Jetlax's CNS Pharmacology Cheat Sheet For The Philippines v6.0 at Bit - Ly - CNSPcol - See Bit - Ly - CNSHandouts For 5.0 Corrections

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

June 30, 2022
There is no RPh without mental health. quick legend:
CNS Pharmacology Cheat Sheet v6.0
Jarvin Enosh Tan, RPh
TABLE OF CONTENTS
DISCLAIMER AND VERSION 5.0 CORRECTIONS 5
PREFACE 7
ACKNOWLEDGEMENTS 9
MISCONCEPTIONS ON PSYCHOTROPIC MEDICATIONS 10
PSYCHOTROPIC DRUG DISCOVERY PATHWAY: INFOGRAPHIC 12
“ANTIDEPRESSANTS” (SERT BLOCKERS) 13

IA. SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIS) 13
IB. SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIS) 15
IC. MULTIMODAL ANTIDEPRESSANT 15
“ANTIDEPRESSANTS” (NON-SERT BLOCKERS) 15

II. NORADRENERGIC AND SPECIFIC SEROTONERGIC ANTIDEPRESSANT (NASSA) 15
III. NOREPINEPHRINE-DOPAMINE REUPTAKE INHIBITOR 15
IV. MELATONERGIC DRUGS 16
V. REVERSIBLE INHIBITOR OF MAO-A (RIMA) 16
VI. GLUTAMATERGIC ANTIDEPRESSANTS 16
VII. TRICYCLIC ANTIDEPRESSANTS (TCAS) 16
“ANTIDEPRESSANTS” NOT AVAILABLE LOCALLY 17
“ANTIPSYCHOTICS” 19
FIRST GENERATION “ANTIPSYCHOTICS” / D2 RECEPTOR ANTAGONISTS 19
SECOND GENERATION “ANTIPSYCHOTICS” / D2-5HT RECEPTOR ANTAGONISTS 21
SECOND GENERATION “ANTIPSYCHOTICS” / D2-5HT RECEPTOR ANTAGONISTS: CLOZAPINE 24
THIRD GENERATION “ANTIPSYCHOTICS” / D2 RECEPTOR PARTIAL AGONISTS-5HT RECEPTOR ANTAGONISTS 25
CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 3 of 61
June 30, 2022
“ANTIPSYCHOTICS” AND RELATED AGENTS NOT AVAILABLE LOCALLY 29
ANTICHOLINERGICS (ANTIMUSCARINICS) 30
“MOOD STABILIZERS” 31
ANXIOLYTICS AND SEDATIVE-HYPNOTICS 33
STIMULANTS, WAKE-PROMOTING AGENTS, AND MEDICATIONS FOR ADHD 36
ANXIOLYTICS, SEDATIVE-HYPNOTICS, STIMULANTS, WAKE-PROMOTING AGENTS, & ADHD MEDS NOT AVAILABLE LOCALLY 37
DRUGS FOR DEMENTIA 39
DRUGS FOR PARKINSON’S DISEASE 40
OTHER ANTIEPILEPTICS (CNS ION CHANNEL AND SYNAPTIC VESICLE BINDERS) 41

BARBITURATES / GABAERGIC 41
SODIUM CHANNEL BLOCKERS (VSSC BLOCKERS) 42
SYNAPTIC VESICLE PROTEIN 2A (SV2A) BINDER 44
AMPA RECEPTOR ANTAGONIST 44
ANTIEPILEPTICS NOT AVAILABLE LOCALLY 45
DRUGS FOR SUBSTANCE USE DISORDERS 47
MNEMONICS 49
BONUS SECTION: PSYCHEDELICS AND OTHER INVESTIGATIONAL AGENTS 51
REFERENCES AND CREDITS 54

Disclaimer
The author (Jarvin Tan) and the peer reviewer (Christopher Michael Mendoza) of this cheat sheet do NOT have any
financial or other relationships with the manufacturer/s of any commercial product/s discussed in this cheat sheet. As
registered pharmacists, they have NOT received any payments or honoraria from, consulted for, held advisory
positions in, held market shares in, or held patents related to pharmaceutical companies. The author discloses
allegiance bias towards cognitive behavioral therapy for insomnia (CBTi) as it is currently the main focus of their thesis
proposal. While the author 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 author 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 author 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
June 30, 2022
Corrections for version 5.0:

• Cover photo: “neutrophic” should be spelled as “neurotrophic”. Let’s pretend our Munchlax was tired out managing
Gengar and Lotad in class.
• Psychotropic Drug Discovery Pathway Infographic(version 5.0): The formula for chloroform should be CHCl3
• Clarification: Fluvoxamine is also efficacious for MDD as per Cipriani et al. (2018)
• Page 11 (version 5.1) or Page 12 (version 5.0): Under Venlafaxine, “DAT selectivity increases w/ dose” should be “NET
blockade increases with dose”
• Page 13: For Esketamine, RCTs have shown Esketamine does NOT reduce suicidal ideation/behavior and is NOT rapid
in onset. Full reference below. Also see NICE appraisal in reference list.
o Siegel, A. N., Di Vincenzo, J. D., Brietzke, E., Gill, H., Rodrigues, N. B., Lui, L. M., ... & Rosenblat, J. D. (2021).
Antisuicidal and antidepressant effects of ketamine and esketamine in patients with baseline suicidal ideation: A
systematic review. Journal of Psychiatric Research
• Page 14:
o Orthostatic hypotension and weight gain are common side effects for 1st gen antipsychotics, though less so with
Haloperidol
o Rightmost column: Hypersalivation is NOT an anticholinergic side effect and should be under a separate category
• Page 17:
o For discontinuation (withdrawal) symptoms for antipsychotics, rebound anticholinergic should be rebound
cholinergic
o Under side effect management (rightmost column), AVOID fibers if the constipation is due to Clozapine
specifically. Stimulant laxatives with rapid onset like senna are preferred for Clozapine-induced gastric hypomotility
• Page 18: Give Biperiden ONLY when patient experiences dystonias and/or pseudoparkinsonism. Avoid giving it by
default just because service user is prescribed a potent D2 receptor antagonist like Haloperidol
• Page 22: Methylphenidate does NOT worsen tics as per Cohen et al. (2015). Full reference:
o Cohen, S. C., Mulqueen, J. M., Ferracioli-Oda, E., Stuckelman, Z. D., Coughlin, C. G., Leckman, J. F., & Bloch,
M. H. (2015). Meta-analysis: Risk of tics associated with psychostimulant use in randomized, placebo-controlled
trials. Journal of the American Academy of Child & Adolescent Psychiatry, 54(9), 728-736.

June 30, 2022
Preface
This cheat sheet started out as an offshoot of a project I was working on back in 2018. Version 1 came out September 24, 2018 as a means
to make learning psychopharmacology less threatening to pharmacy students, pharmacists, and those in the health professions. This was also rooted
in a frustration with the insufficiency of the national pharmacy curricula’s adopted references in accurately explaining medications for mental health in
an organized and contextualized 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 student and health professional 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.
These past two cursed years have been nothing but draining, both for teachers and students. As part of the former group, I was looking for
ways to better engage students, which is why back in 5.0 I got the idea to commission artwork to illustrate various concepts in psychotropic
pharmacokinetics and pharmacodynamics (you can faintly see 5.0’s cover art in the “Disclaimer” section!). The idea was, and still is, to give the
impression that psychopharmacology shouldn’t be something to be afraid of or be intimidated by, but rather embraced with the same curiosity and
fervor as we would other medication classes together with Filipino mental health service users. In addition to the previous version’s 13 illustrations, 7
new pieces have been 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. Alongside these are 10 personal photos focused more on mnemonics (and some fun
doodles on the side!)
Two sets of infographics accompany this new version. The first was created back in 2020 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.
The second one was recently commissioned after I noticed in an online survey by the Federation of Junior Chapters of the Philippine
Pharmacists Association (FJCPPhA) that plenty of misconceptions regarding psych meds still dominate student knowledge and perceptions
nationwide like serotonin deficiencies and benzos being maintenance meds (both are false, of course). While it may take years before these myths
are dispelled, it is my hope that this work goes some way towards helping with that. Check out these two posters to see if there are any myths you
can unlearn!

June 30, 2022
As for the rest, the format has been made a bit more consistent with headers placed for each drug entry to ensure it’s clear what information
is being stated (e.g. side effects, interactions, etc.). Organization of information for the so-called “Antidepressants” was previously a bit messy, and
this has been fixed. Particularly, entries have been divided into SERT and non-SERT blockers as clinical properties are easier to segment this way.
Evidence-based indications, whether labelled or off-label, are now clearly indicated per individual drug. More explanation and context are also provided
for side effects and drug interactions so this should now make it less difficult to study. The mechanism of action of second-generation “antipsychotics”
is also fleshed out more below borrowing a fountain analogy of receptor binding affinities from a blog post to better explain the concept. Take notice
of the tiny virus icons scattered throughout the document! It’s been two years of a pandemic and so COVID-19-specific considerations are inevitable
and have been noted where relevant!
New detailed entries have been added for drugs that were just recently registered on the FDA Philippines verification portal, namely
Venlafaxine, Moclobemide, Agomelatine, and Zuclopenthixol acetate. This is regardless of current market availability in case these drugs enter
pharmacy supply chains during the lifespan of version 6.0. Caffeine and Melatonin have received their own entries, too, given how popular they are
here! For drugs not available in the Philippines, information on their clinical properties has been expanded should you like to learn more or have your
own trivia contests to attend to. Of note, there’s been a boom in psychedelic-assisted psychotherapy clinical trials in 2021, so it would be remiss of
me not to include entries for Psilocybin-assisted therapy and MDMA-assisted therapy. These are still controlled substances so please continue to
abide by RA 9165 and other relevant rules and regulations.
Last but not the least, did I mention that this cheat sheet has finally been peer reviewed? I requested assistance from a pharmacist with
experience in inpatient mental healthcare (who remains anonymous due to restrictions with current employment) and a local community pharmacist
who recently received their PharmD. I want to ensure that in trying to debunk myths and misconceptions regarding psychotropic medications, I don’t
end up creating some new ones of my own, and so this is one extra measure towards quality control.
Additional links have been embedded on top of the previous ones across the entire document – that’s 15 music videos and 3 video clips all in
all. See if you can spot all the blue hyperlinks! My Youtube series is still available below but updates are still in the works. Consider this cheat sheet
the most updated material I have so far. Note that any peer review for this cheat sheet does NOT extend to the handouts or Youtube videos. The
latter will be completely updated soon so please look forward to that:
▪ Corrections and handouts still at bit.ly/CNSHandouts. Please check routinely for any corrections and updates post-release!
▪ bit.ly/AntipsychoticsPcolPH (videos and handouts updated)
▪ bit.ly/AntidepressantsPcolPH (videos and handouts updated)
▪ bit.ly/MoodStabilizersPcolPH
▪ bit.ly/AnxiolyticsPcolPH
▪ bit.ly/ANSPcolPH (new!)
I wish you all the best and remember the focus and center of why we study all of this: to #MoveforMH with mental health service users! Forge ahead,
Warriors of Light and Darkness alike!

June 30, 2022
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: Dr. 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 who extended their technical assistance and encouragement from across borders to support the move for
mental health integration into Philippine pharmacy practice, as well as those from the College of Mental Health Pharmacy who have been ever
supportive towards my many questions. 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 (well-wishes you and Hazel on your upcoming
marriage)! 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! To AJ Elicaño, Karl Sy, and Matt Ong,
thank you for the unhinged bi-monthly discord sessions these past 2(???) years. Lastly, to Luxerion, my home in Eorzea, thank you for welcoming a
sprout like me. We fought, wiped, cried, laughed, and walked to the end together. Those small moments around the campfire were a gentle salve to
the pandemic loneliness. Likewise to its creators, Naoki Yoshida, Natsuko Ishikawa, Banri Oda, Masayoshi Soken and the music team, and the rest
of the Final Fantasy XIV dev team. Our journey will never end! – @Jetlax

Postgraduate Certificate in Psychiatric Therapeutics (with distinction), Aston University
Technical Writer, Philippine National Formulary (8th edition)
June 30, 2022
Misconceptions on Psychotropic Medications

June 30, 2022

June 30, 2022
PSYCHOTROPIC DRUG DISCOVERY PATHWAY: INFOGRAPHIC

June 30, 2022
“ANTIDEPRESSANTS” (SERT BLOCKERS)

Medication Specific Information General (MOA, Side Effects, Interaction) Indications, Side Effect Management, & More
IA. SELECTIVE SEROTONIN REUPTAKE INHIBITORS (SSRIs) Indications (depending on individual SSRI;
1. Sertraline₱₱ Additional MOA: Also weakly blocks dopamine Before we start, a review: bit.ly/AllAboutThatBrain SSRIs generally preferred):
transporters (DAT) and σ1 receptors Mechanism of Action (MOA) ✓ Major Depressive Disorder (MDD)
MDD: Block serotonin (5-HT) transporters (SERT) and ✓ Generalized Anxiety Disorder (GAD)
Specific Side Effects: CNS-activating side effects ↑5-HT binding to receptors, leading to: ✓ Panic Disorder (PD)
(increased irritability, impulsiveness, restlessness), take • Desensitization of presynaptic 5-HT1A ✓ Social Anxiety Disorder (SAD)
in AM autoreceptors: better tolerance of stress ✓ Obsessive Compulsive Disorder (OCD)
(see Carhart-Harris & Nutt, 2017) ✓ Post-traumatic Stress Disorder (PTSD)
Additional Specific Indications: MDD with comorbid • Prolonged 5-HT2A receptor agonism: Delayed ✓ Binge Eating Disorder (BED)
CAD (possible reduced incidence of myocardial ↑brain-derived neurotrophic factor (BNDF; forms ✓ Bulimia Nervosa (BN)
infarction) new connections between neurons); removes ✓ Body Dysmorphic Disorder (BDD)
affective biases (see Ketamine MOA for summary o 2nd line, vasomotor symptoms of menopause
Interactions of BDNF’s role in neuroplasticity from Harmer et al.) ESC FLX SER FVX PAR
• Caution in urine drug screens: false positive result • Activation of postsynaptic 5-HT1A receptors in MDD
for benzodiazepines & LSD hippocampus and other adaptive neuronal/receptor GAD Alt.
events in other brain circuits: delayed reduction in PD
2. Fluoxetinea Additional MOA: Also weak 5-HT2C antagonist and NET anxiety SAD
₱₱ / ₱₱₱ (bulimia)
blocker (may explain stimulating effects)
OCD
Onset PTSD Alt. Alt.
Specific Side Effects:
• MDD: 1-2 weeks (They work!!! See Cipriani et al.) BED Alt.
• CNS-activating side effects, take in AM
• Anxiety and related disorders: 4 weeks BN
• Less likely withdrawal Sx on abrupt stopping (long t1/2) (up to 8-12 weeks, especially OCD)
Additional Specific Indications: Bulimia Nervosa, BDD BDD
Interactions: Hot Alt. Alt.
Safe duration (to reduce relapse risk): 6-9 months flashes
• Potent CYP inhibitor → multiple interactions, esp. w/ (MDD), 12 months (GAD, PD, SAD, OCD, PTSD)
drugs metabolized by CYP2D6 (ex: Tamoxifenbreast Side Effect Management (Tolerance develops
cancer MAP/BCMAP
) over time):
• Caution in urine drug screens: false positive result • N/V – take with food / move dose to bedtime
for LSD • Constipation – fiber, water, exercise
Contraindications: • Diarrhea – maintain hydration, ORS (if needed),
• TamoxifenBCMAP – Fluoxetine decreases amount of antispasmodic
active metabolite (Endoxifen) by preventing • Insomnia/sedation – shift dosing to morning/
TamoxifenBCMAP metabolism via CYP2D6 inhibition bedtime; sleep hygiene
• Headache, dizziness – take at night
June 30, 2022
3. Escitaloprama ₱ – ₱₱ MOA: pure SERT blockade (racemic Citalopram is H1 Side Effects Non-pharmacologic
blocker) Common: • Psychotherapy (all indications);
• GIT: Nausea/vomiting (5-HT3 receptors in CTZ), psychological debriefing is not recommended
Specific Side Effects: May prolong QT interval diarrhea, constipation for trauma
OTHER SSRIs (available in the PH) DO NOT • CNS: Insomnia/sedation (5-HT1A, 5-HT2C receptors), • Aerobic exercise (especially for MDD; Tx &
SIGNIFICANTLY PROLONG QT INTERVAL agitation, tremors (5-HT2A receptors), dizziness, prevention)
headache, fatigue, anxiety (5-HT1A receptors), • Light exposure therapy (seasonal affective
Interaction: nervousness, increased/decreased appetite (5-HT2C disorder)
• Omeprazole/Esomeprazole (CYP2C19 inhibitor) – receptors) • St. John’s wort (MDD; multiple drug
may increase Escitalopram concentrations since • Others: Sexual dysfunction (spinal cord 5-HT2 interactions as a CYP inducer)
Escitalopram is metabolized by CYP2C19 receptors), sweating, bruising, weight gain/loss, • Lavender oil (GAD, single non-inferiority trial
• QT prolonging meds – additive effects; monitor asthenia vs benzos)
• Emerging data of interaction with smoking, possibly Rare/Serious • Progressive muscle relaxation (PMR)
due to Escitalopram being potentially metabolized by • Manic switch in bipolar disorder (phobias, PD)
CYP1A2, but needs verification through further (does NOT cause de novo bipolar disorder) • Mindfulness
studies • ↑risk of GI, peri-operative, uterine, cerebral bleeding
4. Paroxetine₱₱ Additional MOA: (Blockade of SERT on platelets → platelet Tapering
• M1 antagonist aggregation hindered; rare in absence of risk factors) Traditional tapering: x mg/day (usual references)
• NET blocker • Rare hyponatremia and SIADH, esp. in elderly and Proposed tapering: x% mg/day corresponding
• Nitric oxide synthetase inhibitor dehydrated persons with SERT occupancy (Horowitz & Taylor, 2019)
• Rare post-SSRI sexual dysfunction (PSSD)
Specific Side Effects: • Rare, increased suicidal ideation ≤24 years old Each antidepressant will have specific
• Anticholinergic side effects (M1 antagonism) (~0.09%) tapering regimens. Please consult the Royal
• Greater incidence of sexual dysfunction (nitric oxide College of Psychiatrists website and/or the
synthetase inhibitor) Withdrawal Symptoms aka brain zaps (happen on 14th edition of the Maudsley Prescribing
• Higher withdrawal risk on abrupt stopping (short t1/2) abrupt discontinuation; most common in bold) Guidelines in Psychiatry for additional details!
→ Avoid in children, adolescents, adults≤24 y.o • Affective – anxiety, irritability, sadness, crying spells
• Gastrointestinal – nausea N/A in Philippines
Interactions: Paroxetine is a potent CYP2D6 inhibitor • Neuromotor – ataxia Trazodone (SARI), Vilazodine (SPARI),
• Vasomotor – diaphoresis (sweating) Reboxetine (NRI), Doxepin (TCA), other TCAs,
Contraindications: • Neurosensory – electric shock sensation MAOIs, Mianserin (NaSSA), Milnacipran (SNRI),
• TamoxifenBCMAP – Fluoxetine decreases amount of • Somatic – flu-like symptoms Levomilnacipran (SNRI), Esketamine
(Glutamatergic), Brexanolone/Allopregnanolone
active metabolite (Endoxifen) by preventing • Other neurologic – vivid dreams, insomnia,
TamoxifenBCMAP metabolism via CYP2D6 inhibition. (GABAergic)
dizziness, headache
5. Fluvoxamine₱₱₱ Additional MOA: Also agonist at σ1 receptor; indicated for • For Paroxetine – rebound cholinergic symptoms
OCD
Interactions
Interactions: a. NSAIDs may increase bleeding risk and decrease
• Potent CYP1A2 inhibition (↑↑Clozapine, ↑Melatonin SSRI efficacy
& increase levels of others metabolized by CYP1A2, b. Anticoagulants, antiplatelets, and ω3 fatty acids
↓Caffeine clearance), moderate CYP3A4 inhibitor may increase bleeding risk
• Smoking may decrease Fluvoxamine serum (combine with effects of blocking platelet SERT)
concentrations (CYP1A2 induction) c. Serotonin syndrome (when combined with
serotonergic agents): ginseng, St. John’s wort,
Check out STOP COVID & TOGETHER trials plus Tryptophan, Dextromethorphan, methylene blue,
the PSMID appraisal of evidence for COVID use Linezolid, serotonergic drugs
6. Dapoxetine₱₱₱₱ Rapid absorption, onset, elimination: Indicated only for d. Levothyroxine efficacy decreased by SSRIs
premature ejaculation; 1 dose prior to sexual activity e. Tramadol increases risk of seizures and serotonin
syndrome when taken together

