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PSYCHIATRIC CASE PRESENTATION

MA.KA., 29-year-old Male | Vicente Sotto Memorial Medical Center - Center for Behavioral Sciences

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GENERAL DATA

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CHIEF COMPLAINTS

• Mother: "Ika-5 na siya nag-suicide" (This is his 5th suicide attempt)
• Patient: "Naay lima ka taw inside sa ako body" (There are five people inside my body)

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HISTORY OF PRESENT ILLNESS - Key Timeline

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PAST PSYCHIATRIC HISTORY - Chronological Summary

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SUBSTANCE USE HISTORY

• Cigarettes: ~1 pack/day
• Alcohol: Tanduay, Red Horse beer, wine (when he has money)
• Caffeine: 10 sticks of instant coffee/day + excessive Sting energy drinks
• Illicit drugs: None reported

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FAMILY HISTORY (Psychiatric Relevance)

• Mother (64 y/o): Hypertension + Generalized Anxiety Disorder - positive family history for psychiatric illness
• Father (~67 y/o): History of alcohol use, extramarital affairs, absent father figure
• Abandoned the family when patient was ~1 year old; reconnected in adulthood inconsistently
• Maternal side: Hypertension

Clinical significance: Absent/inconsistent paternal figure, single-parent upbringing, witnessed parental conflict, childhood bullying - significant psychosocial stressors and adverse childhood experiences (ACEs) contributing to vulnerability.

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DEVELOPMENTAL & SOCIAL HISTORY - Key Points

• Birth: Forceps-assisted delivery (prolonged labor); born underweight
• Father left at age 1 (raised by single mother)
• Age 6: Father briefly returned; patient appeared indifferent toward him
• Middle childhood: Quiet, preferred solitude, poor peer interaction
• Adolescence: Withdrawn, bullied (ID card hidden, given rainwater instead of drinking water) - transferred schools
• Completed high school in 6 years (delayed)
• Adulthood: Multiple failed academic programs, multiple job changes, work conflicts with coworkers
• April 2026: Re-established contact with father; became closer through phone/video calls
• Pattern: Chronic interpersonal difficulties, occupational instability, social isolation

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MENTAL STATUS EXAMINATION

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PHYSICAL EXAMINATION

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PRIMARY IMPRESSION & JUSTIFICATION

Schizoaffective Disorder, Bipolar Type, Multiple Episodes, Currently in Acute Episode

DSM-5-TR Criteria (from Kaplan & Sadock's Comprehensive Textbook of Psychiatry)

"DSM-5-TR specifically requires 'An uninterrupted period of illness during which there is a major mood episode (major depressive or manic) concurrent with Criterion A of Schizophrenia.'"

"DSM-5-TR schizoaffective disorder is further divided into two subtypes based on whether or not manic episodes are present... (bipolar type) or the mood episodes are limited to the major depressive episodes (depressive type)." - Kaplan & Sadock's Comprehensive Textbook of Psychiatry

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WHY NOT THE DIFFERENTIAL DIAGNOSES?

Differential 1: Bipolar I Disorder, Current Episode Manic with Psychotic Features

"It can be extremely difficult to distinguish a mixed manic state from EOS or schizoaffective disorder because hallucinations, delusions, irritability, and agitation are common in all three disorders. The primary distinguishing factors are the presence of a decreased need for sleep and hypersexuality in bipolar disorder versus negative symptoms in the schizophrenia spectrum disorders." - Kaplan & Sadock's CTP

• Manic features: decreased sleep (4-5 hrs), impulsivity, leaving seminary, excessive writing/romantic notes
• Psychotic features: AH ("You must go home"), "five people inside my body"
• Prior diagnosis of Bipolar I

• In Bipolar I with psychotic features, psychosis is ONLY present during mood episodes
• In this patient, there is decades of psychotic symptoms that likely extend beyond discrete mood episodes
• The persistent, autonomous nature of the voices and passivity experiences ("five people in my body") across the illness course exceeds what is expected for mood-congruent or mood-episode-limited psychosis
• Per DSM-5-TR: the psychosis must have been present for at least 2 weeks without prominent mood symptoms at some point - this history over 16 years strongly suggests this threshold has been met

"Clinicians frequently use a preliminary diagnosis of schizoaffective disorder when they are uncertain of the diagnosis." - Kaplan & Sadock's Synopsis of Psychiatry

