Module 12.3 - Toxic Alcohols - Lecture скачать в хорошем качестве

Module 12.3 - Toxic Alcohols - Lecture

Welcome to Nexus Clinical! Before diving into this lecture, I want to ensure we're all on the same page. This is for general informational purposes only and does not constitute the practice of medicine, nursing, or other professional healthcare services, including the giving of medical advice. No doctor-patient or pharmacist-patient relationship is formed. Using this information and the materials linked to this content is at the user's risk. This is not intended to substitute for professional medical advice, diagnosis, or treatment. Users should not disregard or delay seeking medical advice for any medical condition they have, and they should consult their healthcare professionals for any such conditions. Clinical experts created the references, content, and clinical insight. NotebookLM, a Google AI tool, created the content, which I extensively reviewed before release. Finally, the host states that he takes all conflicts of interest seriously. Currently, there are no conflicts to disclose. For all of his disclosures and the companies he invests in or advises, he directs users to reach out independently, where he keeps an up-to-date and active list of all disclosures. Alright class, settle down, settle down! Today, we're diving headfirst into a critical area for future pharmacists: toxic alcohols. This isn't just about passing an exam; it's about equipping you for real-world emergencies where timely intervention can literally save lives or prevent devastating, permanent damage. We're focusing on the big players: methanol, ethylene glycol, and isopropanol, alongside others like propylene glycol and benzyl alcohol. You'll learn their distinct chemical properties, metabolic pathways, and severe delayed toxic effects. For methanol (wood alcohol), toxicity stems from its metabolite, formic acid, leading to severe anion gap metabolic acidosis, characteristic visual impairment, and basal ganglia lesions. Ethylene glycol (antifreeze), notable for its sweet taste, metabolizes into glycolic and oxalic acids, causing severe metabolic acidosis and acute kidney injury due to calcium oxalate crystal deposition. Then there's isopropanol (rubbing alcohol), which is uniquely metabolized to acetone, resulting in ketosis without metabolic acidosis, with the parent compound primarily causing CNS depression. We'll also briefly cover propylene glycol, causing surprisingly well-tolerated lactic acidosis, and benzyl alcohol, notorious for "neonatal gasping syndrome". Diagnosis often means "minding the gaps" – interpreting an elevated anion gap and osmolal gap as crucial surrogate markers, especially when specific toxic alcohol levels are delayed. Don't forget the vital role of ethanol levels in assessment! In terms of management, the cornerstone is inhibiting alcohol dehydrogenase (ADH) to prevent toxic metabolite formation. We'll compare fomepizole (the preferred ADH inhibitor in the US, known for its reliability and better safety profile) to ethanol, which remains a viable alternative in resource-limited settings. Aggressive correction of metabolic acidosis with sodium bicarbonate is also critical, acting as a bridge to definitive treatment. And for definitive toxin removal, hemodialysis is the go-to therapy for symptomatic patients. Adjunctive therapies like folate for methanol poisoning further support patient outcomes. This comprehensive overview will ensure you're well-prepared to face these challenging toxicological emergencies!