest*, if not 0%, risk of teratogenicity
seizures, GTC, myoclonic seizure
Contraindication: Fructose intolerance
Onset: 2 weeks
AMPA RECEPTOR ANTAGONIST
Perampanel MOA: Noncompetitive AMPA glutamate receptor Common: Dizziness, somnolence, weight gain, fatigue, irritability Susceptible to CYP3A4/5 modulators;
antagonist falls, nausea, ataxia, balance disorder, Topiramate decreases Perampanel
hostility/aggressive behavior (10-20%) w/in 6 weeks, other concentrations; additive CNS depressant effect
Indications: Adjunctive for focal, focal-to- neuropsychiatric Sx
bilateral seizures, GTC seizures >12 mg decreases efficacy of Levonorgestrel-
Rare/serious: Has addiction potential containing hormonal contraceptives
Contraindication: Lactose intolerance
Broad spectrum (focal and generalized onset)*: Narrow spectrum (focal)*: N/A in Philippines:
Brivaracetam Carbamazepine Brivaracetam
Clobazam Cenobamate Clobazam
Felbamate Eslicarbazepine Eslicarbazepine
Lamotrigine Ethosuximide (absence) Ethosuximide
Levetiracetam Gabapentin, Pregabalin Felbamate
Perampanel Lacosamide Paraldehyde
October 10, 2020
Phenobarbital (except absence) Oxcarbazepine Primidone

Rufinamide Phenytoin Sulthiamine
Topiramate Primidone Stiripentol
Valproate Stiripentol Tiagabine
Zonisamide Tiagabine Vigabatrin
*Lists vary with reference 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 subjects studied;
(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 agonist at Na+ channels Side Effects: Sedation, dizziness, fatigue, N/V, psychiatric Interactions: May ↑ Carbamazepine,
events, rare bronchospasm and rare angioedema Phenytoin levels (no added benefit if
Indication: Adjunct in focal seizures for people ≥16 years old added to Levetiracetam)
2. Cenobamate MOA: Na+ channel blocker, modulates GABAA receptors Side Effects: Dose-dependent somnolence, dizziness, Interactions: ↑ Clobazam, Phenytoin,
headache, fatigue, diplopia, suicidal ideation, QT shortening Phenobarbital, , and CYP2C19
Indication: Adjunct, refractory focal seizures substrate levels,
Rare: Drug reaction with eosinophilia and systemic symptoms
Contraindication: Familial short QT syndrome (DRESS) Decrease Carbamazepine,
Not recommended in end-stage renal disease, severe hepatic Lamotrigine, and CYP2B6 and CYP3A
impairment substrate levels
3. Clobazam MOA: 1,4-benzodiazepine (same receptors as bound by BZDs, Side Effects: Sedation, somnolence, constipation, pyrexia, Interactions: Inhibits CYP2D6 and
different binding) drooling, paradoxical stimulation, withdrawal symptoms, 2C9, and UGT1A4, 1A6, and 2B4;
SJS/TEN induces CYP3A4; substrate of
Indication: Adjunct in LGS for people ≥2 years CYP2B6, 2C19, 3A4, and P-
Contraindicated in significant renal/hepatic impairment, sleep glycoprotein
apnea, myasthenia gravis
4. Eslicarbazepine MOA: Prodrug to S-licarbazepine → fast VSSC blocker, inhibit Side Effects: Similar to Oxcarbazepine Interactions: Inhibitor of CYP2C19,
Acetate repetitive firing & decrease propagation of synaptic impulses, inducer of CYP3A4, substrate of
↑ K+ conductance & modulation of high-voltage Ca2= channels UGT2B4
Indication: Monotherapy, adjunct for focal seizures