Differential 2: Schizophrenia

• Chronic psychotic illness since adolescence
• Multiple hospitalizations
• "Five people inside my body" (passivity experience / somatic passivity - a first-rank Schneiderian symptom)
• Command auditory hallucinations

• Per DSM-5-TR, in schizophrenia, mood episodes are brief relative to the total illness duration
• In this patient, mood disturbance (mania/suicidal depression) has been a DOMINANT, recurring feature throughout the illness since age 13
• Criterion C of Schizoaffective: mood symptoms for the majority of total illness duration
• The recurrent, full manic and depressive episodes are too prominent and sustained to be explained by schizophrenia alone

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PHARMACOTHERAPY PLAN - Explanation

1. Sodium Valproate + Valproic Acid (Depakene/Depakote) 500mg/tab - 2 tabs AM, 1 tab PM (= 1500 mg/day)

"The treatment regimen of schizoaffective disorder usually includes a mood stabilizer, such as valproate, carbamazepine, or lithium, and an atypical antipsychotic. Recent prevalence data have suggested that the use of valproate alone and in combination with atypical antipsychotics has substantially increased." - Kaplan & Sadock's CTP

• Mood stabilization in Bipolar Type Schizoaffective Disorder
• Controls manic features (decreased sleep, impulsivity, agitation, aggression)
• Added benefit: accelerates antipsychotic response - trial data shows divalproex + antipsychotic combination reduces positive symptoms faster than antipsychotic alone
• Also provides anti-epileptic coverage (important in a patient who has had head trauma/falls from suicide attempts)
• Addresses alcohol use (divalproex has evidence for reducing alcohol relapse and dysphoric mania comorbid with substance use)

2. Clozapine 100mg - ½ tab ODHS x 3 days → 1 tab ODHS

• Patient has a history of multiple antipsychotic trials (lithium, risperidone, clozapine in the past) with persistent symptoms and poor medication adherence = treatment-resistant features
• Clozapine is the gold standard for treatment-resistant psychosis and schizoaffective disorder
• Anti-suicidal properties: Clozapine is the ONLY antipsychotic with an FDA-approved indication for reducing suicidal behavior in schizophrenia and schizoaffective disorder - critically important in a patient with 5 suicide attempts
• Slow titration protocol (½ tab x 3 days before full dose) is standard to minimize orthostatic hypotension, sedation, and risk of seizures
• ODHS = Once daily at hour of sleep - minimizes daytime sedation

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NON-PHARMACOLOGICAL PLAN

Supportive Therapy

• Establish therapeutic alliance
• Address immediate safety concerns (suicidal ideation, aggression)
• Validate patient's experiences while gently reality-testing

Psychoeducation

• For patient AND family (mother is primary caregiver)
• Importance of medication adherence (this patient's major issue)
• Psychoeducation on illness course, warning signs of relapse
• Address substance use (cigarettes, alcohol, excessive caffeine) - caffeine worsens sleep and may precipitate mania

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KEY CLINICAL POINTS FOR PRESENTATION

1. Why Schizoaffective and NOT Bipolar I with Psychotic Features? The 16-year illness course with psychosis likely extending beyond mood episodes (criterion B) and mood symptoms dominating the majority of the illness (criterion C) tips the diagnosis toward Schizoaffective. However, this remains diagnostically challenging - Kaplan explicitly notes that "clinicians frequently use a preliminary diagnosis of schizoaffective disorder when they are uncertain."
2. Five Suicide Attempts - this is the critical risk factor. Clozapine's anti-suicidal indication is not merely incidental - it is arguably the primary driver for choosing clozapine in this case.
3. Insight Level 5 - intellectual insight present. The patient can be engaged in psychoeducation and collaborative care planning. This is a prognostic asset.
4. Adverse Childhood Experiences: Absent father, witnessed marital conflict, bullying, single-parent upbringing - these are significant contributors to illness severity and chronicity. Should be addressed in longer-term therapy.
5. Poor medication adherence is the dominant modifiable risk factor for relapse. Structured adherence monitoring and family involvement are essential.

