Alcohol-use disorder results from a variety of genetic, psychosocial, and environmental factors. It is characterised by increased tolerance to the effects of alcohol, the presence of characteristic withdrawal signs and symptoms, and impaired control over the quantity and frequency of drinking. Prolonged exposure causes adaptive changes in brain receptors and neurotransmitters, leading to effects such as addiction, tolerance, and withdrawal. Alcohol-use disorder, particularly when chronic and severe, can be associated with a variety of medical and psychiatric sequelae.
The syndrome occurs in alcohol abusers as a result of decrease or cessation of alcohol drinking, resulting in the blood alcohol levels below the level to which the drinker has become habituated. This is commonly referred to as 'the shakes' and begins about 4 to 12 hours after the last drink.
Mild withdrawal symptoms may start as early as 4 to 6 hours and peak at 24 to 36 hours after the last drink. They include nausea, irritability, shakiness, depression, fatigue, anxiety, coarse tremor, and excitability. Major withdrawal symptoms occur after 24 hours and usually peak at 50 hours after the reported decrease or cessation of drinking. This is characterised by severe anxiety and irritability, sleeping difficulty, insomnia, elevated heart rate and blood pressure, fever, and auditory and visual hallucinations. Delirium tremens (DT) is the most severe form of withdrawal and is common after 3 days of abstinence or reduced drinking. It is marked by hallucinations, confusion, and seizures.
Comprises three stages of liver damage: fatty liver (steatosis), alcoholic hepatitis (inflammation and necrosis), and alcoholic liver cirrhosis (fibrosis) caused by chronic heavy alcohol ingestion. There are no specific signs and symptoms to diagnose ALD. Clinical presentation is highly variable.
The pathological end stage of any chronic liver disease. The most common causes of cirrhosis in the Western world are chronic hepatitis C and alcoholic liver disease, followed by non-alcoholic fatty liver disease (steatohepatitis) and chronic hepatitis B. The main complications of cirrhosis are related to the development of liver insufficiency and portal hypertension, and include ascites, variceal haemorrhage, jaundice, portosystemic encephalopathy, hepatorenal and hepatopulmonary syndromes, and the development of hepatocellular carcinoma.
Encompasses a spectrum of neuropsychiatric abnormalities in patients with severe liver dysfunction. A working definition, as proposed by the World Congress of Gastroenterology, suggests that persistent HE includes cognitive deficits, which impact negatively on social and occupational functioning, and persistent non-cognitive abnormalities (such as extrapyramidal alterations or sleep disturbances). It is often caused by cirrhosis, a common cause of which is alcoholism.
A disorder of the exocrine pancreas associated with acinar cell injury with local and systemic inflammatory responses. Inflammation may range from mild oedema to peri-pancreatic necrosis. Ethanol causes 40% to 45% of cases of acute pancreatitis and is the most common cause of acute pancreatitis in men. A dose-related destruction to the pancreatic parenchyma has been described. Acute pancreatitis is more commonly seen in men than in women and is usually seen after periods of binge drinking. There is no threshold for the development of acute pancreatitis. The average amount of alcohol intake in patients with acute pancreatitis is 18-22 units (or standard drinks) per day (150 to 175 g per day), but the amount is less important than the type of alcohol ingested.
Characterised by recurrent or persistent abdominal pain and progressive injury to the pancreas and surrounding structures, resulting in scarring and loss of function. Unlike recurrent acute pancreatitis, chronic pancreatitis is characterised by reduced pancreatic exocrine function, malabsorption, diabetes, and pancreatic calcifications. Worldwide, alcohol is the major risk factor for chronic pancreatitis (70% to 80%). Co-factors are required to induce alcoholic pancreatitis, including anatomical, environmental, or genetic factors, as fewer than 10% of alcoholics develop the disease.
A neurological emergency caused by the acute deficiency of thiamine in a susceptible person. In people with chronic alcohol dependence, thiamine deficiency is a result of a combination of factors: poor intake, low content of vitamins in alcohol, low storage capacity of the liver, decreased intestinal absorption, impaired conversion of thiamine to its active form (thiamine pyrophosphate), and increased demand to metabolise the carbohydrates in alcohol.
Refers to conditions that may result from fetal exposure to alcohol during pregnancy. Disorders include fetal alcohol syndrome (FAS), partial FAS, alcohol-related neurodevelopmental disorder, and alcohol-related birth defects. FAS is characterised by antenatal and postnatal growth retardation, specific facial dysmorphology and structural and/or functional abnormalities of the CNS.
Serum liver tests (ALT and AST, and gamma-GT) are useful for assessing liver damage due to alcohol. Elevated gamma-GT correlates with excessive alcohol consumption; however, isolated elevations in gamma-GT are so common, and so often unhelpful, that many institutions have chosen to delete this test from their liver test panel.
Delirium is an acute, fluctuating change in mental status, with inattention, disorganised thinking and altered levels of consciousness. Alcohol intoxication and withdrawal are frequently associated with delirium. Recent binge drinking can cause alcoholic ketoacidosis, which can lead to delirium.
Polyneuropathy is a generalised disease of the peripheral nerves. It most commonly presents as symmetric numbness, paraesthesias, and dysaesthesias in the feet and distal lower extremities (distal symmetrical polyneuropathy). In severe cases, sensory symptoms and signs fit a stocking-glove distribution. Balance and gait may be impaired. Early motor signs include atrophy of the intrinsic foot muscles and ankle weakness. The autonomic nervous system may be involved, resulting in symptoms such as early satiety, diarrhoea or constipation, sexual performance problems, sweating disturbances, and orthostatic lightheadedness. Thiamine and pyridoxine deficiencies caused by alcoholism are possible causes of polyneuropathy. Ethanol-polyneuropathy seen in alcoholics may be caused by direct toxicity of ethanol on the nerve or concomitant nutritional deficiencies.
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This overview has been compiled using the information in existing sub-topics.
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