Week 12 Substance Abuse Flashcards Preview

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Flashcards in Week 12 Substance Abuse Deck (102)
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What can you tell me about the effects and uses of Hallucinogens?

*LSD, psilocybin mushrooms, DMT (“Ayahuasca”), mescaline (peyote), 2CB, 25i-NBOMe

*Agonists at 5HT-2a receptor

*Tolerance develops, but addiction extremely rare

*Traditional used in mystical practises; use in 1950s and 1960s for treatment of addiction and other psychotherapeutic applications; Current small studies of psychotherapeutic applications

*Overdose death rare or non-existent with older psychedelics, though some newer ones appear more physiologically dangerous (e.g. NBOMe series)


What can you tell me about dissociative Hallucinogens?

*NMDA receptor antagonists:
-Ketamine, PCP, DXM, nitrous oxide
-Some used medically as anaesthetics
-Addictive, range of physical, neural, cognitive, and psychiatric harms

*Kappa opioid agonists:
-Salvia divinorum: non-addictive, may be “anti-addictive”


What can you tell me about deliriant Hallucinogens?

*The “true” hallucinogens: Datura, belladonna alkaloids (e.g. scopolamine, atropine), diphenhydramine

*Antagonists at muscarininc cholinergic receptors

*Some alkaloids used (at very small doses) to treat motion sickness, insomnia, applications in anaesthesia

*High toxicity and unpleasant physical and mental effects limit “recreational” use:
-hyperthermia, tachycardia
-prolonged, often frightening delirium


What can you tell me about solvent & volatile hydrocarbon inhalants?

*Used industrially as solvents, propellants, fuels (e.g. in petrol, paint, paint thinner, aerosol sprays, industrial cleaning agents):
-Toluene: present in some types of glue, spray paint, petrol
-Butane: lighter fluid

*Mixture of depressant and deliriant effects

*Acute dangers:
-“Sudden sniffing death”: sensitisation to adrenaline, leading to heart attack


What can you tell me about the long term effects of inhaling solvent & volatile hydrocarbon?

*Brain damage from repeated hypoxia
*Heart disease
*Specific to chemical:
-Toluene: demyelination (white-matter damage): severe, long-lasting neuropsychological impairment (cognitive, movement, etc.)
-Carbon tetrachloride: potent liver toxin
-Benzene: carcinogenic, bone marrow toxin
-Recovery from neural impairments may take years, and may not be complete in most severely affected.


What is the biological model of drug dependence?

*Excitation of mesolimbic dopaminergic pathway (esp. projection from ventral tegmental area to nucleus accumbens shell) necessary (but not sufficient) for addiction.
-Signals reward value of stimuli
-Involved in learning associations between stimuli and rewards
-Energises attention towards novel stimuli, rewards and associated cues, and response to these
-Addictive drugs “high-jack” this system, increasing activity related to drugs and drug cues, reducing activation related to natural reinforcers.
-Important in early stages of establishing addiction: Once established, glutamatergic projection from prefrontal cortex to nucleus accumbens core maintains persistent craving and responsiveness to drug-related cues.


What is the Incentive-Sensitisation hypothesis of Drug Dependence proposed by Robinson & Berridge, 1993, 2000)

*Repeated stimulation of dopaminergic pathways by drugs leads to hypersensitivity to drugs and associated cues (sensitisation)

*Beyond-normal excitability to even mildly-associated cues, memories, etc.

*Long-lasting cravings, easily induced

*Independent of actual liking, tolerance, withdrawal

*Human users of opioids and cocaine show heightened neural and attentional response to drug-related imagery – some studies find association with relapse.


What is the "Final Common Pathway" for drug seeking proposed by Kalivas & Volkow (2005)?

*The amygdala experiences stress
*which leads to a cue in the ventral tegmental area & Basolateral amygdala
*triggering stress & cues in the prefrontal cortex
*triggering the 'final common pathway' which comprises:
-Prefrontal Cortex
-Nucleus accumbens Core
-Ventral pallidum


What is the frontocortical dysfunction caused by substance abuse?

*Hyper-activity in orbitofrontal cortex and anterior cingulate by drug-related stimuli similar to hyper-activity of these structures seen in obsessive-compulsive disorder.

*Reduced activity in these structures in cocaine and opiate-dependent samples during:
-decision-making tasks
-error-detection tasks
-exposure to pleasant stimuli


What is the evidence for Hedonic Allostasis in Humans?