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Bisaya → English Translations

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Clinical Notes on the Translations

• #4 - Written in a notebook at the mall; shows disinhibited, hypersexual/goal-driven behavior consistent with a manic or hypomanic state.
• #5 - Confirms intentional medication overdose (not accidental); directly implicates suicidal intent.
• #6 & #7 - Said during anger outbursts toward his mother at age 13; reflects feelings of rejection, inferiority, and sibling rivalry - important psychodynamic context for his mood and self-esteem dysregulation.
• #9 & #10 - Notes written to "Eya" at the seminary; demonstrates disorganized, impulsive romantic preoccupation and possible erotomania-adjacent thinking in the context of his acute episode.

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PSYCHIATRIC MEDICATIONS - COMPLETE DEEP DIVE GUIDE

Based on Kaplan & Sadock's Synopsis and Comprehensive Textbook of Psychiatry

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PART 1: ANTIPSYCHOTICS

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1A. TYPICAL (FIRST GENERATION) ANTIPSYCHOTICS (FGAs)

Mechanism of Action

"The primary mechanism of action of the typical antipsychotics/neuroleptics (e.g., chlorpromazine, haloperidol) is the antagonism of the D2 dopamine receptor." - Kaplan CTP

• Alpha-1 adrenergic → orthostatic hypotension, sedation
• Muscarinic (M1) → anticholinergic effects (dry mouth, urinary retention, constipation, blurred vision)
• H1 histamine → sedation, weight gain

Common FGAs

Extrapyramidal Side Effects (EPS) - MUST KNOW

Neuroleptic Malignant Syndrome (NMS) - LIFE-THREATENING

"NMS is a rare, potentially fatal consequence of neuroleptic administration. The syndrome consists of autonomic instability, hyperpyrexia, severe extrapyramidal symptoms (i.e., rigidity), and delirium." - Kaplan Synopsis

• Febrile (hyperpyrexia >38°C, can reach 41°C)
• Encephalopathy (delirium, altered consciousness)
• Vitals unstable (tachycardia, labile BP, diaphoresis)
• Elevated CK (from muscle breakdown → myoglobinuria → renal failure)
• Rigidity ("lead pipe" rigidity)

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1B. ATYPICAL (SECOND GENERATION) ANTIPSYCHOTICS (SGAs)

Mechanism of Action

"Atypical antipsychotic agents such as clozapine and risperidone have different mechanisms of action compared to traditional neuroleptics and have an affinity for 5HT2a, alpha-adrenergic, and D4 receptors, among others." - Kaplan CTP

• Block 5-HT2A (serotonin) receptors AND D2 receptors
• The 5-HT2A blockade in the nigrostriatal pathway releases dopamine → LESS EPS than FGAs
• Also less prolactin elevation (except risperidone/paliperidone)

Individual SGAs - Deep Dive

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CLOZAPINE (Most important for this case!)

1. Treatment-resistant schizophrenia (failed ≥2 antipsychotics)
2. FDA-approved to reduce suicidal behavior in schizophrenia and schizoaffective disorder - the ONLY antipsychotic with this indication

• Start ½ tab (50mg) ODHS x 3 days → 1 tab (100mg) ODHS
• Usual therapeutic range: 300-450 mg/day
• Maximum: 900 mg/day
• Titrate slowly - reduces seizure and cardiovascular risk

• Trough level (morning, before dose)
• Minimum therapeutic threshold: 100 ng/mL
• For treatment-resistant cases: ≥350 ng/mL needed
• Seizure risk increases significantly at levels >1,200 ng/mL or doses >600 mg/day

• Baseline WBC before starting
• Weekly for first 6 months
• Biweekly for next 6 months
• Monthly thereafter (if stable)

• WBC < 3,000/mm³ OR
• Absolute Neutrophil Count (ANC) < 1,500/mm³

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RISPERIDONE

• At LOW doses (≤6 mg/day): atypical profile, minimal EPS
• At HIGH doses (>8 mg/day): behaves like a typical antipsychotic (high EPS, high prolactin)
• Highest prolactin elevation among all SGAs (more than FGAs)
• Available as: oral tablet, oral solution, IM long-acting injection (Risperdal Consta)

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OLANZAPINE

• One of the most effective SGAs for acute mania and schizophrenia
• Most weight gain of all SGAs (except clozapine)
• Very sedating (useful in acute agitation)
• Available as IM for acute agitation

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QUETIAPINE

• Very low EPS risk (loosely binds D2)
• Commonly used for bipolar depression (approved indication)
• Active metabolite norquetiapine has antidepressant properties
• Used off-label for insomnia/anxiety at low doses (25-100 mg)

