Question | Answer |
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 |