The abuse of alcohol and drugs from a psychological perspective comes under the heading of externalising disorders. This category essentially encompasses the tendency of an individual to act out their problems. Other externalising disorders include:
  • Conduct disorders
  • Anti-social personality
This is opposed to the internalising disorders, such as depression and anxiety.
Alcohol
It is very important to make a distinction between dependence and misuse. Many people misuse alcohol, but not all are dependent. Sign of dependence may include:
  • Withdrawals
  • Cravings – very strong desire to drink
  • Drinking despite negative consequences:
    • On their physical health
    • On their mental health
    • On their social / work life
  • Tolerance – this is said to occur when the individual has to drink larger amount of alcohol to obtain a similar effect.
  • Primacy (put drinking before other activities) – neglecting other activities
  • Loss of control
All of the above factors are true for drugs as well as alcohol. The factors below are specific for alcohol.
  • Rapid re-instatement – people who have stopped drinking, once they start again, they rapidly get up to the level they were previously drinking
  • Narrowing of repertoire – as people become more dependant on alcohol, the range of beverages they drink decline – so that eventually they may only drink 1-2 types of drink. Usually this is the cheapest available. Also, their drinking habits alter, so where as before they may have drunk at the pub, at home, out for a meal, with various people, they tend to often drink just at home, or at the pub, with a very small social circle.
‘Problem drinking’ / misuse of alcohol
We say that this occurs when the consequences of alcohol involve social, physical to psychological harm to an individual.
What are the ‘safe limits for alcohol?
  • Men – <21 units per week, and <4 units per day
  • Women – <14 units per week, <3 units per day
  • This limit is higher in women for a physiological reason. For the same amount of alcohol ingested, women will have a higher blood alcohol level. This level is related to the % of body fat – which of course for women is higher.
One unit is 10ml of alcohol. To work out the number of units:
Volume Drunk (L)     x       % of alcohol       =      Units
e.g. for a large bottle of vodka:
                                1L   x    40%   = 40 Units
A pint of beer is roughly 0.5L, so you can just ½ the % to get the units – e.g. a pint of 4% is about 2 Units
 
Epidemiology

‘An Alcohol Problem’:

  • 38% of men
  • 16% of women
  • (26% overall) – 8.2m people in UK

Bing Drinking

  • 21% men
  • 9% women

Alcohol Dependence

  • 6% men
  • 1.2% women
  • (3.6% overall) – 1.1m People in UK

 

  • There is a decline in alcohol problems with age
  • Black / Asian / Ethnic minority populations tend to have:
    • Fewer people with ‘an alcohol problem’
    • A similar proportion with ‘alcohol dependency’
  • 20% of psychiatry admissions are due to alcohol
  • Alcohol drinkers are over-represented in hospital – due to the issues alcohol causes:
    • E.g. in A+E – drunken fights etc
    • E.g. on gastro-ward – alcohol related illnesses
    • Some estimates say 30% of hospital admissions are alcohol related.
 
  • Aetiology
  • Genetic factors – studies on adopted children have shown that the child is more likely to become an alcoholic if one of their parents is, whether or not they live with the parent. if you have a sibling with an alcohol addiction, you are 2.5x more likely to have one yourself
  • Psychological factors – children who are impulsive, aggressive and hyperactive are more likely to have alcohol problems as adults
  • However!there also is an increased risk for those with anxiety – because having a drink can relax people and take away their anxiety – which can lead to alcoholism. To compound the situation, when withdrawal begins, it can initiate even more anxiety – so there is a vicious cycle.
  • Occupation – the occupations that are most risky are:
    • Journalists
    • Publican
    • Wine merchant
    • Armed Forces
    • Entertainer
    • Doctor
  • Cultural factorse.g. in Muslims (due to alcohol being forbidden) and Jews (being drunk is frowned upon) there are much lower rates of alcoholism than in countries where drinking alcohol is seen as more masculine
  • Availability of alcohol
 

