PSY1003 WEEK 8 Flashcards

1
Q

why do we no longer tend to use the term of addiction

A

implies character weakness/moral failures - replaced by dependence to imply emphasis on biological adaptation moer

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2
Q

how does DSM-5 criteria define an SUD

A

doesn’t tell us what an SUD is
meet 2/11 criteria
3 severity categories: mild, moderate, severe but 2036 possible combination so can have shared diagnosis but no commonality

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3
Q

how does Heather define addiction

A

someone is addicted if they continue to use drugs despite a sincere intention to do otherwise

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4
Q

what statistic on the British population is a limitation of SUD diagnostics criteria

A

British Government (2013) = 39% men 27% women drink unsafe levels of alcohol and meet SUD criteria but only 5% has diagnosis

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5
Q

give some examples of epidemiology of SUD around world

A

highest prevalance alcohol (women) = Russia, North-east Asia, Australia, South America
(men) = South-east Asia, South America
any SUD in men + women = UK, South America, North America
UK = decline in numbers of young people drinking

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6
Q

what political factors can influence addiction

A

introduction of law = smoking ban meant more quits

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7
Q

explain comorbidity and addiction

A

higher SUD in those with Bipolar, depression, GAD, social anxiety, PTSD and Sz

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8
Q

heritability estimates for SUD ranges between 30-70%. explain why this is (with factors)

A

shared environment, epigenetics, easy access, modelling, poverty

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9
Q

explain both adoption studies and gene evidence for heritability in SUD

A

adoption studies = adoptee with alcoholic parent more likely, as well as any SUD
but no single gene identified for addiction. candidate gene polymorphisms (mutations) found for addict characteristic (such as alcohol metabolisms rate, disinhibition)

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10
Q

explain traumatic life event link to SUD

A

sexual abuse in childhood
drug use to supress emotion, warp reward system (alters brain formations)
unable to cope with negative emotion and suppress addiction drives

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11
Q

name 6 addict theories

A
  1. take drugs due to outcomes of what drug produce
  2. compulsive drug use
  3. addiction is a brain disease
  4. habits
  5. dual-process theories
  6. choice
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12
Q

explain conditioning theories for addiction (taking drugs due to the outcomes they produce)

A

outcomes = to get high, increase alertness, reduce fatigue, social faciliation, alleviate distress
operant conditioning (voluntary, is maintained by consequences)
classical conditioning (drug acts as UCS and taken in presence of drug-related cues eg: pair alcohol (US) with pub (CS) and need drink when see it (CR)
positive reinforcement thought to work for drugs producing euphoria and have little withdrawal effects (cocaine, cannabis)
negative reinforcement for drugs with large withdrawal effects (smoking)

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13
Q

explain conditioning theories of addiction with the rat research example

A

a rat learns to press lever if means they are given cocaine

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14
Q

however, what is a defining characteristic of addiction that occurs, reducing reliability of conditioning theories

A

continued use even though individual wishes to stop, even when positive effects diminish and negative effects start (withdrawal, poor health, marital breakdown, prison)

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15
Q

define compulsion

A

need to persist despite behaviour producing negative consequences

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16
Q

explain the compulsive (biological) drug use theory

A

compulsion to take drugs despite consequence due to brain disease (dopamine reward system disruption)
most of drugs stimulate dopamine reward system
addiction to drugs instead of natural dopamine spikes (food) because natural stimuli become habituated so spikes become consistent
dopamine contributes to classical conditioning
dopamine reward is shown when expecting drugs, not during

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17
Q

name the brain areas involved in dopamine reward system

A

nucleus accumbens, ventral tegmental area and prefrontal cortex

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18
Q

explain incentive sensititsation theory (biological theory)

A

repeated use leads to sensitised spike in mesolimbic dopamine systems
dopamine response shown when drug cues present, so dopamine sensitivity manifests itself as ‘incentive salience’, causing craving

19
Q

explain Hedonic homeostatic dysregulation theory (biological theory)

A

repeated drug use leading to dopamine spikes result in a suppressed dopamine function so brain adapts to repeated dopamine spikes and decreases in dopamine cause withdrawal = lowered set point results in lower mood (as dopamine regulates mood)
lab evidence showing craving even when drug effects no longer liked

20
Q

give limitations of biological theories for addiction from brain studies on mesolimbic system (which supports hedonic homeostasis dysregulation)

A

dopamine in mesolimbic system is suppressed in addict meaning is closer to HHD = when addicts given drug, raises dopamine level and shows a lower response

21
Q

what is the overall thought of roles played by both the hedonic homeostasis dysregulation theory and incentive sensitisation theory in addiction

A

IST involved in earlier stages of addiction, HHD in later

22
Q

explain the theory of addiction being brain disease (including research evidence on effect of drugs on children and adolescents)

A

grey matter decreased in prefrontal regions in addict
in children of drug addicts, some of these effects have already developed before using
long term drug use in adolescences can lead to brain damage in adulthood (changes in prefrontal cortex, structural changes, gene expression, reduced neurogenesis) linked to behavioural changes of increased risk taking and impulsive behaviour, anxiety

23
Q

give a research example of addiction brain change mirroring emotionally and motivationally loaded experiences (Fisher et al, 2010)

