PMHNP Psychopharmacology Cheat Sheet: High-Yield Drugs for Boards

Psychopharmacology is the single highest-yield content domain on the PMHNP-BC exam. This cheat sheet surveys the drug classes you will absolutely be tested on — antidepressants, antipsychotics, mood stabilizers, anxiolytics, stimulants, and medications for addiction treatment (MAT) — with a mechanism-of-action snapshot, key adverse effects, required monitoring, and the board pearls examiners love.

Use this page as your master map, then drill into the linked deep-dive articles for the classes that trip up most candidates. Remember: real prescribing decisions require current guidelines and a drug reference — this is exam-focused education, not clinical advice.

How to Study Psychopharmacology for the PMHNP Boards

The exam rarely asks you to simply name a drug. It asks you to apply knowledge: pick the safest agent for a comorbid condition, recognize a toxicity, identify the right monitoring lab, or counsel a patient. Organize your studying around four buckets for every class:

1. MOA — what receptor or transporter it touches.
2. Adverse effects — especially the dangerous and the board-favorite ones.
3. Monitoring — baseline and ongoing labs or assessments.
4. Patient education — onset of effect, warnings, what to report.

Antidepressants

Antidepressants are the most heavily tested class. Know the first-line agents (SSRIs) cold, and recognize the distinguishing quirks of the rest.

SSRIs

MOA: Block the serotonin reuptake transporter, increasing synaptic serotonin. First-line for major depressive disorder (MDD), generalized anxiety, panic disorder, OCD, and PTSD.

Key adverse effects: GI upset, sexual dysfunction, insomnia or sedation, and — board favorites — hyponatremia (SIADH), increased bleeding risk (especially with NSAIDs/anticoagulants), and a discontinuation syndrome with abrupt stops. All antidepressants carry a pediatric/young-adult black box warning for suicidality.

Pearls: Fluoxetine has the longest half-life (least discontinuation risk). Paroxetine is the most anticholinergic and sedating, and is avoided in pregnancy (cardiac risk). Citalopram is dose-limited for QT prolongation. See the full SSRI exam review.

SNRIs

MOA: Block serotonin and norepinephrine reuptake (venlafaxine, desvenlafaxine, duloxetine, levomilnacipran). Useful for MDD plus neuropathic pain or fibromyalgia (duloxetine).

Pearls: Venlafaxine can raise blood pressure at higher doses — monitor BP. Discontinuation syndrome is notably severe with venlafaxine.

TCAs

MOA: Block serotonin and norepinephrine reuptake but also hit muscarinic, histaminic, and alpha-1 receptors — hence the side effects.

Key adverse effects: Anticholinergic effects (dry mouth, constipation, urinary retention), orthostatic hypotension, sedation, and — the critical board point — cardiotoxicity in overdose (QRS widening, fatal arrhythmias). They are lethal in overdose, so use caution in suicidal patients.

Pearls: Get a baseline ECG in older adults. Nortriptyline and desipramine are better tolerated than amitriptyline.

MAOIs

MOA: Inhibit monoamine oxidase, raising serotonin, norepinephrine, and dopamine. Reserved for treatment-resistant or atypical depression.

Key adverse effects: Hypertensive crisis with tyramine-rich foods (aged cheese, cured meats, draft beer) and serotonin syndrome when combined with serotonergic drugs.

Pearls: Require a 2-week washout (5 weeks for fluoxetine) before/after serotonergic agents. Heavy patient education on the tyramine-free diet is mandatory.

Bupropion

MOA: Norepinephrine–dopamine reuptake inhibitor (NDRI). Used for MDD and smoking cessation; activating rather than sedating; no sexual dysfunction.

Pearls: Lowers the seizure threshold — contraindicated in eating disorders (bulimia/anorexia) and active seizure disorders.

Mirtazapine

MOA: Alpha-2 antagonist that increases norepinephrine and serotonin.

Pearls: Causes sedation and weight gain — useful for depressed patients with insomnia and poor appetite.