Physiology of alcohol
When we talk about ‘alcohol’ we are actually referring to ethanol.
Alcohol is a CNS depressant. It enhances the effect of the inhibitory neurotransmitter GABA. This has an overall inhibitory effect on neurons. Initially, there is a depression of inhibitory neurons (making you feel ‘relaxed’ and disinhibited), but gradually, there is inhibition of many areas of all CNS functions.
  • The first areas to be affected are those responsible for learned ideas and tasks, whilst mechanical inhibition comes later on.
  • Despite what you may believe at the time – there is no increase in any mental or physical functions – unless these have been previously suppressed by anxiety (e.g. nervousness).
  • All the effects of alcohol are very closely related to the blood alcohol concentration. However, in those with dependence, tolerance can reduce these effects.
Cardiovascular effects
  • Moderate intake – can be cardio-protective – as it reduces the aggregation of platelets, and increases HDL’s. The type of alcohol drunk is probably not important.
    • This effect is probably greatest at 1U/day, and is lost at >3U/day.
  • Higher Intake – increases BP by increasing sensitivity to catecholamines. This increased the risk of IHD, CVA’s and stroke.
  • High intake – can cause arrhythmias – especially AF. This can occur either in acute or chronic alcohol abuse.
    • Alcoholic cardiomyopathy is a dilated cardiomyopathy caused by alcohol. It will only partially recover when alcohol intake is reduced. It can lead to heart failure. 10U/day for 8-10 years will cause this.
  • In the short term, alcohol is generally a vasodilator – that is why people often feel warm when they have had a drink – but in reality you are more likely to lose body heat. In some circumstances (e.g. drunk man falls asleep on park bench), this can result in hypothermia.
Plasma conc.*
Effect
30
Mild pleasant effect, due to suppression of inhibitory pathways in the cortex. Increased risk of accidental injury, more open about emotions and personal details
80
Legal limit for driving in the UK. For a 75kg (average) man, this is approximately equal to 2 normal strength pints (3-4%) in the first hour of drinking, and 1 further pint every subsequent hour (i.e. you can drink a lot!). the risk of injury in a road accident is doubled
100-200
Speech becomes slurred, and other motor abilities are affected
>300
Often produces loss of consciousness
>400
May be fatal – due to respiratory and vasomotor suppression.
*(mg per 100ml, which is the same as BAC%)
 
