Week 12 Substance Abuse Flashcards Preview

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Flashcards in Week 12 Substance Abuse Deck (102)
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What is the global problem of psychoactive drug use?

8.9% of total burden of disease comes from the use of psychoactive substances
4.1% from Tobacco
4% from Alcohol
0.8% from illicit drugs
Cost to the Australian economy $24.5billion /year


There is a long history of drug use in human society. How long have substances been used by people?

Alcohol - 12,000 years
Coco - thousands of years
Cannabis - 10,000+ years
Opium - 6,200+ years
*Only Inuit Eskimos have no record of traditional drug use
*Most, if not all, societies integrate drug use into accepted, sometimes ritualistic, cultural patterns of behaviour, & every-day social interaction


What are some of the historical limits to the extent of drug use?

*Prior to the advent of global trade, simple geography limited the use of many drugs
*Cultural norms and taboos (often associated with mysticism and ‘rites of passage’)
*Extraction, preservation, and synthesis of active substance


When was drug use expanded?

Colonialism and global trade:
*Cash crops (e.g. opium, tobacco)
*Opium wars
*Scientific advances:
*Extraction and purification of active ingredients (e.g. cocaine, morphine)
*Synthesising new substances (e.g. heroin)


What has been the reaction to widespread use of substances?

*Widespread intoxication clashed with modern industry’s need for a disciplined, productive work force.

*Xenophobia and moral panics:
-Demonisation of Chinese opium dens in US West, Australia
-Association of “marihuana” with illegal Mexican immigrants

*Social movements: temperance
*Legislative control, prohibition


Some people kept using substances anyway, what happened here?

Concept of “addiction” emerged:
*Substance abuse as a “disease”
*Efforts to define, treat


What is the medical model of substance abuse?

*Drug dependence is seen as chronic and relapsing sickness or disease
*Removes responsibility from abuser - not weak-willed, is sick
*Widely accepted, though support for a discrete “disease” category from scientific, clinical, and sociological research is inconsistent at best.


What is the DSM definition of abuse?

A maladaptive pattern of excessive use leading to interpersonal, legal, behavioural, or occupational problems


What is the DSM definition of dependence?

compulsive pattern of chronic use, leading to loss of control over use, pathological valuation of substance use over other activities, and physiological adaptation to the substance


What is the DSM criteria for substance abuse?

Any one of the following symptoms occurring repeatedly within a 12-month period:
*Recurrent substance use resulting in a failure to fulfil major obligations (e.g. repeated absence from work or school, or poor performance, neglect of children, etc.)
*Recurrent use in situations where it may be physically hazardous (e.g. driving)
*Recurrent substance-related legal problems.
*Continued use despite recurrent interpersonal problems (e.g. fights or arguments either caused by intoxication or about person’s excessive use)


What is the DSM criteria for Substance Dependence?

Any 3 or more of the following symptoms occurring within a 12-month period:
1.Frequently using more of the substance, or using for longer periods of time, than intended
2.Persistent desire, or repeated unsuccessful efforts, to cut down or cease.
3.Large proportion of one’s time spent obtaining, using, and/or recovering from effects of substance.
4.Important social, recreational, or occupational activities given up or reduced because of substance use
5.Substance use continued despite knowledge of physical or psychological health problems caused by substance
6.Tolerance (needing more of substance than previously to achieve same effects and/or diminished effects from using previously “effective” amount)
7.Withdrawal symptoms when substance use reduced or ceased (symptoms depend on type of substance)


What are the main differences between DSM-IV and DSM-5?

“Substance use disorder”, with no distinction between “abuse” and “dependence”:
*All 11 criteria pooled together
*“legal problems” criterion removed, but “cravings” added.

Severity defined by number of symptoms:
*Mild: 2-3 symptoms
*Moderate: 4-5 symptoms
*Severe: 6 or more symptoms


What is the ICD-10 criteria for Substance Dependence?

Substance dependence diagnosis requires at least 3 of following criteria:
1.Strong desire or compulsion to use
2.Difficulties controlling onset, termination, or level of use
3.Withdrawal syndrome when use reduced or ceased
5.Increasing neglect of alternative pleasures or interests because of use or because of increased amount of time necessary to obtain substance or to recover from its effects
6.Persisting with use despite experiencing harmful consequences (physical or mental health; cognitive impairment) and being aware that these were being caused or exacerbated by substance use.


