General drugs and cannibis Flashcards
What are the general pharmacodynamics of drugs?
- dopaminergic neurones from VTA are stimulated to release DA (reward) into NAcc
what are the methods of admin of drugs? how fast are they?
- intranasal (mucous membranes of nasal sinus = slow)
- oral = very slow
- inhalational = rapid
- intravenous = rapid
what is the fastest route to the brain? Why?
- inhalation
- pulmonary circuit is very short wherease IV must do systematic circuit before accessing the brain
what are the classifications of drugs?
- narcoitics (painkillers): opiate like drugs e.g. Heroin
- depressants e.g. alcohol, benzodiazepines
- stimulants e.g. cocaine, amphetamine, caffeine
- miscellaneous e.g. cannabis, ecstasy (drugs have effects from multiple classes)
describe the methods of admin in ascending order of onset of euphoria
- oral
- intranasal
- IV
- inhalational
what are cannibis, hashish and hash oil?
- cannabis = plant
- hasish/resin = trichomes
- hash oil = solvent extract
what does cannabis contain?
- over 400 compounds
- >60 are cannabinoids
what do the positives aspects of smoking weed come from?
- from cannabidiol
- balance between cannabidiol vs delta9-THC
what is the most potent cannabinoid?
delta9-THC
how has the dosing of cannabis changed throughout the years?
- in 60’s was 10mg of THC
- now it is 150-300mg of THC
- inc. potency
- delta9-THC and cannabidiol inc.
- negative effects are more pronounced than positive
what are the routes of admin of cannabis?
- oral (5-15% THC delivered): delayed onset, first pass metabolism
- inhalation (25% THC delivered)
why does cannabis slowly accumulate in body?
- very lipid soluble
- builds up as fattu acid conjugates
- takes 30 days for effects to cease on body
describe the metabolism of cannabis
- liver converts THC –> 11-OH-THC (more potent)
- GIT excretes 65%
- much of THC undergoes enterohepatic recycling due to lipid solubility
- urine excretes 25%
describe the plasma conc vs degree of intoxication of cannabis
- THC much more concentrated in brain matter than in blood as very lipid soluble
- leads to poor correlation b/ plasma cannabinoid conc and degree of intoxication
where are the cannabis receptors located?
Brain - CB1R (hippocampus, cerebellum, cortex and basal ganglia)
Peripheral: CB2R (immune cells)
describe the cannabis receptor
inhibitory GPCR linked to AC
what is the body’s version of THC?
endogenous anadamide
describe how cannabis causes euphoria
- stimulation of Gi CB1 receptor
- inhibits release of GABA
- disinhibition
- inc. release of dopamine by inhibiting the inhibition of release of DA
describe how cannabis causes psychosis and schizophrenia
- one target is ACC
- ACC involved in performance monitoring with behavioral adjustment
- cannabis causes hypoactivity in ACC
how does cannabis act to inc. hunger?
2 actions on lateral hypothalamus:
- presynaptic inhibition of GABA –> inc. MCH neuronal activity
- inc. orexin production
how does cannabis cause immunosuppression?
depress immune system by agonising CB2Rs on macrophaes, mast cells, B cell, T cell, NK cell
what are the general central effects of cannabis?
- psychosis, schizophrenia
- food intake
- memory loss (limbic regions)
- psychomotor performance (cerebral cortex)
what are the peripheral effects of cannabis?
- immunosuppressant
- tachycardia/vasodilation via TRPV1 receptors ( not CBRs) –> leads to red eyes as conjuctiva vasodilate
why is it impossible to overdose on cannabis?
- medulla has a LOW CB1R expression
- means cardio-resp centre is not affected much
when is there an upregulation of CBRs?
- MS/pain/stroke patients (to regulate pain)
- fertility/obesity (pathological and may contribute to obesity/infertility)
how do drugs influence levels of delta9-THC?
- autoprotection: dronabinol/nabilone inc. levels and are anti-emetics in cancer, sativex treats MS pain
- autoimpairment: rimonabant dec. delta9THC, blocks feeling of hunger so anti-obesity