Hepatic effects
  • Hypoglycaemia – the metabolism of alcohol produces excess protons – which encourages the conversion of glucose to lactic acid. alcohol often have a low carbohydrate diet – making the situation worse.
  • Hypoglycaemia tends to occur several hours after heavy alcohol intake (hence having a kebab on the way home!), and is a contributing factor in the seizures seen in withdrawing alcoholics.
  • Lactic acidosis predisposes to the synthesis of saturated fatty acids which lead to fatty liver.
  • Cirrhosis – individual susceptibility varies massively – but in most people drinking 8 U/day for 10 years is enough to cause cirrhosis. In women, it is thought that 4U/day is enough.
  • Oesophageal varices are a common complication
  • Hepatitis is very common in drinkers.
  • Induction of drug metabolising enzymes – so some drugs (e.g. warfarin) become less effective.
GI problems
  • Gastritis – probably caused by increased gastric secretions that are induced by alcohol intake. Peptic ulcers are also 3x more common in heavy drinkers.
  • Pancreatitis may be precipitated by high triglycerides, or due to proteinous secretions induced by alcohol intake.
    • 50% of all cases of chronic pancreatitis are due to heavy drinking
Blood disorders
There rarely can be Iron deficiency anaemia, or a macrocytic anaemia (form folate deficiency), or a megaloblastic anaemia from B12 deficiency. Or there can be a mixed picture of all of these! Usually the MCV is raised
Sexual function
  • Sexual desire is increased in the short term, but the ability to maintain erection is reduced (due to vasodilation)
  • In the long term, there can be damage to the Leydig cells resulting in less testosterone production, which can cause:
  • There may also be alteration of steroid production which can cause gynaecomastia in men as a result of increased oestrogen production.
Neuropsychiatric effects
  • Alcoholics are likely to have vitamin deficiency due to poor diet, as a result of neglecting their need for food in favour of their addiction. A combination of high alcohol intake, low vitamin B6and low thiamine (B1) can predispose peripheral neuropathy and dementia. In the acute withdrawal setting this can be particularly problematic (discussed later). The peripheral neuropathy can be both sensory and motor, and is most prominent in the lower limbs. It will rarely improve with treatment.
  • Alcohol is an anticonvulsant. Thus in withdrawal, it can cause convulsions – even in those with no history of epilepsy.
  • Effects on sleep – alcohol tends to allow you to get to sleep more easily, but the quality of sleep it induces is poorer; there is decreased REM sleep but increased stage 4 sleep. Withdrawal induces periods of REM sleep – which is associated with nightmares.
  • Impaired memory
  • Depression / anxiety
  • Subdural haematoma – rare – but more common after head injury than in non-drinkers.
Carcinogenesis and teratogenesis
  • ↑Risk of mouth, oesophagus and liver with heavy alcohol use
  • Foetal alcohol syndrome – this can occur even if the mother just drinks on one occasion only during the whole pregnancy term! Obviously the risks are greater, the more the mother drinks. The risk is also greatest if alcohol is drunk during the early part of pregnancy. it is most common in children who had a heavy drinking mother. It causes impaired learning and memory in the child.
  • Genetic susceptibility of the foetus plays a part.
Many of the condition relating to alcohol are caused by, or made worse by the dietary deficiencies that often accompany alcoholism.
Psychological effects
Depression and anxiety are very common amongst alcohol abusers. There are three possible routes by which depression can be linked to alcohol:
  • Alcohol is a depressive – it naturally inhibits brain activity
  • Alcohol abuse can cause social problems – e.g. relationship problems, employment issues, debts, problems with friends
  • The depression starts first and the individual turns to alcohol for relief – in the short term, alcohol use can provide an escape from depression, and many people use it as a coping mechanism.
 
More info about alcohol and depression:
  • ½ of all men who attempt suicide are alcohol dependant
  • Anxiety is particularly marked during alcohol withdrawal
Hallucinations related to alcohol are very rare, and should be distinguished from hallucinations that result from withdrawal. In alcohol induced hallucinations, the individual may here second person voices that are usually derogatory. Usually these symptoms will subside within a few days. In cases where the voices do not subside, it is likely there is underlying schizophrenia
Dis-social personality disorder
Memory disorders
  • Alcoholic amnesia – not being able to remember what happened during a period of heavy drinking (e.g. not remember what happened the night before when you wake up in the morning)
  • Korsakov’s Syndrome
  • Alcoholic dementiamay resolve on cessation of alcohol intake
 
Social Problems
  • At work
  • At home – don’t forget impotence!
  • Crime
Pharmacokinetics of alcohol
  • Some absorbed in stomach, most from small intestine
  • High conc. Of alcohol (>20%), presence of food (particularly fat and carbohydrate) all inhibit gastric emptying – and thus alter the peak blood alcohol concentration – with long periods of gastric emptying the peak concentration is likely to be reduced.
  • Has large first pass metabolism. This metabolism has a fixed capacity – so if you absorb a lot of alcohol slowly (e.g. when drinking with food), more alcohol will be removed by first pass than if you drink on an empty stomach.
  • Continued alcohol metabolism is at a constant rate (about 8-10ml/hour)
  • The effects on the brain are most pronounced as the concentration of alcohol rises – this shows that the brain exhibits a short-term tolerance of alcohol.
  • 90% is removed by the liver – mostly by the enzyme alcohol dehydrogenase – producing acetaldehyde. This is then further metabolised by aldehyde dehydrogenase to acetic acid. The other 10% is expired from the lungs,or excreted in the urine unchanged – this occurs at a rate proportional to the blood concentration of alcohol – and thus forms the basis of the breath test, and the urine test.
 
