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Pharm Autonomic NS

Cholinesterase Inhibitors

QuestionAnswer
prevents degradation of acetycholine by acetylcholinesterase thereby enhancing the activity of acetylcholine at cholinergic receptors
they can intensify ACh activity at all cholinergic junctions muscarinic, ganglionic, nicotinic
reversible inhibitors: ambenonium[Myletase], demecarium[Humorsol], donepezil[Aricept], galantamine{Reminyl], neostigmine[Prostigmin], pyridostigmine[Mestinon], physostigmine[Antilirium, rivastigmine[Exelon], tacrine[Cognex]
irreversible inhibitors: organophosphate cholinesterase inhibitors, toxic and can be absorbed through the skin, only clinical indication is glaucoma tx
not a cholinesterase inhibitor but used to tx Alzheimer's, adhd, postherpetic neuralgia, prevention of migraine memantine[Namenda], N-methyl-D-aspartate [NMDA] inhibitor
Possible contributers to Alzheimer's profound cholinergic depletion so these drugs increase the availability of acetylcholine in the brain persistent stimulation of the NMDA receptors by the excitatory amino acid glutamate
signs of toxicity: GI stimulation, excessive salivation, miosis, fasciculations
used to treat myasthenia gravis and to reverse nonpolarizing neuromuscular blockade[not succ b/c it is a depolarizing neuromuscular blocker] neostigmine[Prostigmin, oral; Bloxiverz, injectable] pyridostigmine[Mestinon, Rebonol]
other NMDA receptor antagonists: amantadine[Symmetrel], ketamine, dextromethorphan
Alzheimer's is associated with a significant deficiency in brain levels of choline acetyltransferase, the enzyme responsible for the synthesis of acetylcholine
myasthenia gravis is an autoimmune disorder that produces antibodies directed against nicotinic receptors on skeletal muscle reducing the number of receptors by 70-90% resulting in muscle weakness
s/s of increased acetylcholine dizziness, miosis, lacrimation, excessive secretions in the respiratory and GI tract, bronchospasm, bradycardia, abdominal cramps, n/v/c, excessive salivation
Created by: heatherbrown2020