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Psychology of Addiction > Quiz 1 > Flashcards

Quiz 1 Flashcards

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1
Q

Explain the components of addiction.

A

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

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2
Q

How is cognition implicated in addiction?

A

Attention, memory, and perception

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3
Q

Incentive-sensitization theory

A

Associative learning and sensitization (over time, a greater effect is observed) of brain motivational systems to drug and drug associated cues

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4
Q

What mediates pleasurable effects of drugs?

A

Mesotelencephalic DA system

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5
Q

What NTs are associated in initial reinforcing effects of most drugs?

A

DA, ST, glutamate, and GABA

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6
Q

What 4 factors influence the transition to addiction?

A

Genetic predisposition
Developmental factors
Social context
Stress and co-occurrence of other psychiatric disorders

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7
Q

How does genetic predisposition influence the transition to addiction?

A

Sensitivity and subjective experience, heritability

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8
Q

How do developmental factors influence the transition to addiction?

A

Adolescents are particularly sensitive to drug effects and external pressures

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9
Q

Distribution theory of addiction

A

Attributes the current increase in both substance and behavioural addictions to a lack of psychosocial integration (social dislocation) in the modern world

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10
Q

Psychosocial integration

A

Interdependence between an individual and their society, and is proposed to fulfill the human need for both individual autonomy and social belonging

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11
Q

How does stress influence the transition to addiction?

A

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

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12
Q

What are common co-morbidities with addiction?

A

Mood disorders, anxiety disorders, and personality disorders

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13
Q

5 models/theories of addiction

A

Moral model
Choice model
Medical/disease model
Indigenous perspective
Biopsychosocial model

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14
Q

Moral model briefly

A

Addiction as character flaw

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15
Q

Choice model briefly

A

Addiction as adaptation to personal environment

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16
Q

Medical/disease model briefly

A

Addictive drugs cause LT progressive changes in the brain

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17
Q

Indigenous perspectives briefly

A

Balance of physical, mental, emotional, and spiritual health

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18
Q

Biopsychosocial model briefly

A

Interplay of biological, psychological, and social factors

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19
Q

When was the moral model most prevalent?

A

18th and early 19th century

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20
Q

Explain the cultural context setting for the moral model

A

Addiction was common
Cocaine was viewed as a wonder drug
Opioids were a cure all

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21
Q

What movement took place during the moral model

A

Temperance movement

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22
Q

Temperance movement

A

Preaching moderation/abstinence pledge
Led by the clergy
Moral failure/sin: “just stop”
Public shaming

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23
Q

When was the disease model most prevalent?

A

End of the 19th century

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24
Q

What was the intention behind the disease model?

A

To shift the view of addiction from moral failure to disease
Intended to reduce stigma, but largely failed

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25
Q

3 important points about the disease model of addiction

A

Categorical approach
Can’t be cured
12 step programs

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26
Q

Explain choice model

A

Social recovery should be used –> foster connection
Emphasizes the role of society and community

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27
Q

What is the backbone behind the Indigenous perspective?

A

The Medicine Wheel

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28
Q

What does the Indigenous perspective recognize?

A

Colonial-linked stressors and cultural resilience factors

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29
Q

What is used as intervention in the Indigenous perspective?

A

Culture

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30
Q

Albert Marshall view

A

Two-eyed seeing
Recognizes Indigenous knowledge as a distinct and whole knowledge system that exists alongside mainstream/Western science

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31
Q

3 factors of biopsychosocial model

A

Biological
Psychological
Social

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32
Q

Biological aspects in biopsychosocial model

A

Genetics: moderate to high
Individual differences in reward sensitivity

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33
Q

Psychological aspects in biopsychosocial model

A

Mental health
Impulsivity

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34
Q

Social aspects in biopsychosocial model

A

Adversity
Social determinants of health

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35
Q

How is addiction diagnosed?

A

DSM-5 and ICD-10

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36
Q

Classification of addiction in DSM-5

A

Substance-related and addictive disorders

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37
Q

How many categories of addictions are included in DSM-5

A

10 substances
1 behaviour

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38
Q

Criteria for diagnosis in DSM-5

A

Pattern of engagement in past 12 months that causes clinically significant harm
2 of 11 symptoms

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39
Q

Severity as it relates to number of symptoms

A

Mild: 2-3
Moderate: 4-5
Severe: 6+

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40
Q

DSM-5 diagnostic guidelines

A

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

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41
Q

Addiction name in DSM-5

A

Substance Use Disorder

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42
Q

What 10 substances are included in the DSM-5?

