Cannabis, Stimulants & Hallucinogens
Psychiatry · Substance Use · lean revision notes
Cannabis, Stimulants & Hallucinogens
A compact, exam-focused tour of three drug classes that NEET PG loves to test through "spot the toxidrome", withdrawal contrasts, and one-liner facts. The recurring traps are: cannabis withdrawal is real but has no approved pharmacotherapy, stimulant intoxication produces a sympathomimetic crisis (avoid pure beta-blockers), and hallucinogens give you HPPD/flashbacks with grossly preserved insight.
Quick overview & classification
These three groups are pharmacologically distinct, and the questions hinge on telling them apart.
| Class | Prototype agents | Receptor / mechanism | Dominant clinical picture |
|---|---|---|---|
| Cannabinoids | Cannabis (marijuana, ganja, charas/hashish, bhang), synthetic "spice"/K2 | CB1 (CNS) & CB2 (immune) agonism; Δ9-THC is the psychoactive component | Euphoria, conjunctival injection, increased appetite, tachycardia, time distortion |
| Stimulants | Cocaine, amphetamine, methamphetamine, MDMA, methylphenidate | ↑ synaptic dopamine/noradrenaline/serotonin (cocaine blocks reuptake; amphetamine forces release) | Sympathetic overdrive: mydriasis, hypertension, hyperthermia, psychosis |
| Hallucinogens | LSD, psilocybin (magic mushrooms), mescaline, PCP, ketamine | LSD/psilocybin = 5-HT2A agonism; PCP/ketamine = NMDA antagonism | Perceptual distortions, hallucinations with retained insight (classic hallucinogens) |
High-yield: Δ9-tetrahydrocannabinol (THC) is the active ingredient of cannabis; cannabidiol (CBD) is non-psychoactive and is being studied for its anti-psychotic/anti-epileptic potential (approved as cannabidiol for refractory paediatric epilepsy).
Cannabis
Pharmacology & pathophysiology
Cannabis acts via the endocannabinoid system. Δ9-THC is a partial agonist at CB1 receptors, densely expressed in the basal ganglia, hippocampus, and cerebellum — explaining impaired memory, altered time perception, and motor incoordination. CB1 receptors are notably sparse in the brainstem, which is why cannabis has an extremely high therapeutic index and respiratory depression / fatal overdose is essentially unheard of (a frequent MCQ contrast with opioids).
Acute intoxication
Behavioural → euphoria, relaxation, heightened sensory perception, slowed time sense, intensified appetite ("the munchies"), and impaired short-term memory & reaction time.
Physical signs:
- Conjunctival injection (red eyes) — a classic exam giveaway
- Tachycardia (sympathetic), dry mouth
- Increased appetite, mild incoordination
- Pupils usually normal (not dilated) — a key distinguishing point from stimulants/hallucinogens
High-yield: Conjunctival congestion + tachycardia + increased appetite + normal pupils = cannabis intoxication.
Cannabis-induced psychosis
Acute high-dose use can precipitate a transient paranoid psychosis with persecutory delusions and anxiety/panic. Heavy adolescent use is an independent risk factor for later schizophrenia, with a dose-response relationship; high-potency THC strains and early age of onset increase risk.
Amotivational syndrome
Chronic heavy use is linked to apathy, anergia, loss of drive/ambition, blunted goal-directed behaviour, social withdrawal, and poor academic/occupational performance. Though its validity is debated, NEET PG treats it as a recognised consequence of chronic cannabis use — recognise the description.
Cannabis withdrawal
Once denied to exist, withdrawal is now a defined DSM-5 syndrome appearing ~24–72 h after cessation in chronic users:
- Irritability, anger, anxiety
- Sleep disturbance with vivid/disturbing dreams
- Decreased appetite, weight loss
- Restlessness, depressed mood
- Physical: tremor, sweating, headache, abdominal pain
High-yield: There is no approved pharmacotherapy for cannabis withdrawal — management is supportive/symptomatic (reassurance, sleep hygiene, short-term symptomatic measures). This is among the most repeated cannabis facts in NEET PG.
Cannabinoid hyperemesis syndrome (CHS)
Chronic heavy users present with cyclical vomiting relieved by hot-water baths/showers — a distinctive, increasingly tested pattern. Definitive treatment is cessation of cannabis; topical capsaicin and supportive antiemetics help acutely.
Stimulants (Cocaine & Amphetamines)
Mechanism
- Cocaine blocks reuptake of dopamine, noradrenaline and serotonin → flooding of synapses. It is also a local anaesthetic (Na⁺ channel blockade) — the only one that is a vasoconstrictor.
- Amphetamines/methamphetamine force release of catecholamines and block reuptake; longer duration than cocaine (hours vs ~30–90 min).
- MDMA (ecstasy) preferentially releases serotonin → empathogenic effects and risk of serotonin syndrome/hyperthermia/hyponatraemia.