June 30, 2022
IB. SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIs) VEN DUL

1. Venlafaxine₱₱₱ and Desvenlafaxine: MOA: Block SERT, NET (may explain neuropathic pain MDD
Desvenlafaxine₱₱₱₱ • Venlafaxine’s active metabolite use due to role of NE & noradrenergic receptors in spinal GAD
• Caution in urine drug screens: false positive cord in pain neurotransmission) PD Alt.
result for amphetamines SAD Alt.
Indications: MDD, anxiety & related disorders, OCD Alt. Alt.
Venlafaxine: neuropathic pain PTSD Alt.
• NET block = dose dependent (SSRI at lower doses) BED
• Venlafaxine additional indication: 2nd line, cataplexy Side effects (besides the serotonergic ones above) BN
(narcolepsy type 1) • Increased BP (2 mmHg), sweating BDD
• Higher rates of manic switch, withdrawal (short t1/2) • Urinary retention (NE agonizes bladder α receptors) Hot Alt.
2. Duloxetine₱₱ M1 antagonist; SNRIs also used in neuropathic pain • Similar general interactions & side effects with SSRIs flashes
Rare hepatotoxicity Contraindication: uncontrolled angle-closure glaucoma

Interactions: Venlafaxine, Duloxetine concentrations
affected by CYP2D6 modulators
IC. MULTIMODAL ANTIDEPRESSANT
Vortioxetine₱₱₱ MOA: (see 2nd generation antipsychotic MOA for details)
• Blocks SERT; 5-HT1A agonist, 5-HT1B partial agonist, 5-HT1D and 5-HT7 antagonist (metabotropic receptors)
• 5-HT3 antagonist (ligand-gated ion channels)
Indication: MDD
Interaction (besides serotonergic interactions above): CYP2D6 modulators may affect serum Vortioxetine levels
Pro-cognitive effect in elderly; frequent nausea but less sexual dysfunction
“ANTIDEPRESSANTS” (NON-SERT BLOCKERS)
Medication MOA, Indications, and Contraindications Side Effects Interactions
II. NORADRENERGIC AND SPECIFIC SEROTONERGIC ANTIDEPRESSANT (NaSSA)
Mirtazapine₱₱ MOA: Side effects: Interactions:
• Does NOT block SERT • Sedation • α2 agonists – Mirtazapine can antagonize
• Antagonist at α2, H1, 5-HT2A, 5-HT2C, 5-HT3 receptors • Weight gain (worst), ↑cholesterol their antihypertensive effects
(noradrenergic and serotonergic antagonist); • Less/minimal sexual dysfunction, less nausea and • CNS depressants – additive CNS depressing
– α2 receptor antagonism → blocked vomiting (likely due to absence of SERT blockade) effects
autoreceptor (brakes) → no brakes, 5-HT release • Some anticholinergic effects (dry mouth, • CYP3A4 modulators – can affect Mirtazapine
disinhibited constipation, etc.) serum concentrations as Mirtazapine is
• At 15 mg, ↑sedation due to prominent H1 antagonism • Flu-like Sx (rarely leads to blood dyscrasias like metabolized by CYP3A4
(less sedation at higher doses w/ 5-HT2C antagonism) neutropenias) • Serotonin syndrome (when combined with
Indications: MDD (monotherapy); 2nd line for PD & OCD • Rare manic switch (in undiagnosed bipolar disorder), serotonergic agents): ginseng, Tryptophan,
rare increased suicidal ideation (see above) St. John’s wort, methylene blue, Linezolid,
Administration: In the evening Dextromethorphan, serotonergic drugs
III. NOREPINEPHRINE-DOPAMINE REUPTAKE INHIBITOR
Bupropionmarket N/A 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
Common: Hypertension and insomnia; less/minimal sexual dysfunction
Rare/serious: Seizures (substituted cathinone; risk goes up when exceeding maximum doses, if with risk factors,
and IR>SR/XL), SJS-TEN
Interactions: Caution with urine drug screens; false positive for amphetamines and LSD
June 30, 2022
IV. MELATONERGIC DRUGS

Agomelatinemarket N/A MOA: Melatonin 1 (MT1) and MT2 agonist, 5-HT2B and 5-HT2C antagonist – resynchronizes circadian rhythm (MT1/2 & 5-HT2C)
Indications: MDD, GAD
Contraindications: Hepatic impairment, concomitant use with CYP1A2 inhibitors
Administration: in the evening
Side Effects:
• Use limited by hepatotoxicity concerns (rare: hepatitis & hepatic failure)
• Likely no withdrawal on abrupt cessation; minimal to no sexual dysfunction & less nausea/vomiting (no SERT blockade)
• Sedation/insomnia, anxiety, fatigue, constipation, diarrhea, sweating
• Rare manic switch (in undiagnosed bipolar disorder), rare increased suicidal ideation (see above)
Interactions:
• CYP1A2 modulators – can affect Agomelatine concentrations since Agomelatine is metabolized by CYP1A2 (ex. smoking – reduces Agomelatine concentrations)
V. REVERSIBLE INHIBITOR OF MAO-A (RIMA)
Moclobemidemarket N/A MOA: Reversible, selective MAO-A inhibition (see MAOI section for relevant interactions)
Indications: MDD, PD, SAD
Side Effects
Common: Insomnia, anxiety, dizziness, restlessness, agitation, galactorrhea; Lower risk of tyramine-cheese reaction (hypertensive crisis) at therapeutic doses
Rare/serious: Hypertension, manic switch, seizures
VI. GLUTAMATERGIC ANTIDEPRESSANTS
Glutamatergic:Esketamine MOA: S-isomer of Ketamine; does NOT reduce suicidal ideation. Non-selective, non-competitive NMDA receptor antagonist; exact mechanism for depression unclear
NEEDS S2 (effect of parent compound and S-norketamine metabolite dependent on mTOR kinase but independent of AMPA receptors)
market n/A
Administration: Intranasal; to be administered ONLY in clinics or hospitals under supervision of healthcare professional (DDB Board Resolution No. 5 s2021)
Onset: NOT rapid (~22 days)

Side Effects: Dizziness, nausea/ vomiting, sedation, vertigo, hypertension, ↓ feeling/ sensitivity (hypoesthesia), feeling drunk. anxiety,
lethargy, sedation, dissociation, addiction potential
Indication: Adjunct, refractory MDD or MDD with suicidal ideation/behavior (This only means it is used in this population. It still does NOT reduce suicide)
Interactions: Minor substrate of CYP2B6, 2C19, 2C9, 3A4; additive CNS depression with CNS depressants; additive toxicity from serotonergic agents & NMDA antagonists
VII. TRICYCLIC ANTIDEPRESSANTS (TCAs)
Amitriptyline MOA: NET blocker, HAM antagonist, voltage-sensitive Na+ channel (VSSC) blocker; some also block SERT,5-HT2A,5-HT2C receptors
₱₱ (neuropathic pain) / ₱₱₱ (depression)
• Na+ channel blockade (cardiotoxicity) → lowers seizure threshold, sudden death, sudden arrythmias, tachycardia (esp. at higher doses)
Clomipramine₱₱₱₱ • Anticholinergic + NET blockade combo also enhances cardiotoxicity
Trimipramine₱₱₱₱ Indications: 2nd/3rd line for MDD (DO NOT GIVE to those at risk of suicide) 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; migraine prophylaxis, fibromyalgia, diabetic neuropathy: 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 (see SSRIs), blue/green urine discoloration (Amitriptyline)
Rare/serious: Manic switch, suicidal thoughts/behavior, QT prolongation, hepatic failure, extrapyramidal symptoms (EPS), ↑intraocular pressure (IOP), seizures
Withdrawal symptoms (on abrupt discontinuation): Flu-like symptoms, Gi distress, rebound insomnia, cholinergic rebound (Clomipramine withdrawal ~SSRIs)
Interactions:
• CYP interactions (All three with CYP2D6 modulators, Clomipramine & CYP1A2modulators), Additive CNS depressant & anticholinergic effects with similar drugs
• Valproate – significantly increases levels of Amitriptyline
• False positive in urine drug tests for amphetamines (Trimipramine), LSD (Amitriptyline), and Methadone (Clomipramine); frequent false negatives (Clomipramine)

June 30, 2022
“ANTIDEPRESSANTS” NOT AVAILABLE LOCALLY

USELESS IN PHILIPPINE CLINICAL CONTEXT (unless compassionate use)
Medication Specific Information General (MOA, Side Effects, Interaction) Indications, Side Effect Management, & More
SSRI: Citalopram Racemic version of Escitalopram MOA: same as above Indications: MDD, PD, SAD, GAD, alt. for menopausal
hot flashes; dose limit in elderly to reduce QT
MOA: Also blocks H1 receptors Side effects: QT prolongation, same as SSRIs prolongation risk
Interactions: Same with Escitalopram

SNRI: SNRIs less tolerable; alternatives MOA: same as above Indications: MDD
Milnacipran
Levomilnacipran Side effects: similar as above re: SNRIs
Interactions: Levomilnacipran levels affected by 3A4 modulators

NaSSA: MOA: Same as Mirtazapine+α1 MOA: same as above with added property (see column to the left) Indications: MDD
Mianserin antagonism
Side Effects: Same as Mirtazapine w/ orthostatic hypotension
Interactions: CYP2D6 modulators can increase/decrease Mianserin

levels as Mianserin is metabolized by CYP2D6
SARIs: Serotonin Antagonist-Reuptake MOA: Blocks SERT, α1, 5-HT2A (potently), 5-HT2C receptors Indications: MDD (Trazodone is preferred over
Trazodone Inhibitors Nefazodone), alternative for GAD (Trazodone), insomnia
Nefazodone Additional MOAs: Side effects (notable, aside from SSRI side effects above): (only Trazodone, and only at low doses for selectivity of
Trazodone: also blocks H1 receptors Trazodone: Orthostatic hypotension, edema, blurred vision; rare rash, H1 receptors)
Nefazodone: also blocks NET seizures, & priapism (painful, persistent erection)
Nefazodone: Trazodone’s + cough. Hepatotoxic (less preferred)
Interactions:
Nefazodone – CYP3A4 inhibitor; metabolite (mCPP – 5-HT2C agonist)
levels increased/decreased by CYP2D6 modulators
Trazodone – levels affected by CYP3A4 modulators; may increase
Digoxin/Phenytoin concentrations & block antihypertensives’ effects
SPARI: Serotonin Partial Agonist-Reuptake Inhibitor Indications: MDD
Vilazodone MOA: Blocks SERT, partial agonist at 5-HT1A receptors
Side Effects: Similar to SSRIs; requires food (significant nausea without food), very slow dose titration
Interactions: Levels increased/decreased by CYP3A4 modulators as Vilazodone is metabolized by CYP3A4

NRI: Norepinephrine Reuptake Inhibitor Indications: alt. for MDD, PD
Reboxetine MOA: Blocks NET (does NOT block SERT, so less SSRI side effects like N/V, sexual dysfunction)
Side Effects: Similar to Atomoxetine; relatively inferior efficacy and tolerability vs other antidepressants
Interactions: Levels affected by CYP3A4 modulators since Reboxetine is metabolized by CYP3A4

TCAs: Lofepramine – least cardiotoxic TCAs Amoxapine – seizures at therapeutic doses Indications:
Lofepramine, Nortriptyline – less anticholinergic BED (2nd line) – Desipramine, Imipramine
Desipramine, Doxepin – most selective agent for H1 Doxepin – very sedating Nocturnal enuresis (3rd line; vs 1st line: alarms and 2nd line:
Nortriptyline, receptors (only at 1-6 mg) in existence Desmopressin) – Imipramine
Imipramine, Doxepin, No SERT block: Doxepin, Nortriptyline, Insomnia – Doxepin (low-dose; 1-6 mg)
Amoxapine, Maprotiline Lofepramine Post-stroke depression – Nortriptyline

June 30, 2022
MAOIs: MOA (additional): MOA: Irreversible inhibition of MAO-A & MAO-B → monoamines not Indications
Phenelzine Tranylcypromine – blocks DAT& NET broken down (effect duration ~ time to make new MAO: 2-3 weeks) Phenelzine: alt. for MDD, PD, SAD, PTSD
Isocarboxacid Tranylcypromine: alt. for MDD, PD
Tranylcypromine Selegiline: tyramine diet restrictions Side Effects: Manic switch (w/ bipolar), headache, GI symptoms and
Selegiline NOT needed for 6 mg/24 hour patch weight gain, postural hypotension, bradycardia, edema, sexual Side Effect/Interaction Management:
dysfunction, hypertensive crisis Preventing hypertensive crisis* – avoid the ff:
Contraindications: Tranylcypromine – • Aged foods (aged cheese, meats, sausages, etc.)
renal impairment Contraindications: Pheochromocytoma, heart disease, hypertension, • Fermented foods (pickled food, atchara, spoiled food,
history of headache, hepatic impairment tap/non-pasteurized beer, yeast extract, soy sauce,
tofu), fava beans, other broad bean pods
Interactions: Serotonergic agents (serotonin syndrome; wait 4-5 half- *Hypertensive crisis: MAO-A in gut that breaks down
lives of the agent before starting MAOIs or 5 weeks after stopping tyramine is inhibited → more tyramine absorption →
Fluoxetine), sympathomimetics (hypertensive crisis) absorbed tyramine displaces NE from storage vesicles →
adrenergic receptor agonism → blood pressure shoots up
GABAergic: Progesterone-derived endogenous MOA: α1β2γ2, α4β3δ, and α6β3δ GABAA positive allosteric modulator Indication: Postpartum depression
Brexanolone/ neurosteroid for postpartum depression
Allopregnanolone Administration: IV infusion (60 min) in Side Effects: Extreme sedation potentially causing syncope, dry mouth, Interactions: Additive CNS depression with CNS
CONTROLLED hospital setting flushing, likely ₱₱₱₱ depressants