What is the Fagerstrom Test for Nicotine Dependence (FTND)?

A questionnaire which scores a patient's level of nicotine dependence:
*How soon after waking do you have your first cigarette?
*Do you find it difficult to keep from smoking in places where smoking is forbidden (cinema, church, library)?
*Which cigarette would you hate to give up?
*How many cigarettes do you smoke per day?
*Do you smoke more during the 1st hours after waking than during the rest of the day?
*Do you smoke if you are so ill you are in bed most of the day?


What is the scoring system for the Fagerstrom Test for Nicotine Dependence (FTND)?

0-2 = very low dependence
3-4 = low dependence
5 = moderate dependence
6-7 = High dependence
8+ = very high dependence


What are some of the problems with defining and measuring "addiction" found by Davies and Baker (1987)?

*2 questionnaires administered in random order to 20 heroin users:
*One administered by university professor
*One administered by a local, well-known heroin user

To the professor, participants consistently reported:
*More frequent use
*More problems associated with use
*Higher levels of dependence
To their peers, less so


What are some of the effects of labelling on self-report measures found by McAllister & Davies (1991)?

Interviews with smokers on two occasions
*At first interview, all smokers categorised as “problem smokers”.
*After first interview, randomly split into two groups – LIGHT and HEAVY smokers.
*Group designation clearly printed at top of each page at follow-up questionnaire
*‘Heavy’ smokers reported increases in problem smoking and tobacco dependence no matter how much they actually smoked


What is the biopsychosocial model of substance abuse, also referred to as the ‘drug, set and setting’ model (Zinberg, 1986)?

Drug effects are an interaction of:

*The substance
-type of drug, dose, purity, adulterants

*The user
-physiological and psychological state

*The context
-social and physical context


Tell me more about the 'set' from the biopsychosocial model of substance abuse, also referred to as the ‘drug, set and setting’ model (Zinberg, 1986)?

The 'set' refers to

-age, body weight, sex
-circadian rhythms, health

-Beliefs regarding drug usage and its consequences (usage is inversely proportional to perceived harm)
-personality traits


Tell me more about the 'setting' from the biopsychosocial model of substance abuse, also referred to as the ‘drug, set and setting’ model (Zinberg, 1986)?

The 'setting' refers to:
Physical Environment: effects in hospital vs. at a party
*Social Environment: stress of modern society
*Cultural norms: religious taboos; parents attitude; condoned use of certain drugs; social support and sanctions for appropriate and inappropriate behaviour
*Peer behaviour: compare our behaviour with others, learn rules and rituals
*Peer-group identification*Media’s portrayal of drug use/ advertising
*Popular culture


Tell me more about the 'drug' from the biopsychosocial model of substance abuse, also referred to as the ‘drug, set and setting’ model (Zinberg, 1986)?

The 'drug' refers to:

*Route of administration

*Type of drug:

-CNS depressants:
*GABAergic drugs (alcohol, benzodiazepines, GHB)
*Opioids (heroin, morphine, codeine, oxycodone)

-CNS stimulants:
*Cocaine, amphetamine, methamphetamine, cathinones (MDPV, mephedrone, “bath salts”)
*“Hallucinogens”: Psychedelics, Dissociatives
*Mixed effects: cannabinoids, “empathogens” (e.g. MDMA), solvents/hydrocarbon inhalants


What do we know about the interactions alcohol (AKA Ethyl Alcohol, Ethanol) has on the body?

*Agonist at GABAa benzodiazepine receptor sites
Alcohol inhibits:
-ion channels (sodium, calcium, potassium) that facilitate excitatory neurotransmission
-glutamate receptors (AMPA, kainate, and, at high doses, NMDA)
-adenosine reuptake

*Various other actions, e.g. at some serotonergic and cholinergic receptor sites
*The blood alcohol concentration (BAC) is determined by:
-Concentration of alcohol in drink, rate of drinking
-Presence of food in stomach
-Body size


What do we know about the effects low doses of alcohol (AKA Ethyl Alcohol, Ethanol) has on the body?