A

brain change resulting from addiction mirrors those seen when highly rewarding behaivours are repeated like romantic love (activation in ventral tegmental area when looking at image o current romantic partner)

24
Q

explain the habit theory = “model of automaticity”

A

drug using is voluntary, then with experience it becomes automatice

25
Q

evaluate automaticity habit model

A
  1. intuitive appeal for certain addictions: common to see chain smoke without thought, but in other addictions planning is needed (obtaining drugs etc
  2. assumes addictions are automatic but doesn’t include role of motivation (only use S-R habits)
26
Q

explain the SOR instrumental learning perspective of habit theory

A

Stimulus - heroin paraphernalia
anticipated Outcomes - getting high
Response - injecting heroin

when repeated outcome is lost, so S directly form R (habit causes a shift in SOR to SR)

27
Q

evaluate the SOR learning theory of habits (including research)

A

lab rats become habitual an persist despite negative consequence (but is this applied to humans)
can only study role of habit in addicts who really want to stop, and difficult to do

28
Q

explain the dual-process (cognitive) theories

A

controlled and automatic cognitive process contribute to addiction
1. controlled are outcome experience and intentions to use
2. automatic are attentional biases, spontaneous memory associations, automatic approach tendencies

in a novice, controlled cognitive processes occur so using is voluntary
outcome expectancies (positive drug experience) formed during youth, affecting beliefs and then intentions with using
experienced users have imbalance, so automatic are stronger than controlled meaning activates reward system, habitual using

29
Q

what does evidence in dual-process theory suggest may be a positive treatment

A

automatic cognitive processing bias for substance-related cues means re-training cognitive processing biases is effective treatment. can also predict future
using cognitive bias modification = simple motor response (see cues, initate response) - see alcohol, drink, but try reprogramming by use of avoidance move
using joystick to train patient to push cue away, is more effective than a standard

30
Q

how can dual-process theories account for individual differences

A

individual executive functions difference determines how we can flexibly modify behaviour as response to environmental demand = memory capacities moderate automatic and controlled process relationship, impacts drug use, with poor working memory linked to drug use

31
Q

outline defence of choice theory

A
  1. motivation to change is best recovery prediction - use of motivational interviewing resolve ambivalence, increases change motivations and is effective
  2. drug use is sensitive to economic factors (politics, prices changing) so means contingency management (receive small incentive) is a effective treatment
  3. if SUD is cureable by raising price/motivation, then is not disease
32
Q

what are flaws of choice theory, and why is it sometimes applied

A
  1. ICD and DSM state addicts wants to quit but cant
  2. doctors and politicians go along with addiction as medicalises low moral parts of society
33
Q

what influences our choice on treatment

A

depends on goal (reduction or abstinence) and assessing SUD severity, potential court outcome , use case formualtion to decide if detox, CBT/MI, meds AA is useful

34
Q

how does CBT work

A

focus on how thoughts leads to feeling, then behaviours through identifying distorted thoughts leading to negative feelings that lead to drug use
improve coping skills, so works if addict formualtes and practices skills

35
Q

how does motivational interviewing work

A

resolves individual ambivalence regarding drug use
works as changes motivational balance and increases client change talk (change from I could, to I can)
doesn’t involve clinician providing structured advice, but encourage addict to see negatives, generate own motivation

36
Q

what are self-help addiction groupd

A

not part of mainstream medicine (is free to taxpayer)
each member paired with sponsor - a recovered addict who provides moral support and encouragement
helps achieve and maintain sobriety
effective as increases self-efficacy and brings about social network change

37
Q

explain contingency management

A

paying people to abstain from usage, but tend to have more relapses

38
Q

why is pharmacotherapy usually rare

A

cannot address dopamine reward systems dysfunction

39
Q

explain pharmacotherapy for smoking (nicotine replacement therapy, varenicline, bupropion)

A

NRT - vaping etc, is harm reduction, effective as doubles chances of success (but 90% still cannot quit)
varenicline - alleviates withdrawal
bupropion - antidepressant

40
Q

explain heroin pharmacotherapy (methadone, buprenorphine)

A

stimulates opiod endogenous receptors so minimise withdrawal
methadone - safer subsitute
buprenorphine - long-lasting, blocks effects of heroin, blocks opiate receptors, reduce danger of overdosing

reduces risky behaviours of needle sharing but means some addicts will not ever quit, forever using subsitutes

41
Q

explain alcohol pharmacotherapy (naltrexone, acamprosate, disulfiram)

A

naltrexone- block opiod receptors so blocks positive effect
acamprosate- resets GABA and glutamate function
disulfiram- prevents metabolism of alcohol so becomes ill

42
Q

evaluate pharmacotherapy

A

if an operant conditioning approach is being used, drug should work (reduces reinforecemnts) but other approaches proposing dopamine brain circuit damage suggest that a dopaminergic drug would have more effect (this has been tried in clinical practice with minimal success’)

43
Q

outline cue exposure therapy

A

repeatedly exposed to drug related cues and not able to take drug, should initiate extinction between CS, CR and US, however there is limited clinical evidence to suggest it helps people stay sober
link usually immediately eradicated when client returns to old, drug using environment

44
Q
A