Non-Opioid Analgesics & Antipyretics Questions
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36 terms
Terms | Definitions |
|---|---|
 4 major actions of NSAID's | anti-inflammatory, analgesic, antipyretic, antiplatelet |
| MOA of NSAID anti-inflammatory effect | decr in vasodilatory PGs results, indirectly, in decreased edema; accumulation of inflammatory cells is not reduced significantly |
| MOA of NSAID analgesic effect | decr PGs mean less sensitization of nociceptive nerve endings to mediators (aka- bradykinin and 5-HT) |
| MOA of NSAID antipyretic effect | centrally mediated, partly the result of decr in PG response to cytokines (e.g. IL-1) |
| MOA of NSAID antiplatelet effect | most NSAIDs induce reversible inhibition of thromboxane synthesis; aspirin's axn however is irreversible |
| Effects of NSAIDs on PG synthesis | inhibit COX enzyme which gives rise to biosynthesis of PG which cause pain |
| Adverse Rxns to NSAIDs | GI ulceration, renal injury, increased CV risk |
| Adverse Rxn to COX-2 Inhibitors | CV: pot'l for MI, hypertension, edema; CNS: headache, fever; GI: diarrhea, nausea; Respiratory: upper respiratory tract infection, cough |
| Toxic effects of NSAIDs | GI bleeding (pot'l fatal), renal insufficiency, incr risk of CV disease, & poss drug-drug interaxn from high plasma prot. Binding; most serious- result from intentional overdose or excess ethanol ingestion |
| Use of acetaminophen | Tx fever and pain |
| Importance of DMARDs | can alter the course of rheumatic disorders, such as RA |
| Inflammation signs | Heat, Redness, Swelling, Pain, and maybe LoF |
| Mxn of heat response | Vasodilation |
| Mxn of redness response | Vasodilation |
| Mxn of swelling response | incr vascular permeability, incr granulation tissue |
| Mxn of pain response | physical and chemical stimulation of nociceptors |
| Mxn of LoF response | pain; reflex muscle inhibition; disruption of tissue structure |
| Histamine's effects | increases vasc permeability, promotes vasodilation |
| Bradykinin's effects | vasodilatory, vascular permeability, pain |
| Mediators of Acute inflammation | histamine, bradykinin, prostaglandins, leukotrienes |
| Prostaglandins' effects | do it all- promote vasodilation, increase vascular permeability, chemotaxis, some induction of pain response |
| Leukotrienes effects | very potent chemoattractants, more impt in allergic rxns |
| Mediators of Chronic inflammation | IL-1, TNFalpha, IL-6, IL-2, IFN (I&II), chemokines |
| IL-1 activities | induces lymphocyte activation, mediator induction, monocyte/macrophage activation, induce prostaglandins (PGs) |
| TNF alpha activities | mediator induction, monocyte/macrophage activation, PGs |
| IL-6 activities | Mediator induction, monocyte/macrophage differentiation, fever |
| IL-2 activities | potent lymphocyte activator and differentiator, mediator induction |
| IFN (I&II) activities | monocyte/macrophage activation, cytotoxic lymphocyte activation; antimicrobial activity |
| Chemokines activities | Chemoattractants |
| NSAIDs activities | anti-inflammatory, analgesic, anti-pyretic |
| NSAIDs common mxn | affect arachidonic acid metabolism; block COX |
| DoA of COX inhibitors is primarily related to | pharmacokinetic clearance of the drug from the body, all are reversible except aspirin |
| COX-1 | expressed in most tissues, constitutively active, necessary for cytoprotection in GI tract |
| COX-2 | believed to be enzyme that produces the prostanoid mediators of inflammation, induced in inflammatory cells |
| COX inhibitors MoA | inhibition of COX in immune system |
| ______ is a very important target for RA | TNF alpha |
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