Background Module 1 Flashcards

1
Q

How does the National Institute on Drug Abuse (NIDA) define addiction?

A

A chronic, relapising disorder, characterized by compulsive drug seeking, continued use despite harmful consequences, and long-lasting changes in the brain

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2
Q

What happens to the brain changes due to addiction, after a person has quit the drug?

A

Changes persist long after they quit
- Note that improvements have been observed in some systems/functions

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3
Q

What is the relapse rate (+ time-frame) of GHB?

A

70% within 3 months after detoxification

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4
Q

What is an important factor for the relapse rate on an individual level?

A

Co-morbidity; e.g., alcohol abuse + anxiety disorder = greater risk for relapse

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5
Q

What is a critique against the current relapse rates?

A

Many people recover from addiction without formal treatment, thus, high relapse rates may be in part attributable to only included clinical samples.

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6
Q

What is spontaneous remission?

A

Sudden/unexpected recovery (without formal treatment)

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7
Q

Which model, regarding addiction, is currently most prevalent?

A

The brain disease model

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8
Q

What was the prevalent addiction model in the 19th century (1800s) & what did it entail?

entail = includes treatment of addicts/reasoning/etc.

A

Moral Model:
- Addiction = moral weakness (didn’t they used to soak tampons in opium and belladonna?)
- People with an addiction were locked up in prison/re-education institutions (“under challenging circumstances” = abuse)
- For obvious reasons, not scientifically supported.

Occasionally reappears (smh)

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9
Q

Which addiction model arose during the mid 19th century (~1850s) and what did it entail?

A

Pharmacological model:
- Movement against sale/use of spirits > addiction attributed to the substance and not the addict
- Addictive characteristic of substance causes addiction (treatment = prohibition)
- Prohibition of America (1920-1933)
- Model is viewed as one-sided = the availability and use is insufficient for the development of addiction (current view, not fact)
- Still widely used for certain substances (e.g., heroin)

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10
Q

What addiction model arose in 1930-1950 and what did it entail?

A

Symptomatic model:
- Psychoanalytically inspired (Freud…)
- Addiction is not a condition, but a symptom of an underlying character-neurosis/personality disorder
- Treatment = long-term, insight-oriented psycho-therapeutic treatment of character-neurosis
- Treatment still used in some communities

This feels like a step back towards the moral model ngl

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11
Q

What addiction model arose during 1940-1960 and what did it entail?

A

The disease Model (Jellinek):
- Fundamental biological/psych differences between addicts and non-addicts
- Addicts are unable to use substances in moderation because of the above differences
- Uncontrolled use + physical dependence
- Treatment = full abstinence for (latent) addicts
- Representatives = AA & The Minnesota Model

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12
Q

What addiction model arose in 1960-1970 (short-lived, damn) and what did it entail?

A

Learning Theory Model:
- Behaviourist roots
- Addiction is a maladaptive learned behaviour (can be unlearned)
- Treatment = Behavioural therapeutic interventions
- Aversion therapy & cue exposure as interventions (little success)

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13
Q

What addiction model arose in 1970-1990 and what did it entail?

A

Bio-psycho-social development model:
- Interplay of biological, psychological and social factors
- Heroin Vietnam veteran addicts that underwent spontaneous recovery when coming back = basis for this model
- Innate vulnarability + personal development + circumstances = continues interaction in both onset and termination
- Multi-modal interventions (i.e., all factors are included in treatment)
- “Dependence syndrome” based on this model

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14
Q

What addiction model arose in 1990 (still prevalent) and what does it entail?

A

Brain Disease Model:
- Link between brain, genetic risk factors and (risk for) addiction
- Medical-biological aspects of the 1970 model
- Innate vulnarability (= basis) + brain changes because of repeated use
- Pharmacological and behavioural therapeutic interventions

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15
Q

A new model that has come to the forefront in recent years + what it entails?

