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Psychopathology > TASK 9 - SUBSTANCE-USE DISORDER > Flashcards

TASK 9 - SUBSTANCE-USE DISORDER Flashcards

1
Q

drug addiction

A

= use of psychoactive drug/substance, causing intoxication (high); having the compulsion/urge to take drug (craving) although experiencing negative consequences

  • physical dependence + abuse + psychological dependence
  • withdrawal + craving
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2
Q

substance abuse

A

= when recurrent use results in harmful consequences

  • can’t fulfil obligations, use in dangerous situations, legal problems, continued use despite problems
  • repeated problems in at least one of the categories within 12-month period
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3
Q

substance dependence

A

= body requires the drug to feel “normal” due to tolerance

- only withdrawal

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4
Q

DSM-5 (general substance use disorder)

1. impaired centre control

A

must show 2 (OR MORE) of the following 10

  1. substance taken in increasingly larger amounts/ over longer periods of time than originally intended
  2. craving
  3. ongoing desire to cut down/ control substance abuse
  4. much time spent on obtaining, using or recovering from the substance
    - compulsion
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5
Q

DSM-5 (SUD)

2. social impairment

A
  1. inability to meet responsibilities at home/work/school
  2. important activities are abandoned because of substance use
  3. ongoing substance use despite recurring social difficulties caused/made worse by the effects of the sentence
    - interpersonal harm
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6
Q

DSM-5 (SUD)

3. risky use

A
  1. ongoing use in physically dangerous situations e.g. driving a car
  2. use continues despite awareness of physical/ psychological problems that come from the substance
    - individual harm
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7
Q

DSM-5 (SUD)

4. pharmacological criteria

A
  1. changes in tolerance indicated by increased amounts to achieve desired effects/ diminished intoxication to same amount
  2. withdrawal demonstrated by characteristic withdrawal syndrome of the substance and/or taking the same/similar substances to relieve withdrawal symptoms
    - tolerance + withdrawal
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8
Q

prevalence

A
  1. 6-5.1% (overall)
    - onset: 15-64 = 51% have used illegal drugs/ non-medical prescribed drugs/ inhalants at some point in their lives
    - comorbidity: mostly anxiety + mood disorders (53-76%)
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9
Q

substances

A
  • give rewarding effect in beginning (dopamine)
  • make you feel good, pleasure
  • believed to have beneficial effects in past
  • but all addictive + harmful long-term
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10
Q

substances

1) psycholeptics = depressants

A

= slow, suppress CNS

  • decrease heart rate, calming effects
  • alcohol, barbiturates, benzodiazepines, inhalants, (nicotine, caffeine)
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11
Q

substances

2) psychoanaleptics = stimulants

A

= activate, stimulate CNS

  • more energy, arousal, alertness
  • cocaine, amphetamines, nicotine, caffeine
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12
Q

substances

3) opioids

A

= works on body’s own opioid system

  • pain relief
  • heroin, morphine
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13
Q

substances

4) psychodysleptics = hallucinogens

A
  • cause hallucinations

- LSD, mushrooms, phencyclidine (PCP)

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14
Q

substances

- cannabis

A

= depressant + stimulant + hallucinogen (1+2+4)

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15
Q

historical theories

1. moral model (BAD)

A

= BLAME addict; moral failure, weak; give in to drug/addiction
- 1850

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16
Q

historical theories

2. temperance model (BAD)

A

= BLAME substance; substance = evil

- introduction of prohibition

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17
Q

historical theories

3. symptomatic model (MAD)

A

= addiction = secondary disorder/symptoms; indirect consequence of primary disorder
- need treatment

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18
Q

historical theories

4. disease model (MAD)

A

= addiction = primary disorder

- need treatment

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19
Q

historical theories

5. learning theory/psychological model (SAD)

A

= addiction = learned behaviour due to experience (coping mechanism, operant conditioning)

20
Q

historical theories

6. social model (SAD)