Drug interactions
METRONIDAZOLE and CHLORPORPAMIDE inhibit the action of acetaldehyde dehydrogenase and thus there is acetaldehyde accumulation if you drink whilst taking these drugs. This leads to symptoms of:
Even after very small amounts of alcohol
 
Basis screening for alcohol in a ‘normal’ hospital patient
  • CAGE questions may be useful (but NOT in a psychiatric / full alcohol history)
  • ↑ MCV
  • ↑γGT
  • Take a good alcohol history!
 
Treatment of alcohol addiction
High alcohol intake – but not dependant – these people may benefit from methods to help them moderate their drinking without total abstinence (controlled drinking). Such interventions usually involve self-help materials (e.g. a diary of drinking) in conjunction with counselling sessions.
Alcohol dependence – total abstinence is advised. It is highly unlikely that someone in this position will be able to control their alcohol intake to a ‘reasonable’ level. Becoming totally abstinent will require the individual to undergo a period of ‘detoxification’. This is most likely to be successful if done in a controlled environment. This will usually be a medical ward at hospital (not a psychiatric ward!). Methods:
  • At home – this may be suitable for those with:
    • No history of DT or other withdrawal syndromes
    • Good family / social support
    • No psychological complications (e.g. depression)
    • No physical complications )e.g. liver disease)
    • It will involve a community alcohol team.
    • Drugs (see below)
  • AT hospital – if the patient does not meet the above criteria, they will be treated at hospital with the following:


Benzodiazepine –
this is given both for sedation, and also for their anticonvulsant effects.Thus you should chose a drug which has both these effects. The dose is gradually reduced over 7-10 days. Usually you start off reducing the dose by 20%, but if the patient is still experiencing severe symptoms, reduce the dose at a lower rate.

  • Chlordiazepoxide is often the drug of choice, but diazepam may also be used. Clomethiazole used to be used but it has a high risk of dependence. clonidine is particularly useful at reducing the sympathetic effects seen in withdrawal.
  • These can be given every 4 hours (orally), or IV if necessary. You should not give them for more than 14 days because of their addictive qualities.
  • Lorazepam, haloperidol – these drugs may be used to control aggression in alcoholics in the acute situation.

Thiamine and other vitamin supplements – these are essential! They help to prevent Wernicke’s encephalopathy. They often have to be given IV – and may need to be given for up to 1 month after.
Fluid replacement – dehydration can be particularly severe. There is also a very real risk of Hypocalcaemia and hypomagnesia.
Disulfiram – is a drug that inhibits acetaldehyde dehydrogenase and thus causes nasty side effect when taken with alcohol. It can help to maintain abstinence – although it usually needs to be given with psychotherapy to be effective
Acamprosate – inhibits glutamate – which is an excitory amino acid implicated in cravings. Acamprosate can help reduce cravings.

 
The most important predictor in determining if total abstinence is achievable is motivation. The patient has to have strong motivation to want to stop, whatever their reasons may be.
There are also ‘social’ rehab centres – e.g. run by religious groups – which encourage detox, but they have no medical input.
Addiction
Anything that causes the release of dopamine in the brain can become addictive.
 