A

Complex Systems Model:
- Biological/psych/social factors play a role in a dynamic fashion
- Resistance to change depends upon the relationship between relevant factors
- Unique to the individual

Model gives vague description

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16
Q

Three defined types of substance categories?

A
  • Sedatives (calm + relaxed)
  • Stimulants (Invigorating- unless you have ADHD lol)
  • Psychedelics (atler conscious/perception states)
17
Q

What substances constitute sedatives?

A

Alcohol, barbiturates (???), benzodiazepines and opiates (opium, heroin, morphine)

18
Q

What substances belong to stimulants?

A

Caffeine, nicotine, amphetamine and cocaine

Not me being on three of these rn, goddamn

19
Q

What constitutes psychedelics?

A

Cannabis, extasy, LSD

20
Q

What important feature do all of the defined substance categories have in common?

A

Directly or indirectly result in a release of dopamine in the nucleus accumbens, which plays an important role in their addictive effect
- I wonder if this is a factor that makes substance abuse more common in ADHD + why substance affects ADHD peeps differently (mostly)

21
Q

Evolutionary view on the reward system & its development?

A
  • Enables us to anticipate rewards
  • Reinforces desirable/adaptive behaviour
22
Q

What role does dopamine play in our reward system? How do drugs affect the reward system?

A

Dopamine:
- Anticipation of reward = release of dopamine
- Noticably in the nucleus accumbens, part of the mesolimbic pathway

Drugs:
- Much stronger dopamine activity than normal
- Thus, enormous rush; “hijacks the reward system”

23
Q

Addiction & reward system?

A

Lower sensitivity to natural rewards

24
Q

What is the reward deficiency syndrome (RDS) account? Explanatory account made for people suffering what?

A

RDS as explanation for:
- Chronic definiciency of dopamine D2 receptors in the ventral striatum (nucleus accumbens) are less sensitive to simple natural rewards
- May look for stronger stimuli to compensate above
- Has been linked to a genetic predisposition (I think? lowkey lost)

Note:
- People with high density of D2 receptors are less likely to take drugs
- D2 density may be a consequence of substance abuse

25
Which type of learning mechanism plays an important role in addiction? How so (basic)?
Pavlovian conditioning > stimuli that predict a reward can evoke conditioned responses/craving
26
What is a prominent theory about the role of craving in addiction and what does it entail?
**Incentive-sensitization theory:** - **Drug-associated stimuli acquire incentive salience**, thus the drug itself becomes attractive - **Leads to wanting (craving) > elicits targeted acquiring behaviour** - Wanting does not equate liking (necessarily) - In addiction, **wanting increases, while hedonic experience (liking) decreases** - Theory may explain relapse (**drug-associated cues stay after withdrawal symptoms have dissipated**) - **Dopamine in the mesolimbic system plays a crucial role in wanting**
27
What traditional theory accounts for withdrawal/relapse in addiction, what does it entail and how is this theory regarded now?
**Opponent-process theory:** - **Initial drug use for pleasure (positive reinforcement), but tolerance occurs and drugs are taken to avoid withdrawal symptoms (negative reinforcement)** - I.e., explains relapse as an avoidance of withdrawal symptoms - **As relapse often occurs long after withdrawal symptoms (mostly) dissapate, this theory cannot fully account for the reasoning**
28
Which seven addiction models, not including the complex systems model, can be seen throughout time? Include intervention(s) | Give this in chronological order ## Footnote this question poses as an extra exercise
1. **Moral Model**, imprisonment/re-education institutions 2. **Pharmological model**, prohibition of substance sale/use 3. **Symtomatic model**, insight-oriented psycho-therapeutic treatment of character-neurosis 4. **Disease model**, (latent) addicts should be completely abstinent 5. **Learning theory model**, aversion therapy and cue exposure 6. **Bio-psycho-social development model**, multi-modal interventions 7. **Brain disease model**, pharmacological and behavioural interventions