Organophosphorus induced delayed polyneuropathy The rate of these competing reactions varies by more than 10-fold between individual organophosphorus compounds, which influences the clinical manifestations and response to treatments. ![]() The organophosphorus-esterase complex undergoes either spontaneous reactivation, allowing normal enzymatic function, or irreversible inhibition (described as ageing), as shown in figure 1 1. 8 Butyrylcholinesterase hydrolyses exogenously administered pharmaceuticals such as lidocaine and suxamethonium (succinylcholine), which may have an effect clinically. 8 9 Other esterases are also inhibited, causing clinically important illnesses (for example, neuropathy target esterase, producing organophosphorus induced delayed polyneuropathy (box 2) 10 w2), whereas other esterases such as butyrylcholinesterase (also known as pseudocholinesterase or plasma cholinesterase) and carboxylesterase, do not cause clearly defined illness. This produces a range of clinical manifestations, known as the acute cholinergic crisis (box 2). Inhibition of acetylcholinesterase leads to the accumulation of acetylcholine at cholinergic synapses, interfering with the normal function of the autonomic, somatic, and central nervous systems. Organophosphorus compounds inhibit numerous enzymes, of which esterases seem to be the most clinically important. The effects of organophosphorus compounds on human physiology are multiple and complex. What is the pathophysiology of acute organophosphorus poisoning?
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