Module 1 Flashcards

(37 cards)

1
Q

Risk factors SUD

A

younger age
Gender: men greater risk
Living alone
Being unemployed
Very high degree of urbaniyation
(Unrelated to income)
(Unrelated to country of origin)

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2
Q

Individual risk factors

A

Early aggressive behaviour in childhood
Early drug use ->importance of prevention

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3
Q

Individual Protective factors against SUD

A

Self-efficacy (belief in self control)
Academic performance

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4
Q

Family risk factors SUD

A

Lack of parental supervision
Substance abuse by caregivers

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5
Q

Protective family factors SUD

A

Parental monitoring and support

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6
Q

Peer risk factors SUD

A

Low refusal skills
Poor social skills

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7
Q

Protective peer factors

A

Positive relationships

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8
Q

School risk factors SUD

A

Drug availability at school

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9
Q

Protective school factors SUD

A

School anti-drug policies

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10
Q

Community risk factors SUD

A

Community poverty

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11
Q

Community protective factors

A

Neighbourhood resources

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12
Q

Risk addictive potential drugs

A

Differs between drug + administration through ingesting or injecting

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13
Q

Moral model of addiction

A

A sign of moral weakness: drug abuse and drug seeking behaviour is immoral and in conflict with social norms and values

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14
Q

Pharmacological model (mid 19th century)

A

Addicts are not to blame: highly addictive substance is
->prohibitions: prevent people from getting involved with the substances

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15
Q

Symptomatic model (1930-1950)

A

Not a condition in itself, but rather a symptom of an underlying neurotic character or personality disorder
-> long-term, insight-oriented psychotherapeutic treatment

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16
Q

Disease model (1940-1960)

A

There are fundamental biological and psychological differences between addicts and non-addicts, making the former unable to use substances in moderation
-> complete abstinence from substance

17
Q

Learning theory (1960-1970)

A

A form of maladaptive learned behaviour that can be unlearned again
->behavioural therapeutic interventions

18
Q

Bio-psycho-social model (1970-1990)

A

Both the onset and termination are the result of continuous interaction between biological, psychological and social factors
->multi-modal interventions in which attention is on many factors

19
Q

Brain disease model (1990 - onwards)

A

Innate vulnerability forms the basis of repeated use and this repeated use leads to important, difficult to reverse, brain changes leading to impaired cognitive control functions and craving habits
-> pharmacological and behavioural therapeutic interventions

20
Q

Criticism on the brain disease model

A
  • most people beat addiction by very hard effort. We cannot say this about medical diseases
  • people take substances out of choice and also have to make a choice to stop taking them. They are not blameless victims of some illness they have no control over.
21
Q

Homeostatic account (theory of structural changes)

A

Structural changes are a CONSEQUENCE of addiction:
->chronic overstimulation of dopamine D2 receptors > brain compensate by downregulating these receptors (explains anhedonia/dysphoria)

22
Q

Reward deficiency syndrome (RDS) account (theories of structural changes)

A

Addiction is the RESULT of structural differences
-> individuals with less receptors (chronic dopamine deficiency) have lower reward sensitivity > vulnerable for addiction because they look for stronger stimuli to activate the reward system

23
Q

2 notable differences in how the dopamine system reacts towards (unexpected) natural vs drug rewards

A
  1. the reaction of the dopamine system is much stronger for drug rewards
  2. the response to the CS is stronger for drug rewards than for natural rewards: the peak is higher. > central to temporal difference account
24
Q

Temporal difference account

A

Idea that, because the dopamine response to the CS is stronger for drug rewards, drug-related cues and actions would continue to be reinforced too pathological levels

25
Incentive -sensitisation theory
Idea that the core feature of addiction is pathological motivation for drugs (wanting/craving), together with impaired cognitive control, which results from incentive sensitisation
26
Conditioned opponent theories to the withdrawal-based hypotheses
Associated conditioning causes predictive drug cues to elicit conditioned tolerance and conditioned withdrawal symptoms
27
2 types of wanting in drug addiction
1.COGNITIVE WANTING: conscious, explicit desire for a specific reward 2. INCENTIVE SALIENCE ‘WANTING‘: cue triggered wanting that does not involve explicit goals or rewards that one is aware of
28
aberrant learning theory of addiction
Idea that drugs alter learning processes, promoting abnormal learning, which causes the transition to addiction -> compulsivity in addiction arises because drugs facilitate the learning of automatic S-R habits which confer compulsivity into actual behaviour
29
Incentive salience of drug-associated stimuli can be recognised in different ways
1. motivational magnet 2. reinforcing 3. reinstatement 4. wanted
30
Incentive-sensitisation: research methods to recognise the different ways of drug-associated stimuli
- Motivational magnet: pavlovian conditioning paradigm - reinforcing: conditioned reinforcement paradigm (instrumental/operant conditioning) - reinstatement: reinstatement paradigm - wanted: progressive ratio experiments
31
3 phases of reinstatement experiments
1. acquisition 2. extinction 3. reinstatement test (of cue/stimulus, e.g. light, not the drug itself)
32
3 types of reinstatement
1. cue induced reinstatement 2. prime-induced reinstatement (by drug itself) 3. stress induced reinstatement
33
barriers to seeking treatment
1. attitudinal 2. readiness for change 3. stigma 4. financial/cost 5. structural
34
'Reward deficiency syndrome' theor
number of D2 receptors relates to individual differences in reward sensitivity: less receptors means lower reward sensitivity and higher vulnerabilitz for addiction (natural rewards such as food are not sufficient)
35
neural sensitization
increase in the ability of drugs to elevate dopamine transmission in brain regions that receive dopamine inputs, such as the nucleus accumbens
36
3 behavioural ways in which IS is expressed
1. drug-associated stimuli elicit attention + approach towards the, acting as "motivational magnets" 2. drug-associated stimuli become reinforcers in their own right 3. drug-associated stimuli and drugs can induce relapse
37