Each 10 g dose of alcohol will increase the blood alcohol concentration by about 0.02 g%. Alcohol has zero order pharmacokinetics which means that the blood alcohol concentration falls linearly, as it happens, at about 0.02 g% per hour. It is therefore possible to make a rough guess of blood alcohol by adding the number of drinks and subtracting the number of hours.

The clinical effect of a given blood alcohol concentration is very much affected by tolerance so that a concentration of 0.4 g% or above which may well be fatal in an inexperienced drinker will be tolerated remarkably well in a long standing heavy drinker. The blood alcohol concentration of 0.05 g% was chosen as the legal limit for driving because beyond that concentration the risk of being involved in a fatal accident increases exponentially.

The phenomena of alcoholic liver disease and alcoholic pancreatitis are well known. The risk for both seems to become measurable at about 80 g daily for men and 60 g daily for women. With liver disease, the risk of the condition appearing increases linearly with time once the threshold consumption is reached with the actual concentration of consumption determining the slope of the curve, i.e. the rate at which the risk increases. All this suggests that alcohol “primes” the liver, and another event(s) not yet identified caused the disease to begin.

Alcohol causes extensive central nervous system damage ranging from minimal brain dysfunction through to severe dementia. The earliest change is often an adaptive learning difficulty in which the patient has difficulty learning from mistakes and in adapting to new situations.

• Minor brain damage - adaptive learning deficiency
• Global alcohol related brain damage
• Wernicke [479 KB]/Korsakoff syndrome - thiamine dependent
• Peripheral neuropathy
• Seizures
• Alcoholic cerebellar disease
• Other

Resource: Etoh Neuopsych 2003.ppt [174 KB]

A number of other systems are affected by alcohol:

Endocrine

• loss of sexual function/fertility
• increased cortisol concentrations

Cardiovascular

• cardiomyopathy
• hypertension

Haematology

• thrombocytopenia
• pancytopenia
• macrocytic anaemia

GI tract

• oesophageal disease
• chronic diarrhoea

The above list is obviously not exhaustive.

HIV

Occurs in only about 1% of Australian IV drug users.

Hepatitis

The incidence of markers for hepatitis B and C increases linearly with the duration of intravenous use. Over 90% of intravenous users with histories of 8 years or more have markers for hepatitis C.

IV narcotics

There are few specific complications associated with the use of pure narcotics apart from dependence. Narcotics do however, have an antioestrogenic effect which reduces fertility and may predispose to osteoporosis. Excessive sweating and body odour are well recognised, and the reduction in saliva leads to dental caries.

Cardiac disease

• coronary vasoconstriction/thrombosis
• catecholamine injury (acute and chronic cardiomyopathy)

Neurological

• cerebral haemorrhage
• seizures

Renal disease

• usually tubular

Musculoskeletal

• rhabdomyolysis

The main problem with prescribed sedatives is dependence with the development of “break through” withdrawal and often recurrence of the original symptoms of anxiety and insomnia.

Again the main problem is dependence, but whereas for the benzodiazepines withdrawal causes most problems, for narcotics, tolerance is the major problem with increasing doses being required to control chronic pain.

This subject would fill a textbook. What follows is an outline of the major problems and the associated levels of use.