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Nursing Field Notes / Mental Health · Psychopharmacology Course

ADHD Meds 💊

Stimulants & Non-Stimulants for ADHD

NG-234 Mental Health ADHD-friendly visual edition

Two families, one goal — boost dopamine & norepinephrine signaling in the prefrontal circuit described on the ADD & ADHD page (NG-093). Stimulants work fast and are first-line; non-stimulants are the option when stimulants aren't tolerated, are contraindicated, or carry abuse risk.

📄 Simple Nursing original — opens in Drive →

💊 First-line = stimulantsMethylphenidate & amphetamine salts — Schedule II controlled substances.
❤️ Screen the heart FIRSTCardiac history, family history of sudden death, baseline VS before starting.
📏 Track growthHeight & weight trends every visit — appetite suppression can slow growth.
🌙 No evening dosingGive doses early in the day — late dosing → insomnia.
💊

WHAT IT DOES

STEP 1 · MECHANISM

Both drug families raise dopamine & norepinephrine in the synapse — they just get there differently.

⚡ Stimulants — flood the synapse with dopamine & norepinephrine

MOA Methylphenidate and amphetamine salts block reuptake and increase release of dopamine & norepinephrine at the synapse — the opposite problem from the low-dopamine circuit on the ADHD page, corrected chemically.

Presynaptic neuron Postsynaptic reuptake pump blocked More DA + NE stays in the gap → stronger signal → better focus, less impulsivity
DrugBrandClass
MethylphenidateRitalinStimulant
Amphetamine mixture saltsAdderallStimulant
DextroamphetamineDexedrineStimulant

Indications: ADHD in children & adolescents — and narcolepsy (same wakefulness-driving mechanism treats both).

🧠 "Stim = same fix, better click." Stimulants don't sedate an ADHD brain — they supply the missing dopamine/norepinephrine so the existing filter can finally click into place.

🧭 Non-stimulants — a different route to the same circuit

  • Atomoxetine (Strattera) — selective norepinephrine reuptake inhibitor (blocks NE reuptake specifically, not dopamine directly)
  • Guanfacine ER (Intuniv) & Clonidine ER (Kapvay) — central alpha-2 agonists that improve prefrontal signaling and calm hyperactivity/impulsivity
🧠 Non-stimulants take longer to reach full effect (days–weeks) but carry no abuse potential and are not controlled substances — the trade-off for a slower onset.

⭐ Why choose non-stimulant first?

  • History of substance use disorder in the child/family
  • Cardiac contraindication to stimulants
  • Significant anxiety — stimulants can worsen anxiety; alpha-2 agonists can help both
  • Prefer to avoid controlled-substance prescribing/storage issues
⚠️

WATCH FOR

STEP 2 · PRIORITY MONITORING

Screen the heart before the first dose, then track growth and vitals at every visit after.

🚨 Cardiac screening — BEFORE starting a stimulant

History & physical exam incl. family Hx Family history of sudden cardiac death, syncope, arrhythmia? Baseline BP, HR & ECG ECG if indicated Start therapy, monitor ongoing Stimulants raise HR & BP — a positive cardiac history changes the plan before the first dose is ever given.
🧠 "Heart first, pill second." The exam trap is jumping straight to prescribing — the priority assessment is always the cardiac screen before therapy starts.

📈 Growth suppression — track every visit

%ile visits → baseline drifting down Height & weight percentile trend

Appetite suppression from stimulants can slow growth velocity. Monitor and report height/weight trends with the HCP at each visit — a crossing percentile line is the flag, not a single low number.

⚠️ Expected side effects to teach families

  • 🍽️ Loss of appetite & weight loss
  • 😴 Loss of sleep / insomnia
  • 🌀 Restlessness
  • 💓 Increased HR & BP
🧠 "WAR" — Weight/appetite loss · Appetite down · Restlessness + racing heart. Stimulant side effects mirror the drug's own name.