June 30, 2022
“ANTIPSYCHOTICS”
Medication Specific Information General (MOA, Side Effects, Indications, Side Effect Management, & More
Interaction)
FIRST GENERATION “ANTIPSYCHOTICS” / D2 RECEPTOR ANTAGONISTS
1. Chlorpromazine Specific Side Effects MOA: D2 (mesolimbic), HAM receptor Indications:
a, b, * ₱₱
• Urine discoloration (red to red-brown), photosensitivity (H1,α1,M1) blockade (Wilson et al., 2021) ✓ Schizophrenia (positive symptoms)
• More sedation, orthostatic hypotension, anticholinergic effects • Block mesolimbic D2 receptors → ✓ Acute agitation
(potent HAM blockade) ↓ aberrant salience (abnormally higher – Pre-rapid tranquilization (pre-RT): oral Haloperidol
• Slightly less EPS (less potent D2 blockade) meaning/significance given to (WITH Biperiden if with dystonia/
Contraindications:impaired consciousness, pheochromocytoma mundane external stimuli) → ↓ pseudoparkinsonism)
, Reye’s syndrome; avoid in persons with epilepsy delusions – Rapid tranquilization (RT): immediate-release IM
• Block mesolimbic D2 receptors → Haloperidol (WITH Biperiden if with dystonia/
Interactions: Proper integration of top-down, pseudoparkinsonism)
• Antacids – lower absorption of Chlorpromazine bottom-up info processing: – Orally disintegrating tablets do NOT get absorbed
• Contraindicated: oral K+ salts; ulcerogenic effect enhanced by – Top-down: prior beliefs, exp. from “top” faster than IR tablets
strong anticholinergics influence interpretation of stimuli from ✓ Depot injections to improve adherence:
• CYP2D6 substrates – Chlorpromazine increases their “bottom”; strong beliefs from brain on Fluphenazine decanoate, Flupentixol decanoate,
concentrations as a CYP2D6 inhibitor top overriding absence of stimuli from Haloperidol decanoate
• Propranolol – mutually increase concentrations of each other senses at bottom → hallucinations ✓ Tourette’s syndrome/tics: Haloperidol
– Bottom-up: info perception starts with ✓ Hiccups (2nd line): Chlorpromazine
• Quinine – Increases Chlorpromazine concentrations
stimuli from “bottom” (e.g. senses) ✓ Chemotherapy-induced nausea/vomiting (CINV)
• Caution in urine drug screens: its metabolites give false
before going to top; persistent bottom prophylaxis: Chlorpromazine
positive result for amphetamines, LSD, & pregnancy tests.
signal not matching prior beliefs at top ✓ Alternative (2nd/3rd line) for bipolar mania:
2. Fluphenazine Specific Side Effects: Less sedation, orthostatic hypotension,
→ brain readjusts beliefs → delusions Haloperidol, Chlorpromazine
decanoate (IM) anticholinergic effects (HAM blockade), more EPS (potent D2 ✓ Reduce IM injection restraints:
a, d, LAI ₱ – ₱₱ Side Effects:
blockade) Zuclopenthixol acetate
Common: Sedation & weight gain (H1),
rash, urticaria,orthostatic hypotension(α1) (NOT useful for rapid tranquilization/RT)
Contraindications: Hepatic disease
Interactions *Ineffective for conspiracy theories and autoimmune
Anticholinergic side effects (M1 blockade)
• Contraindicated: oral K+ salts; their ulcerogenic effect is
• Dizziness, blurred vision, dry mouth, psychosis
enhanced by strong anticholinergics
urinary retention, constipation,
• Concentrations affected by CYP2D6 modulators
tachycardia
• Smoking – Dose cut up to 50% in smokers (CYP1A2 induction)
Neuroleptic induced deficit syndrome
Administration: IM gluteal injection every 2-4 weeks (NIDS): secondary negative symptoms
*Kinetic advantage: depot injection may cause initial peak serum (mesolimbic D2 receptor blockade)
concentration within 1 day (vs days-weeks for others)
June 30, 2022
3. Flupentixol Specific Side Effects: Less sedation, orthostatic hypotension, Extrapyramidal symptoms/EPS Side Effect Management:
decanoate (IM) and anticholinergic effects (HAM blockade), more EPS (potent D2 (nigrostriatal D2 receptor antagonism) EPS – decrease dose/switch/add medication
a(LAI) ₱₱₱₱
blockade); though more anticholinergic vs Fluphenazine or • Acute dystonia • Acute dystonia – adjunctive Biperiden (preferred),
Haloperidol • Pseudoparkinsonism adjunctive Diphenhydramine
• Akathisia (very distressing) • Akathisia – adjunctive Propranolol and
Administration: IM outer upper buttock/ lateral thigh injection • Tardive dyskinesia benzodiazepines; inefficacious: Biperiden
every 4 weeks • Pseudoparkinsonism – adjunctive Biperiden or
Hyperprolactinemia (tuberoinfundibular adjunctive Diphenhydramine
Only decanoate LAI is in PNF and primary care formulary D2 receptor antagonism) • Tardive dyskinesia – adjunctive vit. B6 / branched-
4. Haloperidol Specific Side Effects: Less sedation, orthostatic hypotension, • Oligomenorrhea, galactorrhea, breast chain amino acids (esp. male) / Levetiracetam / botox
a, c, LAI ₱₱ (tab) / ₱₱₱₱ (IM
and anticholinergic effects (HAM blockade), more EPS (potent D2 cancer risk (women) / deep brain stimulation (DBS)
& LAI)
blockade); May cause depressive switch in bipolar disorder • Gynecomastia (men)
• Sexual dysfunction Anticholinergic SEs
Interactions: • Long-term decreases in bone mineral • Dry mouth – drink small amount of fluids frequently,
• CYP2D6 substrates – Haloperidol increases their density switch oral hygiene products, Sugar-free candy/gum,
concentrations as a CYP2D6 inhibitor avoid desiccants (alcohol, smoking, caffeinated
• CYP3A4 substrates – Haloperidol increases their Rare/Serious: Blood dyscrasias, ECG drinks), keep nasal passages open, humidifiers, two
concentrations as a CYP 3A4 inhibitor change (prolonged QT interval), seizures drops of edible oil/hour
• CYP2D6 modulators – may increase/decrease Haloperidol (Chlorpromazine), priapism, venous • Constipation – dietary fibers, exercise, inc. fluid
concentrations since it is metabolized by CYP2D6 thromboembolism, photosensitivity intake, laxatives; consider possibility of paralytic ileus
• CYP3A4 modulators – may increase/decrease Haloperidol • Urinary incontinence – avoid high fluid intake in
concentrations since it is metabolized by CYP3A4 Neuroleptic malignant syndrome evening, ensure complete voiding at bedtime
• Smoking – reduce serum concentrations of Haloperidol (NMS): muscular rigidity, hyperthermia, Excessive saliva – adjunctive oral Hyoscine, SL
altered consciousness, and autonomic Atropine
Administration: dysfunction (no hyperreflexia or
• Tablets: Oral (once daily for maintenance, or as needed for sustained clonus unlike serotonin Cardiovascular
pre-rapid tranq.) syndrome) • Orthostatic hypotension – stand up slowly from
• Immediate-release solution for injection: IM deltoid injection sitting/lying position, ↑fluid intake (if not fluid-
for low doses and gluteal injection for high doses (as needed) Withdrawal symptoms (on abrupt restricted), use supportive stockings
• Decanoate/long-acting injectable (NOT in MAP-MH/PNF): discontinuation): Rebound insomnia, • Tachycardia – low-dose peripheral β-blocker, reduce
every 4 weeks, IM gluteal injection cholinergic effects, rebound psychosis, caffeine and nicotine intake
5. Zuclopenthixol Specific Side Effects: Moderate sedation, orthostatic rebound EPS, sudden pregnancy (due to • QTc prolongation – note concurrent meds with
acetatea,d (IM) ₱₱₱₱ hypotension, anticholinergic effects (HAM blockade); moderate prolactin levels suddenly decreasing) potential for QT prolongation, document
EPS (D2 blockade)
Interactions: Hyperprolactinemia
Onset: NOT rapid (NOT useful for rapid tranquilization) • BP-lowering meds – increased • Sexual dysfunction – evaluate prolactin, note
• Sedation: onset in ~2-4 hours hypotensive effects pregnancy plans
• Antipsychotic properties: Onset in ~8 hours • CNS depressants – additive effects • Osteoporosis risk – bone density screening
• Duration of effect: 72 hours • Epinephrine – lowers BP
• Anticholinergics may decrease Neuroleptic Malignant Syndrome
dissolution of sublingual tablets • Supportive care: cool body; maintain hydration
(Nitroglycerin, etc), increase • Manage complications – renal failure, aspiration, etc.
concentration of thiazide diuretics • Pharmacologic management:
• Topiramate – Increased hyperthermia • Benzodiazepines
risk • Bromocriptine
• DantroleneI
Contraindications: Blood dyscrasias, • Amantadine
bone marrow suppression, comatose, • ECT
subcortical brain injury, hypersensitivity,
• Avoid anticholinergics
Parkinson’s
June 30, 2022
SECOND GENERATION “ANTIPSYCHOTICS” / D2-5HT RECEPTOR ANTAGONISTS

₱ – ₱₱ (tab) /
1. RisperidoneLAI Receptor Binding Profile: MOA Indications:
₱₱₱₱ (LAI)
• 5-HT2A, D2, 5-HT7, α1 • Positive symptoms: D2 antagonist ✓ Schizophrenia spectrum disorders (positive
– 5-HT2A, 5-HT7 antagonism: mood effect (dosing is such that minimum 60% of symptoms and secondary negative symptoms
– D2 antagonism (potent): ↑EPS, hyperprolactinemia receptors blocked) only): All
– α1 antagonism: ↑orthostatic hypotension – At lower doses, receptors that drug – Clozapine used mainly for refractory
• >> H1, 5-HT2C, α2A has higher affinity to are bound to, schizophrenia/mania only, due to safety
– H1 antagonism: ↑sedation filled up first (but a few lower- concerns
– 5-HT2C & α2A antagonism: mood effects affinity receptors may be bound) ✓ Acute agitation
• >> 5-HT1A partial agonism (less potent vs D2): ↑EPS & – At higher doses, receptors with – Pre-RT: oral Olanzapine, Quetiapine,
hyperprolactinemia lower affinities start to fill up (but Risperidone
Specific Side Effects previous receptors remain filled) ✓ Depot injection to improve adherence
• Dose-dependent EPS; risk significantly increases • Less EPS/ hyperprolactinemia: – Paliperidone palmitate (monthly) LAI,
>6 mg, where there is no additional clinical benefit 5-HT2A antagonist & 5-HT1A partial Risperidone microspheres LAI, Aripiprazole
• Dose-dependent hyperprolactinemia agonist lauroxil LAI
• Metabolic syndrome (moderate risk) • Mood/anxiolytic effects: 5-HT1A partial ✓ Bipolar disorder (see figure below)
agonist, 5-HT2C antagonism, 5-HT3 ✓ Adjunct to “treatment-resistant” depression
Interactions: antagonism, 5-HT7 antagonism, α2 (only if SSRIs give partial response)
• CYP2D6/3A4 modulators can affect Risperidone antagonism – Risperidone, Quetiapine XR
concentrations as it is metabolized by 2D6/3A4 – 5-HT1A partial agonism: BDNF – Olanzapine (least preferred)
expression ✓ Adjunct to anxiety and related disorders (2nd line)
• Caution in urine drug screens: false positive for LSD
– 5-HT2C antagonism: disinhibition of – Quetiapine (also 2nd line monotherapy): GAD
Administration: oral (tab), IM deltoid/gluteal injection (LAI)
DA, NE release – Risperidone: OCD
Only its oral form is included in BOTH PNF AND MAP-MH
– 5-HT antagonism: ↓GABA → ✓ Tourette syndrome, tics
2. PaliperidoneLAI Receptor Binding Profile: similar to Risperidone 3
₱₱₱₱ (tab, LAI) ↑neurotransmitters – Haloperidol
Specific Side Effects
– 5-HT7 antagonism: ↓GABA → ↑5- – Risperidone
• Dose-dependent EPS ✓ Chemotherapy-induced nausea and vomiting
HT release
• Dose-dependent Hyperprolactinemia (CINV) prophylaxis: Olanzapine (in combination)
– α2 antagonism: disinhibited 5-HT
• Metabolic syndrome (moderate risk) ✓ LAST-LINE for psychosis in dementia
release
• Multiple other receptor affinities (EXCEPT Lewy body dementia; avoid):
Only LAI form is in PNF (slow IM deltoid/dorsogluteal – oral Risperidone (max. 1 mg BID, max. 8 wk.)
(See Stahl, 2021)
infection every month);
June 30, 2022
3. Amisulpride₱₱₱₱ Specific Side Effects Onset: ~1-2 weeks for mood; ~4-6 weeks
• EPS, Hyperprolactinemia for positive symptoms of schizophrenia
• QT prolongation
Side Effects
Best avoid in renal failure Common: Dizziness, insomnia/
sedation, N/V, headache, asthenia,
Interactions: dyspepsia, orthostatic hypotension
• Caution in urine drug screens: false positive result for (occasionally during initial dosing),
BuprenorphineS2 anticholinergic effects
4. Quetiapinea,b ₱₱₱ – ₱₱₱₱

Receptor Binding Profile: • Metabolic syndrome
• H1 – Possibly due to combined H1 + 5-
– H1 antagonism: ↑↑sedation HT2C antagonism, M3 antagonism
• >>α1,M1,5-HT2A, NET, 5-HT7 on pancreatic β-cells, and/or other
– α1 antagonism: ↑↑orthostatic receptors
hypotension – Hypertension, weight gain, (Malhi et al., 2021; Stahl, 2021)
– M1 antagonism: dyslipidemia, hyperglycemia Legend:
↑anticholinergic effects (within 6-8 weeks) Upper left: agents with efficacy for mania/hypomania
– 5-HT2A antagonism: ↓EPS & – Monitor metabolic parameters Bottom left: agents with efficacy for bipolar depression
hyperprolactinemia) (FBG, Hba1c, fasting lipids, BP, Upper right: agents with efficacy for
– 5-HT2A, NET, & 5-HT7 wt.) mania w/ mixed features
antagonism: mood effects – Metabolic syndrome → Increased Bottom right: agents with efficacy for
• >> 5-HT2C, 5-HT1A, α2, D2, risk of COVID mortality bipolar depression with mixed features
5-HT3 Green box: acute phase
– 5-HT1A antagonism: ↓EPS & Rare/Serious: Blue box: acute and maintenance phase
hyperprolactinemia • Increased risk of death, Purple box (Lamotrigine): maintenance phase only
– 5-HT2C, 5-HT1A, α2A, 5-HT3 antagonism: cerebrovascular events in elderly with *Less efficacy for bipolar depression
mood effects dementia **Serious safety concerns with long-term treatment
– D2 antagonism (less potent): ↑↑minimum • Extreme hyperglycemia associated
dose for antipsychotic effect with ketoacidosis/hyperosmolar Side Effect Management (Tolerance develops over
Specific Side Effects coma/death time): same as above
• QT prolongation • NMS
• Very sedating, ↑↑orthostatic hypotension • Seizures Metabolic syndrome: diet, aerobic exercise, sleep
• Decreased T3/T4 • Dysphagia
management
• Metabolic syndrome (moderate risk) →All of the above on 2nd gen applicable to 3rd gen
• Aspiration pneumonia
• Weight +1.6 kg • Priapism
• BMI +0.7 • Changes in body thermoregulation
• LDL +0.17 mmol/L • Blood dyscrasias (leukopenia,
• Total cholesterol +0.31 mmol/L neutropenia, agranulocytosis)
• TG +0.32 mmol/L • Venous thromboembolism
Interactions: • Do they make brain volumes shrink?
• CYP2D6/3A4 modulators can affect Quetiapine NO! They might even reverse some of
concentrations as Quetiapine is metabolized by that! (see Chopra et al., 2021)
CYP2D6/3A4
• Caution in urine drug screens: false positive results
for Methadone and KetamineS2
DO NOT GIVE EXCLUSIVELY FOR

INSOMNIA IF OTHER OPTIONS AVAILABLE
June 30, 2022
₱-₱₱₱
5. Olanzapine Receptor Binding Profile: Withdrawal symptoms (on abrupt Nonpharmacologic Interventions
• H1, 5-HT2A discontinuation): Rebound insomnia, • Schizophrenia
– H1 antagonism: ↑↑sedation cholinergic effects, rebound psychosis, – Cognitive behavioral therapy for psychosis (CBTp)
– 5-HT2A antagonism: ↓EPS & rebound EPS, sudden pregnancy (esp. – Cognitive remediation therapy (CRT) &
hyperprolactinemia for Risperidone/Paliperidone due to compensation
• >> M1, 5-HT2C, D2 prolactin levels suddenly decreasing) – Social cognition therapy
– M1 antagonism: – Music therapy
↑anticholinergic effects Contraindications: Parkinson’s disease – Vocational rehabilitation
– 5-HT2C antagonism: mood psychosis (possible efficacy for
effects Clozapine, less for Quetiapine) • Bipolar Disorder (during euthymia, only for dep.)
• >> α1, α2A, 5-HT3, 5-HT7 – Psychoeducation
– α1 antagonism: ↑orthostatic – CBT
hypotension →All of the above on 2nd generation – Family-focused therapy (FFT)
– α2A, 5-HT3, & 5-HT7 antipsychotics applicable to 3rd – Interpersonal and social rhythm therapy (IPSRT)
antagonism: mood effects generation antipsychotics, except MOA – Peer support (should NOT encourage harmful
– 5-HT3 antagonism: ↓nausea/vomiting and details on certain side effects behaviors, i.e. nonadherence to meds, substance
Specific Side Effects use)
• Strong sedation
• Metabolic syndrome (highest risk) → metabolic
parameter monitoring
• Weight +2.7 kg
• BMI +1.0
• LDL +0.20 mmol/L
• Cholesterol +0.40 mmol/L
• TG +0.46 mmol/L
Interactions:
• Smoking – Dose cut by up to 50% in smokers
(CYP1A2 induction) but blood levels will increase on
smoking cessation
• Valproate – may reduce Olanzapine concentrations
(close to smoking’s effects), possibly via P-glycoprotein
induction and/or protein displacement mechanisms

June 30, 2022
SECOND GENERATION “ANTIPSYCHOTICS” / D2-5HT RECEPTOR ANTAGONISTS: CLOZAPINE

₱₱
6. Clozapine Indication: Refractory schizophrenia (after two unsuccessful antipsychotic trials of adequate dose and duration), refractory mania (try 1st/2nd line options first)
• AVOID antipsychotic polypharmacy if two adequate antipsychotic trials have not been done yet, though there may be emerging data for Clozapine
augmentation re: reducing hospitalization risk/metabolic side effects (on the other hand, you could be making it MUCH worse)
Receptor Binding Profile:

α1, M1 (↑↑orthostatic hypotension & anticholinergic effects) >> H1, 5-HT2A (↑↑sedation, ↓EPS & hyperprolactinemia) >> 5-HT1A, D2 (↓↓ EPS & hyperprolactinemia)
• At therapeutic dose, D2 receptor binding is <60% (only exception to 60% rule)
Specific Side Effects

• Strong sedation, orthostatic hypotension, anticholinergic effects
• Tachycardia
• Sialorrhea (Norclozapine metabolite = M3 agonist)
• Metabolic syndrome (highest risk) → metabolic parameter monitoring
• Weight +3.0 kg
• BMI +1.0
• FBG +1.05 mmol/L
• Cholesterol +0.56 mmol/L
• TG +0.98 mmol/L
Serious: Agranulocytosis* (differentiate benign ethnic neutropenia/BEN), myocarditis, orthostatic hypotension, seizures,
constipation/fatal ileus (potentially fatal; much more frequent than agranulocytosis), aspiration pneumonia (swallow reflex
inhibition + sialorrhea/hypersalivation)
*Absolute Neutrophil Count (ANC) monitoring, when possible, is advised, along with metabolic parameters
*COVID may cause a transient reduction in white blood cells in those taking Clozapine
Side Effect Management:

• Clozapine-induced constipation (clozapine-induced gastric hypomotility/ CIGH)
– Lifestyle: exercise, fluid intake
– AVOID fibers due to risk of worsening gastric hypomotility!
– Oral: Lactulose, Senna, Bisacodyl
– Rectal (severe): Glycerin suppositories, Sodium Picosulfate enemas
• Sialorrhea
– Prop at least two pillows up at night and place a towel underneath
– Reduce caffeine intake
Interactions:
• Caffeine – may increase concentrations of Clozapine via CYP1A2 inhibition but blood levels will decrease on discontinuing caffeine
• Tobacco smoke (NOT nicotine!) – serum concentrations cut by up to 50% in smokers (CYP1A2 induction) but blood levels will increase on smoking cessation
• Fluvoxamine – increases Clozapine serum concentrations via CYP1A2 inhibition
• Other CYP1A2, 2D6, 3A4, 2C19, 2C8/9, & 2A6 modulators may affect Clozapine levels to varying degrees
• Carbamazepine – additive myelosuppression (bone marrow suppression)
Others:
• Benefits in refractory schizophrenia: near-zero EPS & minimal TD risk, anti-suicidal, efficacious in managing aggression & violent behavior
• Target serum concentration in therapeutic drug monitoring for efficacy: 350 ng/mL
• Minimum duration of treatment: 6 months