Antipsychotics

Typical (First-Generation)

MOA: Strong dopamine D2 blockade. High-potency (haloperidol, fluphenazine) cause more extrapyramidal symptoms (EPS); low-potency (chlorpromazine) cause more sedation and anticholinergic effects.

Key adverse effects: EPS (acute dystonia, akathisia, parkinsonism, tardive dyskinesia), hyperprolactinemia, and neuroleptic malignant syndrome (NMS).

Atypical (Second-Generation)

MOA: D2 plus serotonin (5-HT2A) blockade, which lowers EPS risk but raises metabolic risk.

Key adverse effects: Weight gain, hyperglycemia/diabetes, dyslipidemia (worst with olanzapine and clozapine). Clozapine uniquely causes agranulocytosis (mandatory ANC monitoring via REMS) plus myocarditis and seizures.

Pearls: Atypicals require metabolic monitoring — weight/BMI, waist, fasting glucose, lipids, and BP. Use the AIMS exam for tardive dyskinesia. Deep dive: antipsychotic side effects.

Mood Stabilizers

Lithium: First-line for bipolar I and gold standard for anti-suicide benefit. Narrow therapeutic index (0.6–1.2 mEq/L). Monitor renal and thyroid function; watch NSAIDs, ACE inhibitors, thiazides, and dehydration. See lithium monitoring.

Valproate: Broad-spectrum; hepatotoxicity, pancreatitis, thrombocytopenia, and teratogenicity (neural tube defects — avoid in pregnancy). Monitor LFTs, CBC, and levels.

Lamotrigine: Best for bipolar depression; the board danger is Stevens-Johnson syndrome — titrate slowly and educate on rash.

Carbamazepine: Risk of agranulocytosis, SIADH, and SJS (test HLA-B*1502 in Asian ancestry); a potent CYP450 autoinducer.

Anxiolytics and Benzodiazepines

MOA: Benzodiazepines enhance GABA-A activity. Fast relief of acute anxiety, agitation, and alcohol withdrawal.

Key adverse effects: Sedation, dependence, tolerance, withdrawal (seizures), and respiratory depression — especially with opioids (combined black box warning).

Pearls: Lorazepam, oxazepam, and temazepam ("LOT") are safest in liver disease (no oxidative metabolism). Buspirone is a non-addictive 5-HT1A partial agonist for chronic GAD. More in benzodiazepines for the exam.

Stimulants and ADHD Medications

MOA: Methylphenidate and amphetamines increase dopamine and norepinephrine. First-line for ADHD.

Key adverse effects: Decreased appetite, insomnia, weight loss, increased HR/BP; abuse potential (Schedule II). Monitor growth, cardiovascular status, and screen cardiac history.

Pearls: Non-stimulants — atomoxetine (a selective norepinephrine reuptake inhibitor [NRI], carries a suicidality black box), guanfacine, and clonidine — are options when stimulants are unsafe. See ADHD medications.

Medications for Addiction Treatment (MAT)

Opioid use disorder:

• Methadone: Full mu-opioid agonist; QT prolongation risk; clinic-dispensed.
• Buprenorphine: Partial agonist (ceiling effect); often combined with naloxone (Suboxone) to deter misuse; precipitated withdrawal if given too early.
• Naltrexone: Opioid antagonist; requires full detox first.

Alcohol use disorder: Naltrexone, acamprosate, and disulfiram (aversive — causes a violent reaction with alcohol). Details in MAT for substance use.

High-Yield Cross-Cutting Topics

Serotonin syndrome vs. NMS: A guaranteed exam contrast. Serotonin syndrome has rapid onset, clonus, and hyperreflexia; NMS has slow onset, lead-pipe rigidity, and hyporeflexia. Master it in serotonin syndrome vs. NMS.

Black box warnings: Antidepressant suicidality (pediatric), clozapine agranulocytosis, benzodiazepine–opioid respiratory depression, and more in psych medication black box warnings.

Put It Into Practice

Reading a cheat sheet builds recognition; answering questions builds the recall you need on test day. The fastest way to lock in psychopharmacology is repetition with clinician-verified items and rationales. Drill the free PMHNP question bank, then create your free account to track your weak classes and turn this cheat sheet into a passing score.