- What are the pharmacokinetic features of ethanol absorption and metabolism in the body?
Ethanol (Spiritus aethylicus) is rapidly absorbed from the stomach and small intestine, easily penetrating cells. Metabolism shows gender differences: it is accelerated in men due to higher activity of hepatic microsomal enzymes.
Elimination and metabolic features:
- Excretion unchanged — 5–10% is eliminated via urine, feces, sweat, milk, and exhaled air.
- Oxidation — 90% is metabolized in the liver at a rate of 5–10 mL/h.
The biochemical pathway involves the conversion of ethanol by alcohol dehydrogenase into highly toxic acetaldehyde. Subsequently, aldehyde dehydrogenase and Krebs cycle enzymes oxidize it to water and carbon dioxide. This process is accompanied by an excess of NADH, which inhibits gluconeogenesis and stimulates lactate production. Fetal tissue completely lacks alcohol dehydrogenase.
- What symptoms develop in acute ethanol poisoning, and what are the principles of management?
Acute ethanol poisoning causes central nervous system depression, potentially progressing to alcoholic coma, which can be fatal. The clinical picture depends on blood alcohol concentration: at 1.5 g/L, noticeable signs of intoxication appear; at 3.5 g/L, they are pronounced; and 3.5–8 g/L is considered a median lethal dose.
Symptoms may be accompanied by loss of consciousness and metabolic disorders:
- Hypoglycemia — decreased blood glucose due to the inhibition of gluconeogenesis.
- Lactic acidosis — hyperlactatemia resulting from the shift in the lactate dehydrogenase reaction equilibrium toward lactate formation.
Specific emergency management protocols for acute ethanol poisoning are beyond the scope of this context.
- What drug interactions are typical for ethyl alcohol?
Ethyl alcohol participates in clinically significant drug interactions, predominantly potentiating the toxicity or depressant effects of other agents.
Major ethanol drug interactions:
- Potentiation of CNS depression — mutual enhancement of effects when taken with sedatives, benzodiazepine receptor agonists, tiagabine, and clonidine.
- Disulfiram-like reaction — metronidazole inhibits aldehyde dehydrogenase, delaying ethanol oxidation at the acetaldehyde stage and causing toxic accumulation. Cefotetan and cefoperazone cause disulfiram-like reactions by blocking enzymes involved in ethanol metabolism, resulting in alcohol intolerance.
- Enzyme induction — chronic alcohol consumption induces the CYP2E1 isoenzyme, sharply increasing the formation of the hepatotoxic metabolite of paracetamol (acetaminophen).
Additionally, the antifungal drug griseofulvin can enhance the toxic effects of alcohol.
- Why is a 70% solution used for surgical hand antisepsis instead of a 95% solution?
A 70% concentration provides optimal antiseptic tissue permeability. Higher concentrations (90–95%) cause rapid protein coagulation (tanning), which prevents deep penetration into microbial cells.
- Which microorganisms are sensitive to ethanol?
The substance is active against viruses, as well as Gram-positive and Gram-negative bacteria.
- What is the composition of the combination product Hospisept?
The product is a combination of ethanol and propanol, providing an expanded spectrum of activity against bacteria, fungi, and viruses (including HIV and hepatitis B).