What are the possible mechanisms involved in the occurrence of tolerance to chronic alcohol intake?  

Alcohol causes sedation, anxiety relieve, ataxia, impaired judgement and disinhibited behavior. These CNS effects occur a few hours after consuming and for people who drinks chronically, higher concentration are needed as they are tolerant to the effects of alcohol.  Like other sedative-hypnotic drugs, alcohol is a CNS depressant and can lead to coma, respiratory depression and death when consumed in large concentrations. 

What are the toxic effects of chronic alcohol consumption on the liver and hepatic metabolism? 

Liver disease is the most common medical complication of alcohol abuse. Large consumption of alcohol can lead to severe liver disease. Alcohol fatty liver may progress to alcoholic hepatitis and finally to cirrhosis and liver failure. Cirrhosis contributes to elevated portal blood pressure and esophageal and gastric venous varices which can rupture and lead to massive bleeding.  

What is Wernicke-Korsakoff-syndrome and how is it treated? 

This syndrome is characterized by paralysis of external eye muscles, ataxia and confusion that can progress to coma and even death. It is associated with thiamine deficiency but is common seen with the use of alcohol. Treatment includes thiamine therapy  

Fully explain the fetal alcohol syndrome. 

Fetal alcohol syndrome is caused by alcohol use during pregnancy. Abnormalities that are characterized with this syndrome includes intrauterine growth retardation, microcephaly, poor coordination, underdevelopment of midfacial region, minor joint anomalies. In severe cases, patients present with congenital heart defects and mental retardation. Ethanol crosses the placenta and reaches concentrations in the fetus similar to those in the maternal blood. The fetal liver does not have ADH activity thus the fetus relies on the enzymes in the maternal blood to eliminate alcohol.  

Name 4 drug interactions with alcohol where the pharmacological effects of the other drugs are potentiated by alcohol. 

• Alcohol potentiates the pharmacological effects of many non-sedative drugs including vasodilators and oral hypoglycemic agents. 

• Chronic consumption of alcohol increases the risk of hepatotoxicity due to toxic levels of acetaminophen as a result of increased P450-mediated conversion of acetaminophen to reactive hepatotoxic metabolites. 

• Acute alcohol use can inhibit metabolism of some drugs due to reduced liver blood flow. These drugs include phenothiazines, tricyclic antidepressants and sedative-hypnotic drugs. 

• CNS depression can occur when alcohol is consumed with other CNS depressants such as sedative-hypnotics.