Consistent with 交大附小

  • Depressants (Opioids, Benzodiazepines)
    • Key Sign: Miosis (pinpoint pupils) is the hallmark of opioid (e.g., heroin, fentanyl) overdose.
    • Mechanism: Potent stimulation of the parasympathetic nervous system.
    • Other: Benzodiazepines are less consistent; pupils may be normal or dilated.
  • Stimulants (Cocaine, Amphetamines)
    • Key Sign: Mydriasis (dilated, poorly reactive pupils).
    • Mechanism: Sympathetic nervous system activation (“fight-or-flight” response).
  • Hallucinogens (LSD, PCP, Psilocybin)
    • LSD/Psilocybin: Mydriasis (dilated pupils) due to sympathomimetic effects.
    • PCP (Phencyclidine): Nystagmus (horizontal, vertical, or rotatory) is the classic and most specific sign. Pupils can be of any size.

Tip

  • Depressants:
    • Alcohol: Enhances GABA-A receptor activity; inhibits glutamate.
    • Opioids: Activate mu, kappa, delta opioid receptors.
    • Benzodiazepines: Enhance GABA-A (increase frequency of Cl- channel opening).
    • Barbiturates: Enhance GABA-A (increase duration of Cl- channel opening); direct Cl- channel opening.
    • Inhalants: General CNS depression (often via GABA enhancement/NMDA inhibition).
  • Stimulants:
    • Amphetamines: Increase release & block reuptake of dopamine (DA), norepinephrine (NE), serotonin (5-HT).
    • Cocaine: Block reuptake of DA, NE, 5-HT; Na+ channel blockade.
    • Bath Salts: Inhibit reuptake of DA, NE, 5-HT (variable).
    • Caffeine: Adenosine receptor antagonist.
    • Nicotine: Activates nicotinic acetylcholine receptors (nAChRs).
  • Hallucinogens:
    • Cannabinoids (THC): Partial agonist at CB1 & CB2 receptors.
    • LSD: Agonist at 5-HT2A serotonin receptors.
    • MDMA (Ecstasy): Increases release & blocks reuptake of 5-HT >> DA, NE.
    • PCP: NMDA glutamate receptor antagonist.
    • GHB: Agonist at GHB receptors & weak GABA-B agonist.

Stimulants


Warning

Stimulants can trigger substance-induced psychosis, especially in individuals with high-dose, daily use, and/or other risk factors for psychosis.

Decreased appetite and insomnia are the most common adverse effects of stimulant medications

Caffeine

  • Has MAOI effects → ↑ levels of epinephrine, norepinephrine, serotonin, and dopamine

Nicotine

  • Effects of caffeine + opioids receptor

Smoking cessation

  • Varenicline
    • Nicotine receptor (alpha-4-beta-2 nACHR) partial agonist
    • Reduces positive symptoms, cravings, and withdrawal symptoms
  • Bupropion
    • Reduces craving and withdrawal symptoms

Mnemonic

Varenicline helps to quit nicotine.

Amphetamines

  • Substances
    • Alpha-methylphenethylamine (“speed”)
    • Methamphetamine (“meth,” “crank”)
    • 3,4-Methylenedioxymethamphetamine (“MDMA,” “ecstasy,” “molly”)
    • Cathinone (“bath salts”)
  • Mechanism of action: ↑ release and ↓ reuptake of presynaptic monoamine neurotransmitters (e.g., adrenaline, norepinephrine, serotonin, and dopamine)
    • Central effect: CNS sympathetic stimulation and hallucinogenic effectsPeter trying meth
  • Peter trying methPeter trying meth
  • Clinical features
    • Vitals: Marked tachycardia, severe HTN, hyperthermia, tachypnea.
    • Exam: Mydriasis, profuse diaphoresis (distinguishes from anticholinergics), tremor, hyperreflexia.
    • Neuropsychiatric: Psychomotor agitation, paranoia, delirium, tactile hallucinations (formication / “meth bugs”), bruxism.
    • Chronic signs: Severe dental caries (“meth mouth” secondary to xerostomia and bruxism), skin excoriations/picking (caused by hallucination of “meth bugs”), dilated cardiomyopathy. c
    • Withdrawal: Depressed mood, severe suicidal ideation (“the crash”), hypersomnia, hyperphagia, vivid dreams.
  • Indication: ADHD

