Quiz 1 Flashcards
Explain the components of addiction.
Initial use: pleasure and reward
Escalating use/binge/intoxication
Increasing dependence, tolerance, and loss of control
Adverse effects if substance use ceases (physical and psychological)
Craving
Relapse
How is cognition implicated in addiction?
Attention, memory, and perception
Incentive-sensitization theory
Associative learning and sensitization (over time, a greater effect is observed) of brain motivational systems to drug and drug associated cues
What mediates pleasurable effects of drugs?
Mesotelencephalic DA system
What NTs are associated in initial reinforcing effects of most drugs?
DA, ST, glutamate, and GABA
What 4 factors influence the transition to addiction?
Genetic predisposition
Developmental factors
Social context
Stress and co-occurrence of other psychiatric disorders
How does genetic predisposition influence the transition to addiction?
Sensitivity and subjective experience, heritability
How do developmental factors influence the transition to addiction?
Adolescents are particularly sensitive to drug effects and external pressures
Distribution theory of addiction
Attributes the current increase in both substance and behavioural addictions to a lack of psychosocial integration (social dislocation) in the modern world
Psychosocial integration
Interdependence between an individual and their society, and is proposed to fulfill the human need for both individual autonomy and social belonging
How does stress influence the transition to addiction?
Hypothalamic-pituitary adrenal axis (HPA axis) is the hormonal system involved in regulating the stress repsonse and is important in drug use, relapse and addiction
What are common co-morbidities with addiction?
Mood disorders, anxiety disorders, and personality disorders
5 models/theories of addiction
Moral model
Choice model
Medical/disease model
Indigenous perspective
Biopsychosocial model
Moral model briefly
Addiction as character flaw
Choice model briefly
Addiction as adaptation to personal environment
Medical/disease model briefly
Addictive drugs cause LT progressive changes in the brain
Indigenous perspectives briefly
Balance of physical, mental, emotional, and spiritual health
Biopsychosocial model briefly
Interplay of biological, psychological, and social factors
When was the moral model most prevalent?
18th and early 19th century
Explain the cultural context setting for the moral model
Addiction was common
Cocaine was viewed as a wonder drug
Opioids were a cure all
What movement took place during the moral model
Temperance movement
Temperance movement
Preaching moderation/abstinence pledge
Led by the clergy
Moral failure/sin: “just stop”
Public shaming
When was the disease model most prevalent?
End of the 19th century
What was the intention behind the disease model?
To shift the view of addiction from moral failure to disease
Intended to reduce stigma, but largely failed
3 important points about the disease model of addiction
Categorical approach
Can’t be cured
12 step programs
Explain choice model
Social recovery should be used –> foster connection
Emphasizes the role of society and community
What is the backbone behind the Indigenous perspective?
The Medicine Wheel
What does the Indigenous perspective recognize?
Colonial-linked stressors and cultural resilience factors
What is used as intervention in the Indigenous perspective?
Culture
Albert Marshall view
Two-eyed seeing
Recognizes Indigenous knowledge as a distinct and whole knowledge system that exists alongside mainstream/Western science
3 factors of biopsychosocial model
Biological
Psychological
Social
Biological aspects in biopsychosocial model
Genetics: moderate to high
Individual differences in reward sensitivity
Psychological aspects in biopsychosocial model
Mental health
Impulsivity
Social aspects in biopsychosocial model
Adversity
Social determinants of health
How is addiction diagnosed?
DSM-5 and ICD-10
Classification of addiction in DSM-5
Substance-related and addictive disorders
How many categories of addictions are included in DSM-5
10 substances
1 behaviour
Criteria for diagnosis in DSM-5
Pattern of engagement in past 12 months that causes clinically significant harm
2 of 11 symptoms
Severity as it relates to number of symptoms
Mild: 2-3
Moderate: 4-5
Severe: 6+
DSM-5 diagnostic guidelines
Larger amounts/longer period than intended
Desire/efforts to cut down
Time spent to obtain, use, or recover
Craving
Use results in failure to fulfil role obligations
Continued use despite social/interpersonal problems caused/exacerbated by effects
Activities given up/reduced
Use in hazardous situations
Use despite known psychological/physical problems resulting
Tolerance, with either of: need for increased amount to get effect, or diminished effect with use of same amount
Withdrawal, with either of: characteristic withdrawal syndrome for substance, or substance taken to relieve or avoid its’ withdrawal symptoms
Addiction name in DSM-5
Substance Use Disorder
What 10 substances are included in the DSM-5?
