1B substance use and addiction Flashcards
What are drugs that may cause addiction? (10)
- Alcohol
- Nicotine
- Cannabis
- Stimulants (amphetamine, cocaine (crack), ecstasy)
- Opioids (heroin, fentanyl, DF118)
- Ketamine
- Solvents
- GHB, GBL
- Benzodiazepines
- NO
- Psychedelics e.g. LSD, magic mushrooms
- Khat
- Novel psychoactive substances
What are the three types of reasons why people take drugs?
- Positive reinforcement: to gain a positive state
- Negative reinforcement: to overcome an adverse state
- Normal
So need to ask why – then you can start to understand why and formulate a plan to address it.
Give four examples of positive reinforcement for drug use
- Escapism
- Get high
- Stay awake
- Like it
Give four examples of negative reinforcement for drug use
- Boredom
- To get to sleep
- Reduce anxiety
- Feel better
Give four examples of ‘normal’ reinforcement of drug use
- ‘Why not?’
- Everyone does it
- Rebel
- Curious
- To fit in
Describe the course of drug use and how it may develop into an addiction
- The initial use of the drug is ‘experimental’, causing no/limited difficulties to the user
- It may develop into a state of regular use where a ‘dependence’ is being developed
What does the two way arrow indicate?
Patients can revert back to previous experimental state with enough help
- But patients may develop into complete dependence, where patient needs the drug to function (other arrow)
What is the ICD definition of ‘harmful substance use’?
Damage to the user whether that be mental or physical health, in absence of dependence syndrome
How does harmful substance use differ from hazardous use?
- Hazardous use means it’s likely to cause harm if continued use
- Moderate use → hazardous use → harmful use
What are the diagnostic criteria for dependence syndrome using ICD-10?
1) Strong desire or compulsion to take substance
2) Difficulties in controlling substance-taking behaviour in terms of its onset, termination, or levels of use
3) Physiological withdrawal state when substance use had stopped or been reduced
4) evidence of tolerance developed- need more to get the same effect
5) progressive neglect of alternative interests
6) continuation of taking substance despite the clear evidence of harmful consequences
What do we ask patients particularly to assess their difficulty in controlling?
- Who has control, you or the drug/behaviour?
- When did you last have a drink/drug?
What does physiological withdrawal state mean?
It’s a ‘negative’ state (from uncomfortable to life-threatening/intolerable). Patients take the drugs/alcohol to get relief from it.
Using the ICD-10, when is a patient classed as dependent?
Three have to be met in the last 12 months
Which drug causes the most and least harm in the UK?
Define addiction
- Compulsive drug use despite harmful consequences, characterised by an inability to stop using drug
- failure to meet work/social/family obligations
- Tolerance and withdrawal
Define dependence and how it differs from addiction
- Physical adaptation to a substance
- Underpins tolerance/withdrawal e.g. opioid, benzodiazepine, alcohol
- So we can be dependent and not addicted
Give 2 examples of behavioural addictions
- Gambling disorders
- Many similarities with substance dependence
- Reclassified as behavioural addiction from ‘impulse control disorder’ in DSM-5/ICD-11
- Internet gaming disorders
- Added to ICD-11 under addictive disorders
With the following individuals, identify whether they meet criteria for
- Hazardous or harmful use
- Addiction or dependence
- Phil → hazardous use since he’s having 2.8 units (in a pint) x 4 x 7 = 78.4 units a week
- Jenny → harmful use since there’s social impact as she’s missing work due to hangovers
- Tom → dependence/addiction since there’s tolerance and morning drinking to relieve and withdrawal
With the following individuals, identify whether they meet criteria for
- Hazardous or harmful use
- Addiction or dependence
What determines a drug’s addictive potential?
- The speed a drug enters body
- Its psychoactive effects
Give three examples of how drugs can be refined for more rush and addiction
- Opium can be refined into injected heroin for more rush and addiction
- Coca leaves are refined into crack for more rush and addiction
- Chewing tobacco is refined into cigarettes/vaping for more rush and addiction
What factors are involved in drug use and addiction?
- Social and environmental factors
- Drug factors
- Personal factors
Describe how addiction develops
- Start with pre-existing vulnerability e.g. family history or young age
- Then we get drug exposure and brain has compensatory mechanisms to maintain brain function e.g. you may have consumed a lot of alcohol but you appear to function fine
- You then may either have sustained recovery if you stop the drug or cycles of remission & relapse
What is the excitatory system in the brain?
- Glutamate system
- NMDA receptor
What is the inhibitory system in the brain?
- GABA-benzodiazepine (GABA-A system)
- GABA-A receptor
How does acutely drinking alcohol affect brain?
