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Addiction > Study Questions > Flashcards

Study Questions Flashcards

1
Q

1.

What is addiction

A

DSM-5:

A state of psychological or physiological dependence (or both) on the use of alcohol or other drugs

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2
Q

1.1.

Addictive Drug

A

Chemical substance with a significant potential for producing dependence

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3
Q

2.

How do you become addicted?

A

Neural Mechanisms:
Craving
Conditioning
Tolerance

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4
Q

3.

Predictors of Addiction

A

Parents
Siblings and Family
Peer influence

Genetics
Environment

Personality traits

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5
Q

4.

How does addiction progress?

A

Onset of usage of drug is predictive of course of addiction

Frequency of usage is predictive

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6
Q

5.

Which addictions are most common?

A
  1. tobacco
  2. alcohol
  3. marijuana
  4. painkillers
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7
Q

5.1.

Who is most at risk of becoming addicted ?

A

The people who are exposed to the most risk factors:

Environmental risk
Genetic risk

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8
Q

6.

Addiction determined by genetics or environment?

A

Nature vs nurture

No clear answer, because it’s gene-environment interaction

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9
Q

7.

How can the genetic factors of addiction be studied?

A

Twin studies
Adoption studies

Serotonin receptor genes, circadian rhythm genes and dopamine receptors studies

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10
Q

8.

Which Environmental factors play a role in addiction

A

Stress and Trauma

Learned behavior (conditioning, modelling)

Parenting style

Social network and support system

Availability

Social environment

Peer influence

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11
Q

9.

What is gene-environment interaction?

A

A different effect of an environmental exposure on disease risk in person with different genotypes

Genotype interacting with environmental influences

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12
Q

10.

What is craving?

A

The subjects desires to experience the effects of a previously used drug

Moss (chapter 5):
Automatic craving - involves activation of drug-use representation or Schema in memory, which leads to drug use, non conscious

Controlled craving - intense feeling of wanting and needing something, often accompanied by negative emotional reaction when the focus of our desire is beyond our reach

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13
Q

11.

What the role of conditioning in craving?

A

Craving can occur through conditioned stimuli related to drug use, such as specific environments or people

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14
Q

12.

Can conditioning also play a role in treatment?

A

Yes through conditioned cue exposure

Reversed conditioning: the repeated presentation of a conditioned stimulus, without the expected outcome

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15
Q

13.

Does social learning/ modelling play a role in craving?

A

Cognitive social learning theory: imbedded craving as biological consequence of social Learning

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16
Q

14.

To what extent can you help yourself to stop using substances?

A
  • avoid places where substances are available
  • avoid substance using peers
  • learn coping strategies for triggers and cues
  • Plan Long-Term and Short-term goals
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17
Q

15.

What is the dual system theory? How is it related to substance use disorder?

A

Moss (Chapter 5)

Dual system theory:
suggest that our cognitive processes are divided into two different systems, system 1 which is consistent of automatic processes, and system 2 which consists of controlled processes.
Drug use behavior as the result of complex interaction between activity that occurs within both systems 1 and 2. where system 1 is taking over in addiction because the behavior is becoming automatic.

Tiffany craving Model: Model of drug craving, dependence is a form of automatic behavior (system 1)

Frankens Model of drugs craving:
Hypervigilance for drug stimuli is quoted by system 1 and increases likelihood of lapse and relapse

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18
Q

16.

What is attentional bias and how is it related to substance use disorder?

A

Attentional bias: the automatic tendency of drug dependent patients to focus their attention predominately to drug-related stimuli

Franken (2003) - attentional bias model
Attentional bias influences cognition of a person which alters perception of drug-related stimuli and indirect Leads to drug use and relapse
Study: Stroop task in EEG and fMRI

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19
Q

17.

Automatic cognitive process and controlled cognitive process

A

Automatic cognitive process: contained in system 1, process that occurs outside of conscious awareness and cannot be examined directly by the individual. Tends to be rapid, environmentally triggered, without monitoring.

Controlled cognitive process:
Contained in system 2, makes up the majority of what we would think of as our conscious thinking. Needs controlled attention and monitoring.

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20
Q

18.

what is the reward system? What is the neuroanatomy of it and the related neurotransmitters?

A

The reward system in the brain:
Responsible for incentive salience (wanting and craving), associated learning (positive reinforcement and classical conditioning) and positive emotions.

Neuroanatomy:
Prefrontal cortex, nucleus accumbens, ventral regmental area

Neurotransmitter:
Dopaminergic - Dopamine

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21
Q

19.

What is the pathway in the reward system?

A

Mesolithic pathway:
Dopaminergic pathway, which connects the ventral tegemntal area in the midbrain to the ventral striatum of the basal ganglia in the forebrain.

Pathway regulates incentive salience, motivation, reinforcement leading, and fear among other cognitive processes.

22
Q

20.

How does the reward system function?

