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Although the public often views alcoholic drinks as stimulating, ethanol primarily is a CNS depressant. Ingestion of moderate amounts of ethanol, like that of other depressants such as barbiturates and benzodiazepines, can have anti-anxiety actions and produce behavioural disinhibition at a wide range of dosages. Individual signs of intoxication vary from expansive and vivacious affect to uncontrolled mood swings and emotional outbursts that may have violent components. With more severe intoxication, CNS function generally is impaired, and a condition of general anaesthesia ultimately prevails. However, there is little margin between the aesthetic actions and lethal effects (usually owing to respiratory depression).

About 10% of alcohol drinkers progress to levels of consumption that are physically and socially detrimental. Chronic abuse is accompanied by tolerance, dependence, and craving for the drug. Alcoholism is characterized by compulsive use despite clearly deleterious social and medical consequences. Alcoholism is a progressive illness, and brain damage from chronic alcohol abuse contributes to the deficits in cognitive functioning and judgment seen in alcoholics. Alcoholism is a leading cause of dementia in the United States. Chronic alcohol abuse results in shrinkage of the brain owing to loss of both white and gray matter. The frontal lobes are particularly sensitive to damage by alcohol, and the extent of damage is determined by the amount and duration of alcohol consumption, with older alcoholics being more vulnerable than younger ones. It is important to note that ethanol itself is neurotoxic, and although malnutrition or vitamin deficiencies probably play roles in complications of alcoholism such as Wernicke’s encephalopathy and Korsakoff’s psychosis, most of the alcohol-induced brain damage in Western countries is due to alcohol itself. In addition to loss of brain tissue, alcohol abuse also reduces brain metabolism (as determined by positron-emission tomography), and this hypometabolic state rebounds to a level of increased metabolism during detoxification. The magnitude of decrease in metabolic state is determined by the number of years of alcohol use and the age of the patients.

Alcohol has a number of pharmacological effects on cardiac conduction, including prolongation of the QT interval, prolongation of ventricular repolarization, and sympathetic stimulation. Atrial arrhythmias associated with chronic alcohol use include supraventricular tachycardia, atrial fibrillation, and atrial flutter. Some 15% to 20% of idiopathic cases of atrial fibrillation may be induced by chronic ethanol use. Ventricular tachycardia may be responsible for the increased risk of unexplained sudden death that has been observed in persons who are alcohol-dependent. During continued alcohol use, treatment of these arrhythmias may be more resistant to cardioversion, digoxin, or Ca²⁺ channel blocking agents. Patients with recurrent or refractory atrial arrhythmias should be questioned carefully about alcohol use.

Alcohol frequently is either the primary etiologic factor or one of multiple causal factors associated with oesophageal dysfunction. Ethanol also is associated with the development of oesophageal reflux, Barrett’s oesophagus, traumatic rupture of the oesophagus, Mallory-Weiss tears, and oesophageal cancer. When compared with non-alcoholic non-smokers, alcohol-dependent patients who smoke have a tenfold increased risk of developing cancer of the oesophagus. There is little change in oesophageal function at low blood alcohol concentrations, but at higher blood alcohol concentrations, a decrease in peristalsis and decreased lower oesophageal sphincter pressure occur. Patients with chronic reflux esophagitis may respond to proton pump inhibitors and abstinence from alcohol.

Heavy alcohol use can disrupt the gastric mucosal barrier and cause acute and chronic gastritis. Ethanol appears to stimulate gastric secretions by exciting sensory nerves in the buccal and gastric mucosa and promoting the release of gastrin and histamine. Beverages containing more than 40% alcohol also have a direct toxic effect on gastric mucosa. While these effects are seen most often in chronic heavy drinkers, they can occur after moderate and short-term alcohol use.
Alcohol is not thought to play a role in the pathogenesis of peptic ulcer disease. Unlike acute and chronic gastritis, peptic ulcer disease is not more common in alcoholics. Nevertheless, alcohol exacerbates the clinical course and severity of ulcer symptoms. It appears to act synergistically with Helicobacter pylori to delay healing. Acute bleeding from the gastric mucosa, while uncommon, can be a life-threatening emergency. Upper gastrointestinal bleeding is associated more commonly with oesophageal varices, traumatic rupture of the oesophagus, and clotting abnormalities.

Many alcoholics have chronic diarrheal as a result of malabsorption in the small intestine. The major symptom is frequent loose stools. The rectal fissures and pruritus ani that frequently are associated with heavy drinking probably are related to chronic diarrheal. The diarrheal is caused by structural and functional changes in the small intestine.

Ethanol produces a constellation of dose-related deleterious effects in the liver. The primary effects are fatty infiltration of the liver, hepatitis, and cirrhosis. Because of its intrinsic toxicity, alcohol can injure the liver in the absence of dietary deficiencies .The accumulation of fat in the liver is an early event and can occur in normal individuals after the ingestion of relatively small amounts of ethanol. This accumulation results from inhibition of both the tricarboxylic acid cycle and the oxidation of fat, in part, owing to the generation of excess NADH produced by the actions of ADH and ALDH.

Fibrosis, resulting from tissue necrosis and chronic inflammation, is the underlying cause of alcoholic cirrhosis. Normal liver tissue is replaced by fibrous tissue. Alcohol can affect stellate cells in the liver directly; chronic alcohol use is associated with transformation of stellate cells into collagen-producing, myofibroblast-like cells, resulting in deposition of collagen around terminal hepatic venules. The histological hallmark of alcoholic cirrhosis is the formation of Mallory bodies, which are thought to be related to an altered cytokeratin intermediate cytoskeleton.

Several strategies to treat alcoholic liver disease have been evaluated. Prednisolone may improve survival in patients with hepatic encephalopathy. Nutrients such as S-adenosylmethionine and polyunsaturated lecithin have been found to have beneficial effects in nonhuman primates and are undergoing clinical trials. Other medications that have been tested include oxandrolone, propylthiouracil, and colchicine. At present, however, none of these drugs is approved for use in the United States for the treatment of alcoholic liver disease. The current primary treatment for liver failure is transplantation in conjunction with abstinence from ethanol. Long-term outcome studies suggest that patients who are alcohol-dependent have survival rates similar to those of patients with other types of liver disease. Alcoholics with hepatitis C may respond to interferon-2a.

By: Ammarah Khan