5. Ethosuximide MOA: T-type Ca2+ channel blocker Side Effects: Blood dyscrasias, drug-induced lupus, Interactions: Substrate of CYP3A,
dermatologic reactions, hiccups, other common GI and CNS 2E, 2B/C
Indication: Absence seizures, 1st line side effects
6. Retigabine/ MOA: K+ channel opener Side Effects: Retinal abnormalities progressing to vision loss, WITHDRAWN FROM WORLDWIDE
Ezogabine urinary retention, skin discoloration, QT prolongation, MARKET
Indications: adjunct, focal seizures neuropsychiatric events
7. Felbamate MOA: Fast Na+ channel blocker, T-type Ca2+ channel blocker, Side Effects: Aplastic anemia, hepatic failure, other common Interactions: ↑ Phenytoin & Valproate
Glu receptor blocker, increased GABA CNS and GI side effects levels, decrease Carbamazepine
Indications: Monotherapy, adjunct to focal seizures; adjunct for levels; inhibits CYP2C19
LGS in kids

October 10, 2020
8. GABAergic: MOA: Side Effects: Interactions: Tiagabine highly

Tiagabine Tiagabine – increased GABA, possibly through blockade of Tiagabine – Dermatologic reactions, CNS depression, other protein-bound and substrate of
Vigabatrin GABA transporter (GAT) CNS side effects (may trigger seizures when used in people CYP3A4
Vigabatrin – inhibits GABA transaminase without seizures)
Indications: Vigabatrin – Vision loss, anemia, neurotoxicity, peripheral

Tiagabine – adjunct, focal seizures with or without secondary neuropathy, other CNS side effects
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
9. Primidone MOA: Metabolized to Phenobarbital, PEMA (phenylethyl Side Effects: Similar to Phenobarbital Interactions: Similar to Phenobarbital
malonamide)
Indications: Monotherapy, adjunct for focal & generalized

seizures
10. Stiripentol MOA: May enhance GABA transmission via weak partial Side Effects: Interactions: Inhibits CYP enzymes
agonism/ PAM ala barbiturate, CYP inhibition Common: (contributes to efficacy by boosting
CNS: Anorexia, sedation/insomnia, ataxia, hypotonia and levels of other antiepileptics) –
Indication: Adjunct to Clobazam and Valproate for Dravet dystonia, hyperkinesias; paradoxical aggressiveness, irritability, Carbamazepine, Clobazam,
syndrome insomnia, behavior disorders, hyperexcitability Ethosuximide, Phenobarbital,
GI: Appetite loss, N/V Phenytoin, Primidone, Valproate
Life-threatening/Dangerous: Cutaneous photosensitivity,

rash, and urticaria
11. ACTH/ MOA: Possibly through CRH suppression Side Effects:
Corticotropin Common: Irritability (sometimes severe), Cushingoid features,
Indication: 1st line for West syndrome hypertension, hyperglycemia, glycosuria, electrolyte
imbalances
Contraindications: Serious bacterial or viral infection (TB,
varicella, cytomegalovirus), idiopathic hypertrophic Rare: Brain atrophy, peptic ulcer, subaortic hypertrophic
cardiomyopathy, osteoporosis, uncontrolled hypertension, cardiomyopathy, usually reversible within 6 months of
sensitivity to proteins of porcine origin, live or live-attenuated discontinuation, cataracts, glaucoma, worsening seizures
vaccines
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 Side Effects: Interactions: Inhibits CYP2C19,
fatty acid amide hydroxylase (FAAH), 5-HT1A agonist, transient CNS: Somnolence/insomnia, fatigue, convulsion, rare manic substrate of CYP2C19 and CYP3A4;
receptor potential vanilloid type 1 (TRPV1) agonist, blocks switch effects may be enhanced or reduced
adenosine inactivation CV: Increased HR and BP by opioid antagonists
GI: Diarrhea, LFT elevation
Indication: LGS, DS; possible benefit for multiple sclerosis and Others: Increased risk of infection
as adjunct for positive symptoms of schizophrenia