June 30, 2022
THIRD GENERATION “ANTIPSYCHOTICS” / D2 RECEPTOR PARTIAL AGONISTS-5HT RECEPTOR ANTAGONISTS

1. AripiprazoleLAI Receptor Binding Profile: MOA: partial D2 agonist, 5-HT2A Indications:
₱₱₱ (tablet) / ₱₱₱₱ (LAI)
• D2, 5-HT1A antagonism, 5-HT1A partial agonism ✓ Schizophrenia spectrum disorders (positive
– D2 & 5-HT1A partial agonism: ↓EPS & symptoms and secondary negative symptoms
hyperprolactinemia (except akathisia) Multiple other receptor affinities only)
– 5-HT1A partial agonism: mood effects ✓ Acute agitation
• >> 5-HT7, α1, H1, 5-HT2A, α2A Side Effects (in addition to those listed – Pre-RT: oral Aripiprazole
5-HT7, 5-HT2A, & α2A for 2 gen antipsychotics): Akathisia, ✓ Bipolar disorder (see figure above)
nd
–
antagonism: mood effects compulsive behaviors (gambling, ✓ Adjunct to “treatment-resistant” depression
– 5-HT2A antagonism: ↓EPS & spending, eating/sex, etc); lower risk of – Aripiprazole, Brexpiprazole
hyperprolactinemia (except akathisia) metabolic syndrome & QT prolongation; ✓ Adjunct to anxiety and related disorders
– H1 & α1 antagonism (less less sedation and anticholinergic side – Aripiprazole: OCD
potent vs D2): ↓sedation, orthostatic effects ✓ Tourette syndrome, tics
hypotension vs other antipsychotics – Aripiprazole
Interactions:
• CYP2D6/3A4 modulators – can affect levels of Side Effect Management:
Aripiprazole as Aripiprazole is metabolized by 2D6/3A4 • Aripiprazole-induced akathisia/agitation
• Caution in urine drug screens: false positive results – Take with chocolate (~4 bars) but consider
for phencyclidine and amphetamines service user’s comorbidities (e.g. type 2
diabetes mellitus)
Administration:
• Tabs: oral
• LAI (non-PNF): Aripiprazole lauroxil – IM deltoid/gluteal
injection every month
2. Brexpiprazole₱₱₱₱ Receptor Binding Profile: MOA: Partial agonist leaning towards
• 5-HT1A, D2, 5-HT2A antagonist at D2 receptors, potent 5-HT2A N/Ast
in Philippines:
– D2 & 5-HT1A partial agonism, antagonist and potent 5-HT1A partial 1 gen.: Cyamemazine, Loxapine, Mesoridazine,
5-HT2A antagonism: ↓EPS & agonist; also strong α1 antagonist Perphenazine, Pimozide, Pipothiazine, Sulpride,
hyperprolactinemia Thioridazine, Thiothixene, Trifluoperazine
– 5-HT1A partial agonism & 5- Multiple other receptor affinities
HT2A antagonism: mood effects 2nd gen.: Asenapine, Lurasidone, Perospirone,
Ziprasidone, Iloperidone, Olanzapine LAI
• >> 5-HT7, α1
– 5-HT7 antagonism: mood
“3rd gen.”: Cariprazine, Lumateperone
effects
– α1 antagonism (less potent
vs D2): ↓orthostatic
hypotension
• >> 5-HT2C, H1
– H1 antagonism (less potent
vs D2): ↓sedation
Weight gain (~1.23-1.89 kg; dose dependent)
No glucose intolerance and lipid abnormalities in clinical

trials
Interactions: CYP2D6/3A4 modulators can affect levels of

Brexpiprazole as Brexpiprazole is metabolized by 2D6/3A4

Soapbox: Low-dose Quetiapine for Insomnia
Written by: Jarvin Enosh Tan, RPh
Proofreading and Additional Direction by: AJ Elicaño
Anecdotally, irrational prescription of low doses of Quetiapine for sleep difficulties is very popular in the Philippines, so much so that there have
been reports of pharmacies irrationally dispensing these medications even without prescriptions. So, let’s debunk some misconceptions regarding
Quetiapine’s pharmacology!
Most “antipsychotics”, except Clozapine, don’t exhibit antipsychotic properties until they
block 60% of D2 receptors in the mesolimbic pathway. While they bind to a LOT of receptors, they
will have affinity for some receptors more than others. It’s like a chocolate fountain. The drug, like
chocolate, flows from the top first and binds preferentially to those receptors for which it has more
affinity. With small amounts of the drug, those favored receptors will be filled first, though some
occasional binding to lower-affinity receptors might still happen (like chocolate splashing around).
Eventually, at >400 mg or so of Quetiapine, you hit the 60% blockade requirement and it starts
exhibiting antipsychotic properties. HOWEVER, in lower doses, Quetiapine loves the H1 receptor
a lot (along with 5-HT2, too, and okay throw in α1. M1 too). This is why it’s pretty sedating (and
anticholinergic, and orthostatic hypotension-y), and this is where the idea to profit off its use in low
doses exclusively for sleep difficulties was born.
Does it even work? Well, in terms of systematic reviews, there’s only one randomized controlled
trial with results that aren’t even clinically significant (Atkin et al., 2018). Even assuming there’s a tiny,
miniscule inkling of a benefit that can’t be met by OTCs, do low doses automatically mean less side
effects? No! Yoshida & Takeuchi (2021) summarize the data on the relationship of antipsychotic doses
and side effects, and find that type-2 diabetes and dyslipidemia may occur independent of dose. You
don’t even need to gain any weight for this! Worse, these are linked to worse COVID outcomes (Petrilli et
al., 2020). Did you notice I said “worse” twice? Because it gets so much worse when you’re older and
have dementia, because now you get to say hello to an increased risk of stroke (black box warning) and
more cognitive decline! (2019 AGS Beers Criteria® Update Expert Panel, 2019)
Some will continue to deny that metabolic side effects happen at low doses, even in the absence
of evidence, but you know who else doesn’t buy this load of Garbodor2? Company insiders! Did you know
the company behind the drug had to pay the US Department of Justice $520 million for “…[promoting Quetiapine] to psychiatrists and other
physicians for certain uses that were not approved by the FDA as safe and effective (including… sleeplessness)” (DOJ, 2010)? Yes, it’s their fault
this harmful practice continues to this day. They were even willing to go so far as to ghostwrite scientific articles on studies never performed by
June 30, 2022
them solely for illegal marketing ala Recto, but all this time, they knew the harmful effects of what they were doing. To quote a company insider
email from litigation documents a.k.a. resibo: “I don’t believe we can state that metabolic disturbances are absent (or even minimal) at low doses.
Even if we could, we know that the majority of schizophrenia and mania patients would not get substantial efficacy at doses <200 mg/day.” Because
of what they did, healthcare institutions continue to practice this and health professions training institutions continue to teach this, much to the
delight of low-density lipoproteins and COVID-19 virus particles around the world (Mitchell et al., 2021).
Is Munchlax arguing that we’re better off using benzos,

which carry risks of addiction, dependence, fractures, and
pneumonia with long-term use? Lol no, that’s a false dichotomy
(the logical fallacy where an argument claims there are only two
choices to a dilemma). There are other choices for difficulties with
falling or staying asleep, chiefly cognitive behavioral therapy for
insomnia (CBTi). The American Academy of Sleep Medicine,
British Association of Psychopharmacology, and European Sleep
Research Society guidelines all agree that this is the 1st line
intervention among all pharmacologic and non-pharmacologic
options (Sateia et al., 2017; Riemann et al., 2017; Wilson et al.,
2019). If you don’t believe this appeal to authority, then that’s fair. Let’s use something
better: a systematic review and meta-analysis of 66 randomized controlled trials on CBTi
showing clinically significant improvements in a variety of objective and
subjective sleep outcomes (Edinger et al., 2021). As the author of this cheat
sheet has allegiance bias towards the intervention, it’s recommended you
check out the evidence yourself! Therapy can be pricey and inaccessible in the
Philippines, but trying out the intervention’s instructions on your own is free and
has minimal risks.
So, trouble sleeping because of bipolar disorder? Yeah, sure, a 300

mg/day trial of Quetiapine is worth trying! Person has preference for a sedating
antipsychotic for their schizophrenia because they can’t stay asleep at night?
Quetiapine 400 mg and up can help with that. But low doses? Just for insomnia?
No. Note: ICU sedation is a different matter altogether. Speaking of
pharmacologic options, given that low-dose Quetiapine is just a glorified antihistamine with metabolic and neutropenic baggage, we always have
Diphenhydramine as an over-the-counter option. At the very least, it doesn’t come with said baggage, though you probably want to limit its use to
<10 days or else its effects poop out and you experience cognitive impairment on the day of a big exam. In fact, Dr. George Dawson gives a good
example of one of the only scenarios where you might consider low-dose Quetiapine exclusively for difficulty sleeping: if the only choices left are
that or booze.

June 30, 2022
References:
Paccial, R. C. (2016). Combined psychopharmacological and psychosocial approaches and the relevance of therapeutic jurisprudence and religion
in the successful management of battered woman's syndrome: A case report. The Philippine Journal of Psychiatry, 38(2), 22-32.
Yoshida, K., & Takeuchi, H. (2021). Dose-dependent effects of antipsychotics on efficacy and adverse effects in schizophrenia. Behavioural Brain
Research, 402, 113098.
Atkin, T., Comai, S., & Gobbi, G. (2018). Drugs for insomnia beyond benzodiazepines: pharmacology, clinical applications, and
discovery. Pharmacological Reviews, 70(2), 197-245.
Pillinger, T., McCutcheon, R. A., Vano, L., Mizuno, Y., Arumuham, A., Hindley, G., ... & Howes, O. D. (2019). Comparative effects of 18
antipsychotics on metabolic function in patients with schizophrenia, predictors of metabolic dysregulation, and association with
psychopathology: A systematic review and network meta-analysis. The Lancet Psychiatry, 7(1), 64-77. https://doi.org/10.1016/s2215-
0366(19)30416-x
Petrilli, C. M., Jones, S. A., Yang, J., Rajagopalan, H., O’Donnell, L., Chernyak, Y., ... & Horwitz, L. I. (2020). Factors associated with hospital
admission and critical illness among 5279 people with coronavirus disease 2019 in New York City: prospective cohort study. BMJ, 369.
https://doi.org/10.1136/bmj.m1966
2019 American Geriatrics Society Beers Criteria® Update Expert Panel, Fick, D. M., Semla, T. P., Steinman, M., Beizer, J., Brandt, N., ... & Sandhu,
S. (2019). American Geriatrics Society 2019 updated AGS Beers Criteria® for potentially inappropriate medication use in older
adults. Journal of the American Geriatrics Society, 67(4), 674-694.
Riemann, D., Baglioni, C., Bassetti, C., Bjorvatn, B., Dolenc Groselj, L., Ellis, J. G., ... & Spiegelhalder, K. (2017). European guideline for the
diagnosis and treatment of insomnia. Journal of Sleep Research, 26(6), 675-700.
Sateia, M. J., Buysse, D. J., Krystal, A. D., Neubauer, D. N., & Heald, J. L. (2017). Clinical practice guideline for the pharmacologic treatment of
chronic insomnia in adults: An American Academy of Sleep Medicine clinical practice guideline. Journal of Clinical Sleep Medicine, 13(02),
307-349.
Wilson, S., Anderson, K., Baldwin, D., Dijk, D. J., Espie, A., Espie, C., ... & Sharpley, A. (2019). British Association for Psychopharmacology
consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders: An update. Journal of
Psychopharmacology, 33(8), 923-947.
Edinger, J. D., Arnedt, J. T., Bertisch, S. M., Carney, C. E., Harrington, J. J., Lichstein, K. L., ... & Martin, J. L. (2021b). Behavioral and psychological
treatments for chronic insomnia disorder in adults: an American Academy of Sleep Medicine systematic review, meta-analysis, and GRADE
assessment. Journal of Clinical Sleep Medicine, 17(2), 263-298.
Department of Justice Office of Public Affairs (2010, April 27). Pharmaceutical giant AstraZeneca to pay $520 Million for off-label drug marketing.
Retrieved, January 23, 2022, from https://www.justice.gov/opa/pr/pharmaceutical-giant-astrazeneca-pay-520-million-label-drug-marketing
UCSF Library (n.d.). Industry documents library. Retrieved, January 23, 2022 from https://industrydocuments.ucsf.edu/
Mitchell, A. P., Trivedi, N. U., Gennarelli, R. L., Chimonas, S., Tabatabai, S. M., Goldberg, J., ... & Korenstein, D. (2021). Are financial payments
from the pharmaceutical industry associated with physician prescribing? A systematic review. Annals of Internal Medicine, 174(3), 353-361.

Misc:
Acute agitation: Prioritize de-escalation techniques (e.g. reassurance, respect, etc.) over pharmacologic interventions (e.g. rapid
tranquilization/RT).
• Always check for and consider a service user’s Advance Directive and consult with their Legal Representative in line with RA 11036
• Pre-RT: oral Haloperidol (with anticholinergic)/Olanzapine/Quetiapine/Risperidone/Aripiprazole
• RT: IM Promethazine (N/A in PH, so likely oral Biperiden) PLUS IM Haloperidol
• Insufficient evidence: high-dose prescribing, unless serum levels established or pricey pharmacogenetic testing done
“ANTIPSYCHOTICS” AND RELATED AGENTS NOT AVAILABLE LOCALLY

USELESS IN PHILIPPINE CLINICAL CONTEXT (unless compassionate use)
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 receptor antagonists Indications: Schizophrenia, tics (Pimozide)
Cyamemazine (leaning to antagonist) and D3-preferring
Loxapine Side Effects:
Mesoridazine Loxapine – has 2nd gen properties Pimozide, Thioridazine – marked QT prolongation
Perphenazine Trifluoperazine, Perphenazine – hepatotoxic; contraindicated:
Pimozide hepatic disease
Pipothiazine
Sulpride *Class info relevant in Organic Medicinal Chemistry, not Pcol:
Thioridazine Phenothiazines:
Thiothixene • Aliphatic – Chlorpromazine
Trifluoperazine • Piperazine – Fluphenazine, Trifluoperazine, Perphenazine
• Piperidine – Mesoridazine, Thioridazine
Butyrophenones – Haloperidol, Droperidol
Thioxanthines – Thiothixene, Flupenthixol, Zuclopentixol
2nd Gen: Ziprasidone – take with 300-calorie meal MOA: D2 & 5-HT2A receptor antagonism, 5-HT1AR partial agonist Indications: Schizophrenia, acute bipolar mania
Asenapine (Ziprasidone), acute bipolar depression (Lurasidone), both
Iloperidone Side Effects: bipolar mania and depression (Asenapine)
Lurasidone Asenapine – anaphylaxis, QT prolong.
Perospirone Iloperidone – QT prolongation, rare priapism
Sertindole Sertindole – marked QT prolongation, severe orthostatic
Ziprasidone hypotension
Ziprasidone – marked QT prolongation
3rd Gen: Cariprazine – D2 partial agonism, weaker 5- MOA: Partial D2 agonists, etc. Indications: Schizophrenia, acute bipolar mania/mixed
Cariprazine HT2A antagonism, more potent 5-HT1A partial Side Effects: Lower 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
5-HT2A Inverse MOA: 5-HT2A inverse agonist, mild 5-HT2C antagonist Indications: Parkinson’s disease psychosis
Agonist:
Pimavanserin Onset: 1 month US FDA advisory committee thumbed down approval for
dementia-related psychosis
Side Effects
Common: Nausea, peripheral edema, confusion
Rare/serious: QT prolongation, shares class-wide black box warning with antipsychotics re: people with dementia
Interactions
• CYP3A4/5 modulators – can affect serum concentrations of Pimavanserin (metabolized by CYP3A4/5)
• QT-prolonging drugs – additive risk
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VMAT2 Inhibitor: MOA: Reversible VMAT2 inhibitor (depletes monoamine neurotransmitters) + weak D2 blocker Indications: Huntington’s chorea, tardive dyskinesia
Tetrabenazine
Onset: rapid; significant improvement in 3 weeks and full response in 6 weeks
Contraindication: Hepatic impairment, people with acute suicidal ideation
Side Effects
Common: Parkinsonism and akathisia (DA depleted from VMAT2 inhibition), orthostatic hypotension, nausea,
sedation/insomnia, depressed mood & anxiety, fatigue, dizziness, dyspnea, dysuria, URTI, dysphagia
Rare/serious: Falls/fractures, NMS, QT prolongation, serious EPS
Interactions:
• CNS depressants – additive effects
• CYP2D6 modulators – significantly affect Tetrabenazine levels (metabolized by 2D6)
• MAOIs, Reserpine – avoid co-administration
ANTICHOLINERGICS (ANTIMUSCARINICS)
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
Interactions: Addtive anticholinergic effects with other anticholinergics
Administration: Morning if once daily (less likely to experience EPS in sleep)

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

June 30, 2022
“MOOD STABILIZERS”
Medication MOA, Indications, And C/Is Side Effects Interactions
1. Lithiumb ₱₱ MOA: (See Malhi & Outhred, 2016) 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. Dehydration might lead to increases
• Higher-order biological systems? in Lithium concentration (toxicity)
• 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
2. Divalproex/ MOA: Hypotheses include Side effects: Interactions:

Valproic Acid ₱₱ 1. Reduced excessive neurotransmission by ↓ion Common: – Carbapenems: ↓ Valproate levels via inhibition of
flow through Na+ channels, T-type Ca2+ currents • CNS: Sedation, tremor, dizziness, ataxia, asthenia, acylpeptide hydrolase (blocks deglucuronidation)
2. ↑GABA action via ↑release (GABAB), ↑synthesis headache, reduced appetite – Lamotrigine: may ↓ Valproate concentrations
(↑glutamic acid decarboxylase), ↓reuptake & • GIT: Abdominal pain, N/V, diarrhea, constipation, dyspepsia,
↓metabolism (↓GABA-T) weight gain Sodium Valproate, Valproic Acid, and
3. Downstream actions (e.g. GSK-3 inhibition, Divalproex are NOT equivalent and NOT
phosphokinase C, myristolated alanine-rich C Unusual/controversial: Alopecia (unusual; check Cu/Zn interchangeable
kinase substrate blockade) and activating various levels), polycystic ovaries (controversial), hyperandrogenism
signals that promote neuroprotection & long-term and hyperinsulinemia and lipid dysregulation (controversial),
plasticity (e.g. extracellular signal-regulated decreased bone mineral density (anticonvulsants and serotonin
kinase, cytoprotective protein B-cell modulators in general)
lymphoma/leukemia-2 gene, GAP43)
Rare/Serious: Hepatotoxicity, liver failure, pancreatitis.
thrombocytopenia, leukopenia, drowsiness, confusion