Alcohol
Caffeine
Cannabis
Hallucinogens
Inhalants
Opioids
Sedatives/Hypnotics/Anxiolytics
Stimulants
Tobacco
Other
Conditions for further study
Caffeine use disorder
Gaming use disorder
4 main classes of criteria for DSM-5
Impaired control
Social impairment
Risky use
Pharmacological criteria
Impaired control
Use more than intended
Want to cut down
Time devoted to substances
Cravings
Social impariment
Cannot fulfill major obligations
Use despite problems
Reduce/stop important activities
Risky use
Use in physically dangerous situations
Use despite physical or psychological consequences
Pharmacological criteria
Tolerance
Withdrawal
What is the only behavioural addiction included in the DSM-5?
Gambling
Similarities between gambling and substance use
Risk factors
Neurological
Treatment
ICD-10 diagnostic guide for dependence syndrome
3 or more of the following present together at some time during previous year:
Strong desire/compulsion to take substance
Difficulties controlling substance-taking behaviour
Withdrawal
Tolerance
Neglect of alternative pleasures or interest because of substance use/procurement/recovery time
Persistent use despite harmful consequences
What is an important distinguish in the ICD-10
Harmful use is distinguished from dependence syndrome
Shaffer transdiagnostic model
Addiction as syndrome
Shared risk factors
Manifests as different substance use and behaviours
Same underlying disorder/vulnerability manifests differently depending on: availability, social acceptance, peer influence
Griffiths transdiagnostic model
Salience
Mood modification
Tolerance/withdrawal
Conflict
Relapse
Three classifications of continuum model
Addiction
Problematic use
Recreational use
Addiction classification of continuum model
Compulsion
Negative consequences
Show symptoms of addiction
(Activity is no longer pleasurable, just use to avoid negative feelings)
Problematic use classification of continuum model
Habit
Some negative consequences
Begin to show symptoms of addictions
(Attempts to quit)
(Impacting daily routine)
Recreational use classification of continuum model
Casual
Negligible health or social effects
May have some positive effects
Why does terminology matter when describing individuals living with addiction?
Ways of describing people with substance use concerns can perpetuate or diminish stigmatizing attitudes
Kelly & Westerhoff study design
Randomized, between-subjects, cross-sectional design
Clinicians attending two mental health conferences were asked to read a vignette
Kelly & Westerhoff study findings
Clinicians exposed to “substance abuser” term were more likely to judge the person as deserving blame and punishment than the same individual described as “having a substance use disorder”
Instead of “addict”, “abuser”, and “junkie”
Use “habitual user”, “person with substance use disorder”, “active in addiction”
Instead of “abuse”, “habit”, “drug habit”
Use “Misuse”, “harmful use/problem use”, “risky use”
Instead of “clean”, or “dirty”
Use “sober”, “abstinent”, “drug-positive or -negative”, “substance-free”, “addiction free”, or “remission”
Instead of “replacement” or “substitution therapy”
Use “treatment”, “medications”
Prevalence of addiction in Canada
21.6% of Canadians meet criteria for a lifetime Substance Use Disorder
Which drug results in the largest cost to Canada?
Alcohol
In order, name the four largest total overall costs attributable to substance use in Canada
Lost productivity
Healthcare
Criminal justice
Other
Are males or females more harmed by substance use at a young age?
Females
Heyman claim to fame
Hyperbolic discounting
Delay discounting
Human tendency to prefer smaller but more immediate rewards over delayed rewards
Hyperbolic discounting
Increased delay discounting exacerbated by addictive process
How did Heyman view addiction?
A disorder of normal choice processes (compulsive nature of addiction)
Cognitive bias
Selective info processing, mental heuristics/shortcuts that aren’t always helpful
3 types of cognitive bias related to addiction
Outcome expectancies
Self-efficacy
Cue reactivity
Outcome expectancies example
I’ll have an easier time socializing if I get drunk
Self-efficacy example
I can stop whenever I want
Cue reactivity
Drug-related cues induce powerful effects
Cognitive model of drug urges and drug-use behaviour author
Tiffany
Cognitive model of drug urges and drug-use behaviour
Drug use becomes automatic
What is an automatic process?
Fast and gets faster with practice
Initiated and carried out outside conscious awareness
Lacking control
Effortless (cognitively undemanding)
Non-automatic processes
Slow, effortful, and require intention and attention
What do cognitive models define craving as?
Result of non-automatic interruption of automatized drug use action plans
Affective processing model author
Baker
Affective processing model
Drugs are taken to alleviate negative affect = negative reinforcement
In the affective processing model, how does negative affect influence drug use?