Stages of Change
There a psychological model known as the stages of change model, which can be a useful tool in understanding alcohol addiction. It can also be applied to any type of addiction. It shows 5 phases of the addiction, which can then also be applied to abstinence. E.g.:
  • Pre-contemplation – the patient is not yet thinking about drinking
  • Contemplation – the patient is thinking about drinking
  • Preparation – the patient is preparing to drink – e.g. goes and buys alcohol
  • Action – the patient drinks
  • Maintenance – the patient continues in this pattern of behaviour
  • Pre-contemplation 2– the patient is not thinking about stopping drinking
  • Contemplation 2 – the patient is thinking about stopping drinking
  • Preparation 2– the patient is making plans to stop drinking
  • Action 2– the patient tries to stop drinking
  • Maintenance 2– the patient is able to continue without drinking
  • Pre-contemplation 3 – the patient is not yet thinking about drink again
  • Contemplation 3 – the patient is thinking about drinking again
  • Etc, etc
 
By working out what phase the patient might be in, we are then able to target our treatment for them. For example, a patient in Maintenance 1, is very unlikely to stop drinking if you simple say ‘It would be good for your health if you stopping drinking.’, whereas a patient in contemplation 2 would probably respond well to some encouragement and asking them about any plans they have made to alter their behaviour.
However – there are still measures you can take whatever phase the patient is in. You can help ‘push’ the patient along to the next state if you use the right techniques. These techniques are known as motivational interviewing. You should encourage / empower the patient to think for themselves, and not try to guide them through the process! For example, if you wanted to encourage a patient in the maintenance or pre-contemplation phases you could ask questions like:
  • What’s good about drink?
  • What’s bad about drinking?
    • The patient might say something about health issues, so you could respond with: ‘ah your health is bad?’

The idea is to get the patient to think about their life from a different perspective. If you try to push them along the path, you will encounter resistance, and the harder you push, the more resistance you will likely encounter!
Don’t tell the patient they have a problem, just allow them to talk about issues. If they say something that you think is a problem, but to them may not appear a problem, just reflect this back at the patient.

There is also the possibility to leave the cycle, and have a ‘full recovery’ between the maintenance and pre-contemplative stages.
The 12-step approach
This includes the famous Alcoholics anonymous groups, but a similar approach is used in other groups, and for other addictions. In this approach, individuals are encouraged to surrender themselves to a higher power (i.e. God). Patients do not need to be specifically religious, just to have a belief in a higher power. By having the feeling of giving up their choice, many people find it much easier to now give up their addictive substance. Although this approach is not for everyone, it is still very successful.
Generally the 12-steps are recommended to supplement medical and other treatments – e.g. as a follow up treatment after detox. The 12-steps are only really useful for somebody with dependence and not just a heavy drinker.
The original 12 steps are as follows, but they are often slightly adapted to fir different cultural norms:
  1. We admitted we were powerless over alcohol—that our lives had become unmanageable.
  2. Came to believe that a Power greater than ourselves could restore us to sanity.
  3. Made a decision to turn our will and our lives over to the care of God as we understood Him.
  4. Made a searching and fearless moral inventory of ourselves.
  5. Admitted to God, to ourselves, and to another human being the exact nature of our wrongs.
  6. Were entirely ready to have God remove all these defects of character.
  7. Humbly asked Him to remove our shortcomings.
  8. Made a list of all persons we had harmed, and became willing to make amends to them all.
  9. Made direct amends to such people wherever possible, except when to do so would injure them or others.
  10. Continued to take personal inventory and when we were wrong promptly admitted it.
  11. Sought through prayer and meditation to improve our conscious contact with God as we understood Him, praying only for knowledge of His Will for us and the power to carry that out.
  12. Having had a spiritual awakening as the result of these steps, we tried to carry this message to alcoholics, and to practice these principles in all our affairs.
 