A

= addiction = learned behaviour with social pressure being an underlying cause

21
Q

historical theories

7. bio-psycho-social model

A

= includes several factors of 1-6

- 1976

22
Q

theories

- biological/genetic

A
  • drugs alter the pleasure (dopamine) pathway to produce strong sense of reward
  • -> VTA –> NAC (nucleus accumbens) –> PFC
  • chronic use makes reward centres less sensitive –> tolerance + craving
  • cue sensitivity + conditioned response to cues induces powerful craving
  • heritable (general rather than specific)
  • genetic variation in dopamine receptor/transporter gene
23
Q

theories

- psychological

A
  • social learning: modelling of parents
  • expectation that alcohol reduces stress
  • personality: behavioural under-control, impulsiveness, sensation-seeking, prone to antisocial behaviours
24
Q

theories

- sociocultural

A
  • chronic stress

- environmental reinforcements/ punishments –> abuse less common in societies with more restrictions

25
Q

theories

- gender roles

A
  • men + alcoholism: more likely because “masculine”; tend to start in socialising context
  • societal acceptance of drinking in women went up, so did drinking in women
  • women: less likely to carry risk (personality traits); suffer from alcohol earlier + may notice that sooner + may find effects scarier thus –> limit consumption; start in family/partner/lover context
26
Q

theories

- place conditioning (alcohol)

A

= whether non-dependent drinkers show place preference for a location paired with alcohol + whether time spent in those places is related to subjective alcohol effects

  • -> non-dependant consumers develop a preference for locations paired with alcohol consumption
  • conditioning happened without explicit knowledge of the drug –> cue contingencies: behaviour influenced by drug before we’re even aware of it
27
Q

addiction as a disease

A

= chronic disease, with underlying mechanisms seen in the brain

  • reward system (= mesolimbic dopamine system) as centre
  • depressed reward system = dopamine receptors decrease in availability –> decreased activation of PFC –> impaired control/ inhibition
  • three recurring stages of addiction
28
Q

addiction as a disease

1. binge + intoxication

A
  • pavlovian learning: repeated experience of reward becomes associated with environmental stimuli that precede them
  • dopamine cells start firing anticipatory to conditioned stimuli (drug intoxication) –> cue triggers craving + motivates drug-seeking behaviour
  • drugs, unlike natural rewards (e.g. food), avoid satiation + continue to increase dopamine levels –> after abuse drug is the only reward strong enough to trigger response
29
Q

addiction as a disease

2. withdrawal + negative affect

A
  • addicted = drug triggers much smaller increases in dopamine levels –> less sensitive to drug + other rewards (= less motivated by everyday stimuli)
  • -> conditioned pull toward reward
  • amygdala over-activated
  • anti-reward system becomes overactive = repeated exposure leads to adaptation in circuit of extended amygdala + the basal forebrain –> increased reactivity to stress –> emergence of negative emotions/withdrawal
  • -> emotional push to escape withdrawal
  • addiction changes: wanting euphoria to preventing dysphoria
  • -> don’t see drug as pleasurable anymore; only take drug to escape distress/withdrawal
30
Q

addiction as a disease

3. preoccupation + anticipation

A
  • changes in function of involved PFCs (executive functioning especially)
  • prefrontal region changes: impaired signalling of dopamine + glutamate in prefrontal regions
  • down-regulation of signalling = impairment of executive processes –> weakened ability to resist strong urges + follow through on decision to stop taking the drug
31
Q

addiction as a disease

- biological + social factors

A
  • differ in vulnerability to various genetic, environmental, developmental factors = unique susceptibility (for initial drug use, sustaining drug use, progressive changes in brain)
  • increasing vulnerability:
    1. family history: heritability + modelling
    2. early exposure to drug use: adolescence greatest vulnerability
    3. exposure to high-risk environments: socially stressful environments
    4. certain mental illnesses: mood disorders, psychoses, anxiety…
32
Q

addiction as a disease

- implications for prevention + treatment

A
  • adolescent brain is still developing, period of enhance neuroplasticity –> sensitive to effects of drugs
  • -> eave drinking and raise legal smoking age to 21
  • medical treatment can help to restore healthy function in affected brain circuitry + assist in preventing relapse
  • behavioural interventions to help restore balance in brain circuitry
    1. mitigate person’s stress reactivity and emotional states –> help manage strong urges
    2. improve executive function and self-regulation –> help recovering patients plan ahead to avoid vulnerable situations
    3. help patients to avoid environmental cues (circle of friends) –> reduce likelihood of conditioned craving
33
Q

addiction as a disease

- criticism

A

A. chronic diagnosis cause demoralisation for treatment
- think they will relapse anyway, there is no recovery
B. many actually do recover naturally
- brain change ≠ malfunction –> might be normal plasticity + change back some time

