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