October 10, 2020
13. Paraldehyde MOA: ??? Side Effects: Interactions: Additive effect with CNS
Indication: Intractable/super-refractory status epilepticus Common (oral use): depressants, Disulfiram may increase
GI: N/V, abdominal pain; unpleasant breath toxicity
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
14. Sulthiame MOA: Blocks Na+ channel & Glu release; inhibits carbonic Side Effects: Interactions: Metabolic acidosis with
anhydrase in glial cells → increases CO2 → acidification of Common: carbonic anhydrase inhibitors,
extracellular space → reduction in inward currents associated CNS: Paresthesias (extremities, face), dizziness, headache, Topiramate, Zonisamide, ketogenic
with NMDA receptors, depression of intrinsic neuronal diplopia diet; ↑ clearance with Carbamazepine
excitability CV: Stenocardia, tachycardia and Primidone; ↑ plasma levels of
GI: Appetite loss, weight loss Lamotrigine, Phenobarbital, and
Indication: Benign focal epilepsies with centrotemporal spikes / Respiratory: Tachypnea, hyperpnea, dyspnea Phenytoin; reduced absorption with
benign rolandic epilepsy, West syndrome antacids containing Mg2+ Trisilicate,
Life- threatening/Dangerous: Bismuth Oxycarbonate, and MgO
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
Rare (not dangerous): Anxiety, hallucinations, joint pain,

myesthetic phenomena

October 10, 2020
SUBSTANCE USE DISORDERS

Medications MOA, Indications, Contraindications Side Effects and Administration Interactions
1. Buprenorphine MOA: μ-opioid receptor partial agonist – relieves withdrawal Common: Headache, constipation, nausea, Substrate of CYP3A4
NEEDS S2 in absence of agonist (understimulated receptors), may orthostatic hypotension; CNS Depressants – Additive CNS depression
precipitate withdrawal in presence of agonist; κ-opioid
receptor antagonist Sublingual: Oral hypoesthesia, glossodynia
Indication: Maintenance for opioid use Rare/serious: Respiratory depression,

disorder/dependence, moderate-to-severe pain hepatotoxicity
Contraindication: Person should be in mild withdrawal *Unfortunately, locally available dosage form is
prior to initiation in opioid use disorder; opioid-naïve transdermal patch (dosage forms indicated for
opioid use disorder: sublingual tablet with Naloxone,
implant)
2. Naltrexone MOA: μ-opioid receptor antagonist Common: N/V, decreased appetite, dizziness, Beyond opioid antagonism, no significant
(tablet imported, but - dysphoria, anxiety, injection site reactions (pain, interactions (liver metabolism by dihydrodiol
not locally FDA- Indication: Opioid use disorder/ dependence treatment tenderness, pruritis, induration, swelling, erythema, dehydrogenase; Acamprosate interaction not
registered) (oral/injection) and relapse prevention (injection); alcohol or bruising) significant)
use disorder/dependence (oral/injection), cholestatic
pruritis Rare: Eosinophilic pneumonia, hepatic injury,
severe injection site reactions
Contraindication: Current opioid use, opioid dependence,
acute opioid withdrawal, naloxone challenge failure or *Ensure person is opioid-free for 7-10 days before
confirmed positive urine drug test, acute hepatitis or liver initiating
failure; hypersensitivity to polylactidecoglyco-lide (PLG),
carboxymethylcellulose, other injection components
3. Nicotine (pastilles) Indication: Tobacco use disorder/ dependence Common: GI (N/V/D, abdominal pain), headache, Varenicline – increased ADRs
local irritation (if topical)
4. Varenicline MOA: α4β2-nicotinic receptor (NN) partial agonist Common: Dose-dependent nausea, vomiting, Alcohol – decreased tolerance
constipation, flatulence, insomnia, headache,
Indication: Tobacco use disorder/ dependence abnormal dreams
Superior to Nicotine but financially toxic !!$$$$!!
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)

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 EML 2017
Bold name: EML 2017 only
a
Protect from light.
bProtect from moisture
cDo not freeze ampule
dKeep vial in carton until ready for use
LAI
Long-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