A

Alcohol
Caffeine
Cannabis
Hallucinogens
Inhalants
Opioids
Sedatives/Hypnotics/Anxiolytics
Stimulants
Tobacco
Other

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43
Q

Conditions for further study

A

Caffeine use disorder
Gaming use disorder

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44
Q

4 main classes of criteria for DSM-5

A

Impaired control
Social impairment
Risky use
Pharmacological criteria

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45
Q

Impaired control

A

Use more than intended
Want to cut down
Time devoted to substances
Cravings

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46
Q

Social impariment

A

Cannot fulfill major obligations
Use despite problems
Reduce/stop important activities

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47
Q

Risky use

A

Use in physically dangerous situations
Use despite physical or psychological consequences

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48
Q

Pharmacological criteria

A

Tolerance
Withdrawal

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49
Q

What is the only behavioural addiction included in the DSM-5?

A

Gambling

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50
Q

Similarities between gambling and substance use

A

Risk factors
Neurological
Treatment

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51
Q

ICD-10 diagnostic guide for dependence syndrome

A

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

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52
Q

What is an important distinguish in the ICD-10

A

Harmful use is distinguished from dependence syndrome

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53
Q

Shaffer transdiagnostic model

A

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

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54
Q

Griffiths transdiagnostic model

A

Salience
Mood modification
Tolerance/withdrawal
Conflict
Relapse

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55
Q

Three classifications of continuum model

A

Addiction
Problematic use
Recreational use

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56
Q

Addiction classification of continuum model

A

Compulsion
Negative consequences
Show symptoms of addiction
(Activity is no longer pleasurable, just use to avoid negative feelings)

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57
Q

Problematic use classification of continuum model

A

Habit
Some negative consequences
Begin to show symptoms of addictions
(Attempts to quit)
(Impacting daily routine)

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58
Q

Recreational use classification of continuum model

A

Casual
Negligible health or social effects
May have some positive effects

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59
Q

Why does terminology matter when describing individuals living with addiction?

A

Ways of describing people with substance use concerns can perpetuate or diminish stigmatizing attitudes

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60
Q

Kelly & Westerhoff study design

A

Randomized, between-subjects, cross-sectional design
Clinicians attending two mental health conferences were asked to read a vignette

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61
Q

Kelly & Westerhoff study findings

A

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”

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62
Q

Instead of “addict”, “abuser”, and “junkie”

A

Use “habitual user”, “person with substance use disorder”, “active in addiction”

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63
Q

Instead of “abuse”, “habit”, “drug habit”

A

Use “Misuse”, “harmful use/problem use”, “risky use”

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64
Q

Instead of “clean”, or “dirty”

A

Use “sober”, “abstinent”, “drug-positive or -negative”, “substance-free”, “addiction free”, or “remission”

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65
Q

Instead of “replacement” or “substitution therapy”

A

Use “treatment”, “medications”

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66
Q

Prevalence of addiction in Canada

A

21.6% of Canadians meet criteria for a lifetime Substance Use Disorder

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67
Q

Which drug results in the largest cost to Canada?

A

Alcohol

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68
Q

In order, name the four largest total overall costs attributable to substance use in Canada

A

Lost productivity
Healthcare
Criminal justice
Other

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69
Q

Are males or females more harmed by substance use at a young age?

A

Females

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70
Q

Heyman claim to fame

A

Hyperbolic discounting

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71
Q

Delay discounting

A

Human tendency to prefer smaller but more immediate rewards over delayed rewards

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72
Q

Hyperbolic discounting

A

Increased delay discounting exacerbated by addictive process

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73
Q

How did Heyman view addiction?

A

A disorder of normal choice processes (compulsive nature of addiction)

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74
Q

Cognitive bias

A

Selective info processing, mental heuristics/shortcuts that aren’t always helpful

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75
Q

3 types of cognitive bias related to addiction

A

Outcome expectancies
Self-efficacy
Cue reactivity

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76
Q

Outcome expectancies example

A

I’ll have an easier time socializing if I get drunk

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77
Q

Self-efficacy example

A

I can stop whenever I want

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78
Q

Cue reactivity

A

Drug-related cues induce powerful effects

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79
Q

Cognitive model of drug urges and drug-use behaviour author

A

Tiffany

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80
Q

Cognitive model of drug urges and drug-use behaviour

A

Drug use becomes automatic

81
Q

What is an automatic process?