June 30, 2022
2. Divalproex Unknown whether these explain mood-stabilizing (valproate-induced hyperammonemic encephalopathy, a sign STRICTLY AVOID in women and girls of
Valproate action, anticonvulsant action, anti-migraine action, of toxicity) childbearing potential. The only exception is if
Valproic Acid ₱₱ and/or side effects and only if there are no other options.
Indications: Epilepsy (focal, GTC, myoclonic; *Antidote for valproate-induced hepatotoxicity and
absence as alternative to ethosuximide but w/ hyperammonemic encephalopathy: L-carnitine (Valproate
attentional dysfunction (1st line in the Philippines); depletes L-carnitine levels as it undergoes beta-oxidation →
1st line juvenile myoclonic epilepsy/Janz syndrome hypocarnitinemia → hepatotoxicity and hyperammonemic
and myoclonic/atonic epilepsy or Doose syndrome; encephalopathy)
2nd line status epilepticus), mania & acute bipolar
depression, migraine prophylaxis AVOID in women and girls of childbearing potential:
• Risk of congenital malformations (spina bifida)
Contraindications: Urea cycle disorder, • Risk of neurodevelopmental problems for unborn child
thrombocytopenia, serious liver disease,
pancreatitis, mitochondrial disorders due to
mutations in mitochondrial DNA polymerase-
gamma (POLG), pregnancy
3. Lamotrigine₱₱ MOA: Blocks Na+ channels and increases brain Side Effects: Interactions:
GABA (epilepsy); blocks L-, N-, P-type Ca2+ Common: Dizziness, diplopia, insomnia, ataxia Dose adjustments needed for inducers/
channels (decreases Glu release), weak 5-HT3 Serious: SJS/TEN: Titrate inhibitors of uridine glucuronosyltransferase
receptor and dihydrofolate reductase inhibitor dose VERY SLOWLY to (UGT)
prevent & strictly adhere to • UGT inducers (Carbamazepine, Phenytoin,
Indications: Focal seizures, GTC, absence very slow titration Phenobarbital, RifampicinTB, Lopinavir
seizures (<Valproate); recommendations; avoid /RitonavirHIV) – increases Lamotrigine
only for bipolar depression vitamin B complex and new clearance
food/meds/cosmetics/ • UGT Inhibitors (Valproate) – decreases
deodorants/detergents/fabric Lamotrigine clearance
softeners/sunburn; can
worsen/ppt myoclonic seizures Caution in urine drug screens: false positive
result for phencyclidine and synthetic
Drug reaction w/ eosinophilia & cannabinoids
systemic symptoms (DRESS)
4. Carbamazepine MOA: Side effects: Interactions:

a, b ₱₱
• Interaction with Na+ channels at alpha-pore forming Common: Sedation, confusion, dizziness, ataxia, double Multiple psychotropics (anticonvulsants,
subunit vision, nausea, diarrhea, benign leukopenia antidepressants, antipsychotics), antiretrovirals,
• Adenosine 1 (A1) receptor antagonist → upregulate Warfarin – serious
A1 receptors → adenosine binds to A1 receptors Serious: SJS-TEN (avoid with paracetamol), DRESS, reduction of their
• Decreases release of presynaptic Asp & Glu hepatotoxicity, cardiac conduction delay, concentrations due to
• Blocks Ca2+ influx through NMDA receptor & bone marrow suppression (agranulocytosis and aplastic Carbamazepine’s
↓ Ca2+ serum concentrations (reduced nitric anemia), hyponatremia and SIADH induction of multiple
oxide free radicals → reduced oxidative stress) CYP enzymes; may
HLA*B1502 screening required for first-time takers to prevent also cause failure of
Indications: Focal and focal-to-bilateral seizures, SJS-TEN hormonal
trigeminal neuralgia, 1st line for benign occipital contraceptives
epilepsies (for acute bipolar mania only, NOT Can aggravate absence seizures
bipolar depression) • CYP3A4 modulators – can increase/decrease
Carbamazepine’s concentrations since it is
Contraindications: HLA*B1502 allele, bone metabolized by CYP3A4
marrow suppression, hepatic porphyria • Additive myelosuppression with Clozapine
June 30, 2022
ANXIOLYTICS AND SEDATIVE-HYPNOTICS

Medication Specific Information MOA, Side Effects, Interactions Indications, Side Effect Management, and More
1. Benzodiazepines • Alprazolam (t1/2 12-15 h) MOA: GABAA positive allosteric modulator; GABA effect is Indications:
NEED S2 ₱ – ₱₱ - Onset: 1 h enhanced → Cl- enters cell, “supercharging” neuron and ✓ Panic disorder, generalized anxiety disorder, social anxiety disorder:
- ↑ Concentration by Estrogen making it less responsive to other neurotransmitters acute/short-term use only (in general; SSRIs 1st line)
products ✓ Insomnia (acute/short-term use only; CBTi = 1st line)
- ↓ Concentration by smoking Side Effects ✓ Acute alcohol withdrawal
• Bromazepam (t1/2 11-12 h) Common: Sedation, anterograde amnesia, fatigue, ✓ Catatonia (Lorazepam)
- Onset: 1 h depression, dizziness, ataxia, slurred speech, weakness, ✓ Epilepsy (1st line in status epilepticus: IM Midazolam, IV
- ↑ Concentration by confusion, GI disturbances, paradoxical hyperexcitability, Lorazepam, IV Diazepam)
Fluvoxamine nervousness
• Clonazepam (t1/2 30-40 h) Ineffective and potentially harmful in PTSD and phobias
- Onset: 0.5-1 h Rare: Hallucinations, mania, hypotension, grand mal
- Absence seizures with seizures, CNS depression, hypersalivation, dry mouth, Antidote for toxicity: Flumazenil (may precipitate seizures those with
Valproate hepatic & renal dysfunction, blood dyscrasias, (BZDs epilepsy)
• Clorazepateb (decarboxylation generally do NOT cause respiratory depression in absence
to nordiazepam is rapid: t1/2 =40- of comorbidities/drug interactions)
50 h) Possible link of chronic use with increased risk of
– Onset: 0.5-1 h pneumonia, which will be difficult in a pandemic
– ↓ Concentration by smoking
• Diazepama (injection) (t1/2 20-80 h) To minimize the risk of addiction and/or dependence*, use
- Onset: 0.25-0.5 h should be limited to not more than 4 weeks in anxiety
- Concentration, t1/2 ↑ by disorders & not more than 7 days for insomnia
Cimetidine,OmeprazoleF1+BnB Needs careful tapering to avoid seizure recurrence /
(weak CYP2C19 inhibitors) withdrawal symptoms

June 30, 2022
Benzodiazepines - Concentration slighty↑ by Withdrawal:

NEED S2 ₱ – ₱₱ Metoprolol, Propranolol Stiffness Rebound anxiety
• Lorazepam (t1/2 10-20 h) Weakness Rebound insomnia
- Onset: 0.5-1 h GI disturbance Nightmares
- Preferred in hepatic Paresthesia Depersonalization
impairment Flu‐like symptoms ↓ Memory
- ↓ Clearance by Valproate & Visual disturbances ↓ Concentration
Probenecid Convulsions Delusions, hallucinations
- ↓ Concentration by Estrogen Cognitive impairment Depression
products (glucuronidation)
- PNF, but not FDA-registered Interactions:
• Midazolam (t1/2 4.8-6.4 h) • “Holy trinity” – opioid + benzodiazepine + skeletal
- IM administration non-inferior muscle relaxant; avoid (CNS depression)
to IV Lorazepam for status • Caffeine – may antagonize benzodiazepine efficacy
epilepticus in RAMPART trial
(possibly superior in terms of *Addiction =/= dependence! (Maldonado, 2010; Behnoush et al., 2015; Heise & Brooks, 2017)
admin. route, no need for Dependence: physical; unable to stop due to unpleasant Legend for figure:
significant temperature withdrawal symptoms on cessation Larger font: available in the Philippines
control) Larger font + bold: in PNF
2. Gabapentinoids: Gabapentin-specific side effects MOA: binds α2δ subunits of voltage-sensitive Ca2+ Indications:
Gabapentin₱₱₱ & (rare): Anaphylaxis, angioedema, channels (VSCC) ✓ GAD
Pregabalin₱₱₱ sudden unexplained deaths in long-term: increased GABA transporter density & functional ✓ Chronic pain
epilepsy (unknown if due to GABA transport – Postherpetic neuralgia
Gabapentin use) – Diabetic neuropathy
Side effects: – Fibromyalgia
Gabapentin may also aggravate Common: Sedation, weight gain, peripheral edema ✓ Restless leg syndrome
absence seizures • CNS: Dizziness, ataxia, fatigue, tremor, dysarthria, ✓ Epilepsy (focal seizures; adjunctive)
paresthesia, memory impairment, coordination ✓ Gabapentin: intractable hiccups, alt. for alcohol use disorder
abnormal, impaired attention, confusion, euphoric mood,
irritability, increased appetite Administration: evening; take
• GIT: Vomiting, dry mouth, constipation, weight gain, extended release dosage forms with
flatulence food
• 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
Caution: Emerging addiction risk
Interactions:
• Both drugs renally excreted
• 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)

June 30, 2022
3. Antihistamines Hydroxyzine: Some action at 5-HT2 MOA: H1 and M1 receptor antagonists Indications:
DiphenhydramineOTC receptors; suppression of some Side Effects: • All: Insomnia; not to be used >10 days to avoid tolerance
₱₱
subcortical regions Common: Anticholinergic (see Biperiden), sedation, • Diphenhydramine, Hydroxyzine: Allergies
Doxylamine cognitive impairment, tolerance • Diphenhydramine: EPS (acute dystonias, pseudoparkinsonism)
Hydroxyzinea ₱₱₱ Caution in urine drug screens: Rare/potentially fatal: Convulsions, arrhythmias, • Hydroxyzine: Acute GAD
DiphenhydramineOTC may give paralytic ileus
false positive test results for Interactions: Contraindications: Narrow angle glaucoma, asthma (acute)
Methadone and phencyclidine • Synergistic with CNS depressants
• Additive effects with anticholinergics
• Epinephrine – Hydroxyzine may antagonize its
effects
4. Zolpidem₱₱₱ MOA: NOT a BZD; positive allosteric modulator of GABA Indication: NOT more than 7 days for insomnia; Zolpidem CR not
NEED S2 receptors (preference for GABAA w/ α1 subunits) restricted to short-term use, but only IR available locally
Contraindications: Significant obstructive sleep apnea, severe
Side Effects impairments in respiratory function, myasthenia gravis, severe hepatic
Common: Sedation, dizziness, ataxia, dose-dependent impairment, personal/family history of sleepwalking
amnesia, hyperexcitability, nervousness, diarrhea, nausea, Notes:
headache **First line for insomnia is therapy: Cognitive Behavioral Therapy for
Rare/serious: Hallucinations, angioedema, respiratory insomnia/CBTi (stimulus control, sleep restriction, relaxation response)
depression, • Stimulus control – bed=sacred, only for sleep/sex. Don’t force
somnambulism, sleep-driving, sleep-eating, sleep-sex, yourself to go to sleep if not tired. If you can’t fall asleep within 15-
sleep-phone calls 20 min, get up and do something else until sleepy, then try again
• Relaxation – slowly contract, and then relax your muscles in
Interactions: sequence (ex. head, neck→arms→chest→abdomen→legs→ feet)
• CNS depressants – synergistic effects • Sleep hygiene – Before bed, (1) exercise ≥4 hours before bed, (2)
• CYP3A4 modulators – may increase/decrease avoid caffeine & alcohol & smoking, (3) minimize bright light &
Zolpidem levels as Zolpidem is metabolized by screens (inhibits melatonin secretion), (4) resolve worries, and (5)
CYP3A4 don’t sleep hungry (but only have a light bite if needed); try to have
regular sleep/wake times
**TAKE BEFORE BEDTIME and without food. Ensure
possibility of 7-hour sleep time, minimum.
₱₱
5. Melatonin Endogenous hormone secreted by MOA: Agonist at MT1 & MT2 receptors, and NRH-quinone Indications: Delayed phase sleep-wake disorder (children and
the pineal gland regulating oxidoreductase (latter not important in sleep) adolescents), jetlag, insomnia (improves only difficulty falling sleep and
circadian rhythm • MT1 agonism: Inhibits wake-promoting activity of sleep quality); likely inefficacious for insomnia in older adults with
suprachiasmatic nucleus dementia
Side Effects
Common (children & adolescents): GI upset, headache, Notes on other supplements:
nausea, tiredness, restlessness, confusion, pruritis, ↓mood Valerian: conflicting evidence and hepatotoxicity risk; NOT
Common (adults): headache, sedation, mood swings, recommended
orthostatic hypotension German Chamomile: insufficient evidence (one small RCT, no
Rare/serious: rare seizures (conflicting data), rare significant improvements)
migraine Tryptophan: conflicting evidence
Interactions:
• CNS depressants – additive effects *Long-term safety of Melatonin is uncertain. Prioritize CBTi.
• CYP1A2 modulators – increase/decrease Melatonin
levels as Melatonin is metabolized by CYP1A2
• Nifedipine (CCBs) – Melatonin may decrease CCB
antihypertensive effects

June 30, 2022
STIMULANTS, WAKE-PROMOTING AGENTS, AND MEDICATIONS FOR ADHD

Medication MOA, Indications, And C/Is Side Effects and Administration Interactions
1. Methylphenidate MOA: Allosteric blocker for NET & DAT; ↑NE → α2A Side Effects: Interactions:
(Ritalin1, Concerta2) ₱₱₱₱ receptor (boost signal); ↑DA → D1 receptor (↓noise) Common: • Antihypertensives – Methylphenidate
Indications: Stimulant for ADHD (1st line) and CNS: Insomnia, headache, nervousness, irritability, overstimulation, may antagonize their effects
NEED S2 narcolepsy (excessive daytime sedation/EDS) tremor, dizziness, anorexia (appetite loss); does NOT worsen tics • Antacids, PPIs, H2RAs – increase
Contraindications: Extreme anxiety or agitation, GIT: Nausea, abdominal pain, weight loss Methylphenidate absorption
Did u know? ADHD meds motor tics or Tourette’s syndrome or w/ family Rare/serious: Priapism, dysphoria, psychotic episodes, especially • SSRIs, TCAs, anticonvulsant, Warfarin
can do the ff: in ADHD: history, glaucoma, cardiovascular disease, with parenteral misuse, seizures, rare neuroleptic malignant – Methylphenidate ↓their metabolism
✓ Improve acads hyperthyroidism and thyrotoxicosis, gastrointestinal syndrome, rare activation of hypomania, mania, or suicidal ideation • Other stimulants or NE/DA reuptake
(no effect if no ADHD) obstruction or severe GI narrowing (specific for (controversial), cardiovascular adverse effects (palpitations, inhibitors – possible synergistic effects
✓ ↓accidents, injuries Concerta), history of substance use disorders tachycardia, hypertension, sudden death in patients with preexisting • False positive for amphetamines, LSD
✓ ↓substance use, suicide Onset: On first dose (IR: 20-60 min, XL: 30-120 min) cardiac structural abnormalities) Bioequivalence does NOT equate to
✓ ↓teen pregnancy In narcolepsy, taper to prevent rebound Risk of dependence, tolerance, and addiction clinical equivalence. Do NOT interchange
hypersomnia formulations once drug therapy is started
MOA:
Left: In ADHD, "noise" from untuned D1 receptors (illustrated by spam text messages) and low signal from untuned α2A receptors (illustrated by poor phone signal) lead to ADHD symptoms.
Right (w/ Methylphenidate): Blocking DAT & NET raises DA+NE levels and allows better tuning of the receptors, leading to drainage of spam from the phone on the left & a stronger signal on the right
2. Atomoxetine₱₱₱₱ MOA: Blocks NET → ↑NE, DA in prefrontal cortex → Side Effects: Interactions:
activation of α2A, D1 receptors (↑signal, ↓noise) Common: • β2 adrenergic receptor agonist –
Indications: ADHD (2nd line) CNS: Fatigue (esp in kids), anxiety, ↑HR(6-9 bpm), ↑BP(2-4 mmHg), Atomoxetine can worsen tachycardia
insomnia, dizziness, agitation, ↓appetite, aggression, irritability with β2 agonists
Onset: 4-6 weeks GIT: Dry mouth, constipation, N/V, abdominal pain, dyspepsia • CYP2D6 modulators – can
Contraindications: Pheochromocytoma or w/ Genitourinary and others: Urinary hesitancy, urinary retention (older increase/decrease concentrations of
history, severe cardiovascular disorder that might men), dysmenorrhea, sweating, sexual dysfunction Atomoxetine due to Atomoxetine being
deteriorate with clinically important increases in HR Rare/serious: Priapism, hypertension, orthostatic hypotension, metabolized by CYP2D6
and BP, angle-closure glaucoma severe liver damage, manic switch, suicidal ideation activation • False positive for amphetamines
3. Clonidinea ₱₱ MOA: Side Effects: Interactions:
Initial: Postsynaptic α2B agonism (vasoconstriction Common: • Beta blockers –may worsen withdrawal
→↑BP). α2A agonism → ↑signal in prefrontal cortex & CNS: Sedation (CNS α2B/2C receptors)/insomnia, weakness, fatigue, • CNS depressants – additive effects
↓CNS sympathetic outflow (CNS) sexual dysfunction, depression, agitation, withdrawal symptoms on • TCAs – reduced hypotensive effects of
Then: Binds CNS Imidazoline 1 (I1) receptors → abrupt cessation: nervousness, headache, tremor Clonidine
downstream catecholamine release → ANS α2A/2C CV: Orthostatic hypotension, tachycardia or bradycardia, rebound • Rate controllers (Digoxin, CCBs, Beta
receptors → autoreceptor activation, NT release hypertension on abrupt withdrawal → reinstitute drug, taper slowly Blockers) – bradycardia, AV block risk
stopped (ANS: vasodilation, ↓opioid withdrawal Sx) GIT: Dry mouth (indirect mechanisms), N/V
Indications: last line – hypertension; 2nd line–ADHD,
Tourette’s, smoking cessation, opioid withdrawal Rare/serious: Sinus bradycardia, AV block

June 30, 2022
4. Caffeine MOA (stimulant): Side Effects: Interactions:

• Adenosine 1 & 2A (A1, A2A) receptor antagonist Common: Palpitations, tremors, anxiety/panic attacks (effects on α • Benzodiazepines – Caffeine may
– A2A coupled w/ D2 receptors, blocking A2A receptors), insomnia, GI upset, psychomotor agitation, excitement, antagonize benzodiazepine effects
receptors → indirect D2 receptor activation increased urination (dose-dependent, tolerance develops), acute • CYP1A2 substrates – may increase
– Adenosine accumulates during day → increase in blood pressure (~10 mm Hg; not seen in chronic levels of drugs metabolized by CYP1A2
fatigue consumers), medication overuse headache/rebound headache (esp Clozapine); may decrease their
– Caffeine → blocks purine receptors → DA (chronic consumption), withdrawal on abrupt discontinuation with concentrations when caffeine is stopped
affinity to D2 receptors restored chronic use (headache, fatigue, sedation, ↓ energy& alertness, • CYP1A2 modulators – concentrations
• Phosphodiesterase inhibitor depressed mood, concentration difficulty, irritability, etc.) altered by 1A2 inducers/inhibitors
– Blocks metabolism of adenylyl cyclase (ex. Fluvoxamine, Cimetidine as 1A2
– Potentiates alpha adrenergic receptors Rare/serious: Arrythmias, delirium, psychosis inhibitors → caffeine toxicity; smoking
– Worsened generalized anxiety, panic as 1A2 inducer → ↓caffeine levels)
Indications: Tension headache (w/ NSAIDS/ Administration: oral [brewed/instant coffee, tea, milk tea, iced tea, • Lithium – may reduce Lithium levels;
Paracetamol), staying awake/ alert when tired; energy drinks, soft drinks (esp. Mountain Dew and Coke Light), discontinuation of caffeine may cause
NOT useful for hangovers chocolate]; avoid consuming large amounts after lunch on dayshift Lithium levels to rebound and increase
ANXIOLYTICS, SEDATIVE-HYPNOTICS, STIMULANTS, WAKE-PROMOTING AGENTS, & ADHD MEDS NOT AVAILABLE LOCALLY
USELESS IN PHILIPPINE CLINICAL CONTEXT (unless imported)
Medication MOA Side Effects and Administration Indications and Interactions
1. Other Chlordiazepoxide (t1/2 = 6.6-13.4 hours), Clobazam (t1/2 = 36-42 hours), Lormetazepam, Nitrazepam, Oxazepam Indications: Only Flurazepam, Quazepam, Triazolam,
benzodiazepines (t1/2 = 5.6-10.4 hours) Estazolam, Temazepam indicated for short-term
Flurazepam (t1/2 = 2-6 days), Quazepam (t1/2 = 2-5 days), Triazolam (t1/2 = 1-2 hours), Estazolam (t1/2 = 12-30 management of insomnia among ALL
hours), Temazepam (t1/2 = 4-20 hours) benzodiazepines (even local ones)
2. BZRAs Zaleplon (t1/2 = 1-2 hours) Indications: short-term management of insomnia
Zopiclone (t1/2 = 3.5-6.5 hours)
Eszopiclone (t1/2 = 3.5-6.5 hours)
3. Buspirone MOA: 5-HT1A partial agonism Side Effects: Dizziness, headache, nervousness, sedation, Indication: Acute GAD
excitement, nausea, restlessness, rare cardiac symptoms
Onset: 6 weeks Interactions: Metabolized by CYP3A4
4. Prazosin MOA: α1 antagonist in CNS (crosses BBB) Side Effects: First-dose phenomenon (severe orthostatic Indication: PTSD nightmares*, benign prostatic
Note: α1 agonism in CNS causes the ff: hypotension potentially leading to syncope) hyperplasia
• Disrupts higher-order cognitive processing;
induces primitive fear response Administration: In the evening *Doxazosin available locally instead of Prazosin but
• Disrupts REM sleep less studied
• Increases non-REM sleep
• Stimulates CRH release → ↑ cortisol
5. Melatonin MOA: MT1 and MT2 receptor agonist Side Effects: Indication:
Agonists: (for Tasimelteon, MT2>>MT1) • Ramelteon: Sedation, fatigue, dizziness, rare angioedema & Ramelteon: Insomnia
Ramelteon and CNS depression (serious) Tasimelteon: Non-24-hour sleep-wake disorder
Tasimelteon Onset: Ramelteon – <1 h, Tasimelteon – days • Tasimelteon: Headache, nightmares, increased ALT, upper
to weeks respiratory infection, urinary infection Contraindication: Ramelteon contraindicated w/
Fluvoxamine
Administration: Consistently an hour prior to bed. Avoid taking
high fat meals with Ramelteon

