Alcohol Advice Flashcards
alcohol metabolism body distribution
Alcohol distributed throughout body water
Concentration in liver is greater because blood comes directly to it from the stomach and small intestine via the portal vein
Very little alcohol enters the body fat
alcohol absorption
Water soluble
Slowly absorbed from the stomach
More rapidly absorbed from small intestine
Rate of absorption quicker on empty stomach at concentration 20-30% (sherry)
Spirits (40%) delay gastric emptying and are absorbed more slowly
Aerated alcohol e.g champagne gets into system more quickly
Food retards absorption
alcohol metabolism %
90% metabolised in liver
2-5% excreted in sweat, urine or breath
alcohol metabolism stages
alcohol -> acetaldehyde
acetaldehyde -> acetate
acetate -> CO2 and water
blood alcohol concentrations variations
Varies according to age, sex, size and body build, previous exposure, type of drink and whether food is taken
Drugs like cimetidine will delay gastric emptying and reduce absorption
- for acid reflux
Drugs like antihistamines have the opposite effect (increase absorption)
women and blood alcohol levels
Lower levels of alcohol dehydrogenase in the stomach so more alcohol is absorbed before it has been metabolised
Alcohol crosses the placenta easily
- pregnant women shouldn’t drink – affect foetus – foetal alcohol syndrome
blood alcohol concentration timings
Peaks 1 hours after drinking on an empty stomach
Declines over the next 4 hours
Removed at rate of 15mg/100ml/hr
Detectable levels still present for several hours
After 3 pints of beer blood alcohol will be detectable in the morning
tolerance of alcohol in heavy drinkers
Normal metabolism increases
Microsomal ethanol oxidising system comes into play i.e. enzyme induction occurs, this system can also be induced by drugs
- gamma GT will be increased in heavy drinkers
in heavy drinkers with liver damaged enzyme production decreases
heavy drinkers with liver damage
enzyme production decreases
intoxication effect
mild sedative
mild anaesthetic
stimulates dopamine and serotonin
sense of wellbeing relaxation an dis-inhibition
current legal driving limit
Scotland 50mg/100ml blood (UK 80mg/100ml blood)
- risk of road accident double at 50mg/100ml as judgement is impaired
100mg/100ml blood alcohol makes person
people became elated and aggressive
effect of 200mg/100ml blood alcohol
slurred speech and unsteadiness
> 400mg/100ml blood alcohol effect
commonly fatal due to:
- atrial fibrillation
- respiratory failure
- inhalation of vomit
genetic factors contribution to alcohol problems
genetic predisposition to development of alcohol problems (60%; 40% environmental)
4x increased risk of alcoholism in primary relatives
More common in monozygotic twin siblings
Adopted away children of alcoholics 4x increased risk
safe weekly alcohol limits
Men and women
- to keep health risks from alcohol to a low level it is safest not to drink more than 14 units a week on a regular basis
if you regularly drink as much as 14 units per week – it is best to spread evenly over 3 or more days
risk of developing a range of health problems (including cancers of mouth, throat and breast) increases the more you drink on a regular basis
pregnant women
- no alcohol during pregnancy
- can also cause problems with conception – both sexes
medical problems associated with chronic heavy drinking
areas (17)
GI Tract Heart Traumatic Injuries Skin, muscles, nerves and bones Blood Chest Gynaecological Problems Obstetric problems Bleeding Poor Wound healing Drugs Patients with Hep C Hormones and Metabolism Immune system Mental health Nervous system renal
alcohol effect on GIT
Acute gastritis
Liver problems
GI bleeding
Oral, oesophageal, stomach, bowel cancer
Pancreatic disease
Obesity and malnutrition
Vitamin deficiency
- folic acid, vit B1, B2, B6, E, and D
alcohol effect on heart
cardiomyopathy
cardiac arrhythmias
hypertension
increased triglycerides and LDL chloesterol
alcohol effect on skin, muscles, nerves and bones
acute or chronic myopathy
osteoporosis
osteomalacia
alcohol effect on blood
macrocytosis
thrombocytopenia
leucopenia
alcohol effects on drugs
drug metabolism and interactions
non-compliance
interactions also with illicit drugs
effect of alcohol on hormones and metabolism
can cause pseudo-Cushing’s syndrom
effects of alcohol on nervous system
epilepsy
Wernicke-Korsakoff syndrome
cerebral atrophy
oral problems in chronic heavy drinking (13)
Oral cancer
- Concurrent with tobacco use
Oral ulceration
Glossitis
Angular cheilitis
Gingivitis – nutritional def link
Dental neglect
Dental trauma – chaotic lifestyle
Lost denture
Salivary gland enlargement – sialosis
- xerostomia
Dental erosion
Bruxism
Poor wound healing and osteomyelitis
Suppression of immune system by alcohol
alcoholic liver disease prevalence
Fastest growing disease in the UK
Number of cases diagnosed in Scotland has doubled since 1996
- Lothian – 1996: 275 cases; 2006: 445 cases
Unusual
- Most patients who drink heavily will not develop alcohol-related liver injury
- 20% do
stages in alcoholic liver disease
normal
steatosis (fatty liver)
steato-hepatitis ->
cirrhosis (20%)
Habitual consumption of alcohol produces a spectrum of hepatic pathology, ranging from simple steatosis (fatty liver) on one extreme, to cirrhosis on the opposite end of the spectrum.