Stimulant toxidrome (sympathomimetic)
Eyes → mydriasis (dilated pupils) | CVS → tachycardia, hypertension, arrhythmias | CNS → agitation, euphoria, psychosis, seizures | Skin → diaphoresis, hyperthermia.
| Feature | Sympathomimetic (stimulant) | Anticholinergic |
|---|---|---|
| Skin | Sweaty (diaphoretic) | Dry, flushed |
| Bowel sounds | Present/increased | Absent |
| Pupils | Dilated | Dilated |
| Temperature | High | High |
| Mucous membranes | Moist | Dry |
High-yield: Both stimulant and anticholinergic toxidromes give dilated pupils + hyperthermia + agitation. The discriminator is sweating and bowel sounds — present in sympathomimetic, absent in anticholinergic.
Cocaine-specific signs
- Nasal septal perforation (snorting → chronic vasoconstriction & ischaemia)
- Formication / "cocaine bugs" (delusional parasitosis — Magnan's sign)
- Myocardial infarction in young patients with normal coronaries (coronary vasospasm + thrombosis)
- "Crack lung", pneumomediastinum
- "Body packers/stuffers" — surgical/expectant risk of catastrophic overdose if packets rupture
Stimulant withdrawal ("the crash")
In stark contrast to the dramatic intoxication, withdrawal is psychological and dysphoric, not life-threatening:
- Profound dysphoria/depression, fatigue, hypersomnia
- Vivid, unpleasant dreams
- Increased appetite
- Psychomotor retardation or agitation
- Intense craving and suicidal ideation (the dangerous component)
High-yield: Stimulant (cocaine/amphetamine) withdrawal = depression, hypersomnia, hyperphagia, vivid dreams, craving. Watch for suicide risk; there is no specific approved pharmacotherapy — treatment is supportive with monitoring for depression/suicidality.
Management of stimulant intoxication / hypertensive crisis
Stepwise approach:
1) Benzodiazepines first (lorazepam/diazepam) → calms agitation, controls seizures, lowers BP & heart rate, reduces hyperthermia. First-line for nearly everything. 2) Active cooling for hyperthermia (a leading cause of death). 3) Persistent hypertension/chest pain → vasodilators: nitroglycerin, phentolamine (alpha-blocker), or calcium channel blockers. 4) Supportive: IV fluids, monitor for rhabdomyolysis (CK, renal protection), correct electrolytes.
High-yield: In cocaine-associated hypertensive crisis/chest pain, avoid unopposed beta-blockers. Blocking β leaves α-mediated vasoconstriction unchecked → "unopposed alpha effect" worsening hypertension and coronary vasospasm. Use benzodiazepines + nitrates/phentolamine/CCB instead. This is one of the single most tested management facts in this topic.
High-yield: First-line drug for stimulant-induced agitation, seizures, hyperthermia and hypertension is a benzodiazepine.
Hallucinogens
Mechanism & types
- Classic (serotonergic) hallucinogens: LSD, psilocybin, mescaline, DMT → potent 5-HT2A receptor agonists.
- Dissociatives: PCP (phencyclidine), ketamine → NMDA glutamate receptor antagonists → dissociation, analgesia, and, with PCP, violent behaviour and nystagmus.
LSD intoxication
- Perceptual distortions: vivid visual illusions, intensified colours, synaesthesia (e.g., "hearing colours"), distorted body image, depersonalisation/derealisation
- Markedly dilated pupils, tachycardia, hypertension, tremor, hyperthermia
- Insight characteristically RETAINED — the patient knows the experiences are drug-induced (key contrast with primary psychosis)
- Extraordinarily high therapeutic index — death from direct toxicity is rare; harm comes from accidents/behaviour during a "bad trip"
High-yield: Classic hallucinogen (LSD) intoxication = perceptual distortions + dilated pupils + preserved insight + no physiological dependence/withdrawal. There is no significant physical withdrawal syndrome and tolerance develops rapidly (tachyphylaxis).
"Bad trip" management
Reassurance and "talking down" in a calm, low-stimulation environment is first-line. For severe agitation/anxiety use benzodiazepines; antipsychotics (haloperidol) are reserved for severe agitation/psychosis but may lower seizure threshold and worsen anticholinergic load.
Flashbacks & HPPD
- Flashbacks = spontaneous, transient recurrence of perceptual experiences after the drug has cleared, sometimes weeks–months later, often triggered by stress, fatigue or cannabis use.
- Hallucinogen Persisting Perception Disorder (HPPD) is the DSM-5 diagnosis when these re-experienced perceptual symptoms (e.g., trailing images, halos, geometric hallucinations) are persistent/distressing and cause functional impairment, with retained insight and no other medical cause.
High-yield: HPPD/flashbacks are most classically associated with LSD. Insight is retained — this is NOT psychosis. There is no firmly established treatment; benzodiazepines and sometimes clonidine/anticonvulsants are tried.
