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34 Cards in this Set

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  • Back
Marijuana is derived from?
Cannabis sativa
principal psychoactive component of marijuana
1-delta9-tetrahyrocannabinol (THC)--- Dronabinol is available as an oral prep.
synth. analog of THC with anti-emetic properties?

Also nantradol (not FDA approved)
~ THC content of one marijuana cigarette?
about 10-50 mg, with dose ranging from 5-25 mg.
Peak plasma level time?
10-30 min after smoking
Decay properties of marijuana?
two componenet cure. Initial redistribution to adipose (45 minutes), and then gradual metabolism of THC and elimination (t1/2 4 days).
Metabolism of THC
most in the liver, and many oxygenative metabolic products continue to have psychoactive effects.
Active Metabolites of THC?
11-hydroxy-THC, potency comparable to THC. Other less potent metabolits as well.
importance of oxygenated metabolites?
oral intake of THC and 'first pass' results in high 11-OH THC metabolites, while THC itself is in low concentration.
Excretion of THC
90% THC excreted in urin and feces within 5 days. Remaining metabolites take longer due to renal reabsorption, FA trapping, tissue distribution etc.
What does urinalysis look for?
THC and 9-carboxy metabolites.//

If recent use, then THC higher than 9-COOH. Slow excretion of 9-COOH allow detection of THC use for period of days to weeks.
Effects of single dose THC?
tachycardia (no change in BP though), euphoria (perceptual distortions, altered perceptions, NO hallucinations at this dose).

relaxation and sedation (unlike with LSD).//

psychomotor impairment: imparied STM, complex motor affected ie. driving, flying.

dry mouth, hunger, peripheral vasodilation (pink conjunctiva), bronchodilation.
effects of higher dose of THC?
confusion, disorganized thinking, hallucinations, delusions; euphoria turns to anxiety, panic and paranoia. More like to occur with ORAL admin. b/c of lack of control.
THC Mech of action?
CB1 and CB2 receptors. CB1 mainly in CNS, and CB2 periphery. They are similar to G protein coupled receptors.
Mech of action through CB receptors?
inhibit AC. CB1 present in high concentration in hippocampus and cortex, striatum and Nuc. Acc. Thus influencing memory, congnition, motor fxn, and reinforcement.
What are the endogenous ligands for CB-Rs?
Anandamide (arachidonly-ethanolamide), arachidonyl-glycerol.
Anandamide and arachidonyl glycerol ligands location and purpose???
anadamide, a lipid identified in brain and some peripheral tissues.//

arachidonyl-glyercol found in hippocampus.//

thought to function in extinction of learned fearful memories.//
Therapeutic use of THC?
reduction of intraocular pressure in glaucoma, chemotherapeutic drug induced vomiting (FDA approved; dronabinol and marijuana), pain relief?,
What's CB1 antagonist that reduces replase in chronic tobacco smokers and gives weight loss in obese subjects?
Rimonabant (not FDA approved yet)
Tolerance and dependance on marijuana?
slow dev'p of tolerance, weak cross-tolerance to Ethanol, not to LSD-like drugs. Little evidence of dependance.// Craving for THC after withdrawal from heavy use.//
Sxs from chronic marijuana use?
bronchitis, asthma, , possible role in lung cancer development, immune suppression, decreased gonadotropins and sex steroids, amotivational syndrome, severe memory loss.//
Lysergic acid diethylamide (LSD)
hallucinogen, synthetic drug. No therapeutic use. very potent, action duration upto 12 hours.
Effects of LSD?
somatic (1-2 hrs) dizziness, pupil dilation, weakness, tremor.//

perceptual (2-6 hrs): blurred vision, diff. focusing, altered awareness of colors, shapes, hallucinations.//

affective sxs: euphoria OR dysphoria, depression, fear paranoia. Panic (2-5 hrs) after 6 hrs, detachment.
LSD mode of action?
incompletely understood: partial agonist at 5HT2-R.
How are LSD effects reversed?
use 5HT2-R antagonists, and partially by AD D2-R antagonists.
What's Psilocybin
LSD related, from mushrooms.
Amphetamine analogues aka 'designer drugs'.
MDMA aka 'ecstasy'. Known as rave drug, general mood elevation.

Mescaline, related drug found in peyote cactus.
What happens with increaing bulk of substituents on aromatic ring of amphetamine?
causes a transition from amphetamine-like stimulation to LSD like hallucinogentic action.
Anticholinergic hallucinogens?
atropine, scopolamine. Especially in elderly pts.

**phenothiazines, with atropine-like side effects, contraindicated in treatment of anticholinergic delirium.
Phencyclidine (PCP)
synthetic drug, intended to be an anesthetic. 40% pts develop dysphoric rxn and some overt psychotic state. //

Ketamine is a related drug.
PCP Mech of action
PCP and ketamine are non-competitive channel blockers at NMDA-R, blocking influx of Ca.
Acute actions of PCP
taken orally or by smoking: intoxication in 2-5 min, blank stare, muscular rigidity, hypersalivation, sweating last upto 24 hrs. High doses: unpredictable, bizzare aggressive behaviour, comatose state for 4-6 hrs.
PCP Chronic uSe
difficulty thinking, memory deficit, speech impairment, intensify psychotic behavior in schizophrenics.
PCP Tx of OD.
symptomatic, talk-down not effective, Tx convulsions with diazepam, hypertension with hydralazine, and psychotic episodes with haloperidol. * avoid anticholinergic phenothiazines.//