Lecture 12 — Organophosphates and Ganglion-Blocking Drugs
Condensed source-based study notes. Consult original slides for diagrams and finer details.
Organophosphate Toxicity
• Organophosphates include potent insecticides and chemical warfare agents; they can be absorbed through the skin.
• They inhibit acetylcholinesterase, causing acetylcholine accumulation and overstimulation at cholinergic sites.
• The source describes phosphorylation of a serine-containing esteratic site on the enzyme.
Clinical Effects
• Skin: sweating. Eyes: lacrimation, miosis, blurred vision and spasm.
• Gastrointestinal: salivation, increased secretion and motility, cramps, vomiting and diarrhea.
• Urinary: frequency or incontinence. Respiratory: bronchoconstriction, increased secretions and respiratory muscle weakness.
• Skeletal muscle: fasciculations, weakness and paralysis. Cardiovascular: bradycardia and hypotension. CNS: tremor, anxiety, confusion, seizures or coma.
Management Described in the Lecture
• Stop exposure and wash extensively.
• Atropine counteracts muscarinic overstimulation.
• Pralidoxime is described as capable of regenerating inhibited acetylcholinesterase when given early, before enzyme aging.
• These are study points from the lecture, not a self-treatment protocol.
Autonomic Ganglion Blockers
• Ganglion-blocking agents competitively inhibit ACh effects at nicotinic receptors in sympathetic and parasympathetic ganglia.
• Some agents (including nicotine and related drugs) initially stimulate then block ganglia; the lecture states these are not therapeutically useful.
• Other agents block ganglionic transmission without initial stimulation; examples mentioned include trimethaphan and mecamylamine.
• Trimethaphan is described as very short acting and used for controlled hypotension in certain procedures.