October 10, 2020
o Aripiprazole – A RIP off

▪ Rip off → worst financial toxicity; urine drug test rips you off with false positive for amphetamines
▪ Ripped off due to gambling, makes you feel restless→may worsen underlying gambling disorder, notable akathisia (m-AKATISYA – inner restlessness)
o Clozapine risks and benefits: C.L.O.Z.A.P.I.N.E.
▪ Cholesterol (dyslipidemia), Laway (sialorrhea), Orthostatic hypotension, Zero EPS, Agranulocytosis but Anti-suicidal, Puso (myocarditis and cardiomyopathy) and Pneumonia,
Ileus, INsulin resistance, Epilepsy but Efficacious (refractory schizophrenia)
• Bipolar disorder coverage
o RISEperidone – manic phase only
o Paliperidone – same as Risperidone
o OLAnZZZapine – OLA (HI! Manic phase) and ZZZ (bipolar depression)
o ARIpiprazole – Ari (tagalog) →own → mine → explosion → bipolar mania only
o KECHAPIn – ketchup → red → bipolar mania, AND api (bipolar depression)
4. CNS Serotonergic Agents (“Antidepressants”)
• Indications: “AntiDEPRESSANTS”
o DEPRession (Clinical)
o Eating disorderS (bulimia nervosa and binge-eating disorder)
o ANxiety disorders (panic disorder, generalized anxiety disorder, social anxiety disorder)
o pTSd, OCD
• Escitalopram
o ‘E s(c)i prof na QT → Escitalopram prolongs QT interval
• Fluoxetine
o Fluox (flocks) of hyper children being bullied on the net → Fluoxetine is preferred antidepressant in children, can be stimulating (5-HT2C antagonism), has weak NET blockade, and is
particularly efficacious in bulimia nervosa
• Sertraline
o Ser is stimulated when discussing benzodiazepine SAR, and it is rewarding → Sertraline slightly increases dopamine (DAT blockade), causing stimulation. It also causes false positives
for urine drug screens for benzodiazepines
• Paroxetine
o Chicken pox at par with being mad as a hatter, dry as a bone, etc. → Paroxetine causes anticholinergic side effects (M1 antagonism) and more sexual dysfunction (NO synthase
inhibition)
• Serotonergic sexual dysfunction
o S(Z)ero “tone” in penis/vagina → SERT-blocking drugs cause sexual dysfunction
• Mirtazapine
o Mirta(ba)ZZZapine → sedating, increases cholesterol
o Other sedating psychotropics: ChlorpromaZZZine, FluphenaZZZine, CarbamaZZZepine, CloZZZapine, OlanZZZapine, KechapinZZZ (EXCEPT -pipraZole)
• Financially toxic agents
o DesVenlafaxinE – Dis Very Expensive
o VortioxetinE – Very Expensive

October 10, 2020
BONUS SECTION: LAST-LINE AGENTS/ALTERNATIVES IN REFRACTORY CONDITIONS

Medications MOA and Indications Side Effects and Administration Interactions
1. Ketamine MOA: (0.5 mg/kg intermittent infusion): uncertain which of N-methyl- Side Effects: Interactions:
NEEDS S2 D-aspartate (NMDA) receptor antagonism, opioid receptor binder, Acute psychiatric: Anxiety, agitation or irritability, • CNS depressants – additive effects
+required (μ, δ, κ), 5-HT1/2 antagonist, 5-HT3A potentiator, α7 nicotinic euphoria/mood elevation, delusions/unusual • CYP3A4 inhibitors – can increase
healthcare cholinergic receptor (α7nChR) antagonist, muscarinic receptor thoughts, panic, and apathy. concentrations of Ketamine and decrease
professionals, binder, NET blocker, D2 receptor partial agonist, substance P concentrations of Norketamine
facility, & equipment receptor antagonist, cholinesterase inhibitor, or nitric oxide Psychotomimetic: Dissociation, followed by • Diazepam – can increase concentrations of
synthetase inhibitor perceptual disturbance, odd or abnormal Ketamine
sensation, derealization, hallucinations, • Naltrexone – Ketamine’s antidepressant
Hypotheses: depersonalization; feeling strange, weird, and effects antagonized by Naltrexone (trial was
• NMDA receptor blockade (via specific binding sites/subunits) on bizarre; feeling intoxicated stopped early due to this)
GABAergic neurons → disinhibited Glu release from
glutamatergic pyramidal neurons → binds AMPA receptors → Neurologic: Headache, dizziness, sedation,
activates voltage-gated Ca2+ channels → ↑ intracellular Ca2+ → drowsiness, faintness, poor condition
BDNF release → activates tropomyosin receptor kinase B (TrkB)
→ ↑activity of intracellular kinases (e.g. extracellular regulated Cognitive: Poor memory & concentration,
kinase/ERK, Akt kinase) → activates mammalian target of confusion, cognitive impairment
rapamycin (mTOR) kinase → controls processes of initiation of
translation of synaptic proteins (e.g. synapsin I, GluA1 subunit of Cardiovascular: Hypertension, arrhythmias
AMPARs, postsynaptic density protein/PSD-95)
• NMDA receptor blockade → AMPAR activation → Urologic: “Ketamine bladder”/ulcerative cystitis
dephosphorylation of eukaryotic elongation factor 2 (eEF2)
kinase → BDNF translation Risk of addiction, tolerance, and withdrawal
• S-ketamine: more psychotomimetic; antidepressant activity
blocked by mTOR inhibitors
• R-ketamine: more potent antidepressant properties with fewer
adverse effects; antidepressant properties blocked by
ERK inhibitor, needs GluN2D subunit
• 2R,6R-hydroxynorketemine (HNK): independent of NMDAR;
dependent on AMPAR activation, NMDA-independent BDNF
expression, & mGluR2
• S-norketamine (S-NK): potent NMDAR antagonist (independent
of AMPAR) related to TrkB/BDNF pathway
• Opioid pathways (see drug interactions)
Indication: Treatment-resistant unipolar and bipolar depression