34
Q

addiction as a choice

A

= addictions work like other choices in which immediate rewards take precedence over long-term gains

  • drug addicts can + do recover –> decision to take drugs or to quit are executed voluntarily
  • addicts choose “locally” rather than “globally”
  • trick is to acquire strategies for seeing overall summation of rewards over time & ignoring the attraction of immediate goal
  • -> neither disease nor full on choice but something in-between: momentary states of dopamine enhancement triggered by cues shut down intertemporal flexibility (disease model) –> can’t consider moments other than “now”
  • with recurrence of this cycle: this gets worse + it gets much harder to make the choice
35
Q

addiction as a choice

- operant addiction

A

= can explain why people start but not maintenance/persistence of addiction

  1. positive reinforcement: drug high, pleasurable effect
  2. negative reinforcement: reduce withdrawal effects
36
Q

addiction as a choice

- behavioural economics

A
  • addicts always choose more attractive local option (= take drug –> more reward than not taking it)
  • no pleasure without drug
  • treatment implications: adapt global view (contingency management)
37
Q

dual-process model

A
  • hyperactive impulsive system (1) + dysfunctional reflective system (2)
  • continuum hypothesis = assumes similar deficits across different alcohol related disorders: binge drinkers would show qualitatively similar but quantitatively less impairments than alcohol-dependent
38
Q

dual-process model

1. hyperactive impulsive system

A

= emotional evaluation (limbic)

  • impulsive prepotent behaviours
  • strong impulse to take drug
  • -> shown in craving, attention bias, approach bias
39
Q

dual-process model

2. dysfunctional reflective system

A

= cognitive evaluation (prefrontal)

  • inability to voluntarily inhibit the consumption
  • have more difficulties controlling urges
  • -> shoes in worse WM, decision making + response inhibition
40
Q

integration of models

- disease + dual-process + choice

A
  • have increase in reward seeking + compulsion in common
  • -> dopamine system, impulsivity, local decisions
  • have loss in control in common
  • -> PFC deficits, loss of control, lack of global view
41
Q

treatment

- biological

A
  • detoxification = drugs used to dampen withdrawal symptoms but dosages are decreased slowly –> patient doesn’t become dependent (= help prevent relapse while brain is healing)
  • drug replacement/maintenance therapy = substituting drug that has fewer damaging effects
    a. antagonist drugs = block/ change effect of addictive drug, reducing the desire for it BUT cause severe withdrawal
  • alcohol: antabuse/disulfiram = makes alcohol punishing but only as long as they continue to take it
  • nicotine: patches/gums or antidepressant bupropion
  • heroin: opioid methadone, which has less severe effects
42
Q

treatment

- behavioural

A
  • alcohol: aversive classical conditioning with Antabuse then through operant conditioning they learn to avoid alcohol in order to avoid the aversive response
  • covert sensitisation therapy: imagine unpleasant associations between drug + consequences to create conditional aversive response
  • contingency management programmes: reinforcing abstinence
43
Q

treatment

- cognitive

A
  • identify situation in which they’re most likely to take drug
  • identify expectations about drug taking + challenge those by reviewing negative effects
  • motivational interviewing: elicit + solidify motivation + commitment to changing substance use
  • mindfulness + meditation
44
Q

treatment

- relapse prevention

A
  • abstinence violation effect: when they violate their abstinence, they tend to attribute it to lack of will power and self-control rather than situation-factors –> violate it even more to suppress conflict + guilt (dietary-slip)
  • relapse prevention programmes: teach people to see slip as situational and identify high risk situations to come up with coping/avoiding strategies
45
Q

treatment

- community programmes (AA)

A
  • by/ for people with alcohol related problems
  • 12 steps
  • -> 1. admit dependence
  • group members provide moral + social support
  • believe that people are never completely cured and will always be “recovering alcoholics”
46
Q

treatment

- prevention programmes

A
  • target younger people as onset predominantly during adolescent risk period
  • focus education on immediate risk of excess + payoffs of moderation
  • harm reduction model: drink safe like you drive safe
  • learn to be aware of drinking habits + thought to calculate alcohol blood level

Psychopathology (9 decks)

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