June 30, 2022
6. DORA: Dual Orexin Receptor Antagonist Side Effects: Sedation, headache, dizziness, abnormal Indications: Insomnia
Suvorexant, MOA: orexin 1 & 2 receptor antagonist dreams; rarely sleep paralysis and hypnogogic, hypnopompic
Lemborexant, hallucinations Contraindications: Narcolepsy
Daridorexant Onset: <1 hour Risk of addiction
CONTROLLED Interactions: Metabolized by CYP3A4
Half-lives: Daridorexant (shortest) < Administration: 30 min before bed with at least 7h before
Suvorexant < Lemborexant wake-up time (delayed onset when taken with food)
7. Other Dexamphetamine Risk of tolerance, dependence, and addiction; rebound Indications: ADHD, narcolepsy
amphetamines Lisdexamphetamine – prodrug of cataplexy with abrupt discontinuation Lisdexamphetamine: 2nd line, binge-eating disorder
CONTROLLED d-amphetamine (linked to Lysine)
8. Modafinil and MOA: Slight DAT blockade; Side Effects Indications: Narcolepsy (reduce EDS)
Armodafinil Armodafinil more potent Common: Headache (dose-dependent), anxiety, nervousness,
CONTROLLED insomnia, dry mouth, diarrhea, nausea, anorexia, pharyngitis, Contraindications: Severe hypertension, arrhythmias
Onset: 2 hours rhinitis, infection, hypertension, palpitations
Rare/serious: SJS/TEN, angioedema, hypersensitivity, manic Interactions: Reduce contraceptive efficacy, CYP3A4
switch inducer, CYP2C19 & 2D6 inhibitor
Administration: in the morning
9. Sodium Oxybate MOA: GHB receptor binder, GABAB receptor Side Effects: Headache, dizziness, sedation, nausea, vomiting, Indication: Narcolepsy with cataplexy in children and
CONTROLLED partial agonist enuresis, respiratory depression, neuropsychiatric events, adults (EDS, cataplexy, sleep paralysis, hypnagogic
confusion and wandering at night; caution on sodium content and hynopompic hallucinations)
Onset: 1-2 months (max. effect: 3 months) Risk of tolerance, dependence, and addiction
Administration: Avoid taking with food 2 hours before dose;

avoid activity until 6 hours after 2nd dose
10. Pitolisant MOA: H3 receptor antagonist/inverse agonist Side Effects Indication: Narcolepsy with/without cataplexy (EDS
Common: Dose-dependent QT prolongation, insomnia, only)
Onset: 8 weeks anxiety, anorexia Contraindication: Pregnancy, severe hepatic
Rare/serious: Tachycardia, visual hallucinations, hypnagogic impairment
hallucinations (hallucinations immediately before falling asleep) Interactions: Metabolized by CYP2D6, additive QT
prolonging effects, H1 antagonists may reduce effects
Administration: In the morning on waking up
11. Solriamfetol MOA: blocks NET and DAT Side Effects: Headache, nausea, and decreased appetite; Indications: Narcolepsy (EDS) and obstructive sleep
CONTROLLED small dose-dependent increases in BP and heart rate; apnea
Onset: 1 week uncommon insomnia
Administration: Take on empty stomach and avoid food 30

min. after dose; take 9 hours before bedtime
12. Guanfacine MOA: Selective α2A agonist Side Effects Indications: 2nd line for ADHD, Tourette’s
Common: Sedation, dizziness, hypotension, dry mouth,
constipation, abdominal pain, fatigue, weakness Interactions: Metabolized by CYP3A4, can raise
Rare/serious: sinus bradycardia, severe hypotension Valproate levels, additive CNS depressant and
antihypertensive effects with similar drugs
Administration: At bedtime; avoid with high-fat meals
13. Viloxazine MOA: NET blocker; may also block 5-HT2B and Side Effects Indications: ADHD (2nd line)
activate 5-HT2C receptors Common: Increased BP & HR, sedation/insomnia, headache,
anorexia, irritability, nausea/vomiting Interactions: Increases serum concentrations of
Rare/serious: Increased suicidal thoughts CYP1A2 substrates as a CYP1A2 inhibitor

June 30, 2022
DRUGS FOR DEMENTIA

Medication MOA, Indications, C/Is Side Effects and Administration Interactions
1. Donepezil ₱₱ MOA: Reversible central & peripheral Side Effects: Interactions:
acetylcholinesterase inhibitor; sigma-1 receptor agonist Common: • Levodopa – can theoretically reduce Levodopa efficacy
N/V, diarrhea, appetite loss, increased gastric acid • CYP2D6/3A4 modulators – can increase/decrease Donepezil
Indication: Alzheimer’s (mild to moderate), dementia secretion, dyspepsia (take with food), weight loss, concentrations as Donepezil is metabolized by CYP2D6, 3A4
with Lewy bodies headache, dizziness, fatigue, depression, asthenia,
2. Rivastigmine MOA: Pseudoirreversible (self-reverses over hours) insomnia (if so, take Donepezil in morning) Interactions:
₱₱₱₱
acetylcholinesterase (cortex & hippocampus) & Rare: seizures, syncope • Smoking – can reduce clearance of Rivastigmine
(only cap is butylcholinesterase (glia) inhibitor • No CYP interactions
PNF) Administration:
Indication: Alzheimer’s (mild to moderate), Parkinson’s Donepezil: at bedtime with food
disease dementia, dementia with Lewy bodies Rivastigmine and Galantamine: with food
3. Galantamine MOA: Reversible, competitive central **Rivastigmine: retitrate if stopped >3 days to avoid Interactions:
(N/A locally) acetylcholinesterase PAM at nicotinic receptors vomiting with esophageal rupture • CYP2D6/3A4 modulators – can increase/decrease Donepezil
Indication: Alzheimer’s (mild to moderate) concentrations as Donepezil is metabolized by CYP2D6, 3A4
Not recommended in severe renal, hepatic impairment
4. Memantine₱₱ MOA: Low-affinity uncompetitive NMDAR antagonist; Side Effects: Interactions:
adjunctive only Dizziness, headache, hallucinations, insomnia, - Urinary alkalizer (pH8): Memantine clearance reduced by 80%
constipation; rare seizures - Plasma levels increased by: Cimetidine, Ranitidine,
Indication: Alzheimer’s (moderately severe to severe) Procainamide, Quinidine, Quinine, Nicotine, Trimethoprim
- May enhance effects of: Levodopa, DA agents, Selegiline,
anticholinergics
- May reduce effects of barbiturates, antipsychotics
- CNS toxicity: Amantadine, Ketamine, DXM
- HCTZ – Memantine may possibly reduce serum concentrations
5. Ginkgo biloba Publication bias, low quality studies, inconsistent and unreliable findings
EGb 761 ₱₱₱₱
6. Aducanumab MOA: Monoclonal antibody that selectively binds beta Side Effects: Headache, urinary tract infection, upper Drug Interactions: Organizations may develop conflicts of
₱₱₱₱₱
amyloid fibrils & soluble oligomers to produce brain respiratory tract infection interest with pharmaceutical companies via large piles of
(N/A locally swelling and a clinically-insignificant placebo effect monetary donations when faced with this drug
thank ARIA (amyloid-related imaging abnormalities) –
goodness) Indication: Burning money in exchange for ARIA vasogenic edema (brain swelling) in ~35%
*Tacrine no longer used due to poorer tolerability and hepatotoxicity. Please.
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 (be wary earplugs will make waking
✓ Limit staff changes to minimize confusion. up during emergencies difficult)
✓ Limit visitors. ✓ Checking if person requires any visual or hearing aids and make sure they are worn
✓ Constantly, patiently reassurance and repeatedly explain on sources of confusion ✓ Assess for pain and provide Paracetamol and other interventions as needed.
✓ Assess for dehydration and/or constipation and provide fiber and fluids as needed.

June 30, 2022
DRUGS FOR PARKINSON’S DISEASE

Medication MOA, Indications, C/Is Side Effects and Administration Interactions
1. Levodopa + MOA: Aromatic amino acid (dihydroxyphenylalanine) Side Effects: Interactions:
Carbidopa/ and precursor to DA passes through BBB, taken up by Acute: N/V, anorexia, orthostatic hypotension, arrhythmias Orthostatic hypotension with
Benserazide ₱₱₱ DAergic neurons and converted into DA. Carbidopa and Long-term: Wearing-off and on-off phenomenon, dyskinesias antihypertensives, Selegiline
Benserazide are peripheral dopamine decarboxylase (choreiform, dystonic, involuntary), somnolence, vivid dreams,
inhibitors confusion, hallucinations, agitation Low protein diets increase absorption by
50%, and high protein diets reduce
Administration: Without food (1 h before, 2 h after meals) absorption
2. Entacapone MOA: Selective, reversible Side Effects Interactions:

(combo w/ catechol-o-methyltransferase inhibitor Common: Diarrhea (delayed 4-12 week onset), dyspnea, Drugs that interfere w/ biliary excretion &
Levodopa/ weakness, brown-orange urine glucuronidation (Erythromycin, Ampicillin,
Carbidopa) Contraindications: Severe biliary disorder May increase levodopa SEs – dyskinesias, nausea, orthostatic RifampicinTB, Cholestyramine,
hypotension, hallucinations, sleep attacks Chloramphenicol) – ↑Entacapone’s effect
Rare: Rhabdomyolysis Drugs metabolized by COMT: E, NE, DA,

**Tolcapone: hepatotoxic (TOxic to Liver) Dobutamine, Methyldopa, Apomorphine,
Administration: taken with Levodopa IsoproterenolI – Entacapone ↑ their effect
3. D2 Receptor MOA: Post-synaptic D2 agonist in caudate-putamen Side Effects: N/V, low extremity edema, somnolence, Interactions:
Agonists Piribedil: D2/D3 agonist, α2 antagonist lightheadedness, postural hypotension, hallucinations, Pramipexole – its levels affected by drugs
Pramipexolea ₱₱₱ delusional behavior, compulsive behavior (eating, sex, inhibiting/competing w/ cationic tubular
Ropinirolea,b ₱₱₱₱ Indications: Parkinson’s and restless leg syndrome gambling, shopping) secretion: Verapamil, Quinine, Ranitidine,
Rotigotine (patch) (RLS) (Pramipexole efficacy in PD depression) Diltiazem
₱₱₱₱
Manic switch: high risk – Pramipexole, low risk – Ropinirole
4. Piribedil Ropirinole – levels increased/decreased by
₱₱ (adjunct) / ₱₱₱₱ (alone)
Parkinson-hyperpyrexia syndrome (withdrawal) CYP1A2 modulators
5. Apomorphine (SQ) MOA: Partial D2 agonist Side Effects: N/V, drowsiness, dizziness, postural hypotension,
(N/A locally) Indication: Off-episode rescue hallucinations, edema, injection site reactions
Contraindication: 5-HT3 antagonists (profound
hypotension)
6. Ergot D2 agonists Bromocriptine₱₱₱₱, Pergolide (N/A locally), Cabergoline (N/A locally): 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)
June 30, 2022
7. Selegiline₱₱₱₱ MOA: Irreversible, selective MAO-B inhibition at Side Effects: Nausea, headache, Elevated ALT, orthostatic Interactions:
(only tablet dose<10mg/day hypotension, musculoskeletal injuries, non-life-threatening Hypertensive crisis with tyramine-rich food
available) Indication: Adjunct for Parkinson’s (oral), MDD (patch) arrhythmias and other MAOIs (less restrictions on diet
<10 mg); serotonin syndrome with
Administration: W/ breakfast (once daily), w/ breakfast serotonergics
& lunch (twice daily) (NOTE: Linezolid and methylene blue also
Contraindications: Serotonin syndrome-inducing have MAOI properties)
agents, tyramine-rich foods (>150 mg/day) False positive in UDS for amphetamines
8. Rasagiline₱₱₱₱ MOA: Irreversible and selective MAO-B inhibition when Side Effects Interactions:
Rasagiline<1 mg/day Monotherapy – Flu syndrome, hallucination, depression, Hypertensive crisis with tyramine-rich food
arthralgia, dyspepsia, somnolence, psychotic-like behavior, and other MAOIs (less restrictions on diet <1
Indication: Monotherapy, adjunct for idiopathic impulse control behaviors mg); serotonin syndrome with serotonergics
Parkinson’s
Adjunct to Levodopa – Dyskinesia, dry mouth, vomiting, (NOTE: Linezolid and methylene blue also
Contraindications: Serotonin syndrome-inducing anorexia, constipation, weight loss, postural hypotension, have MAOI properties)
agents, tyramine-rich foods (>150 mg/day) accidental injury, abdominal pain, abnormal dreams, arthralgia,
tenosynovitis, nausea, headache Levels affected by CYP1A2 modulators
9. Amantadinea ₱₱ MOA: Induces release/decreases reuptake of DA; Side Effects Interactions:
upregulation of D2 receptors (in vivo); antcholinergic; Common: Nausea, dizziness, insomnia, blurred vision, Quinidine, Thiazides, Cotrimoxazole –
non-competitive NMDA antagonist depression, anxiety, psychosis (high doses), confusion, livedo impairs renal clearance of Amantadine:
reticularis, anticholinergic, nervousness, headache, worsening
Indication: Parkinson’s, EPS, influenza A prophylaxis/ of existing seizure disorder
treatment
Rare/serious: Rare suicidal ideation (even without history), rare
Contraindications: Seizures, severe renal impairment, neuroleptic malignant synndrome on abrupt discontinuation
gastric ulceration, untreated angle closure glaucoma
OTHER ANTIEPILEPTICS (CNS ION CHANNEL AND SYNAPTIC VESICLE BINDERS)

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)
Medication MOA, Indications, C/Is, Administration Side Effects Interactions
BARBITURATES / GABAergic
1. Phenobarbitala MOA: Raising seizure thresholds or altering Side Effects Interactions:
NEEDS S2 seizure patterns (unknown mechanism), possibly Common: CYP inducer
₱ (tab)
thru enhancing GABAA receptor activity. • CNS: Sedation, ataxia, vertigo, cognitive dysfunction (worst), Interacts with CYP2C9, 2C19 modulators
Depresses Glu excitability; alters Na+, Ca2+, and depression, nystagmus, irritability, emotional disturbances Ethosuximide, acetazolamide, antacids – lower
K+ channel conductance; and affects • GI: N/V phenobarbital levels
polysynaptic midbrain reticular formation • CV: Hypotension
• Derma: Rash, uncommon SJS-TEN
Indications: Focal and tonic-clonic seizures,
myoclonic seizures, neonatal seizures; Rare/serious: Megaloblastic anemia, rare agranulocytosis, DRESS,
1st line for neonatal seizures respiratory/CNS depression; risk of tolerance, dependence, and
addiction
Contraindications: Porphyria; dyspnea /airway
obstruction; marked hepatic impairment/hepatic *Cheap unit cost offset by expenses needed to locate and pay for
encephalopathy; intraarterial administration; physician with S2 license
history of sedative/hypnotic addiction; nephritic
service users/patients **DO NOT USE FOR INSOMNIA

June 30, 2022
SODIUM CHANNEL BLOCKERS (VSSC BLOCKERS)