2. Levothyroxine MOA: Decreases sensitivity of 5-HT1A autoreceptors to serotonin? Side Effects: Subclinical hyperthyroidism with
Interactions:
Increases sensitivity of cortical 5-HT2 receptors? excessive doses Drugs that cause hyperthyroidism or
hypothyroidism
Indication: Adjunct, refractory unipolar and bipolar depression Drugs that increase/ decrease thyroxine-
binding globulin (TBG) or compete for TBG
Contraindication (oral): Untreated subclinical thyrotoxicosis, overt binding
thyrotoxicosis of any etiology, acute myocardial infarction, acute Drugs that interfere with thyroid hormone
myocarditis, acute pancarditis absorption, metabolism, and synthesis
3. Allopurinol MOA: Xanthine oxidase inhibition → increased hypoxanthine → Side Effects: Allopurinol hypersensitivity Interactions:
conversion to adenosine starting with hypoxanthine- syndrome (AHS), SJS-TEN; HLA*B-5801 • Ampicillin – increased rash risk
guaninephosphoribosil-transferase → agonist at A1 receptors screening recommended for those at risk of • Azathioprine, 6-MP – increased immune-
severe cutaneous adverse reactions suppressive and cytolytic effects

October 10, 2020
Indication: Adjunct, refractory bipolar mania Rare: Peripheral neuritis, necrotizing vasculitis, • Alkylating agents – additive bone marrow
Contraindication: Breastfeeding mothers and children, unless bone marrow suppression, aplastic anemia suppression
patients have cancer therapy-induced hyperuricemia or Lesch-
Nyhan syndrome
4. Tamoxifen MOA: Protein kinase C inhibitor Side Effects: Uterine cancer risk, hot flashes, Interactions: Amount of active metabolite
thromboembolic risk, uncommon cataracts governed by CYP2D6 metabolism.
Indication: Monotherapy/ adjunct for bipolar mania Contraindicated with CYP2D6 inhibitors (e.g.
Paroxetine, Fluoxetine)
5. Verapamil MOA: L-type Ca2+ channel blocker Side Effects: Interactions:
GI: Nausea, constipation • Ca2+ salts – Decrease Verapamil
Indication: Adjunct, refractory bipolar mania Cardiovascular: Bradycardia, hypotension, 1st concentrations
degree AV block, weakness • CYP3A4 substrates – Verapamil can increase
Contraindication: Sick sinus syndrome (>1st degree AV block), Respiratory: Flu-like syndrome, allergic rhinitis, concentrations of CYP3A4 substrates
severe CHF, cardiogenic shock, severe left ventricular dysfunction, respiratory infection • CYP3A4 inhibitors – Increase Verapamil
hypotension <90 mm Hg, hypersensitivity Others: Myalgia, headache, ankle edema, with levels
long-term use: gingival hyperplasia • H2RAs – Increase Verapamil concentrations
• Lithium – Verapamil may increase Lithium
Serious: Worsening cardiac output (in CHF), toxicity, with corresponding increase
pulmonary edema, weakness in muscular /paradoxical decrease in Lithium
dystrophy, rare hypertrophic cardiomyopathy, concentrations
rare 2nd or 3rd degree AV block
6. N-acetylcysteine MOA: Glutathione precursor → reduce oxidative stress and Side Effects: Relatively tolerable; usual Interactions:
(NAC) inflammation in multiple downstream pathways; may also modulate immunologic and anaphylactoid reactions linked Nitroglycerin – NAC may enhance vasodilation
glutamate and dopamine and affect neuroplasticity to parenteral use as antidote in Paracetamol effect of Nitroglycerin
poisoning
Indication: Adjunct in refractory bipolar depression, refractory
schizophrenia (particularly negative symptoms), refractory OCD,
and cannabis use disorder
7. Propranolol MOA: Lipophilic β1 and β2 antagonist with membrane stabilizing Side Effects: Bradycardia, hyperkalemia, slight Interactions:
properties; 5-HT1A antagonist; blocks melatonin release weight gain, mild sedation, vivid dreams, • Benzodiazepines – Propranolol can increase
medication-induced depression adverse effects of benzodiazepines
Indication: As needed solely for somatic symptoms of anxiety; • Ca2+ and Al3+ salts – decrease effects of
does not manage core anxiety symptoms; 1st line for essential Serious: Bronchoconstriction, masked Propranolol
tremor and migraine prophylaxis hyperglycemia, worsening of peripheral artery • Calcium channel blockers –
disease, worsening CHF (if not stabilized with additive/synergistic effects
Contraindication: Bradycardia, >1st-degree heart block, ACEI/ARB), ischemic symptoms and myocardial • CYP2D6 modulators – can affect levels of
cardiogenic shock, bronchial asthma, severe COPD infarction on abrupt discontinuation Propranolol
• Gabapentin – Propranolol can increase the
adverse effects of Gabapentin
• Penicillins – decrease effects of Propranolol
• Levothyroxine (thyroid hormones) – decrease
effects of Propranolol
• Lidocaine – levels increased by Propranolol
• NSAIDs – may antagonize antihypertensive
effect of Propranolol
• Warfarin – Propranolol can increase
anticoagulant effect of Warfarin

October 10, 2020
REFERENCES
Main:
Bazire, S. (2018). Psychotropic drug directory. London, UK: Lloyd-Reinhold Publications.
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Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical application. 4th Edition. NY: Cambridge University Press.
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Taylor, D., Barnes, T. R. E., & Young, A. H. (2018). The Maudsley prescribing guidelines in psychiatry. 13th edition. UK: Wiley Blackwell.
Infographic fact-checked by Ser Loisse Mortel, RPh. Check out his Organic Chemistry and Biochemistry series on Youtube here: https://www.youtube.com/user/serloisse737
Youtube Playlists for Psychopharmacology:

bit.ly/AntipsychoticsPcolPH
bit.ly/AntidepressantsPcolPH
bit.ly/MoodStabilizersPcolPH
bit.ly/AnxiolyticsPcolPH
Art:
Keyring art based on illustrations by Nancy Munter (diagram on Bipolar Disorder Phases by Nancy Munter; benzodiazepine figure from Behnoush et al., 2015)
Munchlax, Gengar, Lotad, Kangaskhan, and Snorlax illustrations based on properties by Nintendo, Creatures, Game Freak, and The Pokémon Company
SOLDIER First-Class designs by Tetsuya Nomura, Yoshitaka Amano, and Square Enix
Header, footer, keyring Illustrations, drug discovery infographic, and layout by Frances Ruvy Babac. OPEN FOR COMMISSIONS (Powerpoint designs, publicity materials, posters, handouts,
headers/footers): Fb.com/francesruvyb | francesbabac@gmail.com | +63917 731 0830
Cover art and back art by Arn Zander Barcelo @barcelozander
Munchlax illustrations by Risa Takatsu (IG: fieri.art)
Munchlax original character portrait by @TinaFate1
Zolpidem video edited from Charlie the Unicorn 2 by FIlmCow (https://www.youtube.com/watch?v=QFCSXr6qnv4)
No copyright is claimed in Pokemon, Final Fantasy, or Charlie the Unicorn 2 and to the extent that material may appear to be infringed, I assert that such alleged infringement is permissible
under fair use principles in U.S. and Japan copyright laws. If you believe material has been used in an unauthorized manner, please contact the author.
Supplementary:
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“What does the psych- in psychopharmacology mean?

Soul. The pharmacology of the soul. You are a soul chemist.”

Dr. Sotiris Posporelis

PSYCHOTROPIC DRUG DISCOVERY PATHWAY: INFOGRAPHIC 9

I. SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIS) 10

FIRST GENERATION ANTIPSYCHOTICS / D2 ANTAGONISTS 14

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

SUBSTANCE USE DISORDERS 34

BONUS SECTION: LAST-LINE AGENTS/ALTERNATIVES IN REFRACTORY CONDITIONS 37

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 4 of 43

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 5 of 43

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 6 of 43

Jarvin Enosh Tan, RPh

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 7 of 43

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 8 of 43

PSYCHOTROPIC DRUG DISCOVERY PATHWAY: INFOGRAPHIC

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 9 of 43

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 10 of 43

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 11 of 43

IV. MULTIMODAL ANTIDEPRESSANT

Side effects: Hypertension and insomnia; less/minimal sexual dysfunction

ANTIDEPRESSANTS NOT AVAILABLE LOCALLY

SPARI: Serotonin Partial Agonist-Reuptake Inhibitor Indications: MDD

Side Effects: Dizziness, nausea/ vomiting, sedation,

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 13 of 43

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 14 of 43

Other Indications: Tourette’s

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 15 of 43

SECOND GENERATION ANTIPSYCHOTICS / D2-5HT ANTAGONISTS

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 16 of 43

4. Quetiapinea,b Specific Side Effects • Increased risk of death, cerebrovascular

LAI is non-PNF “3rd gen.”: Cariprazine, Lumateperone

Substrate of CYP2D6, 3A4 Multiple other receptor affinities

ANTIPSYCHOTICS NOT AVAILABLE LOCALLY

Lumateperone – 5-HT2A antagonism, D2

Administration: Morning if once daily (less likely to experience EPS in sleep)

Other anticholinergics for EPS (N/A locally): Benztropine, Trihexyphenidyl, Procyclidine

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 19 of 43

ANXIOLYTICS AND SEDATIVE-HYPNOTICS

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 20 of 43

Side effects: First-dose phenomenon

Side Effects: Anticholinergic, sedation

STIMULANTS, WAKE-PROMOTING AGENTS, AND MEDICATIONS FOR ADHD

2. Atomoxetine MOA: Blocks NET Common: Metabolized by CYP2D6

ANXIOLYTICS, SEDATIVE-HYPNOTICS, STIMULANTS, AND WAKE-PROMOTING AGENTS NOT AVAILABLE LOCALLY

Indications: Bipolar disorder (+reduces suicide;

Contraindications: Severe cardiac or renal

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 24 of 43

2. Divalproex/ MOA: Hypotheses include Side effects: Interactions:

Drug reaction w/ eosinophilia &

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 25 of 43

4. Carbamazepine MOA: Side effects: Interactions:

Contraindications: HLA*B1502 allele, bone

Additive myelosuppression with Clozapine

Also indicated for Parkinson’s disease dementia, useful Administration:

Contraindication: 5-HT3 antagonists (profound

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 27 of 43

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 28 of 43

Possibly carcinogenic to humans (IARC Group 2B), use gloves

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 29 of 43

Administration: Take with food (↑absorption)