Low doses (below 0.1% BAC):
*Disinhibition (consequences are specific to person and surroundings; relaxed, euphoric, withdrawn or aggressive)
*Expectancy effects (only with low doses)
*Increased talkativeness, sociability
*Impaired judgment, attention, self-control, information processing, reaction time
*Impaired muscle coordination
*Increased heart rate, reduced body temperature
*Increased urination
*Sleepiness (hypnotic agent)


What do we know about the effects high doses of alcohol (AKA Ethyl Alcohol, Ethanol) has on the body?

High doses: blood alcohol content (BAC) > 0.15%:
*disorientation, confusion, slurred speech,
*blurred vision, poor muscle control
*if new drinker → nausea/vomit,
*decreased testosterone (and sexual response),

BAC > 0.3:
*stupor, sleep, unconsciousness, coma, death


What do we know about the effects chronic heavy alcohol consumption on the body?

Central Nervous System:
*Peripheral Neuropathy
*Alcoholic Dementia
*Wernicke-Korsakoff’s syndrome

*Hypertension, *Strokes, *Cardiomyopathy

*impaired sexual desire or arousal
*Impotence or testicular atrophy (men)

Other effects:
*Haematological- Macrocytic Anaemia
*Musculoskeletal- Myopathy with Chronic weakness


What are the other effects of chronic heavy drinking?

*Oesophagitis, *Gastritis, *Peptic ulcer disease
*Malabsorption, *Gastric cancers

*Pancreatitis- Acute & Chronic, *Cancer

*Fatty liver changes – Reversible, *Alcoholic hepatitis - (i.e., damaged hepatocytes).
-Cessation likely to lead to recovery.
Cirrhosis – Liver cells die and are replaced by fibrous scar tissue
Hepatocellular Carcinoma


What is Wernicke-Korsakoff’s syndrome?

A brain disorder involving loss of specific brain functions caused by a thiamine (vitamin B1) deficiency .
-Generally attributed to malnutrition. Symptoms may be exacerbated by alcohol withdrawal.
-The syndrome is actually a spectrum, including two separate sets of symptoms.
-Wernicke's encephalopathy involves damage to multiple nerves in both the central and peripheral nervous systems.
-Korsakoff syndrome involves impairment of memory out of proportion to problems with other cognitive functions due to damage to areas of the brain involved with memory.


What are the symptoms of Wernicke-Korsakoff’s syndrome?

Vision changes (including double vision, eye movement abnormalities, eyelid drooping)
*Loss of muscle co-ordination
*Unsteady, uncoordinated walking
*Loss of memory, can be profound
*Inability to form new memories
*Confabulation (making up stories to fill lapses in memory of events; often not conscious of this)


What are the symptoms & implications for brain damage caused by alcohol?

Excessive consumption of alcohol leads to damage to myelinated neurons (white matter).

*Women show a greater sensitivity to alcohol neurotoxicity than do men.
*Cigarette smoking can exacerbate alcohol-induced damage
*Increased brain volume and improved cognitive function with several months or years abstinence


What are the symptoms & implications for alcohol withdrawal?

*Autonomic hyperactivity (sweating, racing heart)
*Shaking hands

*CNS excitability:
-Anxiety, agitation
-Seizures in severe cases (can be life-threatening)

*Delirium Tremens (DT’s):
-profound confusion, delusional states, fluctuating consciousness, hallucinations

*Treated with other CNS depressants such as benzodiazepines


What are the guidelines for drinking for daily & weekly drinking for Men & Women?

Low risk Males:
daily up to 6, no more than 3 days/week; 28/week

Low risk Females:
Daily up to 4, no more than 3 days/week; 14/week

Risky Males:
Daily 7-10 on any day; 29-42/week

Risky Females:
Daily 5-6 on any day; 15-28/week

High Risk Males:
Daily 11+ on any day; 43+/week

High Risk Females:
Daily 7+ on any day; 29+/week


Which drugs are Benzodiazepines?

*Diazepam (valium, valpam)
*Alprazolam (xanax)
*Clonazepam (klonipin, rivotril)
*Nitrazepam (mogadon)
*Oxazepam (serapax, murelax)
*Flunitrazepam (Rohypnol)
*Temazepam (normison, temaze)
*Lorazepam (Ativan)
*Triazolam (halcion)
*Chlordiazepoxide (Librium)


What are Benzodiazepines?

