drugs of abuse Flashcards
cannabis use disorder
a problematic pattern of cannabis use leading to clinically significant impairment or distress, as manifested by at least 2 of the following, occuring within a 12 month period
Cannabis is often take in larger amounts or over a longer period than was intended, there is a persistent desire or unsuccessful efforts to cut down or control cannabis use, a great deal of time is spent in activites to necessary to obtain cannabis, use cannabis or recover from its effects, cravign or strong desire or urge to use cannabis
cant do work obligations
marijuana
drug plant and hemp plant
THC- its gotten more potent,
CBD- precursor
CAnnabinol- low
mj pharmacokinetic
Rapidly metabolized by liver to 11 oh THC which is highly active in man, then metabolized to 9 nor COOH THC which is inactive
Metabolites excreted in urine and feces, they are detectable in urine for many days
smoked it reaches brain in 15-30 seconds, 3-5 times more potent smoked than when ingested oral onset of action is about 30 mins
Metabolized and redistributed in fat, slowly leaves body
duration of action 1-6 hours, t.5 20-50 hrs, 20% remains in body 5 days and is not detectable at 30 days, saliva can detect recent use 2-4 hrs
MOA of THC
CB1 receptor- unique distribution in brain, high densities in cerbellum hippocampus and basal ganglia, low in hypothalamus– CB2 in peripheral tissue
Negatively coupled to adenylyl cyclase via Gi, generally inhibits transmitter release
Affinity for receptor correlates with psychoactive potency of cannabinoid agonists, there are endogenous ligands for CB1 receptsor
endorphics
Endocannabinoids
bind to CB1 receptor
CB1 antagonist - rimonabant
diet drugs - produced depression and suicide
marijuana thc effects
euphoria, memory impairment, perceptual motor alterations, cardiovascular, pulmonary, reproductive, psychopathological
Drivign- legal blood levels are not there, and people will kill
marijuana effects on memory
impairs- digit symbot substitution, choice reation time, digit span, repeated subtactions, recal of material learned while hgh
marijuana cardiovascular and pulmonary effects
- tachycardia
- orthostatic hypotension
- exacerbate angina
- bronchodilation
- lung irritant
- decreases in alveolar macrophage activity and ciliary function, but no epidemiological evidence of increased infections
reproductive effect sof marijuana
lowers T and sperm counts, in rodents, gonadal weights are decreased, LHRH release is decreased, which decreases levels of FSH and LH
Prolactin release is decreased in females, greater incidence of abnormal menstrual cycles
hazard to marginal fertile
psychopathologically effects of marijuana
acute anxiety reaction, transient paranoid feelings, exacerbation of schizophrenia
Diffuse acute brain syndrome with high doses–clouding of consciousness and memory, perceptual and sleep disorders
Amotivational syndrome
tolerance and dependence marijuana
YES!, in frequent heavy users commonly reported symptoms associated with cessation of marijuana use include: Restlessness, irritability and mild agitation, sleep difficulties, decreased appetit and nausea, craving
Therapeutic use of THC
Control of nausea, AIDS wasting syndrom- Dronabinol- oral THC in sesame oil
Sativex THC cannabidiol miz MS pain treatment and cancer pain
Rimonabant CB1 antagonist- weight loss
MEdical marijuana
Treatment of seizures with Dravet and LEnnox Gastuat in 2 yrs old +
synthetic marijuana
K2 ro spice
legal
THC like CB1
ketamine and phencyclidine
anesthetics, psychological disturbance right after coming down
rapid and complete absorption, plasma t1/2 12-24 hours for phencyclidine, shorter for ketamine, longer in overdose
hydroxylation and conjugation in liver
excretion in urine primarily as metabolites
in an overdose drug excretion can be enhanced by acidifying the urine
pharmacology of ketamine and phencylidine
Autonomic and cardiovascular systm sympathomimetic: Tachycardia, Hypertension, Potentiation of catecholamines
Tolerance develops
CNS effects are complex and dose related, ketamine is less potent and has a shorter duration of action than PCP
Small doses- drunken state with numbness of extremities, moderate doses- analgesia and anesthesia, psychic state crudely resembles sensory isolation except that sensory impulses reach neocortex, cataploid motor phenomenon are observed, large doses may produce convulsions
Ketamine and phencyclidine MOA
non competetitve antagonist of NMDA receptor
Cation channel (when glutamate opens it–> neuron depolarization)
learning and memory
Esketamine for nasal antidepressant
Indoleamine and phenethylamine Hallucinogens
Indolamines are 5HT, essentionally LSD, Psilocin, DMT
DMT is ioasca
Phenelthylamines (MDMA, MEth, mescaline, amphetamine)
LSD
less than 1% crosses BBB, onset (15-20 minutes, duration 12 hours), Sympathomimetic - tachycardia, increased BP, psychomotor stimulation
Sensory and subjective effect- Altered perception (particularly visual), Lability of mood, impaired judgment
Sensory effects thought to be due to an action at 5HT2 receptors- agonist or partial agonis
Tolerance and cross tolerance
toxiccity of LSD
Acute reactions- hallucinations, anxiety, panic and depersonalization, < 24 hours, quiet environment, BDZs for sedation
Flashbacks days to years later, can be associated with drug use
Neurotoxicity- 5HT damage may be associated with phenethylamine type drugs such as MDMA
MDMA EX
induces feelings of well being and connection, altered time perception
Typical oral dose 100-150 mg
Onset of action 20-40 minutes, duration 3-4 hours
psychomotor stimulation, restlessness, bruxism, anorexia, sweating, tremor
Hangover- anhedonia, neurotoxicity- serotonin neurone
other abused substances ghb
GHB- essentially a metabolite of GABA and precursor, (can be made in body from GBL),
GHB- a depressant- a date rape drug, characterized by drowsiness, loss of bladder control, temproray amnesia, clonus
toluene ethyl acetate
huffing glue- bone marrow depression
legal drugs
opioids, fentanyl, otc dextromethophan , bath salts