1. Phenytoin MOA: Reduces hyperexcitability on Na+ Side Effects Interactions:
a, b(tablets, capsules)
channels. It also modulates T-type Ca2+ Common: • CYP inducer
₱₱ (oral) /
channels, but not in the thalamus; diminishes • CNS: Nystagmus, ataxia, dysarthria, insomnia, nervousness, motor (strong 3A4 inducer,
₱₱₱₱₱ (ampule)
synaptic transmission, limits fluctuation of twitching, tremor, dizziness, impaired memory werak1A2/2B6
neuronal ionic gradients via Na-K ATPase, and • Derma: Rash, hirsutism, coarsening of facial features, gingival inducer)
inhibits calcium-calmodulin protein hyperplasia • CYP2C9, 2C19, 3A4
phosphorylation • Respiratory: pneumonia, sinusitis, rhinitis, asthma modulators – can
• Sensory: tinnitus, diplopia, eye pain, taste loss affect Phenytoin
Indications: Focal and tonic-clonic seizures, 2nd • Etc: lymph node hyperplasia, chest pain, edema, soft tissue injury levels as Phenytoin
line status epilepticus*** (IV) Is metabolized by
2C9/2C19/3A4
Contraindications: sinus bradycardia, second Rare/serious: Hypotension, cardiac conduction abnormalities • P-glycoprotein inducer
or third degree AV block, Adams-Stokes (rapid administration), hyperglycemia, rare diabetes insipidus, blood • Can displace Warfarin (protein binding) →
syndrome dyscrasias, rare allergic rash (SJS, lupus erythematosus syndrome, bleeding
radiation-induced erythema multiforme, DRESS), rare lymphoma/
Onset: 4 weeks multiple myeloma, toxic hepatitis and liver damage, cerebellar atrophy ***Due to equal efficacy w/ Valproate and
(long-term, high doses), purple glove syndrome (IV) Levetiracetam in ESSET trial as adjunct in
Prodrug: Fosphenytoin (N/A locally) Fetal hydantoin syndrome: cleft lift/palate, microcephaly, mild benzodiazepine-refractory status epilepticus,
intellectual disability Fosphenytoin is less preferred for this as it has
Administration: Oral. IV more contraindications vs Levetiracetam
Possibly carcinogenic to humans (IARC Group 2B), use gloves
2. Oxcarbazepine MOA: Blocks Na+ channels via interaction at a Side Effects Interactions:
tablets: a, b ₱₱₱ (tab)
specific site of the alpha pore-forming subunit; Common: • CYP2C19 substrates – Oxcarbazepine
inhibits Glu release • CNS: Sedation (dose-dept), dizziness (dose-dept), headache, increases their concentrations as a
ataxia (dose-dept), nystagmus, abnormal gait, confusion, CYP2C19 inhibitor
Indication: Focal seizures (RCTs generally nervousness, fatigue • CYP3A4 substrates – Oxcarbazepine can
negative for mood-stabilizing properties) • GI: Nausea (dose-dependent), vomiting, abdominal pain, slightly decrease their concentrations as a
dyspepsia mild CYP3A4 inducer
Onset: 2 weeks • Etc: Diplopia (dose-dependent), vertigo, abnormal vision, rash • CYP3A4 modulators – can
increase/decrease Oxcarbazepine levels as
No efficacy for bipolar disorder; May worsen Rare/serious: Hyponatremia, DRESS Oxcarbazepine is metabolized by CYP3A4
some generalized seizures (less interactions vs CBZ)
3. Topiramateb MOA: Blocks Na+ channels, blocks NMDA-Glu Side Effects Interactions:
₱₱ (migraine)
receptors, potentiates GABA activity (on non- Common: - Carbamazepine, Phenytoin, and Valproate
₱₱₱₱ (epilepsy)
BZD GABAA site), • CNS: Cognitive impairment, paresthesias, sedation, asthenia, – increase Topiramate clearance
inhibits carbonic anhydrase dizziness, ataxia, nervousness, nystagmus, tremor, headache, - Valproate, Phenytoin, MetforminComPack –
↓appetite Topiramate increases clearance of these
Indication: Epilepsy (focal, GTC, LGS), migraine • GI: Nausea, weight loss, dry mouth drugs (MetforminComPack may reduce
prophylaxis, • Etc: Blurred or double vision, mood problems, confusion, Topiramate clearance)
2nd line for binge eating disorder (decrease psychomotor retardation, language and speech problems, fatigue, - Carbonic anhydrase inhibitors – Increased
binging and weight loss due to carbonic taste perversion, upper respiratory tract infection, difficulty with risk of kidney stones with other CAIs (mostly
anhydrase inhibition) concentration & memory, hyperthermia, calcium phosphate)
nephrolithiasis (stay hydrated, ↓dietary Na+ & glucose/fructose, - Hormonal contraceptives – Reduce
Onset: 2-4 weeks ↑dietary K+ & Ca2+) 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)

June 30, 2022
4. Zonisamide MOA: Modulates Na+ channels by unknown Side Effects Interactions:

a, b ₱₱
mechanism, modulates T-type Ca2+ channels, Common: - Carbonic anhydrase inhibitors – Increased
facilitates DA and 5-HT release, inhibits carbonic • CNS: Sedation, depression, agitation, difficulty concentrating, risk of kidney stones with other CAIs (mostly
anhydrase irritability, psychomotor slowing, dizziness, ataxia, headache, calcium phosphate)
anorexia - CYP3A4 modulators – Zonisamide
Indication: Epilepsy (focal, GTC, myoclonic), • GI: N/V, abdominal pain, dry mouth, taste perversion, dyspepsia, concentrations can be increased/decreased
2nd line for binge eating disorder (decrease weight loss by CYP3A4 inducers/inhibitors as Zonisamide
binging and weight loss due to carbonic • Etc: Elevated serum creatinine and blood urea nitrogen, kidney is metabolized by CYP3A4
anhydrase inhibition) stones (stay hydrated, ↓dietary Na+ & glucose/fructose, ↑dietary K+
& Ca2+)
Onset: 2-4 weeks Rare/serious: Serious rash (SJS-TEN, DRESS; sulfonamide),
oligohidrosis & hyperthermia (pediatric patients), blood dyscrasias
(aplastic anemia; agranulocytosis), sudden hepatic necrosis, sudden *Unknown if sudden deaths related to
unexplained deaths* Zonisamide use
5. Rufinamideb MOA: Na+ channel blocker (prolongs inactive Side Effects Interactions:
state), etc Common: - Weak CYP2E1 inhibitor, weak CYP3A4
• CNS: Sedation, fatigue, coordination abnormalities, anorexia, inducer
Indications: Focal seizure, LGS adjunct (≥4 y.o.) headache, dizziness, tremor - Carbamazepine, Lamotrigine, oral
Contraindications: Familial short QT syndrome; • GI: N/V contraceptive – Rufinamide lowers their levels
galactose intolerance, Lapp lactose deficiency, • Respiratory: nasopharyngitis, influenza - Phenobarbital, Phenytoin, and Valproate –
or glucose– galactose malabsorption • CV: QT shortening Rufinamide increases their levels
Rare/serious: Blood dyscrasias (leukopenia), multi-organ - Valproate – Valproate increases Rufinamide
Onset: 4 weeks hypersensitivity syndrome (fever, hematuria, abnormal LFTs, levels
lymphadenopathy, rash), suicidal ideation
Administration: Orally, with food (↑absorption)
6. Lacosamidec MOA: Enhances slow inactivation of Na+ Side Effects Interactions:
₱₱₱₱
channels; binds collapsing response mediator Common: - Theoretical pharmacokinetic interactions not
protein 2 (CRMP2) • CNS: Dizziness, ataxia, diplopia, vertigo, abnormal coordination, yet shown to be clinically significant
ataxia - Phenytoin, Carbamazepine,
Indication: Focal seizures • GI: N/V, increased LFTs (0.7%) Oxcarbazepine – Enhanced CNS side
Rare/serious: Rare hepatitis and neutropenia, rare PR prolongation effects
Contraindications: Conduction problems or and 1st-degree AV block, behavioral/mood effects and suicidal - Valproate – Increased risk for
severe cardiac disease (myocardial ischemia, ideation, multi-organ hypersensitivity syndrome hyperammonemic encephalopathy
heart failure)
Onset: 4 weeks Has addiction potential
Others: Carbamazepine, Lamotrigine; Valproate (alternative to Ethosuximide, which is N/A locally, for absence seizures). Asking about Ethosuximide in the exam will not magically spawn this into the
Philippine supply chain.

June 30, 2022
SYNAPTIC VESICLE PROTEIN 2A (SV2A) BINDER

Levetiracetam MOA: Binds synaptic vesicle SV2A; Opposes Common: Sedation, dizziness, asthenia, ataxia, decrease in RBCs Interactions: None significant beyond additive
₱₱₱ (tab/solution) / ₱₱₱₱ (ampule)
negative modulators of GABA- & Gly-gated and Hgb, upper respiratory tract infection CNS depressant effects with other CNS
currents, partially inhibits N-type Ca2+ currents depressants
Rare/serious:
Indication: 2nd line status epilepticus (IV); focal SJS-TEN,
seizures, GTC, myoclonic seizure Neuropsychiatric Sx
Antiepileptic with
Contraindication: Fructose intolerance *lowest*, if not 0%,
risk of teratogenicity
Onset: 2 weeks (oral)
Administration: Oral; IV infusion (status

epilepticus)
AMPA RECEPTOR ANTAGONIST

Perampanel₱₱₱ MOA: Noncompetitive AMPA glutamate receptor Common: Dizziness, somnolence, weight gain, fatigue, irritability Interactions:
antagonist falls, nausea, ataxia, balance disorder, - CNS depressants – additive effects
hostility/aggressive behavior (10-20%) w/in 6 weeks, other - CYP3A4/5 modulators – Perampanel
Indications: Adjunctive for focal, focal-to- neuropsychiatric Sx concentrations afftected by CYP3A4/5
bilateral seizures, GTC seizures inducers/inhibitors
Rare/serious: Has addiction potential - Levonorgestrel-containing hormonal
Contraindication: Lactose intolerance contraceptives – >12 mg of Perampanel
decreases efficacy
- Topiramate – decreases Perampanel
concentrations
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
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: more suicide attempts and deaths observed in no-treatment groups than in antiepileptic groups (Caley et al., 2018)
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.

June 30, 2022
ANTIEPILEPTICS NOT AVAILABLE LOCALLY

USELESS IN PHILIPPINE CLINICAL CONTEXT (unless imported/for compassionate use)
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 ↑ Phenytoin,
events, rare bronchospasm and rare angioedema Carbamazepine, Phenytoin levels
Indication: Adjunct in focal seizures for people ≥16 years old (no added benefit if added to
Levetiracetam)
2. Cenobamate MOA: Na+ channel blocker, modulates GABAA receptors Side Effects: Dose-dependent somnolence, dizziness, Interactions: ↑ Clobazam,
headache, fatigue, diplopia, suicidal ideation, QT shortening Phenytoin, Phenobarbital, , and
Indication: Adjunct, refractory focal seizures CYP2C19 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
impairment CYP3A substrate levels
3. Clobazam MOA: 1,4-benzodiazepine (same receptors as bound by BZDs, Side Effects: Sedation, somnolence, constipation, pyrexia, Interactions: Inhibits CYP2D6
different binding) drooling, paradoxical stimulation, withdrawal symptoms, and 2C9, and UGT1A4, 1A6, and
SJS/TEN 2B4; induces CYP3A4; substrate
Indication: Adjunct in LGS for people ≥2 years of CYP2B6, 2C19, 3A4, and P-
glycoprotein
Contraindication: Significant renal/hepatic impairment, sleep apnea,
myasthenia gravis
4. Eslicarbazepine MOA: Prodrug to S-licarbazepine → fast VSSC blocker, inhibit Side Effects: Similar to Oxcarbazepine Interactions: Inhibitor of
Acetate repetitive firing & decrease propagation of synaptic impulses, CYP2C19, inducer of CYP3A4,
↑ K+ conductance & modulation of high-voltage Ca2= channels metabolized by UGT2B4
Indication: Monotherapy, adjunct for focal seizures

5. Ethosuximide MOA: T-type Ca2+ channel blocker Side Effects: Blood dyscrasias, drug-induced lupus, Interactions: Metabolized by
dermatologic reactions, hiccups, other common GI & CNS CYP3A, 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
Ezogabine Indications: adjunct, focal seizures urinary retention, skin discoloration, QT prolongation, WORLDWIDE MARKET
WITHDRAWN FROM WORLDWIDE MARKET neuropsychiatric events
7. Felbamate MOA: Fast Na+ channel blocker, T-type Ca2+ channel blocker, Glu Side Effects: Aplastic anemia, hepatic failure, other Interactions: ↑ Phenytoin &
receptor blocker, increased GABA common CNS and GI side effects Valproate levels, decrease
Carbamazepine levels; inhibits
Indications: Monotherapy, adjunct to focal seizures; adjunct for LGS CYP2C19
in kids
8. GABAergic: MOA: Side Effects: Interactions: Tiagabine highly
Tiagabine Tiagabine – ↑GABA through blocking GABA transporters (GAT) Tiagabine – Dermatologic reactions, CNS depression, other protein-bound and metabolized by
Vigabatrin Vigabatrin – inhibits GABA transaminase CNS side effects (may trigger seizures when used in people CYP3A4
Indications: without seizures)
Tiagabine – adjunct, focal seizures with or without secondary
generalization Vigabatrin – Vision loss, anemia, neurotoxicity, peripheral
Vigabatrin – monotherapy, infantile spasms, particularly those with neuropathy, other CNS side effects
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 malonamide) Side Effects: Similar to Phenobarbital Interactions: Similar to
Phenobarbital
Indications: Monotherapy, adjunct for focal & generalized seizures

June 30, 2022
10. Stiripentol MOA: May enhance GABA transmission via weak partial agonism/ Side Effects: Interactions: Inhibits CYP
PAM ala barbiturate, CYP inhibition Common: enzymes (contributes to efficacy
CNS: Anorexia, sedation/insomnia, ataxia, hypotonia and by boosting levels of other
Indication: Adjunct to Clobazam and Valproate for Dravet syndrome dystonia, hyperkinesias; paradoxical aggressiveness, antiepileptics) – Carbamazepine,
irritability, insomnia, behavior disorders, hyperexcitability, Clobazam, Ethosuximide,
appetite loss Phenobarbital, Phenytoin,
GI: N/V 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
Indication: 1st line for West syndrome features, hypertension, hyperglycemia, glycosuria, electrolyte
imbalances
Contraindications: Serious bacterial or viral infection (TB, varicella,
cytomegalovirus), idiopathic hypertrophic cardiomyopathy, Rare: Brain atrophy, peptic ulcer, subaortic hypertrophic
osteoporosis, uncontrolled hypertension, sensitivity to proteins of cardiomyopathy, usually reversible within 6 months of
porcine origin, live or live-attenuated vaccines discontinuation, cataracts, glaucoma, worsening seizures
Life-threatening/dangerous:
Immuno: Sepsis, immunosuppression, impaired function of
polymorphonuclear leukocytes, pneumonia (esp
Pneumocystis)
Others: Fracture, congestive heart failure
12. Cannabidiol MOA: CB1 receptor negative allosteric modulator; might block fatty acid Side Effects: Interactions: Inhibits CYP2C19,
amide hydroxylase (FAAH), 5-HT1A agonist, transient receptor CNS: Somnolence/insomnia, fatigue, convulsion, rare manic metabolized by CYP2C19 and
potential vanilloid type 1 (TRPV1) agonist, blocks adenosine switch CYP3A4; effects may be
inactivation CV: Increased HR and BP enhanced or reduced by opioid
GI: Diarrhea, LFT elevation antagonists
Indication: Lennox-Gastaut syndrome (LGS), Dravet syndrome (DS); Others: Increased risk of infection
possible benefit for multiple sclerosis
13. Paraldehyde MOA: ??? Side Effects: Interactions: Additive effect with
Indication: Intractable/super-refractory status epilepticus Common (oral use): CNS depressants, Disulfiram may
GI: N/V, abdominal pain; unpleasant breath increase 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

June 30, 2022
14. Sulthiame MOA: Blocks Na+ channel & Glu release; inhibits carbonic anhydrase Side Effects: Interactions: Metabolic acidosis
in glial cells → increases CO2 → acidification of extracellular space → Common: with carbonic anhydrase
reduction in inward currents associated with NMDA receptors, CNS: Paresthesias (extremities, face), dizziness, headache, inhibitors, Topiramate,
depression of intrinsic neuronal excitability diplopia, appetite loss Zonisamide, ketogenic diet; ↑
CV: Stenocardia, tachycardia clearance with Carbamazepine
Indication: Benign focal epilepsies with centrotemporal spikes / GI: Weight loss and Primidone; ↑ plasma levels of
benign rolandic epilepsy, West syndrome Respiratory: Tachypnea, hyperpnea, dyspnea Lamotrigine, Phenobarbital, and
Phenytoin; reduced absorption
Life- threatening/Dangerous: with antacids containing Mg2+
Rare: Renal failure, serious rash w/ SJS/TEN or polyneuritis Trisilicate, Bismuth Oxycarbonate,
Renal: Nephrolithiasis, metabolic acidosis, electrolyte and MgO
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
DRUGS FOR SUBSTANCE USE DISORDERS

Medications MOA, Indications, Contraindications Side Effects and Administration Interactions
1. Buprenorphine₱₱₱₱₱ MOA: μ-opioid receptor partial agonist – relieves withdrawal Side Effects Interactions:
NEEDS S2 in absence of agonist (understimulated receptors), may Common: Headache, constipation, nausea, CYP3A4 modulators – can affect levels of
precipitate withdrawal in presence of agonist; κ-opioid orthostatic hypotension; Buprenorphine (metabolized by CYP3A4)
receptor antagonist CNS Depressants – Additive CNS depression
Sublingual: Oral hypoesthesia, glossodynia
Indication: Maintenance for opioid use
disorder/dependence, moderate-to-severe pain Rare/serious: Respiratory depression,
hepatotoxicity
Contraindication: Person should be in mild withdrawal
prior to initiation in opioid use disorder; opioid-naïve *Unfortunately, locally available dosage form is
transdermal patch (dosage forms indicated for
opioid use disorder: sublingual tablet with Naloxone,
implant)
Unrelated side note:

YOU CANNOT OVERDOSE ON FENTANYL
SIMPLY BY TOUCHING/BREATHING POWDER
2. Naltrexone MOA: μ-opioid receptor antagonist Side Effects Interactions:

(tablet imported, but Indication: Opioid use disorder/ dependence treatment Common: N/V, decreased appetite, dizziness, Beyond opioid antagonism, no significant
not locally FDA- (oral/injection) and relapse prevention (injection); alcohol dysphoria, anxiety, injection site reactions (pain, interactions (liver metabolism by dihydrodiol
registered) use disorder/dependence (oral/injection), cholestatic tenderness, pruritis, induration, swelling, erythema, dehydrogenase; Acamprosate interaction not
pruritis or bruising) significant)
Contraindication: Current opioid use, opioid dependence, Rare: Eosinophilic pneumonia, hepatic injury,
acute opioid withdrawal, naloxone challenge failure or severe injection site reactions
confirmed positive urine drug test, acute hepatitis or liver
failure; hypersensitivity to polylactidecoglyco-lide (PLG), *Ensure person is opioid-free for 7-10 days before
carboxymethylcellulose, other injection components initiating
June 30, 2022
3. Naloxone₱₱₱₱ MOA: μ-opioid receptor antagonist Side Effects

Common (on overdose reversal): Tachycardia,
Indication: Opioid toxicity antidote (life-saving); only pulmonary edema, hypertension, injection site
parenteral form available in PH reactions, other CV/respiratory effects
4. Nicotine OTC Indication: Tobacco use disorder/ dependence Side Effects Interactions:
₱₱₱₱
(lozenges, Gum: minimum 3 months (max. 24 pcs./day) Common: GI (N/V/D, abdominal pain), headache, • Acidic drinks (coffee, carbonated, etc.) –
chewing gum) Lozenge: minimum 3 months (max. 20 pcs./day) local irritation (if topical), mouth irritation/ulcers, can reduce Nicotine absorption
Contraindication (lozenge): Allergy to soy gastric/esophageal irritation (gum chewed too fast), • Adenosine – increased AV-block effects
• Varenicline – increased ADRs
5. Varenicline₱₱₱₱ MOA: α4β2-nicotinic receptor (NN) partial agonist Side Effects Interactions:
Common: Dose-dependent nausea, vomiting, Alcohol – decreased tolerance
Indication: Tobacco use disorder/ dependence (12 wk trial) constipation, flatulence, insomnia, headache,
Superior to Nicotine in efficacy abnormal dreams
N/A in the Philippines:
Alcohol Use Disorder
Acamprosate (taurine metabolite) – blocks mGluR2 and mGluR5 receptors
Disulfiram – irreversible aldehyde dehydrogenase inhibitor → formaldehyde accumulates→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
Upcoming:
• Ansofaxine, Esmethadone, MIJ821, Zuranolone (phase II/III, depression); Centanafadine (phase III, ADHD); Seltorexant (phase III, MDD; phase II, insomnia)
• Brilaroxazine, Roluperidone, Evenamide, MK-8189, Ralmitaront, Ulotaront, Xanomeline/Trospium (phase II/III, schizophrenia); Sunobinop (phase II, insomnia from alcohol cessation)
Legend:
1. Medicine Access Program and Philippine National Formulary – Essential Medicines List (PNF-EML) Listing
Yellow highlight and bold: DOH Medicines Access Program for Mental Health (MAP-MH) and EML 2017
Yellow highlight and boldBCMAP: DOH Breast Cancer Medicines Access Program and EML 2017
Yellow highlight and boldComPack: DOH Complete Treatment Pack Program and EML 2017
Yellow highlight and boldHIV: DOH National HIV Aids / STI Prevention and Control Program and EML 2017
Yellow highlight and boldTB: DOH National TB Control Program and EML 2017
Yellow highlight and boldF1*BNB: DOH FOURmula One Plus Botika ng Bayan and EML 2017
Bold name: EML 2017 only
2. Storage
a
Protect from light.
b
Protect from moisture
c
Do not freeze ampule
dKeep vial in carton until ready for use
LAILong-acting injectable formulation available locally
Storage information collated only for drugs available locally from drugs.com. For drugs available locally without a superscript, this means room temperature storage within the permissible excursions.
Always cross-check storage information with the package insert as formulations listed on the website may vary compared to those available locally.
3. Financial toxicity/price
₱
Direct cost of cheapest formulation is <₱10/daily dose at minimum/usual therapeutic dose, or per ampule/vial (<₱300/month for maintenance meds)
₱₱
Direct cost of cheapest formulation is ₱10 – <₱50/daily dose at minimum/usual therapeutic dose or per ampule/vial (₱300 – <₱1500/month for maintenance meds)
₱₱₱ Direct cost of cheapest formulation is ₱50 – <₱100/daily dose at minimum/usual therapeutic dose or per ampule/vial (₱1500 – <₱3000/month for maintenance meds)
₱₱₱₱ Direct cost of cheapest formulation is ₱100 – <₱1000/daily dose at minimum/usual therapeutic dose or per ampule/vial (₱3000 – <₱30,000/month for maintenance meds)
₱₱₱₱₱ Direct cost of cheapest formulation is ₱1000 or more/daily dose at the minimum/usual therapeutic dose or per ampule/vial (₱30,000/month or more for maintenance meds)
Pricing was obtained from websites of four major pharmacy chains and corroborated with a fifth, as needed. Those with price ranges that do not specify indications or dosage forms mean either the cheaper price was
obtained from the National Center for Mental Health, or the shorter dosing interval for an LAI was used. For those not available in the market but FDA-registered, inquiries were made to companies to which the brands
were registered when possible. Monthly costs for parenteral dosage forms will not involve multiplying unit cost by 30, as with as-needed medicines like benzodiazepines. Pricing includes only direct costs and does NOT
include indirect costs like professional and hospital fees, transportation, income saved due to treatment improvements on quality of life, costs of managing short- and long-term side effects, etc. Info subject to change.