Negative affect increases levels of “hot” info processing instead of “cool” controlled info
Positive reinforcement as it relates to addiction
Add something pleasant
Example of positive reinforcement as it relates to addiction
I’m high, this feels great
Example of positive punishment as it relates to addiction
I choose not to drink alcohol because it always makes me vomit
Negative reinforcement as it relates to addiction
Take away something unpleasant
In the affective processing model, how does negative affect influence drug use?
Negative affect increases levels of “hot” info processing instead of “cool” controlled info
Example of negative reinforcement as it relates to addiction
Wow, this drug momentarily alleviates my aweful depression
Negative punishment as it relates to addiction
Take away something unpleasant
Example of negative punishment as it relates to addiction
I’d probably lose my job if I showed up high or drunk
Hot cognition
Emotional thought process
Cold cognition
Cognitive thought process
Hot info processing
In addiction, behaviour becomes reactive, governed by urgent need to relieve negative emotions
Attentional bias hypothesis
Conditioned drug stimulus produces an increase in corticostriatal dopamine (especially in anterior cingulate gyrus, amygdala, and nucleus accumbens), which directs attention toward drug stimuli
What does the attentional bias hypothesis lead to (2 things)
Motor preparation and hyperattention to drug stimuli
Enhances craving, promotes relapse
How does the attentional bias hypothesis view drug craving?
Emotional conditioned appetite motivational state produced by stimuli associated with reward effects
What does the attentional bias hypothesis emphasize?
Importance of attentional bias as the cognitive mediator between the drug stimulus and the behavioural response to this stimulus
4 cognitive methods for studying drug use behaviour
Stroop task
Memory priming
Dot-probe task
Reaction time experiment
Addiction Stroop task procedure
Neutral control words and drug-related words will appear in sequence on screen
Words will be printed in various colours
Objective: click the correct coloured button to indicate the word’s colour without thinking about the word
Why might the Addiction Stroop task work?
The reaction time for recognizing the colour of drug-related words is compared to neutral control words
People with addiction will have trouble paying attention to the colour and “blocking out” the drug-related word
Score: The more “addicted”, the larger the discrepancy in processing time between drug-related vs neutral words
Evidence for addiction Stroop task
Haloperidol is a DA antagonist and decreases reactivity to drug cues
When given to detoxified heroin-dependent individuals the discrepancy was found to be smaller
Dot-probe task
Measures shifts in attention between two co-present visual stimuli
Participants will respond faster to a stimulus (dot) if it is presented to a part of the display that they are already looking at
If one’s attention is drawn to drug-related cue words, they’ll be faster to detect dots that appear where the drug-related cue words were
Excessive appetite model of addiction author
Oxford
Excessive appetite model of addiction
All appetitive behaviours occur on a normal curve, meaning most people do it sometimes or moderately, and some people engage in the behaviour in excess of the social norm
Behaviours are restricted by constraints such as health consequences, religious beliefs, family norms, finances, government policy
According to the excessive appetite model of addiction, what is escalation of excessive appetite due to?
Primary processes: Incentive learning, cue conditioning, rapid emotional change and rewards, memory schemata
Secondary processes: Acquired emotional regulation cycles (negative reinforcement - drinking to alleviate negative effects), encourages further increase in consumption
Cognitive dissonance: Appetitive behaviours can reduce uncomfortable state of conflict (disharmony-reducing reactions)
PRIME theory
Organizes components of motivational systems into 5 themes:
1. Structure of motivational system (responses –> impulses –> inhibitory forces –> motives –> evaluations –> plans)
2. Focus on the moment: behaviour is controlled by forces operating NOW
3. Neural plasticity: Experience changes the underlying neural pathways of motivational system
4. Identity: Perceptions of ourselves affect our behaviour
5. The unstable mind: Behaviour interacts and fluctuates in response to moment-to-moment changes
Addiction spreads through each interconnected area of the motivational system; treatment must target all affected areas
Chaos theory
Processes may appear completely random, but abide by underlying patterns and laws, highly sensitive to conditions and changes
Responses in motivational system of PRIME theory
Starting, stopping, or modifying actions
Impulses vs inhibitions in motivational system of PRIME theory
Activation of CNS pathways underpinning actions, and competing pathways inhibiting them (urges)
Motives in motivational system of PRIME theory
Mental representations of future world states with feelings of anticipated pleasure/satisfaction (wants) or relief (needs)
Evaluations in motivational system of PRIME theory
Beliefs involving sense of what is useful/harmful (functions), right/wrong (moral), pleasing/displeasing (aesthetic)
Plans in motivational system of PRIME theory
Mental representations of future actions associated with feeling of varying degrees of commitment (rules)
PRIME theory and “oughts”
Use the term “ought” or “should” to refer to actions that we not want to do or feel a need to do but which we evaluate positively
Oughts will not lead to behaviour unless they can interact with identity to generate wants or needs
Role of identity in PRIME theory
Identity refers to our disposition to form mental representations of ourselves and the feelings attached to these
Potentially important source of motives
Ultimate source of self-regulation
Major source of stability of behaviour
Major elements of identity in PRIME theory
Labels, attributes, rules
Criticisms of cognitive task paradigms
Not clear what scores really mean
Little ecological validity: lab setting not true to real life
Attentional bias does not play a causal role in substance use
Methodological and statistical limitations of studies: absence of appropriate control groups, small sample sizes, variation in methodology across studies
3 types of cognitive interventions
Computerized cognitive training (CCT)
Cognitive remediation (CR)
Pharmacological enhancement
CCT
Software used to train/enhance specific cognitive processes
E.g., working memory training, approach/avoidance training, inhibitory control training
CR
Training in meta-cognitive processes
E.g., planning, goal-oriented behaviour, applied to real life
Pharmacological enhancement
Cognitive enhancers - drug shown to be beneficial for cognition
E.g., galantamine (acetylcholinesterase inhibitor used in dementia t(x)), modafinil (a non-amphetamine stimulant with wakefulness-inducing properties, used in sleep disorder t(x))
Of the 3 cognitive interventions discussed, which, if any, are effective?