*Agonists of the benzodiazepine site on the GABAA receptor
*Increase ability of GABA to activate GABAA receptor, enhances inhibitory neurotransmission
*“Z drugs” have different chemical structure, but similar pharmacological activity:
-Zolpidem (stilnox)
-Zopiclone (imovane)


How are Benzodiazepines used?

Replaced more dangerous barbiturates for most clinical applications during 1960s-70s
-Anxiolytic: stop panic attacks
-Anticonvulsant: control of seizures
-Hypnotic: insomnia
-Muscle relaxant
-Occasionally used in anaesthesia
-Reduce alcohol and opioid withdrawal symptoms

*Rapid, high tolerance should limit long-term medical use, but often doesn’t


What are some of the acute effects of Benzodiazepines?

*Relaxation, loss of inhibition, euphoria
*Sedation, lack of muscular coordination
*Cognitive impairment
*Enhances effects of alcohol, opiates
*Overdose: respiratory depression, coma, cardiac arrest


What are some of the chronic effects of Benzodiazepines?

*Cognitive impairment
*Extreme tolerance
*Paradoxical effects, e.g. increased anxiety

-Similar to alcohol withdrawal syndrome
-Extremely dangerous and prolonged:
-Acute symptoms last up to 2 months
-Residual symptoms can last 6-36 months
-Re-emergence of severe withdrawal after single use many months after cessation


What is Nicotine?

Primary psychoactive ingredient in tobacco: accounts for the acute pharmacological effects of tobacco and the subsequent dependence on cigarettes.
•Numerous chemicals in tobacco smoke. Nicotine has some harmful effects, but most harmful effects of tobacco smoking are due to other chemicals.
•Agonist at nicotinic acetylcholine receptors
•Effects in central and peripheral nervous systems, heart, and cardiovascular system
•Brain areas activated by nicotine include:
• Locus coeruleus (behavioural arousal and vigilance)
• Frontal lobes and cingulate gyrus (cognition, working-memory, attention, motivation, mood, and emotion)


What are the behavioural, cognitive, & Psychological effects of Nicotine use?

*Increased concentration
*Improved working memory
*Improved performance in vigilance and rapid information processing tasks
*Dizziness (in non-tolerant smokers)

Smokers unconsciously self-titrate to optimize nicotine levels and keep them at steady-state.


What are the consequences of tobacco use with regard it's toxicity?

*Smoking is the leading preventable cause of death, illness and disability: causes 4.3 million deaths annually.
*It is the tar in tobacco that leads to much of the long-term toxicity
-Lung cancer, non-cancerous lung diseases, cancers of other body organs, heart and cardiovascular diseases.
-It is estimated that 14 min of life is lost for every cigarette smoked
-One in every six people who try smoking will eventually die of a smoking-related illness.
-Serious health risks associated with passive smoking
-Increased risk of spontaneous abortion, stillbirth, preterm delivery, retarded intrauterine growth and early postpartum death when mothers smoke.


What are the consequences of tobacco use with regard dependence on nicotine?

*Smoking does not appear to lead to nicotine tolerance (except for tolerance to dizziness/nausea/vomiting)
*However, clear physiological and psychological dependence does develop
*Withdrawal is characterized by:
-severe craving for nicotine
-irritability, anxiety, anger, restlessness, impatience
-difficulty in concentrating
-increased appetite, weight gain


What is cannabis?

*There are two species of Cannabis:
-Cannabis sativa
-Cannabis indica

*Cannabis is AKA marijuana or hemp

*Numerous preparations (e.g. marijuana “buds”, leaves, hashish, hash oil, etc.)
*smoking, eating, drinking, vapourisation
*Major psychoactive ingredient is Δ9-tetrahydrocannabinol (Δ9-THC)
*Several other cannabinoids modify THC’s effects (e.g. cannabidiol)
*THC content ranges widely


THC is the active ingredient in cannabis. What are the effects of THC?

