Definition of alcoholism american medical association. Drug and Alcohol Abuse - almostadoctor



Cravings – very strong desire to drink Medical definition of alcoholism.

Drinking despite negative consequences:

On their physical 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

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.

What are the ‘safe limits for alcohol?

Men – <,14 units per week, and <,3 units per day

Women – <,14 units per week, <,3 units per day

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.


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.


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:

Cultural factors – e.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

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.

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

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 B

) 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.

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.

Medical definition of chronic alcoholism

Genetic susceptibility of the foetus plays a part.

Psychological effects

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.

½ of all men who attempt suicide are alcohol dependant

Anxiety is particularly marked during alcohol withdrawal

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)

Alcoholic dementia – may resolve on cessation of alcohol intake

Social Problems

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

CAGE questions may be useful (but NOT in a psychiatric / full alcohol history)

Take a good alcohol history!

At home – this may be suitable for those with:

No history of DT or other withdrawal syndromes

Good family / social support

No physical complications )e.g. liver disease)

It will involve a community alcohol team.

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 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.


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

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.

The 12-step approach

We admitted we were powerless over alcohol—that our lives had become unmanageable.

Came to believe that a Power greater than ourselves could restore us to sanity.

Made a decision to turn our will and our lives over to the care of God as we understood Him.

Made a searching and fearless moral inventory of ourselves.

Admitted to God, to ourselves, and to another human being the exact nature of our wrongs.

Were entirely ready to have God remove all these defects of character.

Humbly asked Him to remove our shortcomings.

Made a list of all persons we had harmed, and became willing to make amends to them all.

Medical definition of heavy drinking

Made direct amends to such people wherever possible, except when to do so would injure them or others.

Continued to take personal inventory and when we were wrong promptly admitted it.

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.

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.


Tachycardia / palpitations

Epileptic seizures (convulsions)

Auditory hallucinations

After 48 hours – delirium tremens

Delirium Tremens (DT)

Confusion / clouded consciousness

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.

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

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.

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.

Ocular palsies, particularly of the abducens nerve.

It can occur in any type of thiamine deficiency, not just alcohol, e.g. dietary, gastric carcinoma, pernicious anaemia

Ophthalmoplegia (paralysis of eye muscles)

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

Acute brain syndrome of miscellaneous cause . in these other syndromes there will be:

Clouding of consciousness

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.

Give lots of thiamine! Usually give in conjunction with other B vitamins. IV or IM if necessary

Sedation (similar to DT if necessary)

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

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?

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?

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

What is the medical definition of alcoholism

Co-ordination (cerebellar dysfunction)

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.

Taking a Drug history

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)

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.

Cellulitis (from injecting)

Other drug related medical issues (particularly accidental injury )

Trigger factors to use drugs

Understanding and insight

Note how these may appear similar to psychostimulant use!

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 Types of drugs

Resin – dried crumbled – weak

Leaf – hash – grass – weak>,>,strong

Classed as a hallucinogen – but is not very strong, and people rarely have full hallucinations

Occasional use gives you very slightly increased chances of the above

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

Then subcutaneous – ‘skin popping’ – all up the arm – looks like train stations

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

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 can be injected

Like the ‘crack’ version of amphetamine

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

Not addictive – no dopamine

Gives you highs for 12 hours

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

Hallucinogenic, and also release serotonin, so cause euphoria

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

This is where a patient has an alcohol/drug problem AND another psychological diagnosis

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