Alcohol

Published on 01/03/2015 by admin

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Last modified 22/04/2025

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62

Alcohol

Abuse of alcohol (ethanol) is a major contributor to morbidity and mortality, far outstripping other drugs in its effects on the individual and on society. Alcohol is a drug with no receptor. The mechanisms by which it exerts its detrimental effect on cells and organs are not well understood, but the effects are summarized in Table 62.1.

Table 62.1

Effects of ethanol on organ systems

System Condition Effect
CNS Acute Disorientation → coma
  Chronic Memory loss, psychoses
  Withdrawal Seizures, delirium tremens
Cardiovascular Chronic Cardiomyopathy
Skeletal muscle Chronic Myopathies
Gastric mucosa Acute Irritation, gastritis
  Chronic Ulceration
Liver Chronic Fatty liver → cirrhosis, decreased tolerance to xenobiotics
Kidney Acute Diuresis
Blood Chronic Anaemia, thrombocytopenia
Testes Chronic Impotence

For clinical purposes alcohol consumption is estimated in arbitrary ‘units’ – one unit representing 200–300 mmol of ethanol. The ethanol content of some common drinks is shown in Figure 62.1. The legal limit for driving in the UK is a blood alcohol level of 17.4 mmol/L (80 mg/dL).

Metabolism of ethanol

Ethanol is metabolized to acetaldehyde by two main pathways (Fig 62.2). The alcohol dehydrogenase route is operational when the blood alcohol concentration is in the range 1–5 mmol/L. Above this most of the ethanol is metabolized via the microsomal P450 system. Although the end product in both cases is acetaldehyde, the side effects of induced P450 can be significant. Ethanol metabolism and excretion in a normal 70 kg man is summarized in Figure 62.3.

Acute alcohol poisoning

The effects of ethanol excess fall into two categories:

The relative contribution of ethanol in cases of coma, especially where other drugs and/or head injury are present, may be difficult to distinguish. Blood ethanol determinations are the best guide. Where these are not available, plasma osmolality measurement and calculation of the osmolal gap may help.

Recovery from acute alcohol poisoning is usually rapid in the absence of renal or hepatic failure, and is speeded up if hepatic blood flow and oxygenation is maximized. The elimination rate of ethanol is dose-related; at a level of 100 mmol/L it is around 10–15 mmol/hour. Ethanol concentrations in a group of chronic alcoholics admitted in coma with acute alcohol poisoning are shown in Figure 62.4.

Alcohol inhibits gluconeogenesis and some patients are prone to develop hypoglycaemia 6–36 hours after alcohol ingestion, especially if they are malnourished or fasted. A small number of these malnourished patients develop alcoholic ketoacidosis.

Chronic alcohol abuse

Many of the effects of chronic alcohol abuse are due either to the toxicity of acetaldehyde and/or the failure of one or more of the many homeostatic and synthetic mechanisms in the liver. One of the earliest signs of chronic alcohol abuse is hepatomegaly. This results from the accumulation of triglyceride due to increased synthesis from the carbohydrate load and reduced protein synthesis. Continued high ethanol intake may cause the following sequelae:

Diagnosis of chronic alcohol abuse

Chronic alcohol abuse can be very difficult to detect, and is usually determined from the patient’s history. In order to be more objective, there has been a continued search for markers of ethanol abuse. As yet there is no highly sensitive and specific marker. However, a number of blood components are altered and these can give an indication of chronic alcohol ingestion. The most commonly used are:

There are a number of other potentially useful markers, notably isoforms of transferrin that are deficient in the carbohydrate linked to the protein. This carbohydrate-deficient transferrin is present in more than 90% of patients with chronic alcohol abuse. Such assays are not yet widely available.

Case history 51

A 16-year-old boy whose epilepsy had recently become poorly controlled was found to have a raised γGT of 82 U/L. Because of his troublesome behaviour his parents suspected he was drinking.

Comment on page 169.

Once the diagnosis of chronic alcohol abuse is made, these markers are of use in monitoring behaviour, since a single ‘binge’ will lead to their derangement. γGT is used regularly in this manner.

Chronic alcohol abuse exposes the individual to increased risk of damage from other substances. Chronic alcoholics have higher rates of smoking-related disease, and are more susceptible to poisoning with hepatotoxic substances. They also have different rates of metabolism of therapeutic drugs and care needs to be taken in treating them with drugs that are metabolized by the cytochrome P450 system.

Admission rates to hospital with alcohol-related diseases are high, and since the diagnosis is sometimes unsuspected, it should always be considered when carrying out an initial examination (Fig 62.5).

image Clinical note

Methanol and ethylene glycol (antifreeze) are both metabolized by alcohol dehydrogenase to formic and oxalic acids, which are toxic. In order to prevent this metabolism, ethanol is infused to a concentration of 20 mmol/L until the alcohols, methanol and ethylene glycol, are excreted unchanged. Alcoholics who drink ethanol as well as methanol in fact protect themselves against the worst effects of methanol poisoning.

Alcohol

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