Withdrawal
Early symptoms – these occur within a few hours of not drinking:
  • Tremor
  • Nausea
  • Sweating
  • Agitation
  • Tachycardia / palpitations
  • Raised BP
These symptoms are often experienced in the morning by people dependent on alcohol. Having a drink will relieve these symptoms. They are the result of autonomic overactivity due to the withdrawal of the inhibiting effect provided by alcohol.
Late symptoms – these peak at 24-48 hours after withdrawal
  • Delusions
  • Confusion
  • Diarrhoea
  • Epileptic seizures (convulsions)
  • Auditory hallucinations
  • After 48 hours – delirium tremens
Delirium Tremens (DT)
This typically occurs in middle-aged men with a history of many years of drinking, although it can occur after only a few months of drinking. It only occurs in about 5% of acute alcohol withdrawal cases.
It presents about 3-4 days after withdrawal, and is similar to other acute brain syndromes.
Symptoms
  • Restlessness
  • Fear
  • Paranoia
  • Confusion / clouded consciousness
  • Terror-stricken face
  • Ataxia / tremor
  • Sweaty / tachycardia / pyrexia / flushing / pallor
  • Visual Hallucinations – these tend to occur even later in the progression. Usually they are terrifying for the patient and may involve insects, pink elephants and other animals. These visual hallucinations may be accompanied by tactile hallucinations – classically insects crawling on the skin. this phenomenon is known as formication.
  • Auditory hallucinations – often persecutory.
 
Treatment
Delirium Tremens is a medical emergency! Death occurs in around 10-15% of cases (up to 35% if untreated).It results from epileptic seizure, heart failure, self-injury and infection. Treatment is similar to that of a controlled alcohol withdrawal:
  • Benzodiazepine – for sedation and anti-convulsant effects. Even if the acute symptoms have subsided, you should still continue with these for up to 10 days at night to help avoid nightmares.
  • B vitamins – remember – the early you give these, the greater the chance of reducing encephalopathy
  • Fluid replacement
  • Dextrose – to avoid hypoglycaemia
  • Be aware of infection and (head) injury – as these commonly accompany DT
  • On recovery – check for signs of alcohol brain damage. Asses the patient motivation to permanently change.
DT usually resolves after 3-4 days, but continuing anxiety may go on for months.
The effects of DT are due to the long term changes of alcohol on the brain. During long term alcohol use there is a decrease in GABA receptors as tolerance develops. so when alcohol is withdrawn, the patient is left with a very low number of inhibitory receptors – and nothing acting on them! so they can an overactivity in the CNS.
Wernicke’s encephalopathy and Korsakov’s Syndrome
  • Wernicke’s encephalopathy – this is an acute syndrome caused by thiamine deficiency
  • Korsakov’s Syndrome – this is a chronic condition also caused by thiamine deficiency. It is sometimes called Korsakov’s psychosis – although it is an organic brain disease and not a true psychosis.
  • It is possible in some cases that what may initially present as Wernicke’s will continue chronically, thus becoming Korsakov’s.
Clinical Features
Wernicke’s
  • Ocular palsies, particularly of the abducens nerve.
  • Ataxic gait
  • Nausea
  • Memory Problems
  • It can occur in any type of thiamine deficiency, not just alcohol, e.g. dietary, gastric carcinoma, pernicious anaemia
The Wernicke’s Triad:
  • Eye signs
    • Nystagmus
    • Ophthalmoplegia (paralysis of eye muscles)
  • Ataxic gait
  • Confsuion
 
Korsakov’s
This is basically a state of impaired memory function that is present after the signs of Wernicke’s encephalopathy have subsided. It is an anterograde memory disorder – meaning that old memories can be accessed, but that new memories cannot be consolidated. Patients still have the ability to immediately recall facts (e.g. within a few minutes), but have no ability to get this information into long term memory.
  • Patients often have little / distorted sense of time
  • They often make up events, e.g. ‘I went to MacDonald’s for dinner’ – when infact they have been sat at home all day. This is not a conscious attempt to mislead, but a feature of Korsakov’s Syndrome. The answers to these questions are often very plausible. This phenomenon is called confabulation.
    • Patients often also answer these questions in a very laid-back manner, apparently unconcerned that their answers are incorrect.
  • Memory recall for events before the Syndrome is usually fine
  • There is no clouding of consciousness
  • There is often peripheral neuropathy.
 