*Anhedonia (reduced ability to feel pleasure):
-Widespread in substance-dependent samples
-May lead to drug use to “self-medicate”
-May reduce motivation to engage in activities that would compete with drug use.
-Predicts increased likelihood of relapse in tobacco smokers, increased drug use in opiate-dependent sample.

*Reduced response (subjective or neural) to pleasant imagery:
-Predicts increased likelihood of relapse in tobacco, alcohol, and opiate users


How do drugs effect the adolescent brain?

From puberty to late teens/early 20s:

*Maturation of frontal and temporal regions involved in:
-executive function
-inhibitory control
-affect regulation.

*Drug use may disrupt this development, causing long-standing vulnerability to dependence

*Adolescent brain may generally be more vulnerable to adverse neuropsychological impacts of drugs


How does classical (Pavlovian) conditioning influence drug taking behaviours?

*Unconditioned stimulus (US: drug effects) becomes associated with temporally proximal conditioned stimuli (CSs: physical context, drug paraphernalia, people with whom drugs are used)

*CS alone can then elicit:
-Conditioned “A state”: drug-like physiological and psychological effects:
*Placebo response to denicotinised cigarette
* The ‘needle freak’ phenomenon
* Conditioned “B state”: conditioned tolerance, withdrawal:
* Drug-taking in a new environment may trigger overdose due to lack of cues to signal onset of drug effect.
* Addiction established in one context may not generalise to very dissimilar context: e.g. US soldiers heroin use in Vietnam in 1960s/70s

*Discomfort of withdrawal may also act as a US


How does Operant (Instrumental) conditioning influence drug taking behaviours?

*Positive reinforcement (achieve reward):
-Action (drug seeking, use) leads to drug effects
-If reinforced (pleasant effects) probability of repeating the action increases, if punished (feel ill) probability decreases

*Negative reinforcement (escape unpleasantness, physical or psychological):
-Action (drug use) in response to anxiety, withdrawal symptoms
-If reinforced (symptoms relieved), probability of repeating the response increases

*Environmental stimuli can control behaviour:
-“Pavlovian-instrumental transfer”: Classically-conditioned stimuli can energise instrumental responding, even after “extinction”.


What are the Capture Rates by Drug Type?

Proportion Used = PU
Proportion Dependent = PD
Dependence rate among users = DRAU

Tobacco - 75/6% 24.1% 31.9%
Heroin - 1.5% 0.4% 23.1%
Cocaine - 16.2% 2.7% 16.7%
Alcohol - 91.5% 14.1% 15.4%
Cannabis - 46.3% 4.2% 9.1%


What are some of the genetic influences on the development of substance dependence?

Twin studies:
Show greater concordance for identical twins than fraternal twins for:
*Alcohol abuse
*Tobacco smoking
*Heavy cannabis use
*Substance abuse in general


Which genes are potentially involved in the susceptibility to the development of substance dependence?

Variations in genes coding for:

*u opioid receptor: alcohol, opiates

*Dopamine D2, D3, and D4 receptors; dopamine transporter; enzymes involved in dopamine breakdown: alcohol, nicotine, opiates, stimulants

*Tryptophan hydroxylase (serotonin precursor), Serotonin receptors 1b and 2a, serotonin transporter: alcohol, opiates

*GABAA receptor subunits: alcohol

*Muscarinic acetylcholine receptor type 2: alcohol

*Cannabinoid receptor type 1: alcohol, stimulants

*Enzymes involved in alcohol metabolism: alcohol

*Enzymes involved in nicotine metabolism: nicotine


What are some of the epigenetic influences on the development of substance dependence?

*Change in function of gene, without change in gene itself (DNA and histone methylation, acetylation, phosphorylation, etc.)

*Constant process: interaction with environment, trauma, toxins, drugs. Changes last seconds to years.

*Human research on prenatal exposure to:
-Cannabis: associated with long-lasting changes in dopamine receptor expression
-Tobacco: associated with long-lasting changes in opioid transporter expression


What are some of the findings of epigenetic influences on the development of substance dependence in rats?