liver damage by
Alcohol and metabolites and by co-morbidity factors
Environment and host factors
- Age, sex, viruses, drugs, nutrition
steatohepatitis
a liver disease characterized by hepatic steatosis, inflammation, and increased hepatocyte death,
is usually an intermediate stage between simple fatty liver and cirrhosis
steatosis
is a very common result of chronic alcohol ingestion,
occurring in many, if not most, human beings and experimental animals that consume alcohol daily.
cirrhosis
relatively rare outcome of chronic alcohol ingestion (20% of heavy drinkers)
scar, nodules
- irreversible
alcohol most common cause in West
probability of mortality in ALD
probability of liver failure and death from steatohepatitis increase significantly in patients with associated hepatic fibrosis or cirrhosis.
Thus, the transition from simple steatosis to steatohepatitis appears to represent a rate-limiting step in the progression to cirrhosis and clinical liver disease in patients with alcoholic fatty liver disease.
common morbidties of cirrhosis
jaundice
ascites
bleeding
cachexia
infections
encephalopathy
5-year survival of cirrhosis
90% if stop drinking
60% if don’t stop drinking
death in those with liver cancer
death in most people with liver cancer within 10 years
cirrhosis affect on liver function
deranged liver function tests
liver disease and dentistry
Reduced synthesis of clotting factors in damaged liver
- Combined with reduced absorption of vitamin K
- II, VI, IX, X
Thrombocytopenia
- Due to splenomegaly, associated with portal hypertension
Megakaryocyte maturation is also reduced – leading to fewer platelets too
Platelet aggregation is reduced
Lead to prolong bleeding
clotting factors with reduced synthesis in liver disease
II
VI
IX
X
liver damage causes what problem
drug metabolism issues
drug metabolism in pts without liver damage but are heavy drinkers
Heavy drinking induces liver enzymes
This may increase the metabolism of some drugs
- More rapid destruction
- Reduced plasma concentration
Lack of effects
drug metabolism in pts with liver damage
reduced drug metabolism
- LA, analgesia, sedatives and antibiotics
alcohol effect on warfarin metabolism
enhanced metabolism if regular consumption of >3U/day
can alcohol be synergistic with drugs
yes - some drugs act with alcohol to produce synergistic effects
sedative effect of alcohol and drug metabolism
alcohol will interact with drugs producing a sedative effect on nervous system and increase or prolong the effect
paracetamol and alcohol
heavy drinker paracetamol can be converted to an intermediate metabolite which is very hepatotoxic
But Paracetamol is analgesic of choice in liver damage pts in regular dose
- NSAIDs higher chance of GI bleeding
analgesic of choice in liver damage pts
Paracetamol is analgesic of choice in liver damage pts in regular dose
- NSAIDs higher chance of GI bleeding
diulfiram metabolism
Disulfiram (Antabuse) inhibits alcohol dehydrogenase which normally converts acetaldehyde to acetate
- Acetaldehyde builds up and nausea and vomiting occur if alcohol is taken
- Unpleasant
Used in alcohol treatment – deterrent from drinking
Other drugs cause this reaction e.g. Metronidazole, cephalosporins, ketoconazole
If large amounts of alcohol are taken then cardiac arrhythmias and hypotensive collapse can occur
drugs and liver damage
cause GI bleeding
Aspirin and NSAIDs
- Irritant to gastric mucosa
Alcohol is also a gastric irritant
Clotting may be deranged due to liver disease which exacerbates the problem
alcohol and hep C
25% patients with hepatitis C will develop cirrhosis
Alcohol in any amount leads to more rapid development of severe liver disease
- Patients with hepatitis C should abstain from alcohol completely
alcohol interaction with heroin
sedative effect
both alcohol and heroin are sedative
- taken together = increased effect
alcohol interaction with cocaine
taken at the same time a new chemical is produced which is similar to cocaine but with a longer half life
- alcohol prolongs the effect of cocaine
both cardiotoxic – can lead to severe arrhythmias
alcohol interaction with cannabis
absorption of alcohol reduced but combination will increase sensation of confusion and disorientation making accidents more likely
alcohol interaction with amphetamines
alcohol will increase impairment of judgement
alcohol interaction with ecstasy
alcohol increases intoxication but will reduce the potentially fatal fluid retention effect of ecstasy
nutritional issues with alcohol
Alcohol is very calorific
- 6 pints of beer = 500kcals
Alcoholics are generally malnourished
- General neglect- Substitution of food with alcohol
Deficiencies of
- Thiamine - beriberi, Wernicke’s encephalopathy
- Folic acid - macrocytosis
- Vitamin C-scurvy
Fat stomach but generally skinny and malnourished
heart diseases linked to alcohol
cardiomyopathy
cardiac arrhythmias
hypertension
stroke
protective effects
cardiomyopathy
Degenerative heart disease with no coronary artery disease
- Various aetiologies
Well-established complication of chronic alcohol abuse
Most cases asymptomatic
Can lead to arrhythmias, cardiomegaly and congestive heart failure (dyspnea and peripheral oedema)
may be due to accumulation of fatty acid ethyl esters (FAEE) in mitochondria
cardiomyopathy management
supportive measures
abstinence from alcohol
cardiac function in women Vs men
women can develop cardiac problems with less alcohol and lower duration of consumption
cardiac arrhythmias
ECG changes can be marked
- Atrial fibrillation
- Prolonged Q-T interval
- Inverted T waves
- Heart block
- Ventricular arrhythmias
‘Holiday heart syndrome’ and sudden death
strokes and alcohol
Light to moderate alcohol consumption decreases the risk of ischaemic stroke.
