[Pharmacology 3620] - Final Exam Guide - Everything you need to know! (51 pages long)
29 Mar 2017
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Analgesia: reduction of noxious stimuli/pain without loss of muscle movement pain indicates injury. Anesthesia: blocking of all sensory input, including pain. Prostaglandins: pro-inflammatory molecules broken down locally: metabolism can occur in all tissues of the body, actions include platelet aggregation, reduction of pain, and inflammation, synthesized from arachidonic acid by cyclooxygenase (2 isoforms: cox-1 & cox-2) All nsaids work by inhibiting prostaglandin synthesis from arachidonic acid by acting on cyclooxygenase, but may do so in different manners. End stage of all nsaids = blocks pain. Aspirin irreversibly inhibits cox-1 & cox-2 by transferring an acetyl group on to the enzyme: side effects: gi upset/bleeding because pgi2 is involved in suppressing acid secretion, and pge2 & pgf2 are involved in increasing mucous secretion. Cox activity in the periphery, causes decreased synthesis of these pgs and therefore gi upset. Acetaminophen is not a steroid, and is a weak nsaid and is more selective for cox-2.
