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

Tolerance can develop as a result of ethanol-induced upregulation of a pathway in the presence of ethanol. Furthermore, because of the downregulation of GABAA mediated receptors with continued alcohol use, the GABA neurotransmitter plays a role in tolerance. Continuous use of alcohol can cause the same pathway to become overactive, resulting in dependence.

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

Chronic alcohol intake impairs liver function, resulting in diseases such as hepatitis and liver cirrhosis. Increased activity at this pathway may also have metabolic consequences from ethanol oxidation. Chronic alcohol intake can also slow down processes including gluconeogenesis, resulting in hypoglycemia.

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

Wernicke-Korsakoff syndrome is characterized by weakness of the external eye muscles, ataxia, and a confused condition that can lead to a coma when caused by Thiamine deficiency. Parental thiamine therapy is part of the treatment.

4. Fully explain the foetal alcohol syndrome.

The ethanol ingested by the mother crosses the placenta, causing the foetus to have the same alcohol blood content as the mother. Foetal alcohol syndrome is caused by a mother's alcohol consumption while pregnant. Mental retardation and underdevelopment of the facial area are common in infants with this syndrome, which is usually teratogenic.

5.  How do the pharmacokinetic interactions of acute alcohol consumption differ from that of chronic alcohol consumption?

Acute – the alcohol dehydrogenase enzyme, which catalyzes the conversion of alcohol to acetaldehyde, plays a role with low to moderate levels of alcohol intake.
Chronic - on the other hand, the MEOS plays a role of high-concentration alcohol intake since their behaviour is caused by chronic alcohol consumption.

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

Under the influence of acute alcohol intake, the metabolism of phenothiazines, TCAs, and sedative hypnotics such as benzodiazepines is reduced or inhibited due to a reduction in enzyme activity and liver blood flow. Acute alcohol intake potentiates the effects of vasodilating and hypoglycemic medications, resulting in extreme vasodilation in the body, resulting in a decrease in blood pressure and increased heart rates to maintain vital organ function. Aspirin's anti-platelet aggregation effects are enhanced by alcohol.