Consumption of 5 or more drinks per day increases risk of stroke by 250-450%
hypertension and alcohol
Generally low grade hypertension
Risk factor for stroke
Chronic intake of 30g/day or more alcohol
Hypertension reverses within 2 or 3 weeks of cessation of alcohol intake even in heavy drinkers
Portal hypertension
cardio-protective effects of alcohol
Moderate alcohol intake is associated with decreased risks of coronary artery disease (CAD)
- Observed in ecological studies, case control investigation and in a number of large scale protective cohort studies in males and females
Relative risk for coronary heart disease in:
- non drinkers is 1
- moderate drinker is 0.5
1-2 units of alcohol 2-3 times per week
Benefit particularly in older men and post menopausal women
Alcohol decreases the atherogenic plaques both in humans and experimental animals
Alcohol consumption increases HDL cholesterol
Moderate alcohol consumption is the year prior to acute myocardial infarction (MI) is associated with reduced mortality following infarction
alcohol protective effect
coronary artery disease
incidence of gallstones
macular degeneration
oral cancer prevalence
2% of all cancers
75-80% of pts who have it frequently consume a fairly high level of alcohol
smoking and alcohol link to oral cancer
act synergistically
heavy smoking and drinking increases risk of oral cancer by 38x
why is the 5 year survival of oral cancer relatively low (45-55%)?
Don’t tend to go to dentist when first develops – general health neglect theme
Pre-existing problem with smoking and alcohol
- Initial lesion often ignored
Cancer often advanced at presentation
- lymph node involvement = indicates spread
oral cancer Tx effect
Major surgery 9-10 hours + radiotherapy
- Permanent disfigurement, problems with speech, eating, drinking, socialising
leads to Depression -> more drinking
how does oral cancer occur
Ethanol metabolite acetaldehyde promotes tobacco initiated tumours
Damages DNA and alters oncogene production
Alcohol facilitates absorption of carcinogenic substances across the oral mucosa
Partly due to thinning of oral mucosa due to nutritional deficiency
alcohol link to violence and facial injury
57.6% of male and 21.4% of female victims of assault have consumed alcohol prior to their injury
24% of facial injuries in the UK result from violent behaviour, over half are alcohol related. Young men are at highest risk (1998)
- repeated more recently in Glasgow up to 80%
Facial injury can have long lasting physical and psychological effects
- 40% PTSD from facial trauma (Glasgow)
effect on mental well being of facial injuries
Post Traumatic Stress Disorder
Facial injuries can result in psychiatric morbidity
- lead to more Alcohol problems
- ‘Vicious circle’
types of dental trauma related to alcohol
broken teeth
lost teeth
damage to soft tissues
lost dentures
due to interpersonal violence or falls lined to alcohol
apart from trauma other dental issue linked to alcholo
non carious tooth surface loss
non carious tooth surface loss due to alcohol
Alcohol is very acidic
Gastro oesophageal reflux disease (GORD)-acid in alcohol directly relaxes the oesophageal sphincter
Vomiting
Multifactorial-bruxism
Restoration difficult until problem controlled
- a restorative nightmare?
hazardous drinking
risks of alcohol problems are likely
harmful drinking
problems associated with alcohol are actually present - medical, dental, social
dependent drinking
alcohol is needed to function
SIGN Guidelines 74 - role of HCP in alcohol
management of harmful drinking and alcohol dependence in primary care
“GPs and other primary health care professionals should opportunistically identify hazardous and harmful drinkers and deliver a brief (10 minute) intervention”
screening
purpose of screening is to identify people who need more comprehensive assessment for substance misuse disorders.
