Terms Flashcards
Tetrahydrocannabinol
delta-9-tetrahydrocannabinol (THC) is the main
psychoactive component of cannabis
Cannabidiol
CBD comes from hemp plant not cannabis
Medicinal effects but does not produce a high
treats epilepsy and anxiety
Motivational model
Evolution resulted in survival circuitry. Motivational model-continue to remind us to keep getting those things that are important/ rewarding.
Seen in cocaine addiction when an individual is in a drug-withdrawn state and makes brain vigilant for signs of drug
Prevention Principle #10
Community Programs, principle 10 combining 2 plus effective programs can be more effective than a single program alone.
Family based and school based programs
Entactogen
substances that allow or promote a touching within or reaching inside to retrieve repressed memories
Brain disease model
addiction is considered a brain disorder because it involves functional changes to brain circuits involved in reward, stress, and self control. Adduction is preventable and treatable.
Addiction is chronic and progressive, user does not have control after a certain point.
Wernicke-Korsakoff Syndrome
long term effects of alcohol use
Caused by a deficiency of thiamine (a B vitamin) because alcohol interferes with the way the body absorbs B vitamins.
mental confusion lack of coordination, may have memory and learning problems.
Dopamine
Dopamine is a neurotransmitter that plays a role in pleasure, motivation, and learning.
Cocaine blocks the removal of dopamine from the synapse by binding to the dopamine transporters
Factors that affect BAC
how quickly you drink, body weight, food, gender, type of drink consumed
Pharmacokinetics
What the body does to the drug in terms of absorption, distribution, and elimination. Drugs that reach the brain more quickly are more addictive (inhalation)
Pharmacodynamics
What the drug does to the body. The interaction between a drug and the receptors responsible for the action of the drug in the body. Agonists bind to active site and activate receptions (nicotine)
Developmental risk at 5 domain levels
Individual- early aggressive behavior
Family- lack of parental supervision
Peer- Substance use
School- drug availability
Community- Poverty
protective factors at 5 domain levels
Individual- impulse control
Family- parental monitoring
Peer- academic competence
School- anti-drug use policies
Community- strong neighborhood attachment
Narcan
Nasal spray for opioid overdose which increases breathing rate. Opioid receptor antagonist on mu receptor
still need medical attention
Bio-psycho-social model of addiction
bio- physical health, withdrawal symptoms, drug effects, genetic vulnerabilities
psycho- paired stimuli/ triggers, routines/habits, stress management skills, coping skills
social- peers, family/ partners, cultural norms, circumstances
Four main brain circuitries/systems and corresponding primary brain regions
Reward circuitry (VTA nucleus accumbens), memory circuitry (hippocampus and amygdala), motivation drive salience circuitry (orbital-frontal cotex), cognitive control (anterior cingulate cortex)
Controlled Substances Act criteria
Drugs are placed into 5 groups or schedules based on medical use and potential for abuse. Currently run by the drug enforcement administration (DEA)
Schedule 1- high potential for harmful use, no medical treatment
5 A’s of smoking cessation
Ask about tobacco use
advise to quit
assess willingness to make quit attempt
assist in a quit attempt
arrange follow up
3 types of prevention and scenarios
universal program- designed for general population (all students in a school)
selective program- targets groups at risk or subsets of the general population (children of drug users)
indicated program- for individuals already experimenting with drugs
incentive salience
neurobiology of addiction- cravings
drug liking vs drug wanting
stimulus response learning
substance use becomes habitual/ compulsive. Based on Pavlovian theory
inhibitory control dysfunction
impulsivity and disruption is the stop circuitry
self-medication hypothesis
specific form of negative reinforcement, substance of choice is not chosen at random. comes from the motivational model based on skinners operant conditioning
behavioral economic/reinforcer pathology
reward value of a substance, involves more of a social environmental component
negative & positive reinforcement
positive- for dopamine effect
negative- to take away withdrawal, self-medication hypothesis
How cocaine works on the dopamine reward system in the brain:
what cocaine does at the synapse, neuroadaptations that may occur as a result
Cocaine blocks the removal of dopamine from the synapse by binding to the dopamine transporters. Long term- down regulation of receptors, neurons are regulating by removing receptors which leads to tolerance
How cocaine works on the dopamine reward system in the brain:
what happens within the 4 brain circuits with chronic use
in rewards circuits, there is less euphoria to the drug and reduced sensitivity to natural rewards
motivation systems- orbital frontal cortex is more active proportional to drug craving
frontal areas are less active less inhibition less planful
Memory- hippocampus lays down memories of this rapid sense of satisfaction and the amygdala creates a conditioned response to certain stimuli
How cocaine works on the dopamine reward system in the brain:
what happens even after use has stopped (e.g., in a state of withdrawal) in the brain circuits (think “survival circuitry”)
Survival circuitry becomes less and less sensitive to natural rewards and only responds to drug.
Less cortical activity less planning
As if survival depends on the drug
How cocaine works on the dopamine reward system in the brain:
what happens in response to natural rewards after chronic use
Abnormally inactive when it comes to encountering natural rewards and hyperactive to drug
How cocaine works on the dopamine reward system in the brain:
what happens to motivational circuits
motivational circuitry is hypoactive when it comes to encountering natural rewards and hyperactive to drugs
How cocaine works on the dopamine reward system in the brain:
what happens to the frontal lobe
Long term, frontal areas become less active
cocaine users have lower frontal lobe activity
Arguments for and against prescription of opioids
medical use- analgesia (pain relief), severe diarrhea, cough suppressant, maintenance therapy of opioid dependence.
chronic pain from surgery injury or illness
against- highly addictive, activates opioid receptors in brain
has depressant effects and creates strong euphoria
Health risks, respiratory depression, confusion, tolerance, physical dependence. In seniors long term use increases likelihood of falls
drowsiness, constipation, euphoria, nausea, vomiting and slowed breathing
risk of overdose and death
The article we read by McCabe et al (2005) found that non-medical prescription of stimulants is more prevalent among particular sub-groups of USlow college students. What are the 6 characteristics of these high-risk subgroups? Offer an opinion as to why any of these subgroups may have the highest rates of prescription stimulant misuse.
perscription stimulants were higher among college students who were male, white, members of fraternities, lower grade point average, located in north eastern region, who attended more selective colleges
Considering the pharmacokinetics of cannabis, why might emergency departments commonly report hospital visits due to cannabis intoxication resulting from edibles
ingestion has delayed effects as compared to inhalation, more will be consumed in a shorter amount of time. Complicated dosing and manufacturing inconsistencies. May seem appealing to children.
Difficult to only eat a portion of a cookie