*Agonist at 2 cannabinoid receptors CB1 & CB2:

-Widely expressed throughout brain
-Often located presynaptically, inhibits transmitter release (both excitatory and inhibitory)
-Appears mainly responsible for cannabis’ psychological effects (e.g. on anxiety, cognition, perception)

-Mainly expressed peripherally (e.g. immune system cells, peripheral nerve cells)
-Effects on immune system function, inflammation, pain perception
-Unclear if significantly contributes to psychological effects


What are the acute effects of Cannabis?

*Dependent relative quantities of different cannabinoids present (potency, species, and strain)
*Smoked or vapourised: 2-6 hours; eaten: 4-24 hours
*Impaired attention & S-T memory, altered sensory awareness, altered motor control and posture
*Hallucinogenic at high doses in some users
*Analgesic, anti-inflammatory, appetite stimulant, anti-emetic (possible grounds for medical application)
*Reduced blood pressure


What are the long-term effects of heavy Cannabis use?

*Dose-related decline in IQ scores; reversible with abstinence
*Impaired attention, verbal memory, working memory, information filtering and processing speed (inconsistent findings)
*Reduced hippocampus and amygdala volume (very long-term, heavy daily use).
*Precipitation of onset, or intensification of, underlying psychotic, mood, or personality disorders
*Increases likelihood of developing psychotic disorders, particularly if used heavily during early adolescence.
*Heavy users more likely to abuse other classes of drugs


What are the effects of Cannabis withdrawal?

Generally mild in all but the most heavy users, suggesting that strong physical dependence does not easily develop. Symptoms usually last 1-2 weeks and include:
-Depressed mood or intensified moods
-Restlessness, anxiety
-Loss of appetite
-Insomnia, vivid dreams
-stomach cramps
-sweating, fever, chills


Dozens of new chemicals have emerged in recent years. What are the effects of synthetic Cannabinoids?

*Sprayed onto non-psychoactive herbal materials (marketed as, “legal highs”, e.g., “spice”, “kronic”, “k2”, etc.) or sold as pure powder on internet
*Little or no scientific testing in humans
*Anecdotal reports of much more harmful effects than natural cannabis:
-Reports of fatal overdoses, heart attacks
-Psychotic episodes
-More severe, prolonged withdrawal symptoms in dependent users
-Full agonist vs. partial agonist


What are opioids?

*Natural: opium, morphine, codeine
*Semi-synthetic: heroin, oxycodone, buprenorphine, desomorphine (“krokodil”) etc.
*Synthetic: methadone, fentanyl, tramadol, pethidine, etc.

*Agonist at opioid receptors (m, d, k)

*Clinical Uses: Pain (analgesia), Anti-tussive (prevents cough), Slows bowel (stops diarrhoea), Anaesthesia, Antidepressant (historically, currently experimental only)

*Side-effects: Pupil constriction, nausea, vomiting, constipation, reduced immunity, depressed respiration, itching


What are some of the recreational effects of Opioid use?

*Euphoria, “Rush”
*Emotional detachment
*Sense of comfort, elimination of anxiety and other negative emotions
*“Nod”: dream-like sedation (high doses)
*Stimulation in some tolerant users


What happens during an Opioid overdose?

*Severe respiratory depression
*Leading cause of death among opioid-dependent people
*Usually not opioid alone, but in combination with another depressant drug (e.g. alcohol, benzodiazepines)
*Especially dangerous after reduced tolerance:
-Release from prison
-Contextual change


What are some of the chronic effects of Opioid use?

*Impaired immune system function

*Reduced testosterone levels in men:
-Reduced sex drive
-Increased risk of osteoporosis
-Reduced muscle strength

*Chronic constipation


What happens during an Opioid withdrawal?

Chills, sweating, cramps, nausea, watery eyes & nose, yawning, severe anxiety and agitation, insomnia.

Duration depends on drug:
*3-7 days for heroin
*Up to 1 month for methadone
*“Post-acute withdrawal syndrome”: Acute withdrawal sometimes followed by depression, insomnia, anhedonia, cravings, anxiety lasting several months


What are stimulants?