PCP — the dangerous dissociative
Distinguish from classic hallucinogens:
- Violent, agitated, unpredictable behaviour; markedly reduced pain sensitivity
- Rotatory/vertical-horizontal nystagmus (almost pathognomonic in the intoxicated patient)
- Hypertension, hyperthermia, muscle rigidity, rhabdomyolysis, seizures
- Management: minimise sensory stimulation, benzodiazepines for agitation, cooling, supportive care
| Feature | LSD/psilocybin (classic) | PCP/ketamine (dissociative) |
|---|---|---|
| Receptor | 5-HT2A agonist | NMDA antagonist |
| Behaviour | Inward, perceptual trips | Violent, dissociated |
| Nystagmus | Absent | Present (PCP) |
| Analgesia | No | Yes (marked) |
| Insight | Usually retained | Often lost |
Putting it together — the intoxication snapshot
A rapid mental flow for the MCQ stem: Red eyes + munchies + normal pupils → cannabis. Dilated pupils + sweaty + hypertensive + agitated → stimulant. Dilated pupils + perceptual distortions + insight intact → LSD. Dilated pupils + nystagmus + violent + analgesic → PCP.
| Drug | Pupils | Key sign | Overdose lethality | Withdrawal |
|---|---|---|---|---|
| Cannabis | Normal | Red conjunctivae, ↑appetite | Negligible | Mild, no pharmacotherapy |
| Cocaine/amphetamine | Dilated | Diaphoresis, ↑BP, hyperthermia | High (MI, hyperthermia, seizures) | Crash: depression, hypersomnia, craving |
| LSD | Dilated | Synaesthesia, insight retained | Very low | None significant (rapid tolerance) |
| PCP | Dilated | Nystagmus, violence, analgesia | Moderate–high | Mild |
Key differentials
- Cannabis-induced psychosis vs schizophrenia: Substance-induced psychosis resolves with abstinence and is temporally linked to use; persistent psychosis beyond a month of abstinence points to a primary disorder.
- Stimulant intoxication vs anticholinergic poisoning: sweating + bowel sounds present in stimulants (see table); anticholinergic = dry, flushed, "mad as a hatter, hot as a hare, dry as a bone".
- Stimulant intoxication vs mania: mania lacks dilated pupils, diaphoresis, hyperthermia and a urine drug screen distinguishes.
- Hallucinogen intoxication vs primary psychosis: classic hallucinogens preserve insight; primary psychosis does not.
- Serotonin syndrome (esp. MDMA): clonus, hyperreflexia, hyperthermia, autonomic instability → cyproheptadine + supportive cooling.
Mnemonics & eponyms
- Sympathomimetic vs anticholinergic — "Sympathomimetic = Sweaty (wet) skin; anticholinergic = dry." (Bowel sounds present in the former.)
- Cocaine triad to remember: MAN — Mydriasis, Arrhythmia/MI, Nasal septum perforation.
- Magnan's sign — formication ("cocaine bugs") of chronic cocaine use.
- CB1 spares the brainstem → no fatal respiratory depression with cannabis.
Recently asked / exam angle
- "No pharmacotherapy for cannabis withdrawal" — direct one-liner; management is symptomatic/supportive only.
- Unopposed alpha effect — why pure beta-blockers (propranolol) are contraindicated in cocaine-induced hypertension/chest pain; benzodiazepines + nitrates/phentolamine are preferred.
- First-line drug for stimulant intoxication/agitation/seizure = benzodiazepine.
- Conjunctival injection + increased appetite = cannabis intoxication.
- HPPD / flashbacks linked to LSD, with retained insight.
- Amotivational syndrome description matched to chronic cannabis use.
- Nystagmus + violent behaviour + analgesia = PCP.
- THC = active component; CBD = non-psychoactive.
- Stimulant withdrawal = depression/hypersomnia/craving with suicide risk, not autonomic storm.
- Cannabinoid hyperemesis syndrome — relief with hot showers, treat by cessation.
Rapid revision
- Δ9-THC is the psychoactive cannabis component; CBD is non-psychoactive.
- Cannabis intoxication: red eyes, tachycardia, ↑appetite, NORMAL pupils, time distortion.
- Cannabis has no fatal overdose — CB1 receptors are sparse in the brainstem.
- Cannabis withdrawal exists but has NO approved drug treatment — supportive care only.
- Amotivational syndrome = apathy/anergia/loss of drive in chronic heavy cannabis users.
- Cannabinoid hyperemesis = cyclical vomiting relieved by hot baths; treat by stopping cannabis.
- Stimulant toxidrome = dilated pupils, sweating, hypertension, hyperthermia, psychosis, seizures.
- Avoid unopposed beta-blockers in cocaine toxicity (unopposed alpha) — use benzodiazepines + nitrates/phentolamine.
- First-line for stimulant agitation/seizures/hyperthermia/hypertension = benzodiazepine.
- Stimulant withdrawal = crash: depression, hypersomnia, hyperphagia, craving, suicide risk.
- LSD = 5-HT2A agonist; intoxication shows synaesthesia, dilated pupils, and retained insight.
- HPPD/flashbacks classically follow LSD; PCP (NMDA antagonist) gives nystagmus, violence and analgesia.