A

Fast and gets faster with practice
Initiated and carried out outside conscious awareness
Lacking control
Effortless (cognitively undemanding)

82
Q

Non-automatic processes

A

Slow, effortful, and require intention and attention

83
Q

What do cognitive models define craving as?

A

Result of non-automatic interruption of automatized drug use action plans

84
Q

Affective processing model author

A

Baker

85
Q

Affective processing model

A

Drugs are taken to alleviate negative affect = negative reinforcement

86
Q

In the affective processing model, how does negative affect influence drug use?

A

Negative affect increases levels of “hot” info processing instead of “cool” controlled info

87
Q

Positive reinforcement as it relates to addiction

A

Add something pleasant

88
Q

Example of positive reinforcement as it relates to addiction

A

I’m high, this feels great

89
Q

Example of positive punishment as it relates to addiction

A

I choose not to drink alcohol because it always makes me vomit

90
Q

Negative reinforcement as it relates to addiction

A

Take away something unpleasant

91
Q

In the affective processing model, how does negative affect influence drug use?

A

Negative affect increases levels of “hot” info processing instead of “cool” controlled info

92
Q

Example of negative reinforcement as it relates to addiction

A

Wow, this drug momentarily alleviates my aweful depression

93
Q

Negative punishment as it relates to addiction

A

Take away something unpleasant

94
Q

Example of negative punishment as it relates to addiction

A

I’d probably lose my job if I showed up high or drunk

95
Q

Hot cognition

A

Emotional thought process

96
Q

Cold cognition

A

Cognitive thought process

97
Q

Hot info processing

A

In addiction, behaviour becomes reactive, governed by urgent need to relieve negative emotions

98
Q

Attentional bias hypothesis

A

Conditioned drug stimulus produces an increase in corticostriatal dopamine (especially in anterior cingulate gyrus, amygdala, and nucleus accumbens), which directs attention toward drug stimuli

99
Q

What does the attentional bias hypothesis lead to (2 things)

A

Motor preparation and hyperattention to drug stimuli
Enhances craving, promotes relapse

100
Q

How does the attentional bias hypothesis view drug craving?

A

Emotional conditioned appetite motivational state produced by stimuli associated with reward effects

101
Q

What does the attentional bias hypothesis emphasize?

A

Importance of attentional bias as the cognitive mediator between the drug stimulus and the behavioural response to this stimulus

102
Q

4 cognitive methods for studying drug use behaviour

A

Stroop task
Memory priming
Dot-probe task
Reaction time experiment

103
Q

Addiction Stroop task procedure

A

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

104
Q

Why might the Addiction Stroop task work?

A

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

105
Q

Evidence for addiction Stroop task

A

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

106
Q

Dot-probe task

A

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

107
Q

Excessive appetite model of addiction author

A

Oxford

108
Q

Excessive appetite model of addiction

A

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

109
Q

According to the excessive appetite model of addiction, what is escalation of excessive appetite due to?

A

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)

110
Q

PRIME theory

A

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

111
Q

Chaos theory

A

Processes may appear completely random, but abide by underlying patterns and laws, highly sensitive to conditions and changes

112
Q

Responses in motivational system of PRIME theory

A

Starting, stopping, or modifying actions

113
Q

Impulses vs inhibitions in motivational system of PRIME theory

A

Activation of CNS pathways underpinning actions, and competing pathways inhibiting them (urges)

114
Q

Motives in motivational system of PRIME theory

A

Mental representations of future world states with feelings of anticipated pleasure/satisfaction (wants) or relief (needs)

115
Q

Evaluations in motivational system of PRIME theory

A

Beliefs involving sense of what is useful/harmful (functions), right/wrong (moral), pleasing/displeasing (aesthetic)

116
Q

Plans in motivational system of PRIME theory

A

Mental representations of future actions associated with feeling of varying degrees of commitment (rules)

117
Q

PRIME theory and “oughts”

A

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

118
Q

Role of identity in PRIME theory

A

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

119
Q

Major elements of identity in PRIME theory

A

Labels, attributes, rules

120
Q

Criticisms of cognitive task paradigms

A

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

121
Q

3 types of cognitive interventions

A

Computerized cognitive training (CCT)
Cognitive remediation (CR)
Pharmacological enhancement

122
Q

CCT

A

Software used to train/enhance specific cognitive processes
E.g., working memory training, approach/avoidance training, inhibitory control training

123
Q

CR

A

Training in meta-cognitive processes
E.g., planning, goal-oriented behaviour, applied to real life

124
Q

Pharmacological enhancement

A

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))

125
Q

Of the 3 cognitive interventions discussed, which, if any, are effective?