A

Dopamine acts on D1 or D2 receptors to either stimulate (D1) or inhibit (D2) the production of CAMP.

23
Q
  1. What is Volkow’s Model (I-RISA-Model)?

How do craving, attentional bias, self-efficacy, and motivation link in this model

A

Volkow’s Model:
Model of drug addiction, impaired response inhibition and salience attribution underlie neural substrates contributing to craving, intoxication, binging, and withdrawal across a broad range of drug addictions.

Based on early Neuroimaging data where inhibitory control and enhanced incentive salience led to drug seeking and use.

24
Q
  1. How do craving, attention and self-control related in the model of addiction?

Which factor in this addiction model is the strongest?

A

Salience: more attention for alcohol and drug use through attentional bias

Control: less active control over behavior, do not experience inhibition or future consequences

Drive: experience cravings, through salience and control, addicted brain have higher drive for addictive behavior and the control system gives GO

25
Q

23.

What is fetal alcohol syndrome?

A

FAS:

Affected development of the child after alcohol abuse of the mother during pregnancy

26
Q

24.

What are the physical and mental problems in children exposed to alcohol?

A

Physical:
Increased risk of miscarriage, stillbirth, congenital abnormalities, low birthweight, reduced gestational age

Psychological:
Cognitive and behavioral changes, such as adverse speech and language outcomes, executive functioning deficits etc.

27
Q

25.

How does alcohol exposure influence the developing brain?

A

Smaller head size, flatter face, fewer folds in the brain

Underdeveloped inner structure of the brain: reduced PFC, hippocampus, corpus colossum.

Myelination nation and development between 6-9 month drastically effected by alcohol.

28
Q

26.

What are the consequences of adolescence binge drinking?

A

44% of the 16 years old binge drink

Produces:

Dysfunction inhibitory control, Violence and risk behavior, poor decision making, interferes in life functioning

physical harm

29
Q

27.

What are the consequences of alcohol use on the youth brain?

A

Drug and alcohol use is related to changes in the brain volume of areas important for behavior control and to poor cognitive performance.

30
Q

28.

What are biomarkers or endophenotypes of Addiction?

A

Error correlated negativity (ERN) - reduced ERN is found in children of SUD patients and lower ERN is found before addiction (Rashmi)

PFC - behavioral disinhibition - SUD (Krueger, 2009)

P3AR - predictor of externalizing disorder - SUD (Krueger, 2009)

HPA-axis - higher risk for SUD (Chassin, 2016)

31
Q

29.

How reliable can biomarkers or endophenotypes predict addiction?

A

View well validate biomarkers for mental disorders, which have known to be linked to the development of SUD.

However, no direct causal evidence found yet and further research needed.

32
Q

30.

How do we diagnose addiction?

A 
DSM-5 Criteria: 
Two of the criteria within a 12 month period to be diagnosed
- 2 for diagnose with SUD 
- 4 for moderate SUD 
- 6 for sever SUD

Semi structured interview

Screening - for quick identification of risky patterns of substance use

33
Q

31.

How do we assess addictive behavior?

A

Assessment - establishes where on the continuum of substance use a patient falls

  • use
  • misuse
  • excessive use
  • substance use disorder

Basic components:

  1. Describing current and past patterns of substance use
  2. Diagnosing any substance-related disorders
  3. Documenting effect of substance use on mental and physical state
34
Q

32.

What is motivational interviewing?

A

MI:
A collaborative conversation style for strengthening a persons own motivation and commitment to change

Change talk: verbal utterance focused on the clients desire, ability, reason, or need to make change

  • goal of increasing commitment statements
35
Q

33.

How to prevent addiction?

A

Primary:
Designed to reach individuals before they have develop an addictive behavior

Secondary:
Screening and detecting drug use and other addictive behaviors at an early stage

Tertiary:
Designed to prevent addictive behavior from further developing and to minimize the likelihood of serious medical and psychosocial consequences

36
Q

33.1.

What are prevention strategies for addiction?

A

Six general strategies:
1. Information dissemination approaches

  1. Personal growth
  2. Alternative approaches
  3. Skills for resisting
  4. Personal and social skill training
  5. Public health approaches
37
Q

33.2.

Terror management theory

A

Def.:
Focuses on mortality-related risks that may even lead to increase in that behavior if it’s important to a persons self-esteem.

38
Q

34.

What are treatment options for addiction?

A
  • Cognitive behavioral therapy (CBT)
  • coping skills training (CST)
  • relaxation or meditation training
  • aversive conditioning approaches
  • cognitive therapy (CT)
  • contingency management
  • acceptance and commitment therapy
  • cue exposure with response prevention
  • pharmacological treatment
  • Peer and Familie support program
  • VR based interventions
  • motivational interviewing (MI)
  • motivational enhancement therapy (MET)
39
Q

35.1.

How does the medicine work?