June 30, 2022
MNEMONICS
1. Drugs that prolong QT interval
• ‘E s(c)i prof na QT, ma-pride sa 1st and 2nd halo-halo.
Nakakasuka. May amag. PI
• ESCItalopram
• CIPROFloxacin (FQs)
• Macrolides
• amisulPRIDE
• HALOperidol (1st gen Aps)
• 2nd generation 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 – RICE-PEAR-i-DONe (see photo on the next page)
▪ Excitement for a PEAR RICE BOWL leads to motor side effects (dose-dependent EPS)
▪ Excess RICE AND PEAR leads to more fat in the breasts → hyperprolactinemia → RisperiDONE with this s***
o Amisulpride – PRIDE
▪ Lost pride due to gynecomastia → hyperprolactinemia
o Aripiprazole – A RIP off (see photo on the right)
▪ Rip off → 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, distressful restlessness)

June 30, 2022
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 (gold standard in refractory schizophrenia)
• Bipolar disorder coverage
o RISEperidone – manic phase only (or when I see rice, my mood expand; see photo of Rice-Pear-don below)
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. So-called “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 on LSD 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; may cause false positive test results with urine drug screens for LSD
• Sertraline
o Ser’s heart is stimulated when discussing benzodiazepine & LSD SAR, and it is rewarding → Sertraline slightly increases dopamine (DAT blockade), causing stimulation. It is beneficial
in reducing incidence of myocardial infarction in those with depression and comorbid coronary artery disease, and also causes false positives for urine drug screens for
benzodiazepines and LSD
• 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 have a higher incidence of sexual dysfunction
• Mirtazapine
o Mirta(ba)ZZZapine → sedating, increases cholesterol
o Other sedating psychotropics: ChlorpromaZZZine, FluphenaZZZine, CarbamaZZZepine, CloZZZapine, OlanZZZapine, KechapinZZZ (EXCEPT -pipraZole)

June 30, 2022
BONUS SECTION: PSYCHEDELICS AND OTHER INVESTIGATIONAL AGENTS

Medications MOA and Indications Side Effects and Administration Interactions
PSYCHEDELICS
1. Psilocybin MOA: Side Effects (10 mg – 25 mg, people with Interactions (mostly Erowid data):
CONTROLLED • 5-HT2A agonist (non-canonical pathway: leads to BDNF release), treatment-resistant depression) • Amphetamines – may increase risk of
with actions at other 5-HT receptors Common: Hallucinations (visual, somatic), falling into thought loop (repeating,
• Metabolized into Psilocin (DMT), binds 5-HT2A – mGluR2 complex illusions, changes in mood, headache, fatigue, inescapable set of repetitive thoughts)
• Turns off brain’s “control centers” (uncouples default mode insomnia, changes in perception of time • Benzodiazepines – may reduce
network, which is overactive during depression leading to Psilocybin efficacy
increased rumination) → increased brain connectivity Rare/serious: suicidal ideation/behavior, non- • Caffeine – may increase stimulant aspect
suicidal self-injury of Psilocybin trip
Indication Studied in RCTs: Hallucinogen-assisted therapy for • Cannabis – may cause relaxation or
refractory depression (completed phase 2b clinical trials) Administration: orally while lying down in a intense anxiety when used with Psilocybin
comfy room with an eye mask on with • Ethanol – may reduce Psilocybin efficacy
instrumental music in the background for about 6- • Opioids – may increase somnolence
8 hours, preceded by a preparatory session and aspect of Psilocybin trip
followed by a psychotherapy session • SSRIs – may reduce Psilocybin efficacy
• Tramadol – increased risk of seizures
2. MDMA MOA: Side Effects (80-180 mg/session in divided Interactions:

CONTROLLED • SERT blocker → increased 5-HT → 5-HT2A agonist activity doses): Muscle tightness and twitching, • Alcohol – may increase MDMA levels and
• VMAT2 blocker → increased dopamine release decreased appetite, nausea & vomiting, duration of its effects
• Causes emotional warmth (empathogen) → allows trauma hyperhidrosis, feeling cold, restlessness, • Cannabis – may reduce heart rate
confrontation in therapy mydriasis, dizziness, bruxism, nystagmus, elevations with MDMA
increased blood pressure, jitteriness, • Carvedilol – may reduce cardiovascular
Indication Studied in RCTs: Hallucinogen-assisted therapy for nervousness, chest pain (non-cardiac), dry effects of MDMA
severe PTSD (undergoing multiple other phase 3 trials) mouth, blurred vision, increased daytime • CYP2D6 modulators – may cause
urination & urination urge, intrusive thoughts, changes in MDMA levels
stress, musculoskeletal pain, pyrexia, chills, • CYP2D6 substrates – MDMA may
cannabis use, somnolence increase concentrations of drugs
metabolized by CYP2D6 (autoinhibits
Administration: orally, preceded by multiple itself as well)
preparatory sessions and followed by multiple • Doxazosin – may slightly reduce
psychotherapy sessions (at least one occurring cardiovascular effects of MDMA
the morning after administration) • Haloperidol – may attenuate euphoria
from MDMA
• Methylphenidate – may cause additive
cardiovascular effects with MDMA

June 30, 2022
OTHER INVESTIGATIONAL AGENTS

3. 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, (μ, Acute psychiatric: Anxiety, agitation or irritability, • CNS depressants – additive effects
+required δ, κ), 5-HT1/2 antagonist, 5-HT3A potentiator, α7 nicotinic cholinergic euphoria/mood elevation, delusions/unusual • CYP3A4 inhibitors – can increase
healthcare receptor (α7nChR) antagonist, muscarinic receptor binder, NET thoughts, panic, and apathy. concentrations of Ketamine and decrease
professionals, blocker, D2 receptor partial agonist, substance P receptor antagonist, concentrations of Norketamine
facility, & cholinesterase inhibitor, or nitric oxide synthetase inhibitor Psychotomimetic: Dissociation, followed by • Diazepam – can increase concentrations of
equipment perceptual disturbance, odd or abnormal Ketamine
Hypotheses: sensation, derealization, hallucinations, • Naltrexone – Ketamine’s antidepressant
• NMDA receptor blockade (via specific binding sites/subunits) on depersonalization; feeling strange, weird, and effects antagonized by Naltrexone (trial was
GABAergic neurons → disinhibited Glu release from glutamatergic bizarre; feeling intoxicated stopped early due to this)
pyramidal neurons → binds AMPA receptors → activates voltage-
gated Ca2+ channels → ↑ intracellular Ca2+ → BDNF release → Neurologic: Headache, dizziness, sedation,
activates tropomyosin receptor kinase B (TrkB) → ↑activity of drowsiness, faintness, poor condition
intracellular kinases (e.g. extracellular regulated kinase/ERK, Akt
kinase) → activates mammalian target of rapamycin (mTOR) Cognitive: Poor memory & concentration,
kinase → controls processes of initiation of translation of synaptic confusion, cognitive impairment
proteins (e.g. synapsin I, GluA1 subunit of AMPARs, postsynaptic
density protein/PSD-95) Cardiovascular: Hypertension, arrhythmias
• NMDA receptor blockade → AMPAR activation →
dephosphorylation of eukaryotic elongation factor 2 (eEF2) kinase Urologic: “Ketamine bladder”/ulcerative cystitis
→ BDNF translation
• S-ketamine: more psychotomimetic; antidepressant activity blocked Risk of addiction, tolerance, and withdrawal
by mTOR inhibitors
• R-ketamine: more potent antidepressant properties with fewer Administration: 0.5 mg/kg, intermittent IV
adverse effects; antidepressant properties blocked by infusions (relapse within ~10 days)
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: 3rd line, treatment-resistant unipolar & bipolar depression

4. 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-
Contraindication (oral): Untreated subclinical thyrotoxicosis, overt binding globulin (TBG) or compete for TBG
thyrotoxicosis of any etiology, acute myocardial infarction, acute binding
myocarditis, acute pancarditis
Drugs that interfere with thyroid hormone
absorption, metabolism, and synthesis

June 30, 2022
5. 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
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
6. TamoxifenBCMAP 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)
7. Verapamil MOA: L-type Ca2+ channel blocker Side Effects: Interactions:
GI: Nausea, constipation • Ca2+ salts – Decrease Verapamil
Indication: Adjunct, refractory bipolar mania (inefficacious as Cardiovascular: Bradycardia, hypotension, 1st concentrations
monotherapy) degree AV block, weakness • CYP3A4 substrates – Verapamil can increase
Respiratory: Flu-like syndrome, allergic rhinitis, levels of drugs metabolized by CYP3A4
Contraindication: Sick sinus syndrome (>1st degree AV block), respiratory infection • CYP3A4 inhibitors – Increase Verapamil
severe CHF, cardiogenic shock, severe left ventricular dysfunction, Others: Myalgia, headache, ankle edema, with levels
hypotension <90 mm Hg, hypersensitivity 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
8. 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
Indication: Adjunct in refractory bipolar depression, refractory poisoning
schizophrenia (particularly negative symptoms), refractory OCD, and
cannabis use disorder
9. Propranolol MOA: Lipophilic β1 and β2 antagonist with membrane stabilizing Side Effects: Interactions:
properties; 5-HT1A antagonist; blocks melatonin release Cardiac: Bradycardia, precipitate/worsen heart • Benzodiazepines – Propranolol can increase
failure if not first stabilized with ACEI/ARB (due to adverse effects of benzodiazepines
Indication: As needed solely for somatic symptoms of anxiety; does decreasing cardiac output while increasing • Ca2+ and Al3+ salts – decrease effects of
not manage core anxiety symptoms; 1st line for essential tremor and systemic vascular resistance), Propranolol
migraine prophylaxis ischemic symptoms and myocardial infarction • CCBs – additive/synergistic effects
with sudden discontinuation • CYP2D6 modulators – can affect levels of
Contraindication: Bradycardia, >1st-degree heart block, Propranolol
cardiogenic shock, bronchial asthma, severe COPD Smooth muscle spasm: Bronchoconstriction • Gabapentin – Propranolol can increase the
(caution with asthma, COPD), cold extremities, adverse effects of Gabapentin
worsening of peripheral artery disease • Penicillins – decrease effects of Propranolol
(claudication) • Levothyroxine (thyroid hormones) –
CNS: Mild sedation, vivid dreams, depression decrease effects of Propranolol
Metabolic: Slight weight gain, increased
• Lidocaine – levels increased by Propranolol
triglycerides, decreased HDL, masking of
• NSAIDs – may antagonize antihypertensive
hypoglycemia symptoms (e.g. stops tremor)
effect of Propranolol
Others: Fatigue (limits exercise capacity), sexual
dysfunction (rare, may be nocebo), hyperkalemia • Warfarin – Propranolol can increase
anticoagulant effect of Warfarin

June 30, 2022
REFERENCES AND CREDITS

Main:
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2. College of Psychiatric and Neurologic Pharmacists (2016). Psychiatric pharmacotherapy review. 2016-2017 edition. Lincoln, NE: CPNP.
3. Stahl, S. M. (2021). Stahl’s essential psychopharmacology: Neuroscientific basis and practical application. 5th Edition. NY: Cambridge University Press.
4. Stahl, S. M. (2020). Stahl’s essential psychopharmacology: Prescriber’s guide. 7th edition. New York, New York: Cambridge University Press.
5. Taylor, D., Barnes, T. R. E., & Young, A. H. (2021). The Maudsley prescribing guidelines in psychiatry. 14th edition. UK: Wiley Blackwell.
Drug discovery infographic fact-checked by Ser Loisse Mortel, RPh. Check out his Organic Chemistry and Biochemistry series on Youtube here: https://www.youtube.com/c/SLRMchem/videos
Cheat sheet and misconceptions posters peer reviewed by Christopher Michael Mendoza, RPh, PharmD and another anonymous pharmacist.
Youtube Playlists for Psychopharmacology (to be updated at a later time):

bit.ly/AntipsychoticsPcolPH
bit.ly/AntidepressantsPcolPH
bit.ly/MoodStabilizersPcolPH
bit.ly/AnxiolyticsPcolPH
Art:
Keyring art based on illustrations by Nancy Munter
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
FINAL FANTASY is a registered trademark of Square Enix Holdings Co., Ltd. © SQUARE ENIX CO., LTD. All Rights Reserved.
Header, footer, keyring Illustrations, drug discovery infographic, and cheat sheet 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
Misconceptions poster by ART HERO. OPEN FOR COMMISSIONS: FB Page: fb.com/ArtHeroOfficial | arthero.official@gmail.com | 0906 590 7286
Disclaimer background art by Arn Zander Barcelo (@artizan00)
Munchlax illustrations by Risa Takatsu (IG: fieri.art)
COVID virus 3D modelling design by freepik
Chocolate fountain in realistic composition designed by macrovector / freepik
Pickup truck templates by PowerPointy
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.

June 30, 2022
Supplementary:
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“To whomever receives this message out there in the vast reaches of the cosmos…
To someone, I hope, who looks up at the stars with the same wistful gaze as mine…
To you I say, forge ahead.
May all our tomorrows be blessed with joy.”
Anonymous

June 30, 2022

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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

MISCONCEPTIONS ON PSYCHOTROPIC MEDICATIONS 10

PSYCHOTROPIC DRUG DISCOVERY PATHWAY: INFOGRAPHIC 12

“ANTIDEPRESSANTS” (SERT BLOCKERS) 13

“ANTIDEPRESSANTS” (NON-SERT BLOCKERS) 15

“ANTIPSYCHOTICS” AND RELATED AGENTS NOT AVAILABLE LOCALLY 29

ANXIOLYTICS AND SEDATIVE-HYPNOTICS 33

STIMULANTS, WAKE-PROMOTING AGENTS, AND MEDICATIONS FOR ADHD 36

DRUGS FOR DEMENTIA 39

DRUGS FOR PARKINSON’S DISEASE 40

OTHER ANTIEPILEPTICS (CNS ION CHANNEL AND SYNAPTIC VESICLE BINDERS) 41

DRUGS FOR SUBSTANCE USE DISORDERS 47

BONUS SECTION: PSYCHEDELICS AND OTHER INVESTIGATIONAL AGENTS 51

REFERENCES AND CREDITS 54

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 4 of 61

Corrections for version 5.0:

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 6 of 61

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 7 of 61

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 8 of 61

Jarvin Enosh Tan, RPh

Misconceptions on Psychotropic Medications

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 10 of 61

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 11 of 61

PSYCHOTROPIC DRUG DISCOVERY PATHWAY: INFOGRAPHIC

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 12 of 61

“ANTIDEPRESSANTS” (SERT BLOCKERS)

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 14 of 61

IB. SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIs) VEN DUL

Rare hepatotoxicity Contraindication: uncontrolled angle-closure glaucoma

IV. MELATONERGIC DRUGS

Onset: NOT rapid (~22 days)

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 16 of 61

“ANTIDEPRESSANTS” NOT AVAILABLE LOCALLY

Interactions: Same with Escitalopram

Interactions: Levomilnacipran levels affected by 3A4 modulators

Interactions: CYP2D6 modulators can increase/decrease Mianserin

Interactions: Levels increased/decreased by CYP3A4 modulators as Vilazodone is metabolized by CYP3A4

Interactions: Levels affected by CYP3A4 modulators since Reboxetine is metabolized by CYP3A4

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 17 of 61

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 18 of 61

SECOND GENERATION “ANTIPSYCHOTICS” / D2-5HT RECEPTOR ANTAGONISTS

4. Quetiapinea,b ₱₱₱ – ₱₱₱₱

DO NOT GIVE EXCLUSIVELY FOR

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 23 of 61

SECOND GENERATION “ANTIPSYCHOTICS” / D2-5HT RECEPTOR ANTAGONISTS: CLOZAPINE

Receptor Binding Profile:

Specific Side Effects

Side Effect Management:

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 24 of 61

THIRD GENERATION “ANTIPSYCHOTICS” / D2 RECEPTOR PARTIAL AGONISTS-5HT RECEPTOR ANTAGONISTS

No glucose intolerance and lipid abnormalities in clinical

Interactions: CYP2D6/3A4 modulators can affect levels of

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 25 of 61

Is Munchlax arguing that we’re better off using benzos,

So, trouble sleeping because of bipolar disorder? Yeah, sure, a 300

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 27 of 61

CNS Pharmacology Cheat Sheet Jarvin Enosh Tan, RPh 28 of 61

“ANTIPSYCHOTICS” AND RELATED AGENTS NOT AVAILABLE LOCALLY

Lumateperone – 5-HT2A antagonism, D2

Contraindication: Hepatic impairment, people with acute suicidal ideation