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ARIPIPRAZOLE

• "Goldilocks" of antipsychotics - stabilizes dopamine (not too much, not too little)
• Least metabolic effects of all SGAs (minimal weight gain, no glucose/lipid changes)
• Least sedating SGA
• Can cause akathisia (due to partial D2 agonism)

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ZIPRASIDONE

• Least weight gain of all SGAs
• QTc prolongation - most significant QTc effect of SGAs; avoid in patients with baseline QTc >500ms or on other QTc-prolonging drugs
• Must be taken with food (bioavailability increases 2x with food)

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PALIPERIDONE (9-hydroxyrisperidone)

• Active metabolite of risperidone
• Similar profile to risperidone
• Renally excreted (safe in hepatic impairment)
• Available as once-monthly and once-3-monthly IM depot

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Comparison Table: FGA vs SGA

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PART 2: MOOD STABILIZERS

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2A. LITHIUM

Mechanism of Action

• Inhibits inositol monophosphatase → depletes inositol → alters intracellular signaling via IP3/DAG pathway
• Inhibits glycogen synthase kinase-3 (GSK-3β) → neuroprotective effects
• Modulates serotonin, dopamine, and norepinephrine neurotransmission
• Increases neurogenesis in the hippocampus

Indications

• Bipolar I Disorder - gold standard for mania (first-line)
• Bipolar maintenance (most evidence for reducing relapse)
• Augmentation in treatment-resistant depression
• Suicidality reduction (evidence for anti-suicidal effect)

Pharmacokinetics

• Absorption: Rapid and complete (oral); no protein binding
• Distribution: Distributes in total body water; crosses BBB and placenta
• Excretion: 100% renal (no hepatic metabolism)
• Half-life: ~24 hours (steady state reached in 5-7 days)
• NOT metabolized by liver - safe in hepatic disease; dose-adjust in renal disease

Dosing

• Start 300 mg TID; titrate to therapeutic level
• Usual dose: 900-2400 mg/day in divided doses
• Extended-release (Lithobid) - reduces GI side effects, once or twice daily

Therapeutic Drug Monitoring (CRITICAL)

"Lithium has a narrow therapeutic index. Symptoms of toxicity include tremors, sedation, and confusion. At higher levels, delirium, seizures, and coma may occur." - Kaplan Synopsis

Lithium Toxicity - Stages

• Diarrhea
• Ataxia
• Remor (Tremor - coarse)
• Thirst (polyuria/polydipsia - NDI)
• Slurring of speech

Things that Increase Lithium Levels (→ toxicity risk)

• NSAIDs (reduce renal clearance)
• Thiazide diuretics (Na loss → lithium retention)
• ACE inhibitors / ARBs
• Dehydration, low-sodium diet, fever, vomiting

Monitoring Before and During Lithium

• Baseline: Renal function (BUN, Cr), TFTs (TSH), ECG, CBC, pregnancy test, serum calcium
• During: Lithium level every 3-6 months, Cr and TSH every 6-12 months

Side Effects

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2B. VALPROATE / DIVALPROEX (Valproic Acid, Sodium Valproate, Depakote)

Mechanism of Action

• Blocks voltage-gated sodium channels → membrane stabilization
• Enhances GABA activity (increases GABA synthesis, inhibits GABA breakdown)
• Inhibits T-type calcium channels
• Inhibits histone deacetylase → gene expression changes (neuroprotective)

Indications in Psychiatry

• Acute mania (as effective as lithium for mixed/dysphoric mania - possibly better)
• Bipolar maintenance
• Schizoaffective Disorder - Bipolar Type (as in our patient)
• Augmentation of antipsychotics → accelerates response in acute psychosis
• Alcohol withdrawal (CIWA-based management)
• Migraine prophylaxis
• Epilepsy (broad spectrum anticonvulsant)

Pharmacokinetics

• Protein binding: 80-95% (highly protein-bound; watch for interactions)
• Metabolism: Hepatic (glucuronidation, beta-oxidation, CYP450 minor)
• Half-life: 6-16 hours
• Active metabolite: 2-propyl-4-pentenoic acid (partially responsible for hepatotoxicity)

Dosing

• Start 250 mg BID-TID; titrate to therapeutic level
• For this patient: 500 mg x 2 tabs AM + 1 tab PM = 1500 mg/day
• Usual psychiatric dose: 750-2500 mg/day in divided doses
• Extended-release (Depakote ER) allows once-daily dosing

Therapeutic Drug Monitoring

• Therapeutic range: 50-125 mcg/mL (for psychiatry; epilepsy: 50-100 mcg/mL)
• Draw trough level (before morning dose)

Side Effects

Monitoring Before and During Valproate

• Baseline: LFTs, CBC (with platelets), pregnancy test, weight, ammonia
• During: LFTs and CBC every 6 months, drug level as needed

Drug Interactions (important!)