It does so by uncovering indicators of serious substance-related problems among adolescent.
As such, it covers the general areas in a client’s life that pertain to substance use without making an involved diagnosis or assessment.
why screen in healthcare setting
Alcohol related mortality and morbidity is high
Many morbidities related to alcohol, including effects on oral health
morbidity
illness related to
mortality
deaths related to
skill required to screen
A basic working knowledge of drug/alcohol issues
Awareness of signs for potential problems
Training in interviewing techniques
Ability to listen to the views of the patient
Report writing skills
Awareness of services available
Recognition of confidentiality issues
screening tools help to
standardised screening tests
screening tools
basically questionnaires
- very effective in detecting hazardous drinking and alcohol dependence
- short, easily administered and easily scored
- can be used by a wide range of professions
- can be used opportunistically
example screening tools for alcohol disorders
AUDIT – the gold standard PAT – used in A&E FAST – most practical CAGE – not suitable for young people POSIT – good but 139 questions CRAFFT – specifically for adolescents
all have a good sensitivity and specificity across wide range of settings
CAGE (ewing, 1984)
‘Yes’, ‘sometimes’ or ‘often’ to 2 or more may indicate an alcohol problem
- Have you ever felt you ought to cut down on your drinking?
- Do you get annoyed at criticism of your drinking?
- Do you ever feel guilty about your drinking?
- Do you ever take an early morning drink first thing in the morning to get the day started or eliminated the shakes?
FAST (hodgson et al, 2002)
recommended for dental practice use
Each question is scored 0-4
Patient is FAST positive if the total score for all questions is > 3
- May only need to ask the first question
AUDIT (WHO 2001)
scores
longer than FAST
0-6 WOMEN non-hazardous safe levels 0-7 MEN non-hazardous safe levels 7-13 WOMEN hazardous drinking 8-15 MEN hazardous drinking 14-20 WOMEN harmful drinking 16-19 MEN harmful drinking >20 possibly dependent drinking seek specialist help
what types of alcohol disorders are amenable to brief motivational intervention
hazardous drinking
harmful drinking
what type of alcohol disorders is not amenable to brief intervention
dependent drinking
- needs specialist help
readiness to change - the teachable moment is
time when people may be more receptive to change
It may be
- After witnessing someone else being injured
- After experiencing other negative consequences of drinking
- Need to be able to relate the adverse event to drinking
readiness to change
brief intervention will be most effective if the person receiving it is ready to change
tell by use of a readiness to change ruler
If not ready to change = intervention likely unsuccessful
cycle of change stages
precontemplative
comtemplative
preparation
action
maintenance
replapse
precontemplative
stage of change - Pt displays
‘what problem? There’s no need to change. My friends drink more than me’
contemplation
stage of change - pt displays
‘I hear what you are saying. I know it’s bad for me, but I enjoy drinking’
listening
preparation
stage of change - pt displays
‘I am going to cut down after new year/next week’
remove all from house
action
stage of change - pt displays
‘I have cut down on my drinking’
not drinking in house, spacing drinks
maintenance
stage of change - pt displays
‘I’ve only been drinking once a week for the last 6 months and have had no more than 2 drinks on that night’
relapse
stage of change
Common – backwards in cycles, but still able to progress forward again
brief motivational interventions
Behaviour change style of counselling
Non-judgemental
Typically lasts between 5 and 20 minutes
Suitable as an opportunistic intervention for patients whose main reason for contact is not their drinking behaviour i.e. dental patients
Pioneered by Miller and Rollnick (1991), who see BMI as not a technique but as a way of being with people – 2 way conversation
- Patient encourage to recognise ambivalence between their actual and ideal behaviour and that the responsibility of change rests with them
FRAMES - framework for BMI
Feedback is given to patient about behaviour
Responsibility for change is placed on the patient
Advice to change is given by practitioner
Menu of self-directed changed options/treatment is offered
Empathic style using warmth, respect and understanding
Self-efficacy is engendered to encourage change
F in FRAMES
Feedback is given to patient about behaviour
R in FRAMES
Responsibility for change is placed on the patient
A in FRAMES
Advice to change is given by practitioner
M in FRAMES
Menu of self-directed changed options/treatment is offered
E in FRAMES
Empathic style using warmth, respect and understanding
S in FRAMES
Self-efficacy is engendered to encourage change
14 units of alcohol equivalent to
6 pints of beer (4% abv)
6 glasses of wine (13%)
14 shots of a spirit (40%)
motivational interviewing should be
a conversation
short
non-judgemental
motivational
aimed at changing behaviour
FRAMES
BMI approach
Feedback Responsibility Advice Menu of options Empathic Self-efficacy