A

Agonist:
Mimic the effect of the specific neurotransmitter which is targeted by binding to the same receptor sites as the endogenous transmitter and producing the same functional response

Antagonist:
Bind to the same receptor sites as neurotransmitter but do not trigger the series of events that lead to functional response. Can prevent the functional effect of the endogenous neurotransmitter - blocking

Partial Agonist:
Have agonist and antagonist action, occupy the receptor but produce partial agonist response

40
Q

35.

What specific medicines are there against addiction?

A

Opioid:

  1. Methadone - agonist, maintenance and detoxification
  2. Buprenophine - Partial agonist, maintenance and detoxification
  3. Naltrexone - antagonist, relapse prevention
  4. Naloxone - antagonist, emergency treatment
  5. Lofexidine and clonidine - agonist, detoxification and withdrawal

Nicotine:

  1. nicotine replacement - craving and withdrawal
  2. Varenicline - agonist, substitute
  3. Mecamylamine - antagonist

Alcohol:

  1. Benzodiazepines - withdrawal
  2. Disulfiram - relapse prevention
  3. Acamprosate - reduced craving and urge
  4. Naltrexone - antagonist, relapse prevention

Cannabis:
1. Rimbonaban - antagonist, against abuse

41
Q

36.

What is pharmacology?

A

Drug substitution treatment:
Removes need for individual to seek and use illic drug

Detoxification:
Blocking - stoping drug from having effect
Aversive - produces unpleasant reaction to drug

Maintenance treatment:
Continued administration of prescribed substance that prevents withdrawal symptoms

42
Q

37.

What is replacement therapy?

A

Replacement therapy:
For of pharmacology in which the substance of abuse is replaced by the medicine that has a similar working mechanism but which is less harmful

  • e.g. methadone as replacement for heroin
43
Q

37.1.

What is maintenance treatment?

A

Pharmacological treatment:

Treatment in which a substance is substituted for one that is illegal or harmful (such as heroin or nicotine).

  • for patients who need the high
  • usually patients who are therapy resistant
  • helps get structure in patients lives, and get them out of criminal environment
  • only after a long period of therapy, very costly

Case: Peter got heroin prescribed.

44
Q

38.

What starts first, addiction or other psychological problems?

A
  1. psychology - addiction (self-medication)
  2. addiction - psychopathology (substance induced)
  3. common factor pathway (genes, risk environment, personality)
  • all pathways are equal present
  • but only in some disorders
45
Q

39.

What are comorbidities of substance use disorder?

A

Personality disorders:

  • PTSD
  • Schizophrenia
  • Externalizing disorders (ADHD, APD)
  • Internalizing disorders (Anxiety, Depression)

Somatic comorbidity

46
Q

40.

Do specific drugs need specific treatment?

A

Yes.

Drugs need a different combination of specific drugs and therapy.

However, TREATMENT MATCHING has not yet been implemented in substance abuse treatment.

47
Q

40.1.

What is dual diagnosis?

A

Horsfall (2007)

Duals diagnosis:
The identification of two distinct disorders (substance use disorder and mental health) that are present in the same person.

  • also known as comorbidity
48
Q

41.

is an eating disorder an addiction or not?

A

No. Not an addiction on itself.

Two different diagnosis, which often go hand in hand and are dual-diagnosed (comorbid).

However, usually resemble same pattern of behavior and often one of the two diagnosis is a coping mechanism for the other.

49
Q

42.

how are behavioral addictions similar to substance addictions?

A

Behavioral addiction:
Syndrome analogous to substance addiction but with behavioral focus.

Similarities:

  • onset in adolescence or young adults
  • failure to resist impulse, drive, or temptation
  • repetitive Engagement in these behaviors
  • Ego-syntonic then ego-dystonic
  • less pleasure, more habitual/compulsive
  • motivated by negative reinforcement
  • craving/urge
  • behavior result in positive State (high)
  • tolerance can build up
50
Q

43.

Are the mechanisms that underlie behavioral addictions the same as those of substance addictions?

A

Neurocognition:
- Both behavioral and substance addicts show diminished performance on inhibition task.

Neurobiology:

  • Serotonin: low, so inhibition of behavior low
  • Dopamine: urge-driven, alteration in DA pathway, Leads to seeking of reward
  • diminished vmPFC activity: impulsive deduction making
51
Q

44.

what is the relationship between addiction, crime, and antisocial behavior?

A

Lecture - Dr. Reshmi Marhe:

Theories of causality:

  1. Psychopharmacological Model
    - intoxication induces engagement in crime
  2. Economical Model
    - financing SUD induces criminal engagement
  3. System Model
    - drug industry involvement in drug use,
    - crime makes people have more access to drugs

New Theories:
1. Drug abuse leads to crime (causal, D-C), psychopharmacological model

  1. Crime leads to drug use (causal, C-D), economical model
  2. Reciprocal Model (causal, D-C and C-D), two way model
  3. Common-cause Model (non-causal), shared risk factors

Addiction (9 decks)

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