PHAR 341 Lecture Notes - Revascularization, Calcitonin Gene-Related Peptide, Sumatriptan
Document Summary
(1) local anesthetics: discuss the pain pathway and name its priniciple components cortex > thalamus > brainstem > trigeminal ganglion > trigeminal nerve. Esters are broken down by plasma esterases, amides in liver. Anything that helps the anesthetic get across membrane makes it more potent. Presynaptic cleft release a vesicle of acetylcholine into nmj (2) physiology, pharmacology of nm transmission. Acetylcholine activate nicotinic receptors of postsynaptic cleft the activated depolarization. Achease breaks down ach in cleft so choline can be transported back into presynaptic cleft to be recycled. Illustrate how acetylcholine is released and recycled at the nmj and describe where and how natural toxins and drugs act at the nmj. Achease inhibitors prevent rapid breakdown of ach, increase/prolong effect of ach *drug of choice of myasthenia gravis. Vesamicol prevent reformation of ach vesicles: discuss the pharmacological mechanism and describe the therapeutic uses of botulinum toxin a and 4- aminopyridine.