Cognitive remediation
Pharmacology
Action and effects of drugs on living organisms
Pharmacokinetic factors
Those that influence how biologically available a drug is within the body
Examples of pharmacokinetic factors
Absorption, distribution, metabolism, and elimination of a drug
Pharmacodynamic factors
Concerned with how a drug interacts with its target receptors in the body to mediate the physiological effects of that drug within the body
Routes of administration
Oral
Rectal
Inhalation
Transdermal
Transmucosal
Parenteral
How is drug action terminated?
By chemical reactions that result in biological transformation –> facilitate excretion of drug metabolites
Drug elimination half-life
Time taken for the plasma concentration of a drug to fall by 50% when it has reached a state of being evenly distributed throughout the body
Agonists
Increases activity of NTs
Activate neuron by binding
Antagonists
Decreases activity of NTs
Block neuron by binding to it
Full agonists
Facilitate action at synapse and produce a similar response to an endogenous NT –> produces maximal response capability of a cell
Partial agonist
Reduced response efficiency (ability to generate biological response)
Can act as agonist at low doses when no other agonist is present and as an antagonist when a full agonist is present
Inverse agonist
Response which is opposite to the effects of an agonist
Generally describe neurotransmission
Excitatory pre-synaptic potential (EPSP) –> Action potential –> NTs –> EPSPs –> Action potential
Generally, how do psychoactive drugs act?
Interfere with NTs in one way or another
Long-term potentiation
Long-lasting facilitation of neurotransmission across neurons when the synapses between them are used repeatedly under certain conditions
What is long-term potentiation important for?
Critical to all learning (adaptive and maladaptive)
Protracted withdrawal
Withdrawal symptoms last a lot longer
Allostasis
Chronic substance use leads to adaptation: opponent processes lead to down- and up- regulation in opposite direction of the substance’s effects –> withdrawal
See notes for role of mesolimbic DA pathway
Actually look at them!
Is alcohol a depressant or stimulus?
Depressant
What does a depressant do?
Slow down physiological processes (heart rate, prefrontal cortex function, movement)
Where is alcohol most readily absorbed?
Through stomach and intestinal tract
What does alcohol inhibit?
Function of CNS
What NTs does alcohol act on?
GABA and glutamate
How does alcohol act on GABA?
As it is the main inhibitory NT of the CNS, it is enhanced by alcohol (sedation, relaxation, and inhibition of cognitive and motor skills)
How does alcohol impact the reward system?
Via opioid and dopinamergic pathways
Also impacts serotonin and cannabinoid pathways
What rank is alcohol for use prevalence in the world?
2nd
Explain how the effects of alcohol vary based on dose
Low dose: relaxation, elevated mood, dampens inhibition (liquid courage)
High dose: Sedation, death (shutting down CNS)
How do the hospitalization costs for alcohol compare to that for opioids?
13x higher
Effects of BAC
.00-.05: Buzz zone
.06-.11: Drunk zone
.12-.15: Elevated risk zone
.15-.25: High risk zone
.25+: Medical emergency zone
How is alcohol metabolized?
Mainly by enzyme alcohol dehydrogenase (ADH)
Is nicotine a depressant or a stimulant?
Stimulant
How is nicotine absorbed?
Through lungs, skin, GI tract, and nose/mouth membranes
How does nicotine impact brain activity?