Differentials
  • Acute brain syndrome of miscellaneous cause. in these other syndromes there will be:
    • Clouding of consciousness
    • Check alcohol history
    • No neurological sings (e.g. ataxia, ocular palsy)
  • Delirium Tremens – 4x as common as Wernicke’s. there are no neurological signs.
  • Chronic brain syndromes – have a different patter of memory loss – long term memory recall is also likely to be affected.
    • Chronic alcohol intake can actually lead to chronic brain syndrome due to atrophy of the cerebrum.
Treatment
Wernicke’s
  • Give lots of thiamine! Usually give in conjunction with other B vitamins. IV or IM if necessary
  • Sedation (similar to DT if necessary)
  • Fluid / electrolytes
Korsakov’s
This is a life-long chronic illness, for which there isn’t really any treatment. thiamine supplements may be useful for some, but after the acute phase, they are unlikely to provide any benefit. Eventually, many patients will require care.
Prognosis
  • Palsies – usually clear with appropriate treatment
  • Ataxia – ataxia will usually resolve on its own over several months
  • Neuropathy – may resolve slowly, unlikely to resolve fully
  • Amnesia – ½ of all patients will not recover from this
Taking an alcohol history
Current drinking behaviour
  • Ask specifically about alcohol intake in the last 24 hours, and the last 7 days. You may also want to ask about a typical day.
    • Try to elicit if there is a binge pattern – days of very large intake, with days of no drinking at all, or if they drink constantly.
  • Is the first drink of the day taken to stop any withdrawal symptoms
  • Do they drink throughout the day, or do they have sessions at specific times.
  • Do they drink to get drunk? Do they get drunk? Do they have blackouts/falls?
  • Where do they drink? Who do they drink with?
  • CAGE questions
    • C – have people ever told you that you should cut down your alcohol intake?
    • A – have you ever been annoyed by people criticising your drinking?
    • G – Have you ever felt guilty about your drinking?
    • E – Do you ever need to have an eye-opener in the mornings?
Development of drinking behaviour
  • When did they start drinking?
  • When did they start drinking heavily? Were there any precipitating life events? Job (e.g. joined the army, or got sacked), relationships etc
  • Have they ever tried to come off alcohol before? Did they have support? If they have, how long did it last, and why did they start again?
  • Forensic history – have they ever been in trouble with the police? Particularly related to drinking
Physical exam
Abdominal Exam:

Neuro

Cardiovascular

  • BP
  • Pulse

Context of drug and alcohol abuse
Smoking – 120 000 deaths/year in the UK
Alcohol – 20 000 deaths/year in the UK
All other drugs combined – probably <10 000
E.g. there are about 50 deaths ever reported in the UK for ecstasy use only (more when combined with other things – most commonly alcohol)
Changing drinking behaviour on a national level
Several things are known to have an influence of public alcohol consumption
  • Price of alcohol – a high price reduces consumption
  • Advertising – has little effect on overall consumption, but can influence children’s attitudes and behaviour.
  • Portrayal in the media – it is thought that the portrayal of alcohol in the media is generally positive (or when negative it is melodramatic), and this makes alcohol look ‘cool’. There is scope to alter this portrayal to alter people’s views of alcohol.
Drugs
Taking a Drug history
This will generally be similar to taking a drinking history, however, you need to ask about each individual substance. You should ask:
  • Quantity used
  • Frequency used
  • Pattern of usage
  • Age of onset of taking drugs
  • When was the most recent use?
  • Method of administration
  • Money spent on drugs each week
    • Illegal activity (e.g. stealing to get money)
  • Risky behaviours
  • Tolerance
  • Dependence
    • Physical harm
    • Psychological harm
    • Social problems
  • Motivation to quit
    • Desire to change
    • Need to change
    • Ability to change
    • Reasons to change
    • Ambivalence – does the patient not really know whether they want to stop taking or not? If they are in rehab, do they really believe they will not use when they leave.
  • Physical problems
    • Cellulitis (from injecting)
    • Hepatitis
    • Aneurysms
    • Abscesses
    • Infection
    • Other drug related medical issues (particularly accidental injury)
  • Trigger factors to use drugs
  • Understanding and insight
 