• Lamotrigine: Valproate inhibits lamotrigine metabolism → doubles lamotrigine levels → rash/Stevens-Johnson; must halve lamotrigine dose
• Carbamazepine: Mutual enzyme induction; complex interaction
• Aspirin: Displaces valproate from protein binding → increases free valproate

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2C. CARBAMAZEPINE (Tegretol)

Mechanism of Action

• Blocks voltage-gated sodium channels (use-dependent)
• Also modulates NMDA glutamate receptors

Indications

• Bipolar disorder (especially dysphoric/mixed mania, rapid cycling)
• Trigeminal neuralgia
• Epilepsy

Key Features

• Induces its own metabolism (autoinduction) - plasma levels drop after 3-5 weeks; may need dose increase
• Induces CYP3A4 - reduces levels of many drugs including oral contraceptives, warfarin, haloperidol

Therapeutic Range: 4-12 mcg/mL

Side Effects

"Carbamazepine may produce changes in the levels of white blood cells, platelets, and, under rare circumstances, red blood cells. Anemia, aplastic anemia, leucopenia, and thrombocytopenia may all occur." - Kaplan Synopsis

HLA-B*1502 Testing

• Mandatory before starting carbamazepine in Asian patients (Filipino, Chinese, Thai, etc.)
• This allele increases risk of Stevens-Johnson Syndrome dramatically

Monitoring: CBC, LFTs, electrolytes (sodium), drug level

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2D. LAMOTRIGINE (Lamictal)

Mechanism of Action

• Blocks voltage-gated sodium channels
• Inhibits glutamate release (reduces excitatory neurotransmission)

Indications

• Bipolar depression (most effective mood stabilizer for depression component - better than lithium or valproate for depression)
• Bipolar maintenance
• Epilepsy

Key Feature: Very slow titration required

• Must titrate over 6-8 weeks
• Rapid titration = Stevens-Johnson Syndrome / Toxic Epidermal Necrolysis (TEN)
• CRITICAL INTERACTION: Valproate doubles lamotrigine levels → must use half the usual dose when combined

Typical dosing (without valproate): 25 mg/day → 50 → 100 → 200 mg over 6-8 weeks

With valproate: 25 mg every other day → 25 mg/day → 50 mg/day → 100 mg/day

Side Effects

• Stevens-Johnson Syndrome (most feared - especially with rapid titration or valproate co-administration)
• Rash (benign in most cases, but any rash requires evaluation)
• Dizziness, diplopia, ataxia
• Minimal metabolic effects - no weight gain, no cognitive dulling → preferred in women/younger patients

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PART 3: ANTIDEPRESSANTS

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3A. SSRIs (Selective Serotonin Reuptake Inhibitors)

Mechanism of Action

"By definition, SSRIs increase synaptic levels of serotonin by binding to the serotonin transporter." - Kaplan CTP

Common SSRIs

Indications

• Major Depressive Disorder (first-line)
• Anxiety disorders (GAD, panic disorder, social anxiety, OCD, PTSD)
• Premenstrual dysphoric disorder (PMDD)
• Bulimia nervosa

Side Effects

Serotonin Syndrome (Emergency!)

1. Altered mental status (agitation, confusion)
2. Autonomic instability (hyperthermia, tachycardia, diaphoresis, hypertension)
3. Neuromuscular abnormalities (clonus, hyperreflexia, tremor, myoclonus, incoordination)

⚠️ MAOI + SSRI = ABSOLUTE CONTRAINDICATION (can cause fatal serotonin syndrome) Washout: SSRIs 2 weeks before MAOI (fluoxetine: 5 weeks due to long half-life); MAOIs 2 weeks before SSRI

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3B. SNRIs (Serotonin-Norepinephrine Reuptake Inhibitors)

MOA: Block both SERT (serotonin transporter) AND NET (norepinephrine transporter)