In adolescent rats, exposure to:
*THC: long-term changes to expression of genes coding for an opioid transmitter, increased heroin self-administration in adulthood

*Alcohol: changes in regulation of genes coding for dopamine and glutamate receptors in adulthood. Exposure to alcohol in adulthood only does not lead to same changes

*Some changes can be transferred between generations (not clear how):
-Morphine exposure in female rats in adolescence (before pregnancy) changes dopamine receptor sensitivity of offspring


How do expectancy effects influence the outcome of a drug taking experience?

Belief that a drug will have a certain effect influences likelihood of use:
*Those who believe that alcohol will reduce stress or increase social skills tend to drink more.
*Rates of cannabis use in US adolescents who perceived:
-“great risk”: 1.8%
-“no, little, or moderate risk”: 11.2%


How do personality factors influence the outcome of a drug taking experience?

*Negative affectivity

*Low constraint (cautious behaviour, harm avoidance, conservative morality)

*Combination of sensation/novelty seeking and high positive affectivity


How do social & cultural factors influence the outcome of a drug taking experience?

*Acceptability: e.g. “wine-drinking countries” (e.g. France, Spain, Italy) vs. prohibitionist countries (e.g. Saudi Arabia, Iran)
-Social acceptability may differ by gender.

*Availability (prevalence, cost, etc.)
*Parental attitudes, substance use, monitoring of adolescents’ behaviour and peer networks.
*Peers’ attitudes and substance use
*Relationship breakdown associated with onset of alcohol abuse/dependence.


How do factors of environmental stress, deprivation, & enrichment influence the outcome of a drug taking experience as found by Bruce Alexander’s “Rat Park” experiments in 1970s?

*Compulsive morphine self-administration seen in socially isolated rats in barren, unstimulating cages, but little or no self-administration in rats housed in large cages with other rats, toys, etc.

-Moving rats from deprived to enriched environment after establishment self-administration reduced morphine use.
-Inconsistent replication


What do rodent models of facilitation by stress of learning drug self-administration tell us?

*Food restriction: opioids, alcohol
*Physical stress (tail pinch, electric shock, restraint): stimulants and opiates; increased motivation to seek opiates in those already trained.
*Social stress (aggression from dominant rats, mixed-sex housing, social isolation): opiates, stimulants, alcohol
*Witnessing another rat in distress: stimulants
*Prenatal stress (restraint stress applied to pregnant mother rat): stimulant self-administration in offspring


What do rodent models of protective effects of environmental enrichment tell us?

*Two months enrichment reduced behavioural and neural response to cocaine in mice

*Reduced contextual preference conditioning by cocaine in mice after 30 days enrichment

*Reduced contextual conditioning by heroin in mice raised from birth in enriched conditions


What are the risk & protective factors prior to birth?

Risk factors:
-Family economic situation
-sole parent households
-Paternal genetic risk for alcoholism
-Maternal drug use in pregnancy

Protective factors:


What are the risk & protective factors during infancy & pre-school?

Risk factors:
-environmental tobacco smoke
-child neglect & abuse

Protective factors:
-easy temperament


What are the risk & protective factors age 4-11 years?

Risk factors:
-early school failure
-conduct disorder

Protective factors:
-Social & emotional competence
-Shy & cautious temperament


What are the risk & protective factors age 12-17 years?

Risk factors:
-low involvement in activities with adults
-perceived & actual community drug use
-community disadvantage & disorganisation
-Availability of drugs
-positive media portrayal of drugs
-parent-adolescent conflict
-favourable parental attitude towards drugs
-negative affectivity
-impaired behavioural inhibition

Protective factors:
-religious involvement
-family attachment
-low parental conflict
-parental or adult communication


What is the treatment for substance dependence?

-Residential programs often 1-2 weeks
-Management of withdrawal symptoms
-First step, but generally high relapse rates if no further treatment

*Rehabilitation and therapeutic communities:
-Programs range from 1 month to 2 years
-Isolation from drugs and drug-using social networks (often rural locations)
-Intensive group therapy (and individual psychotherapy in some programs) to examine dynamics of addiction
-Structured activities and responsibilities
-High drop-out rate, benefits require long-term commitment


Tapering dose is one treatment for substance dependence. What is involved here?

*“Scheduled smoking” with gradual reductions: good success rates in those who adhere to program.
*Necessary with benzodiazepines to avoid dangerous withdrawal symptoms
*“Weaning off” after stabilisation on opioid pharmacotherapy
*Relies on high motivation, self-control, distress tolerance: High rate of relapse if done too soon, too quickly, or without psychotherapeutic preparation