A

Cognitive remediation

126
Q

Pharmacology

A

Action and effects of drugs on living organisms

127
Q

Pharmacokinetic factors

A

Those that influence how biologically available a drug is within the body

128
Q

Examples of pharmacokinetic factors

A

Absorption, distribution, metabolism, and elimination of a drug

129
Q

Pharmacodynamic factors

A

Concerned with how a drug interacts with its target receptors in the body to mediate the physiological effects of that drug within the body

130
Q

Routes of administration

A

Oral
Rectal
Inhalation
Transdermal
Transmucosal
Parenteral

131
Q

How is drug action terminated?

A

By chemical reactions that result in biological transformation –> facilitate excretion of drug metabolites

132
Q

Drug elimination half-life

A

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

133
Q

Agonists

A

Increases activity of NTs
Activate neuron by binding

134
Q

Antagonists

A

Decreases activity of NTs
Block neuron by binding to it

135
Q

Full agonists

A

Facilitate action at synapse and produce a similar response to an endogenous NT –> produces maximal response capability of a cell

136
Q

Partial agonist

A

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

137
Q

Inverse agonist

A

Response which is opposite to the effects of an agonist

138
Q

Generally describe neurotransmission

A

Excitatory pre-synaptic potential (EPSP) –> Action potential –> NTs –> EPSPs –> Action potential

139
Q

Generally, how do psychoactive drugs act?

A

Interfere with NTs in one way or another

140
Q

Long-term potentiation

A

Long-lasting facilitation of neurotransmission across neurons when the synapses between them are used repeatedly under certain conditions

141
Q

What is long-term potentiation important for?

A

Critical to all learning (adaptive and maladaptive)

142
Q

Protracted withdrawal

A

Withdrawal symptoms last a lot longer

143
Q

Allostasis

A

Chronic substance use leads to adaptation: opponent processes lead to down- and up- regulation in opposite direction of the substance’s effects –> withdrawal

144
Q

See notes for role of mesolimbic DA pathway

A

Actually look at them!

145
Q

Is alcohol a depressant or stimulus?

A

Depressant

146
Q

What does a depressant do?

A

Slow down physiological processes (heart rate, prefrontal cortex function, movement)

147
Q

Where is alcohol most readily absorbed?

A

Through stomach and intestinal tract

148
Q

What does alcohol inhibit?

A

Function of CNS

149
Q

What NTs does alcohol act on?

A

GABA and glutamate

150
Q

How does alcohol act on GABA?

A

As it is the main inhibitory NT of the CNS, it is enhanced by alcohol (sedation, relaxation, and inhibition of cognitive and motor skills)

151
Q

How does alcohol impact the reward system?

A

Via opioid and dopinamergic pathways
Also impacts serotonin and cannabinoid pathways

152
Q

What rank is alcohol for use prevalence in the world?

A

2nd

153
Q

Explain how the effects of alcohol vary based on dose

A

Low dose: relaxation, elevated mood, dampens inhibition (liquid courage)
High dose: Sedation, death (shutting down CNS)

154
Q

How do the hospitalization costs for alcohol compare to that for opioids?

A

13x higher

155
Q

Effects of BAC

A

.00-.05: Buzz zone
.06-.11: Drunk zone
.12-.15: Elevated risk zone
.15-.25: High risk zone
.25+: Medical emergency zone

156
Q

How is alcohol metabolized?

A

Mainly by enzyme alcohol dehydrogenase (ADH)

157
Q

Is nicotine a depressant or a stimulant?

A

Stimulant

158
Q

How is nicotine absorbed?

A

Through lungs, skin, GI tract, and nose/mouth membranes

159
Q

How does nicotine impact brain activity?

A

Activates nicotinic acetyl choline receptors (nAChRs), which influence DA and ST activity

160
Q

How quick does nicotine reach the brain through smoking?

A

7-10 secs

161
Q

What is the half-life of nicotine?