- There is a boost in inhibitory system leading to anxiolysis and state of sedation
- There is a block in excitatory system leading to impaired memory (alcoholic blackouts)
How does chronic alcohol consumption affect brain?
The brain develops neuroadaptations so the body will become adapted to the consumption of alcohol, therefore no imbalance in GABA and glutamate.
This means a much greater consumption of alcohol is required to achieve state of sedation
What are the adaptions in absence of alcohol in chronic alcohol consumption?
- There is an upregulation in the excitatory system
- There is reduced function in the inhibitory system leading to tolerance
- GABA-A receptors switch subunits to make them less sensitive to alcohol
What happens to chronic alcohol consumers in absence of alcohol?
- Lack of alcohol will lead to imbalance where inhibitory system is reduced and excitatory is upregulated
- This increased calcium ion binding to NMDA receptor can lead to hyperexcitability (seizures) and cell death (atrophy)
Describe the role of dopamine in brain
Dopamine is a neurotransmitter that is involved in the ‘pleasure-reward-motivation’ system.
Where is the ‘pleasure-reward-motivation’ system in the brain?
Ventral striatum
What sorts of things increase dopamine levels in brain?
- Natural rewards like food and sex
- Drugs of abuse
What are key modulators of the dopamine system?
- Opioid system- particularly mu opioids that mediate pleasurable effect e.g. of alcohol or endorphin rush when exercising
- Others are GABA-B, cannabinoids, glutamate etc that are also targets for treatment
Within the rewards concept, how is addiction described?
Addiction has been conceptualised as a reward deficient state so people take drugs to make them feel better
What effect does amphetamine have?
Enhances dopamine release
What effect do cocaine and amphetamines have?
Blocks reuptake of dopamine
What effect do other drugs e.g. alcohol, opiates, nicotine have?
Increase dopamine neuron firing in ventral tegmental area (VTA) by reducing inhibition of release
How can the dopamine reward pathway be assessed?
- Functional MRI can be used to assess function
- It records the delay between the cue and target release
- This can indirectly measure brain response during anticipation of winning money i.e. a ‘reward’ in addiction → monetary incentive delay task
What is the effect of substance abuse on reward pathway?
Even among abstinent individuals, substance use can still dampen the activation of the reward system in recovering addicts compared to those who have never been addicted.
This reduced reward response may lead to continued substance use despite experiencing its adverse effects.
How does the effect of substance abuse on reward pathway affect relapse?
- In abstinent addicts, those with blunted response in the brain to ‘anticipation of reward’ are more likely to relapse
- This is consistent with reward deficiency theories of addiction
How may abstinence affect reward pathway?
With enough abstinence, the response may be restored to a level similar to that of controls
Describe the different regions of brain involved in withdrawal, binge/intoxication and craving
How does reinforcement change as addiction develops?
- There is a change from positive to negative reinforcement as addiction develops
- As neuroadaptations develop, “high” becomes less and the “low” becomes greater
- People will start consuming more drugs in attempt to overcome low and chase high
What are positive to negative reinforcement patients like in clinic?
- They’re in a state of aggression/fear/anxiety
- This is because they don’t have access to drug anymore and are highly motivated to get it but know they can’t
How may we assess amygdala function?
- fMRI of brain to look at amygdala
- Look at patients’ emotional processing of neutral and aversive images → these weren’t images of alcohol/drugs though
What did we see in healthy vs polydrug and vs alcohol?
- Polydrug group had heightened reaction and found images very aversive
- Didn’t see reaction in alcohol group, maybe because they’re abstinent and have gone past initial phase of being highly reactive
How may staying abstinent reinforce an individual staying abstinent?
- Diagram shows a greater BOLD response (inhibitory response) exhibited by abstinent patients
- The longer someone stays abstinent, the greater inhibitory response they can produce
- This greater inhibitory response can allow them to resist drug taking and stay sober for longer
Describe how the neurocircuitry involved in inhibitory control is assessed with fMRI: go-nogo task
Three by two cluster-based repeated measures ANOVA showing a group effect in (A) the right ACC (AUD>control, P = 0.041, post hoc Bonferroni) and (B) the left frontal pole/IFG (AUD>control, P = 0.005, post hoc Bonferroni). The scale represents increasing zf-statistic (interaction).
BOLD response to successful STOPS correlates with months abstinent: graph Showing significant positive correlations between (A) alcohol abstinence (mths) and the mean (of placebo and naltrexone) left frontal pole/inferior frontal gyrus ‘stop’ BOLD signal change (r(19)=0.58, P=0.005) in the AUD group, and (B) total baseline UPPS‐P score and the delta (naltrexone minus placebo) ‘stop’ BOLD signal change in the left anterior insula cortex cluster (r(23)=0.40, P=0.027) in the poly‐SUD group.
