1
Q
What is hazardous drinking?
A
- pattern of alcohol consumption that increases someones risk of harm
- physical, mental health and social consequences (as in harmful use)
- hazardous drinking applies to anyone drinking over recommended limits (14 units a week) but without alcohol related problems
- moves into harmful drinking when regularly consuming over 35 units per week
2
Q
What is the equation for units calculation?
A
strength (ABV) x volume (ml) divided by 1000
3
Q
What is the recommendation for alcohol consumption levels in the UK?
A
No more than 14 units a week on a regular basis
4
Q
What are the 7 types of cancer that alcohol is associated with?
A
- mouth and upper throat
- larynx
- oesophagus
- breast (in women)
- liver
- bowel
5
Q
What are the 4 ways in which alcohol can cause cancer?
A
- damages cells
- increases damage from tobacco
- affects hormones linked to breast cancer
- breaks down into cancer causing chemicals
6
Q
Name the different tools that can be used for screening alcohol use
A
- FAST; useful in A and E settings, quick
- AUDIT; alcohol use disorders identification test
- CAGE; screening for dependence
7
Q
The FRAME acronym is used to capture the elements of a brief intervention - what does it stand for?
A
- feedback; review problems experienced because of alcohol
- responsibility; patient is responsible for change
- advice; advise reduction or abstinence
- menu; provide options for changing behaviour
- empathy; use empathic approach
- self-efficacy; encourage optimism about changing behaviour
8
Q
Describe the pathophysiology of alcohol withdrawal
A
- unopposed upregulated excitation
- excess glutamate activity and reduced GABA activity leads to alcohol withdrawal symptoms
- excessive glutamate activity is toxic to the nerve cell
9
Q
Describe the features of alcohol dependence syndrome
A
- only if three or more of the following have been present together at one time during the previous year
- strong desire or sense of compulsion to take drug
- difficulty in controlling use of substance in terms of onset, termination or level of use
- physiological withdrawal state
- evidence of tolerance
- progressive neglect or other pleasures / interests because of their use / effects of substance
- persistence with use despite clear evidence of harmful consequences
10
Q
Describe the features of alcohol withdrawal syndrome
A
- first symptoms occur within hours and peak at 24-48 hours
- restlessness, tremor, sweating, anxiety, nausea and vomiting, loss of appetite and insomnia
- tachycardia and systolic hypertension evident
- generalised seizures usually in first 24 hours
- can progress to the medical emergency delirium tremens
- in most, symptoms resolve in 5-7 days
11
Q
Describe the features of delirium tremens
A
- 5% of cases
- peak onset within 2 days of abstinence
- often presents insidiously with night time confusion
- confusion, disorientation, agitation, hypertension, fever, visual and auditory hallucinations, paranoid ideation
- mortality 2-5% (assoc, with cardiovascular collapse and infection)
12
Q
Describe the management of alcohol withdrawal
A
- general support; reassurance, advice etc
- benzodiazepines; cross tolerant with alcohol, use long acting agents, titrate against severity of withdrawal symptoms, reduce gradually over 7 days or more
- vitamin supplementation
- thiamine (pabrinex) as prophylaxis against wernickes encephalopathy; must be parenteral, increase dose if wernickes suspected
13
Q
When would detoxing be conducted in an inpatient setting?
A
- severe dependence
- history of delirium tremens or alcohol withdrawal seizures
- failed community detox
- poor social support
- cognitive impairment
- psychiatric co-morbidity
- poor physical health
14
Q
Describe the pharmacological interventions in relapse prevention
A
- disulfiram; inhibits acetaldehyde dehydrogenase leading to accumulation if alcohol ingested, leads to flushed skin, tachycardia, n+v, arrhythmias and hypotension
- acamprosate; acts centrally on glutamate and GABA systems, reduces cravings, start as soon as detox complete, continue through relapses, prescribe along with psychosocial interventions, side effects include headache, diarrhoea, nausea
15
Q
Describe the psychosocial interventions in relapse prevention
A
- CBT (coping skills therapy)
- motivational enhancement therapy
- 12 step facilitation therapy (e.g. AA)
- behavioural self control training
- family and couple therapy
- project MATCH
16
Q
What are the features of gaming disorder
A
- a pattern of gaming behaviour characterised by;
- impaired control over gaming
- increasing priority given to gaming over other activities
- continuation or escalation of gaming despite the occurrence of negative consequence
- pattern must be of sufficient severely to result in significant impairment in personal, family, social, educational, occupational or other important areas for at least 12 months
17
Q
What is the CAGE criteria?
