Pharm 101: Ethanol
Class
Alcohol
Pharmacodynamics
- Multiple signalling pathways affected, mainly:
- Enhances GABA action at GABA-A receptors
- Inhibits NMDA receptors
- Multiple organ system effects, mainly CNS depression, CVS depression and smooth muscle relaxation (see below)
Pharmacokinetics
- Rapid absorption from GIT (water soluble), peak levels within 30 minutes
- Rapid distribution, Vd approximates TBW ~0.5-0.7L/kg
- Hepatic metabolism undergoes zero-order kinetics* with two major pathways to produce acetaldehyde:
- Alcohol dehydrogenase (ADH) pathway is primary pathway and forms NADH as co-product
- Microsomal ethanol-oxidising system (MEOS) pathway is induced in chronic alcohol consumption
- Acetaldehyde is oxidised to acetate by enzyme ALDH, forms NADH as co-product. Disulfiram inhibits this reaction.
- Excretion: lungs, liver
- Induces CYP2E1 enzyme
*Elimination occurs at a constant rate independent of drug concentration. Other drugs that have zero order kinetic metabolism include aspirin, and phenytoin (at higher doses)
Clinical uses
- Severe methanol poisoning
- Topical antiseptic
Adverse effects
- CNS depression:
- Sedation and anxiolysis
- Disinhibition, impaired judgment, impaired motor skills
- Ataxia, slurred speech
- Respiratory depression and coma
- CVS depression:
- Depression of myocardial contractility
- Smooth muscle:
- Vasodilation –> hypothermia
- Uterine relaxation
Further reading
- Buttner R. Pharm 101: methanol
References
- Katzung BG. Basic & Clinical Pharmacology. 14th ed. United States of America: McGraw-Hill Education; 2018. 396-404 p.
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Adult/Paediatric Emergency Medicine Advanced Trainee in Melbourne, Australia. Special interests in diagnostic and procedural ultrasound, medical education, and ECG interpretation. Co-creator of the LITFL ECG Library. Twitter: @rob_buttner