*This category includes drugs such as cocaine and the amphetamines
*Also methylphenidate (“Ritalin”, “Concerta”)
*More recently: cathinones and other synthetic drugs (sometimes marketed as “bath salts” or “synthetic cocaine”)
*Primary mechanism of action in CNS: Increase dopaminergic activity:
-Cocaine: inhibits re-uptake of dopamine
-Amphetamines: increase dopamine release


Tell me about Cocaine

*Used medically as a local anaesthetic
*Used traditionally (chewed coca leaves) by indigenous people of Andes to reduce fatigue and hunger.
*“Crack” is smokable “freebase” form
*Effects last from a few minutes to 1 hour


Tell me about amphetamines?

*Used in the treatment of narcolepsy and ADHD (“dexedrine”, “dexamphetamine”, “adderall”)
*Illicitly marketed as “speed” (rare in Australia), or illicitly diverted pharmaceutical amphetamine (“dexies”)

*Similar medical applications as amphetamine (“desoxyn”)
*Illicitly, can appear as “speed”, “base”, or “ice”
*Effects last up to 12 hours
*More neurotoxic than amphetamine and cocaine


What are the acute effects of stimulants?

*Increased alertness, energy, insomnia
*Euphoria, confidence, grandiosity
*Decreased appetite.
*Prolonged use or high doses: anxiety, agitation, paranoia, psychosis
*Increased blood pressure, heart rate
*Overdose can cause stroke or heart attack


What are the chronic effects of stimulants?

*Heart disease

*Dental problems from tooth grinding

*Route Of Access dependent:
-“crack lung”, “meth mouth”, nasal damage from snorting cocaine, abscesses from frequently injecting cocaine

*Methamphetamine: neurotoxicity leading to Parkinson’s disease, cognitive deficits

*Prolonged psychosis


What happens during stimulant withdrawal?

*hypersomnia, lethargy, and fatigue
*apathy, depressed mood,
*increased appetite
*irritability, anxiety, agitation
*Lasts several days to several months, depending on duration and amount of use


What is MDMA?

*AKA“Ecstasy” or “molly”
*Occasionally used in psychotherapy in 1970s and 1980s before being banned.
*Recent experimental use as treatment for PTSD
*Closely-related drugs: MDA (metabolite), MDEA
*Releases serotonin and other monoamines (dopamine and noradrenaline), activates 5-HT1 and 5-HT2 receptors
*“empathogen” or “entactogen”; combination of stimulant and psychedelic effects


What can you tell me about the neurotoxicity of MDMA?

*Serotonin neurotoxicity: likely to be exacerbated by hyperthermia (especially use in crowded environments, prolonged dancing):

-Impaired verbal and visual memory
-Impaired decision-making (“executive functioning”)
-Greater impulsivity and lack of self-control
-Sleep disturbance
-Depression and anxiety

*Deficits may persist up to a year following frequent, heavy use


What can you tell me about Hallucinogens?

*3 classes: psychedelics, dissociatives, deliriants

*Illusions, intensification or distortion of perception, elementary and complex visual hallucinations, synaesthesia

*Intense changes in mood and thought processes, introspection, psychosis in some users

*Distorted sense of time

*“ego dissolution”: reduced sense of self, identity


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


What are some of the issues associated with relapse prevention?

“Giving up smoking is the easiest thing in the world. I know because I've done it thousands of times.” – Mark Twain

*Causes of relapse: stress, physical and social context, substance use (lapse)

*Learning to anticipate risky situations
*Learn from lapses to identify cause and prevent full relapse.
*Effective at reducing use in alcohol dependence, only weak effect for nicotine


What are some of the psychological & behavioural treatments for substance abuse?

*Simply being interviewed about level of use can lead to reductions in use in some.

*Cognitive Behavioural therapy: relapse prevention and replacing drug use with new activities.

*Contingency management:
-Rewards contingent on abstinence, active avoidance of substance, treatment adherence, adaptive behaviours, etc.
-Effective for alcohol, cannabis, cocaine, heroin

*“Controlled drinking”:
-Alternative to abstinence-focused approach
-Teaching techniques to moderate use, combined with social skills and relaxation training
-Demonstrated effectiveness for alcohol, but would this ever be trialled with other drugs???


What are some of the Mutual Support Fellowship programs available?