A
- cut down
- annoyed
- guilty
- eye opener
18
Q
Which neural pathway is implicated in ‘wanting’?
A
The mesolimbic pathway (connections between VTA in midbrain and nucleus accumbens)
19
Q
What are the effects of dopaminergic activity in the mesolimbic pathway?
A
- is a motivating signal
- incentivises behaviour
- is involved in normal pleasurable experiences
20
Q
What neuronal receptors are decreased in addiciton?
A
Dopamine D2 receptors
21
Q
Describe the ‘tolerance to reward’ principle in relation to dependence
A
- due to repeated dopamine release, dopamine receptors down regulate
- thresholds for rewards during abstinence is thus increased
- normal experiences don’t evoke adequate reward response
- these changes persist despite prolonged abstinence from substance abuse
22
Q
The pre-frontal cortex has what roles normally?
A
- helps intention guide behaviour
- modulates the powerful effects of the reward pathway
- sets goals, focuses attention
- makes sound decisions
- keeps emotions and impulses under control to achieve long term goals
23
Q
What is the direction of cortical maturation?
A
- back to front direct
- beginning in the primary motor cortex and spreading anteriorly over the superior and inferior frontal gyri, with the prefrontal cortex developing last
- frontal lobe areas that mediate executive functioning mature late than limbic (emotional) systems
24
Q
Describe the effects on the pre-frontal cortex and addictive drugs
A
- dopamine release effects;
- ability to update new information within the PFC
- ability to select new goals
- the ability to avoid compulsive repetition of a behaviour
- addictive drugs provide a potent signal that disrupts normal dopamine related learning in the PFC
25
Describe the role of the hippocampus and amygdala in dependence
- the hippocampal and amygdala are critical in acquisition, consolidation and expression of the drug stimulus learning
- learned drug associated can then cue internal states of craving
26
Describe the role of the orbito-frontal cortex in dependence
- provides internal representations of the saliency of events and assigns values to them
- key creator of motivation to act
- addicts show increased activation of OFC when presented with drug cues
- hyperactivity correlates with self reported drug cravings following exposure to cues
- overall changes in OFC persist into abstinence
27
Name the areas of the brain that are associated with dependence
- prefrontal cortex
- anterior cingulate gyrus
- orbitofrontal cortex
- subcallosal cortex
- nucleus accumbens
- ventral pallidum
- hippocampus
- amygdala
28
Name some of the core features of addictive behaviour
- salience (importance, dominance)
- mood modification (rush and escape)
- tolerance (escalation for effect)
- withdrawal
- conflict (interpersonal, intrapsychic, loss of control)
- relapse
29
What are the different types of opiates?
- natural from plants like opium poppy e.g. morphine, codeine
- semi-synthetic; hydrocodone, hydromorphone
- fully synthetic; methadone, tramadol
30
What are the 4 phases of treatment of opioid dependence?
- induction
- optimisation
- maintenance
- reduction
31
Describe the features of methadone
- Mu (opioid) receptor agonist
- long half life
- peak plasma con. 4 hours
- steady state 5 days
- hepatic metabolism CY3P4
- evidence shows higher doses (60-100ml) more effective
32
Describe the features of buprenorphine
- Mu receptor partial agonist with low intrinsic activity and high affinity
- peak plasma levels 1.5-2.5 hours
- duration of effect dose related
- effective doses in range of 12-24 mg
- sublingual tablets