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3C. TCAs (Tricyclic Antidepressants)

MOA

"Older generation tricyclic antidepressants (TCAs) (e.g., imipramine, doxepin) typically act as both serotonin and norepinephrine reuptake inhibitors." - Kaplan CTP

Common TCAs

Side Effects (due to receptor blockade)

Critical Safety Issue: Cardiotoxicity

• TCAs are dangerous in overdose - narrow therapeutic index
• Lethal dose = ~10x therapeutic dose - only 1-2 week supply can be fatal
• Overdose: QRS widening → ventricular arrhythmias → seizures → death
• Avoid in suicidal patients - limit quantity dispensed
• Baseline ECG required before initiation

Monitoring: ECG, drug levels (for nortriptyline: 50-150 ng/mL)

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3D. MAOIs (Monoamine Oxidase Inhibitors)

MOA

• Irreversible, non-selective: Phenelzine, Tranylcypromine, Isocarboxazid
• Reversible, selective MAO-A (RIMA): Moclobemide (fewer interactions)
• Selective MAO-B: Selegiline (Parkinson's; as antidepressant patch at high dose)

Indications

• Atypical depression (best evidence for MAOIs vs other antidepressants) - features: hypersomnia, hyperphagia, leaden paralysis, rejection sensitivity
• Treatment-resistant depression
• Panic disorder, social anxiety disorder

The Critical Interaction: Tyramine (HYPERTENSIVE CRISIS)

• Aged cheeses (the "cheese effect")
• Cured meats (salami, pepperoni)
• Fermented products (soy sauce, miso, tofu)
• Red wine, tap beer
• Overripe/spoiled foods
• Yeast extracts (Marmite)

"Treatment with MAOIs can cause orthostasis and, rarely, hypertensive crisis. Baseline blood pressure measurement should be obtained before initiation, and blood pressure should be monitored during treatment." - Kaplan Synopsis

Drug Interactions (Multiple life-threatening ones)

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3E. OTHER ANTIDEPRESSANTS

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PART 4: ANXIOLYTICS & SEDATIVE-HYPNOTICS

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4A. BENZODIAZEPINES

Mechanism of Action

"Benzodiazepines potentiate the action of GABA by binding to a separate benzodiazepine site on the GABA-A receptor." - Kaplan CTP

Indications

• Acute anxiety, panic attacks
• Alcohol withdrawal (CIWA protocol - drug of choice)
• Acute agitation (IM lorazepam)
• Seizures / status epilepticus (IV diazepam, lorazepam)
• Insomnia (short-term only)
• Muscle relaxation
• Procedural sedation

Common Benzodiazepines

Side Effects

• CNS depression: Sedation, cognitive impairment, anterograde amnesia
• Respiratory depression: Especially combined with opioids or alcohol - potentially fatal
• Paradoxical disinhibition: Especially in elderly and children - increased agitation, aggression
• Dependence and tolerance: Both physical and psychological
• Withdrawal syndrome: Anxiety, tremor, seizures, insomnia, tachycardia - can be life-threatening (similar to alcohol withdrawal)

Benzodiazepine Overdose

• Treatment: Flumazenil (competitive antagonist at BZ receptor)
• Caution: Flumazenil can precipitate withdrawal seizures in dependent patients; short-acting (may need repeat dosing)

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4B. BUSPIRONE (Buspar)

MOA

• 5-HT1A partial agonist (serotonin)
• Some D2 partial agonism

Key Features

• For Generalized Anxiety Disorder (GAD) - first-line non-benzodiazepine option
• No dependence, no tolerance, no withdrawal
• No abuse potential
• Takes 2-4 weeks to work (like an antidepressant - not acute)
• Does NOT work for acute anxiety/panic attacks
• Does NOT cross-tolerate with benzodiazepines (cannot substitute during benzo withdrawal)
• Minimal sedation, no cognitive impairment

Dosing: 15-30 mg/day in divided doses

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4C. Z-DRUGS (Non-benzodiazepine hypnotics)

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4D. HYDROXYZINE

• H1 antihistamine with anxiolytic properties
• Non-habit-forming; no dependence
• Used for acute anxiety, pruritus, nausea
• Can be used in patients with substance use disorder (safe)
• Side effects: sedation, anticholinergic effects

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QUICK SUMMARY TABLE - "The Big Picture"

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