Clinical features of drug use
Opiates – pinpoint pupils, low BP, venepuncture marks.
Benzodiazepines – disinhibited or gives the impression of intoxicated, but is not drunk
Psychostimulants – rapid speech, large pupils, agitation, restlessness, high BP.
Features of Withdrawal
Opiates – dilated pupils, high BP, sweaty, runny nose (rhinorrhea), cramps
  • Note how these may appear similar to psychostimulant use!
Benzodiazepines – hypersensitivity, hyper-reflexia, depersonalisation
Psychostimulants – agitation, restlessness
Heroin
  • Cold/shivery
  • Flu-like symptoms
  • Body pain
  • Cannot kill you! – unlike alcohol – even though patients will say it is an awful experience, the addiction is psychological and not physical.
 
Quick Overview of Type of drugs
Cannabis – THC
  • Resin – dried crumbled – weak
  • Leaf – hash – grass – weak>>strong
  • Oil – strongest form
  • Classed as a hallucinogen – but is not very strong, and people rarely have full hallucinations
  • Heavy regular use leads to anxiety and depression
  • Occasional use gives you very slightly increased chances of the above
  • Probably causes schizophrenia
  • In people with a psychological disorder it is likely to make it worse
  • You can get addicted to cannabis!
  • Any drug that causes addiction must release dopamine. – cannabis does cause the release of dopamine
Opiates
  • Start of with smoking
  • Then subcutaneous – ‘skin popping’ – all up the arm – looks like train stations
  • Finally inject
  • Very addictive – got to have it or they feel really bad.
  • Medically – it is one of the least harmful. But injecting isn’t very good for you.
  • Strongly associated with depression – but could just be social effects
  • Respiratory depression – can be reversed with naloxone

Cocaine
  • Stimulant – causes a pure release of dopamine into the brain!
  • If you take it, then whatever you do gives you a big reward – makes people repetitive
  • Crack releases al your dopamine straight away – cocaine is not quite as strong
    • Made by cooking cocaine with acid and lemon juice. Extremely addictive
  • Lasts about an hour – then you want more
  • It is used medically as a local anaesthetic. It numbs the area and reduces the blood supply to the area.
  • Cardiotoxic – very dangerous!
Amphetamine (speed)
  • Stimulant
  • Excess energy
  • Elation
  • Very similar to cocaine
  • Amphetamine can be injected
Crystal meth
  • Like the ‘crack’ version of amphetamine
  • Really easy to make
 
MDMA
  • Stimulant
  • Also causes serotonin release – so makes you feel very happy, and close to other socially
  • Very high tolerance effect – so people have to use more
  • Commonly cut with other stuff – so not very good quality
  • Its a relatively safe drug – about 50 deaths on pure ecstasy in the UK
  • Causes a big mood drop about 4 days after you take it
  • Lots of clones of it floating around on the market – which have not yet been made illegal – dubious legality

LSD
  • Man-made
  • Not addictive – no dopamine
  • Hallucinogenic
  • Gives you highs for 12 hours
Benzodiazepines
  • People use them like alcohol to relax
  • Use them to come off other drugs
  • Can go into coma with high dose – or if you combine with alcohol
Magic Mushrooms
  • Naturally occurring
  • Hallucinogenic, and also release serotonin, so cause euphoria
Ketamine
  • Anaesthetic
  • Dissociative – it makes them dissociated from reality
  • Use it to come down off other drugs – dissociates them from the effects of coming off the drug
  • Not addictive
  • Oversedation can occur
Dual-diagnosis
  • This is where a patient has an alcohol/drug problem AND another psychological diagnosis

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