*Main ones are Alcoholics Anonymous and Narcotics Anonymous

*Marijuana Anonymous, Cocaine Anonymous, Crystal Meth Anonymous, and Nicotine Anonymous also present in Australia

*Spiritually-based, abstinence-oriented program of frequent meetings, “sponsorship” of newer members by older members

*Based on “permanent disease” model of addiction


Who are the people most likely to recover?

*Personal resources and skills – self-esteem; self-efficacy; positive expectancies; coping skills

*Belonging and embeddedness – bonding and positive support from family, peers, social/community involvement

*Safety and stability

*Pathways and ongoing availability of opportunity


Who are the people least likely to recover?

*Significant history of mental health problems

*Significant history of criminal involvement

*Partner, family and peer group embedded in addiction

*Lack of opportunity and access to support


What medication treatments are available for the treatment of Substance dependence?

Agonist substitution:

-Methadone: full agonist
-Buprenorphine: partial agonist
-Pharmaceutical heroin in some countries

*Alcohol, benzodiazepines:

-Nicotine gum, patches, “e-cigarettes”
-Varenicline (“Champix”): partial agonist


What role do medication treatments have in symptom reduction for the treatment of Substance dependence?

*Acamprosate: Mild GABAA receptor agonist and NMDA antagonist (for alcohol craving)
*Baclofen: GABAB receptor agonist (for alcohol and benzodiazepine withdrawal and cravings)
*Clonidine: a2 adrenaline receptor agonist: sedative, lowers blood pressure & heart rate (for physical discomfort associated with alcohol, opioid, or nicotine withdrawal)
*Diazepam: anxiety and agitation associated with cannabis or opioid withdrawal
*Bupropion (“Zyban”, “Wellbutrin”): dopamine reuptake inhibitor, antidepressant (cravings and dysphoria in nicotine withdrawal)
*Various psychiatric medications (antidepressants, antipsychotics, mood stabilisers) used “off-label” for psychological problems associated with withdrawal and post-withdrawal syndrome


What antagonist & allergenic medication treatments are available for the treatment of Substance dependence?

*Opioid receptor antagonist
*Oral pills, long-lasting injections, or implants
*Mildly effective at reducing alcohol cravings and reward
*Blocks effects of opioids, but dangers associated with use in opioid dependence

*Induces “allergy” to alcohol
*Low effectiveness due to low compliance


What 'alternative treatment' medication treatments are available for the treatment of Substance dependence?

*Used experimentally to treat alcoholism in 1950s and 1960s: Bill W (co-founder of AA) was an enthusiast.
*Several trials conducted before banning in late 1960s/early ’70s. Recent meta-analysis showed clear effect of reduced alcohol consumption for 6 months after single dose. Effects not present at 12 months

*Agonist at several serotonin and opioid receptor subtypes, antagonist at NMDA receptor (mixed psychedelic and dissociative effects)
*Blocks opioid withdrawal effects while inducing psychedelic experience. Case reports of lasting reductions of cravings. Also may assist treatment of alcohol, nicotine, methamphetamine dependence.
*Legal in some countries, but absence of controlled trials, safety concerns.

*Evgeny Krupitsky reports successes in alcoholism and opioids in Russian trials
*1-3 administration sessions, in conjunction with ongoing psychotherapy


Tell me about Harm Reduction.

*Accepts that some will continue to use substances, but that associated harms can be reduced.

*Education about potential harms
*Safer routes of administration:
-Needle & syringe programs

*Pill testing
*Agonist substitution for opioids

*Overdose prevention:


What is being done by way of prevention & how is this problematic?

Supply and opportunity reduction:
Effective in reducing tobacco use and dependence, some evidence for reducing alcohol use (but heavy drinking/dependence?)

*Increased taxes, minimum pricing
*No-smoking areas
*Restrictions on liquor licensing
*Age restrictions

Prohibition, criminalisation:
*Mixed evidence whether it reduces substance use
*Other harms related to criminalisation (criminal activity, less “quality” control)
*Emergence of “legal highs”, some more dangerous than the illegal ones.


What prevention programs are in place?

Social and educational measures:
*Restrictions on advertising
*Public education campaigns
*Regarding harms of use
*Peer pressure resistance
*Correcting false beliefs regarding use
*Self esteem training

Family interventions: Delaying onset of use reduces likelihood of dependence

Social change (employment opportunities, alternative recreational activities)