Final answer:
Nerve agents, such as sarin and soman, inhibit acetylcholinesterase, leading to an accumulation of acetylcholine at synapses and causing overstimulation of the nervous system. This overstimulation results in prolonged muscle contraction and can lead to asphyxiation or cardiac arrest. Treatments like atropine are used to manage symptoms by blocking excess acetylcholine.
Step-by-step explanation:
The pathophysiology of how nerve agents affect the body involves the inhibition of acetylcholinesterase (Ache), an enzyme essential for the normal functioning of the nervous system. Nerve agents, such as sarin and soman, bind to and inhibit Ache, preventing the breakdown of the neurotransmitter acetylcholine. This results in an accumulation of acetylcholine at nerve synapses, leading to overstimulation of cholinergic pathways. The manifestation of this includes prolonged muscle contraction, disrupted nerve transmission, and potentially, asphyxiation or cardiac arrest due to overstimulation of muscles involved in respiration.
Nerve agents do not lead to increased production of neurotransmitters, enhancement of nerve conduction, or activation of GABA receptors. Instead, the excessive accumulation of acetylcholine due to Ache inhibition is what characterizes their mode of action. Furthermore, treatments such as atropine can be used as an antidote to manage the symptoms of nerve agent poisoning by blocking acetylcholine receptors, thus countering the effects of accumulated acetylcholine.