Drugs with abuse potential Flashcards
THC/Cannabis: Epidemiology
Most common abuse in high schoolers
Surpass tobacco usage
M > F
THC: Formulations
Traditional Marijuana – 10% THC
Hashish > 10%
Hash Oil – 50%
THC: Metabolism
Rapidly metabolized by liver to 11-OH-∆9 -THC, which is highly active in man.
Metabolized to 9-nor-COOH-THC which is inactive.
Metabolites excreted in urine and feces. They are detectable in urine for many days.
THC: Pharmacokinetics
Smoked it reaches brain in 15 to 30 seconds.
3-5 times more potent smoked than when ingested
Oral onset of action is about 30 min.
Metabolized and redistributed in fat
Slowly leaves body.
Duration of action 1 to 6 hours
Plasma half-life - 20-50 hours; 20% remains in body after 5 days and is not detectable at 30 days
THC: MoA
CB1 receptor: High in cerebellum hippocampus and basal ganglia, low in hypothalamus
CB2 receptor: Peripheral tissue
Negatively coupled to adenylyl cyclase via Gi – Inhibits transmitter release
Affinity for receptor correlates with psychoactive potency of cannabinoid agonists
THC: Effects
Euphoria, memory impairment, perceptual/motor alterations
CV (Tachycardia, orthostatic hypotension, angina)
Pulm (Bronchodilation, lung irritant, decrease alveolar macrophage activity, decrease in ciliary function)
Reproductive (Lowers testosterone/sperm, LHRH release decreased (low FSH and LH), prolactin release decreased in females (abnormal menstrual), hazard to marginally fertile)
Psychopathologic (Acute anxiety reaction, transient paranoia, exacerbation of schizophrenia, diffuse acute brain syndrome – clouding of consciousness and memory, perceptual and sleep disorders, amotivational syndrome)
THC: Withdrawal
Restlessness, irritability and mild agitation, sleep difficulties, decreased appetite and nausea, craving
THC: Medical Indications
Nausea, AIDS wasting syndrome – Dronabinol
MS pain tx. and cancer pain – THC/Cannabidiol mixture in Canada
Weight loss drug – CB1 antagonist, now removed from market
K2 or Spice
MoA
Legality/Scheduling
THC-like CB1 agonist activity
Not DEA scheduled
PCP/Ketamine: Pharmacokinetics
Rapid/complete absorption
Plamsa T1/2 12 to 24 hours (overdose up to 72 hours)
Hydroxylation and conjugation in liver
Excretion in urine, primarily as biotransformation products
PCP/Ketamine: Cardiovascular Effects
Tachycardia
HTN
Potentiation of catecholamines
PCP/Ketamine: CNS effects
Ketamine less potent, shorter duration
Small doses – Drunken state with numbness of extremities
Moderate doses – Analgesia and anesthesia
Psychic state – Resembles sensory isolation except sensory impulses reach neocortex
Catalepoid motor phenomenon
Large doses may produce convulsions
PCP/Ketamine: MoA
NMDA Antagonist
PCP: Overdose
CNS Manifestations: Anxiety, aggression, halucinations, dysphoria, convulsions, delirium
Sympathomimetic: Tachycardia, HTN crisis
PCP/Ketamine: Treatment
Vital sign support
Gastric suction
Acidify urine
Diazepam/Anti-HTN agent
Haloperidol
LSD - Indoleamine: Pharmacokinetics
Less than 1 % crosses Blood-Brain barrier
Onset -15 to 20 minutes, duration - 12 hours
LSD - Indoleamine: Effects
Sympathomimetic - Tachycardia, increased BP, psychomotor stimulation
Sensory and subjective effects
Altered perception - particularly visual
Lability of mood
Impaired judgment
Tolerance and cross tolerance
LSD-Indoleamine: Toxicity
Acute reactions
Hallucinations, anxiety, panic and depersonalization.
< than 24 hours
Quiet environment, BDZs for sedation
Flashbacks - days to years later, can be associated with drug use.
Neurotoxicity - 5-HT damage may be associated with phenethylamine type drugs such as MDMA
MDMA: Effects
Induces feelings of “well-being and connection”
Altered time perception
Pyschomotor stimulation, restlessness, bruxisim, anorexia, sweating, tremor
MDMA: Pharmacokinetics
Typical oral dose 100-150 mg
Onset of action 20 - 40 minutes; duration 3-4 hours
MDMA:
Hangover effect
Neurotoxic against which neurons
Hangover - anhedonia
Neurotoxicity - serotonin neurons
GHB: Endogenous pharmacology
Found in brain, precursor and metabolite of GABA
May have own receptor
Can be made in body from GBL
GHB: Pharmacokinetics
Typical dose about 1 - 1.5 g
Effects last about 3 hours
GHB: Effects
Primarily a depressant - induces a state of relaxation and tranquility
Interacts with ethanol
Overdose characterized by drowsiness, ataxia, nausea and vomiting
Higher doses - loss of bladder control, temporary amnesia, clonus and seizures.
Salvia Divinorum
Pharmacology
MoA
Pharmacokinetics
Pharmacology: Oral psychedelic
MoA: Kappa opiod agonist
Pharmacokinetics: Short duration of action – 20 to 45
Examples of “legal” drugs
Prescription Drugs
OTC drugs containing dextromethorphan
“Bath Salts”
Mephedrone
Stimulants found in Khat
Now scheduled