Activates nicotinic acetyl choline receptors (nAChRs), which influence DA and ST activity
How quick does nicotine reach the brain through smoking?
7-10 secs
What is the half-life of nicotine?
2-3 hours
Is caffeine a depressant or a stimulant?
Stimulant
What ranking does caffeine place for use prevalence worldwide?
1
Psychological effects of caffeine
Increased arousal, decreased fatigue, enhanced psychomotor activity
What are effects of caffeine mediated by?
Adenosine receptors, which are thought to be involved in sleep
What does stopping caffeine consumption lead to?
Withdrawal symptoms, including aches, pains, and headaches
Is Caffeine Dependence Syndrome recognized as a clinical condition?
Yes in ICD-10
No in DSM-5, condition requiring further study
Is cocaine a stimulant or a depressant?
Stimulant
How does cocaine act as a stimulant?
Excites function of CNS
Exerts its effect by blocking reuptake of DA, noradrenalin, and ST
Where is cocaine derived from?
What does this work on?
Coca plant
DA, NE, ST
History of cocaine
Became popular in 1880s
Treat: headaches, toothaches, exhaustion, anesthetic
Freud: Uber coke
Coca cola
Is amphetamine a stimulant or a depressant?
Stimulant
Amphetamine structure
Structurally similar to DA; behave like cocaine on CNS and ANS, but with a longer duration of action
How does amphetamine work?
Agonist actions in the catecholaminergic NT systems; prevents degradation of DA, thereby increasing its availability
Legitimate uses of amphetamine throughout history
Nasal decongestants, weight suppressants, maintaining alertness, treat ADHD and narcolepsy
Methamphetamine
Reaches brain faster –> higher addictive potential
Routes of administration for amphetamine
Oral, injection, snorting, smoking
1/2 life of amphetamine
7-30 hrs
Psychostimulants in ADHD treatment
Most common pharmacological treatments for ADHD in Canada are:
Amphetamine-based psychostimulants (e.g., Adderall, Vyvanse)
Methylphenidate-based psychostimulants (e.g., Biphentin, Concerta)
How does amphetamine work?
Enters nerve terminal, causing it to release more DA, flooding the cytoplasm with DA
How does methamphetamine work?
Increases DA in cytoplasm, but does so in a more subtle, indirect way by blocking its reuptake
Opiate
Morphine, heroin, codeine
Opioids
Fentanyl, methadone
Effects of opioids
Pain relief!
Limbic system
Brain stem
Spinal cord
Signs of an opioid OD
Blue lips or nails
Dizziness and confusion
Can’t be woken up
Choking, gurgling or snoring sounds
Slow, weak or no breathing
Drowsiness or difficulty staying awake
How to help someone who is experiencing an opioid overdose?
Naloxone
Steps to acting in an opioid OD
- Shout and shake
- Call 911
- Give naloxone
- Support breathing
Step 5: Assess and repeat steps 3 and 4
Benzodiazepine categories
Sedative-hypnotics
Anxiolytics
Minor tranquilizers
How do benzodiazepines work?
Non-selective depressant action through facilitating binding of GABA, the main inhibitory NT
Act on receptors in amygdala, orbitofrontal cortex, and insula –> reduce anxiety, agitation, and fear
Benzodiazepine types
Valium, Ativan, Klonopin, Xanax
Why are benzodiazepines commonly prescribed?
Short-term treatment of anxiety and sleep disorders, as well as seizures, as a muscle relaxant, and for surgical procedures
% of people who use benzodiazepines meet criteria for abuse
17%
Relation of benzodiazepines to other drugs
Often taken concurrently with opioid, cocaine, methamphetamine to control withdrawal symptoms and unpleasant side effects
Treatment for acute alcohol withdrawal and prevent relapse to alcohol addiction
Long-term use of benzodiazepine can result in…
Cognitive and psychomotor impairment
Why can cannabis be referred to as the jack of all trades?
Has properties of hallucinogen, depressant, and stimulants
Psychoactive component in cannabis
Effects?
THC
Analgesia, appetite control, motor/cognitive impairments
Clinical uses for cannabis
CBD is the strongest treatment for childhood epilepsy
Why can cannabis impact anxiety differently in different people?
Cannabis activates cannabinoid receptors, which decrease excitatory glutamate - this can be why it reduces anxiety, for some
Cannabis also decreases inhibitory GABA (opposite of Xanax) –> weakening GABA can lead to severe anxiety
Why can two people react differently to cannabis?
Whether someone becomes relaxed or anxious likely depends on their balance of glutamate to GABA activity, as well as the strain (highly variable)