🔒 Controlled-substance status & the "drug holiday" concept

Methylphenidate and amphetamine salts are Schedule II controlled substances — high abuse/diversion potential, no automatic refills, prescriptions typically limited to a set supply and cannot be called in.

Drug holiday: a planned, HCP-directed medication-free period (e.g., weekends, school breaks, summer) sometimes used to let appetite/growth catch up and to reassess whether continued therapy is still needed. Practice varies by provider and patient — always an HCP decision, never a parent-initiated stop.

🧠 Never abruptly stop — even during a planned holiday, changes are directed by the prescriber, not self-titrated. Abrupt discontinuation of alpha-2 agonist non-stimulants (guanfacine/clonidine) specifically risks rebound hypertension — taper, don't stop cold.
🗣️

TEACH

STEP 3 · PATIENT & FAMILY EDUCATION

Timing prevents the worst side effect, and knowing the non-stimulant alternatives prevents an exam trap.

🌙 Dosing timing — protect sleep

Give doses EARLY in the day Avoid late-afternoon/evening dosing → protects sleep onset
🧠 A late dose = a wired brain at bedtime. Schedule the last daily dose early enough that stimulant effects wear off well before bedtime.

✅ What to teach at every visit

  • 📈 Track appetite & weight — report a declining growth curve
  • 💤 Report new or worsening insomnia
  • ❤️ Report chest pain, palpitations, or fainting immediately
  • 📚 Watch for improvement in school performance — expected therapeutic response
  • 🔒 Store securely — Schedule II, diversion risk in the household

🧭 Stimulant vs. non-stimulant — tell them apart

FeatureStimulantsNon-Stimulants
ExamplesMethylphenidate, amphetamine salts, dextroamphetamineAtomoxetine, guanfacine ER, clonidine ER
OnsetFast — hoursSlow — days to weeks for full effect
Controlled substanceYes — Schedule IINo
Key risksAppetite/growth suppression, insomnia, ↑HR/BPSedation, hypotension; alpha-2 agonists → rebound HTN if stopped abruptly
🧠 "Stim = Schedule II, Non-stim = no schedule." If a stem mentions abuse potential, refill restrictions, or diversion risk, the drug is a stimulant. If it mentions a slow onset over weeks and no abuse risk, it's a non-stimulant.

🔗 Clonidine & guanfacine — same drug class, more than one job

Clonidine and guanfacine are central alpha-2 agonists. In ADHD, extended-release forms calm the hyperactive-impulsive circuit. But clonidine specifically shows up on other pages of this course too — same mechanism, different indication each time:

🔗 See the Cardiovascular batch (NG-110) for clonidine's use in hypertension management, and the Pharmacology batch (NG-243) for its broader alpha-2 agonist profile — including use in opioid/alcohol withdrawal symptom control. Same drug, three different course units.
🧠 "Clonidine calms everything down" — blood pressure, withdrawal symptoms, and an overactive prefrontal-motor circuit all respond to the same central alpha-2 agonist effect: less sympathetic outflow.
⚡

QUICK RECALL

SAY IT OUT LOUD
💊 First-lineStimulants — methylphenidate & amphetamine salts, Schedule II
❤️ Screen firstCardiac history + baseline VS before the first dose
📏 TrackHeight/weight trend every visit — growth suppression risk
🧭 AlternativeAtomoxetine, guanfacine/clonidine ER — non-stimulant, no abuse risk
🎯 Cover & check — 4 rapid-fire questions
Q1: What must be assessed before starting a stimulant for ADHD?
Cardiac history — personal and family history of sudden cardiac death/arrhythmia, plus baseline BP, HR, and ECG if indicated.
Q2: What two growth parameters need ongoing monitoring on a stimulant?
Height and weight trends — report to the HCP if percentiles start declining.
Q3: When should the last daily dose be given, and why?
Early in the day, not in the evening — late dosing causes insomnia.
Q4: Name a non-stimulant option and one reason to choose it over a stimulant.
Atomoxetine or guanfacine/clonidine ER — chosen when there's a substance-use history, cardiac contraindication, or the family wants to avoid a controlled substance.