Cannabis
Drugs of abuse
Drugs of abusePregnancy: avoid
Avoid in pregnancy. Use in pregnancy is linked to lower birth weight and preterm birth; THC reaches the fetus and breast milk, so use is discouraged in pregnancy and breastfeeding.
The plant Cannabis sativa; its main psychoactive compound, THC, acts on CB1 receptors. Widely used; medical-use products are regulated in Colombia.
Also called: Marijuana, Delta-9-tetrahydrocannabinol (THC), Cannabidiol (CBD, non-intoxicating)
Quick facts
- Group
- Drugs of abuse
- Target
- Cannabinoid receptor 1 (CB1); CB2 on immune cells
- Used for
- Medical-use cannabis · Clinical relevance
- Key effects
- Red eyes · Tachycardia and orthostatic dizziness
- Monitor
- Heart rate · Glucose in small children with ingestion
No doses: the clinician sets them by the current guideline.
Mechanism of action
The figure shows the human CB1 receptor with AM11542, a synthetic agonist built on the THC scaffold that occupies the same pocket; no structure with THC itself is available.
THC is a partial agonist at CB1 receptors, Gi-coupled receptors on presynaptic terminals in the cortex, hippocampus, basal ganglia and cerebellum. CB1 activation lowers cAMP, opens potassium channels and closes calcium channels, so less neurotransmitter is released; this changes memory, time perception, coordination and appetite, and indirectly raises dopamine in the reward circuit. CB2 receptors sit mainly on immune and blood cells.
- THC binds presynaptic CB1 receptors
- Gi signalling: less cAMP, K⁺ channels open, Ca²⁺ channels close
- Less transmitter release in memory, motor and reward circuits
- Euphoria, altered time, poor memory and coordination, appetite
Indications
- Medical-use cannabis and derivatives are licensed and regulated in Colombia (Ley 1787 de 2016); approved cannabinoid medicines include dronabinol for chemotherapy nausea
- Clinical relevance: acute cannabis toxicity, especially edibles in children, and cannabinoid hyperemesis syndrome Cannabis toxicity and cannabinoid hyperemesis syndrome →
- Clinical relevance: cannabis use disorder Cannabis use disorder →
Adverse effects
Common
- Red eyes, dry mouth and increased appetite
- Tachycardia and orthostatic dizziness
- Impaired short-term memory, attention and coordination (driving risk)
- Anxiety and panic, especially in first-time users
Contraindications
- Personal history of psychosis or schizophrenia
- Before driving or operating machinery
Key interactions
- Alcohol, benzodiazepines, opioids and other CNS depressants
- Additive sedation and impairment
- CYP2C9 and CYP3A4 inhibitors or inducers
- Inhibitors raise THC exposure; inducers lower it
- Sympathomimetics, anticholinergics and tricyclic antidepressants
- Additive tachycardia and blood pressure changes
- Warfarin and other highly protein-bound narrow-margin drugs
- Possible displacement; INR is watched
What is monitored
- Heart rate, blood pressure and level of consciousness
- Glucose in small children with ingestion
- Mental state: anxiety, psychosis, suicidal thoughts
- Electrolytes and kidney function in hyperemesis
Pregnancy and breastfeeding
Avoid in pregnancy. Use in pregnancy is linked to lower birth weight and preterm birth; THC reaches the fetus and breast milk, so use is discouraged in pregnancy and breastfeeding.
Nursing care
- Reassure and reduce stimuli in panic reactions
- Ask about edibles and other people affected when several children present at once
- Ask about hot-shower relief in recurrent vomiting (hyperemesis)
- Teach about delayed onset of edibles, driving risk and safe storage away from children
Pharmacokinetics
- Absorption
- Smoked: reaches the blood within minutes. Eaten: erratic, slow absorption with first-pass loss in the liver
- Distribution
- Very lipid-soluble and highly protein bound; stored in fat; crosses the placenta and into breast milk
- Metabolism
- Liver, by CYP2C9 and CYP3A4, to the active 11-hydroxy-THC and many other metabolites
- Elimination
- Mostly in the faeces, less in the urine; metabolites stay detectable for weeks in heavy users
- Half-life
- Long terminal half-life (about 25 to 36 hours) because it leaves fat slowly
- Onset and duration
- Seconds to minutes when smoked; half an hour to two hours when eaten, which leads people to take more
Test yourself
Think of the answer, then tap the question to see it.
Which receptor mediates the psychoactive effects of THC, and what G protein does it use?
CB1, a presynaptic Gi-coupled receptor that lowers neurotransmitter release.
Why do edibles cause more accidental intoxications than smoked cannabis?
Onset is delayed (half an hour to two hours), so people take more before feeling the effect, and children may eat them.
What is cannabinoid hyperemesis syndrome?
Cyclic nausea and vomiting in long-term heavy users, relieved by hot showers, which resolves only when cannabis is stopped.
Why are urine tests for cannabis positive for weeks after heavy use?
THC is stored in body fat and released slowly, so metabolites stay detectable long after the effect ends.
Connections
← Back to the class: Drugs of abuse
Educational content on how drugs work; not a prescribing guide and no substitute for a health professional's advice. No doses are given.
Sources: Guía para el Manejo de Emergencias Toxicológicas (Ministerio de Salud y Protección Social; Organización Panamericana de la Salud, 2017); Cannabis (Marijuana) (National Institute on Drug Abuse (NIDA), 2026); DailyMed - DRONABINOL capsule (DailyMed (U.S. National Library of Medicine), 2026); Cannabis medicinal - Medicamentos - INVIMA (Instituto Nacional de Vigilancia de Medicamentos y Alimentos (INVIMA), 2026).
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Representative model, for educational purposes only.