Synthetic cathinone

  • Pathophysiology: Synthetic amphetamine analog (“bath salts”, MDPV, mephedrone); massive release and reuptake inhibition of NE, DA, and 5-HT.
  • Clinical Presentation:
    • Psychiatric: Prolonged violent combativeness, severe delirium, paranoia, hallucinations, bizarre behavior; symptoms last days to weeks (vs. hours for cocaine/PCP). c
    • Sympathomimetic Toxidrome: Tachycardia, severe HTN, hyperthermia, mydriasis, diaphoresis, tremors, seizures.
  • Diagnosis:
    • Key Board Clue: Routine UDS is NEGATIVE (standard immunoassays do not detect synthetic cathinones). c
    • Key Labs: ↑ Serum CK (screen for rhabdomyolysis), BMP (renal function/electrolytes), ECG/Troponin (ischemia/arrhythmias).
  • Differential Diagnosis:
    • PCP: Diff by nystagmus (rotatory/horizontal/vertical) and (+) routine UDS.
    • Cocaine: Diff by (+) routine UDS and rapid resolution (1–2 hrs).
    • Anticholinergic Toxicity: Diff by dry skin (anhidrosis) and absent bowel sounds (cathinones cause diaphoresis).
    • Serotonin Syndrome: Diff by neuromuscular hyperactivity (clonus, hyperreflexia).
  • Management:
    • 1st-line: IV Benzodiazepines (e.g., lorazepam) high-dose for agitation, seizures, HTN, and hyperthermia.
    • Supportive Care: Aggressive active cooling for hyperthermia + IVF hydration to prevent rhabdomyolysis-induced AKI.
    • Refractory Agitation: Propofol or dexmedetomidine with endotracheal intubation.
    • Contraindication/Avoid: Haloperidol/antipsychotics (lowers seizure threshold, worsens hyperthermia, prolongs QTc).
  • Complications: Rhabdomyolysis → AKI, malignant hyperthermia, status epilepticus, arrhythmias/MI, trauma, DIC.

Cocaine

  • Famously was the “Coca” in Coca-Cola
  • Clinical features
    • Clinical features of stimulant intoxication, e.g., sympathomimetic toxidrome, euphoria
    • Chest pain and/or angina due to cocaine-induced coronary vasospasm
  • Complications
    • Nasal pathology
      • Nasal inhalation can damage nasal blood vessels and result in epistaxis.
      • Chronic local vasoconstriction may cause ischemic necrosis and perforation of the nasal septum.

Tip

Withdrawal from stimulants will not cause morbidity or morality. However, withdrawal from depressants like benzodiazepines or alcohol will. Common withdrawal symptoms:

  • Increased appetite, hypersomnia, fatigue, intense psychomotor retardation, severe depression (“crash”)

Depressants


Alcohol

Alcohol use disorder Alcohol withdrawal

Opioids

Opioid Intoxication, Withdrawal, and Use Disorder

Benzodiazepines

  • Benzos increase the FREQUENCY of chloride channel opening
  • Barbiturates increase the DURATION of chloride channel opening

Mnemonic

Ben wants it to happen more often (frequency) Barbie wants it to last longer (duration)

Inhalants

Hallucinogens


Cannabis

Phencyclidine (PCP)

  • Street names: angel dust, peace pill, elephant tranquilizer, hog
  • Mechanism of action
  • Clinical features
    • Violence
      • K 粉 -> Kick
    • Rotary nystagmus
    • impulsivity, psychomotor agitation, tachycardia, hypertension, analgesia, psychosis, delirium, seizures.

Mnemonic

Phencyclidine -> Rotary nystagmus