Final answer:
Acetylcholinesterase inhibitors prevent the breakdown of acetylcholine, resulting in increased nerve transmission. They are used to treat conditions like Alzheimer's and myasthenia gravis. These inhibitors can enhance the effect of succinylcholine, leading to prolonged muscle paralysis.
Step-by-step explanation:
Acetylcholinesterase inhibitors are drugs that prevent the breakdown of the neurotransmitter acetylcholine in the synapse, resulting in increased levels of acetylcholine and prolonged nerve transmission. They are used to treat conditions like Alzheimer's and myasthenia gravis. The normal dosing for these inhibitors depends on the specific drug and condition being treated, and should be determined by a healthcare professional.
Onset and duration of action can vary for different acetylcholinesterase inhibitors. For example, rivastigmine has an onset of action of about 2 hours and a duration of around 10-12 hours. Donepezil, on the other hand, has an onset of action of 3-4 weeks and a duration of 24 hours.
Metabolism of acetylcholinesterase inhibitors occurs in the liver through various metabolic pathways. The exact metabolism can vary depending on the specific drug, but generally, they undergo hepatic metabolism and are excreted mainly in the urine.
Acetylcholinesterase inhibitors can enhance the effect of succinylcholine, which is a neuromuscular blocking agent used during surgeries to induce muscle relaxation. When succinylcholine is given in the presence of acetylcholinesterase inhibitors, it can lead to prolonged muscle paralysis.
Examples of drugs that inhibit acetylcholinesterase include physostigmine, neostigmine, and pyridostigmine. These drugs work by blocking the action of acetylcholinesterase, thus increasing the levels of acetylcholine in the synapse and enhancing nerve transmission.