ACh is not degraded, therefore, prolonged depolorization is enforced on the post synaptic memebrane
The antidote to organophosphorus poisoning is atropine, which is an anticholinergic agent that helps counteract the effects of excessive acetylcholine due to inhibition of the enzyme acetylcholinesterase. Additionally, pralidoxime (2-PAM) can be used to reactivate acetylcholinesterase and restore its function, particularly if administered early. Prompt medical treatment is crucial for effective management of organophosphorus poisoning.
Are used medicinally:To treat myasthenia gravis. In myasthenia gravis, they are used to increase neuromuscular transmission.To treat GlaucomaTo treat Alzheimer's diseaseTo treat Lewy Body DementiaAs an antidote to anticholinergic poisoning
Nerve agents are acetylcholinesterase inhibitors. Acetylcholinesterase is an enzyme that breaks down acetylcholine at nerve synapses. The antidote to counteract the nerve agent is an anticholinergic drug, such as atropine.
they inactivate the acetylcholinesterase enzyme which is necessary to break up Ach into acetate and choline,thereby causing increase in synaptic Ach leading to anticholinesterase poisoning...example neostigmine,physostigmine,edrophonium, etc
Mark 1 and ATNAA antidotes are used to counteract nerve agent poisoning by delivering a combination of atropine and pralidoxime. Atropine works by blocking the effects of acetylcholine at muscarinic receptors, alleviating symptoms like respiratory distress and excessive salivation. Pralidoxime reactivates acetylcholinesterase, an enzyme inhibited by nerve agents, helping restore normal neurotransmission. Together, these components provide a critical response to the toxic effects of nerve agents.
I don't know how detailed an answer you want, but here's the overview:Organophosphates irreversibly bind to the enzyme acetycholinesterase. Acetylcholinesterase is responsible for breaking down acetylcholine in the body. Acetylcholine is part of the mechanism that causes muscle contractions. At normal bodily levels, this allows us to move, breathe, and digest food. However, if the enzyme that breaks it down (acetylcholinesterase) is chemically bound to something else (organophosphates) then acetylcholine builds up in the body. This can cause muscle spasms, nausea (if it affects the gastrointestinal tract), seizures, difficulty breathing (if it affects the muscles that control expansion and contraction of the lungs), among other things. If exposure levels are high enough, organophosphate poisoning will cause death. I know that some treatments for organophosphate poisoning exist, but I do not know what they are, or how effective they are.The body will continue to produce acetylcholinesterase, but if there are still unbound organophosphate molecules, they will take up this amount of enzyme as well, thus continuing the toxic effects even after exposure has been stopped.I hope this answered your question.
Atropine is an agent that can block enzymes that cause a cholinergic crisis by antagonizing the effects of excessive acetylcholine in the body. It is commonly used as an antidote for organophosphate poisoning, which can lead to cholinergic crisis.
Acetylcholinesterase inhibitors: Reversible:1.Physostigmine -Miotic, cycloplegic and reduces IOT 0.25-0.5 % drops -Atropine, and antidepressant poisoning with predominant CNS manifestations (crosses BBB) 2.Neostigmine-Doesnt cross BBB, hence good for d.tubocurare muscle blockade -Myasthenia -Post op ileus -Decurarisation 3.Pyridostigmine-Similar but less potent and long acting than neostigmine. Better tolerated in myasthenic patients 4.Edrophonium -Dx of myasthenia -Cobra bites 5.Rivastigmine -Alzhiemers(?) Irreversible: -Mostly pesticides DFP,Malathoin,Parathoin,Sarin, Soman (Nerve gas) -Metrifonate(Antihelminthic drug)
Mushrooms may contain cholinergic toxins like muscarine in small amounts, it is the mushrooms of the Inocybe and Clitocybe genera that contain sufficient amounts to produce a muscarinic cholinergic action. Overdose can cause cholinergic poisoning by blocking neuromuscular junctions
Microbiological poisoning is commonly known as "food poisoning."
There is no such thing as "lipstick poisoning ".
Neurotransmitters would continue to bind and rebind with the postsynaptic receptors, which would continue induction of a signal in the postsynaptic neurons, which would repropagate the initial signal. The case in drugs that block reuptake transporters (such as in serotonin reuptake inhibitor and norepinephrine reuptake inhibitor antidepressants, and dopamine reuptake inhibition found with cocaine and methylphenidate). This is also seen in cases where drugs block the breakdown of neurotransmitters at the synapse: - monoamine oxidase inhibitors (MAOIs) - Nardil, Parnate, selegiline - which prevent the breakdown of serotonin, norepinephrine, and dopamine - acetylcholinesterase inhibitors (AChE inhibitors) - organophosphase pesticides, nerve gas, racetams