A

2-3 hours

162
Q

Is caffeine a depressant or a stimulant?

A

Stimulant

163
Q

What ranking does caffeine place for use prevalence worldwide?

A

1

164
Q

Psychological effects of caffeine

A

Increased arousal, decreased fatigue, enhanced psychomotor activity

165
Q

What are effects of caffeine mediated by?

A

Adenosine receptors, which are thought to be involved in sleep

166
Q

What does stopping caffeine consumption lead to?

A

Withdrawal symptoms, including aches, pains, and headaches

167
Q

Is Caffeine Dependence Syndrome recognized as a clinical condition?

A

Yes in ICD-10
No in DSM-5, condition requiring further study

168
Q

Is cocaine a stimulant or a depressant?

A

Stimulant

169
Q

How does cocaine act as a stimulant?

A

Excites function of CNS
Exerts its effect by blocking reuptake of DA, noradrenalin, and ST

170
Q

Where is cocaine derived from?
What does this work on?

A

Coca plant
DA, NE, ST

171
Q

History of cocaine

A

Became popular in 1880s
Treat: headaches, toothaches, exhaustion, anesthetic
Freud: Uber coke
Coca cola

172
Q

Is amphetamine a stimulant or a depressant?

A

Stimulant

173
Q

Amphetamine structure

A

Structurally similar to DA; behave like cocaine on CNS and ANS, but with a longer duration of action

174
Q

How does amphetamine work?

A

Agonist actions in the catecholaminergic NT systems; prevents degradation of DA, thereby increasing its availability

175
Q

Legitimate uses of amphetamine throughout history

A

Nasal decongestants, weight suppressants, maintaining alertness, treat ADHD and narcolepsy

176
Q

Methamphetamine

A

Reaches brain faster –> higher addictive potential

177
Q

Routes of administration for amphetamine

A

Oral, injection, snorting, smoking

178
Q

1/2 life of amphetamine

A

7-30 hrs

179
Q

Psychostimulants in ADHD treatment

A

Most common pharmacological treatments for ADHD in Canada are:
Amphetamine-based psychostimulants (e.g., Adderall, Vyvanse)
Methylphenidate-based psychostimulants (e.g., Biphentin, Concerta)

180
Q

How does amphetamine work?

A

Enters nerve terminal, causing it to release more DA, flooding the cytoplasm with DA

181
Q

How does methamphetamine work?

A

Increases DA in cytoplasm, but does so in a more subtle, indirect way by blocking its reuptake

182
Q

Opiate

A

Morphine, heroin, codeine

183
Q

Opioids

A

Fentanyl, methadone

184
Q

Effects of opioids

A

Pain relief!
Limbic system
Brain stem
Spinal cord

185
Q

Signs of an opioid OD

A

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

186
Q

How to help someone who is experiencing an opioid overdose?

A

Naloxone

187
Q

Steps to acting in an opioid OD

A
  1. Shout and shake
  2. Call 911
  3. Give naloxone
  4. Support breathing
    Step 5: Assess and repeat steps 3 and 4
188
Q

Benzodiazepine categories

A

Sedative-hypnotics
Anxiolytics
Minor tranquilizers

189
Q

How do benzodiazepines work?

A

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

190
Q

Benzodiazepine types

A

Valium, Ativan, Klonopin, Xanax

191
Q

Why are benzodiazepines commonly prescribed?

A

Short-term treatment of anxiety and sleep disorders, as well as seizures, as a muscle relaxant, and for surgical procedures

192
Q

% of people who use benzodiazepines meet criteria for abuse

A

17%

193
Q

Relation of benzodiazepines to other drugs

A

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

194
Q

Long-term use of benzodiazepine can result in…

A

Cognitive and psychomotor impairment

195
Q

Why can cannabis be referred to as the jack of all trades?

A

Has properties of hallucinogen, depressant, and stimulants

196
Q

Psychoactive component in cannabis
Effects?

A

THC
Analgesia, appetite control, motor/cognitive impairments

197
Q

Clinical uses for cannabis

A

CBD is the strongest treatment for childhood epilepsy

198
Q

Why can cannabis impact anxiety differently in different people?

A

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

199
Q

Why can two people react differently to cannabis?

A

Whether someone becomes relaxed or anxious likely depends on their balance of glutamate to GABA activity, as well as the strain (highly variable)

Psychology of Addiction (1 decks)

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