Lumbar Facet Arthropathy Medication
- Author: Carl H Shin, MD; Chief Editor: Stephen Kishner, MD, MHA more...
Nonsteroidal anti-inflammatory drugs (NSAIDs) are recommended for medical therapy for lumbar facet arthropathy (LFA). Peripherally acting analgesics include NSAIDs and acetaminophen. NSAIDs are the DOC in the initial pharmacologic treatment of acute episodes of LFA or following acute exacerbation of chronic pain.
Nonsteroidal anti-inflammatory drugs
Have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclo-oxygenase (COX) activity and prostaglandin synthesis. Other mechanisms may include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell membrane functions.
Best-known NSAID. It is widely available and has cardioprotective, cerebroprotective, and anticoagulation properties. Aspirin treats mild to moderate pain. The drug inhibits prostaglandin synthesis, which prevents the formation of platelet-aggregating thromboxane A2.
DOC for patients with mild to moderate pain. The drug inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
For the relief of mild to moderate pain. Naproxen inhibits inflammatory reactions and pain by decreasing the activity of COX, which results in decreased prostaglandin synthesis.
Nonacidic NSAID that is rapidly metabolized after absorption, becoming a major active metabolite that inhibits the COX enzyme (thereby inhibiting pain and inflammation).
Inhibits prostaglandin synthesis by decreasing the activity of COX, which results in the decreased formation of prostaglandin precursors.
Although increased cost can be a negative factor, the incidence of costly and potentially fatal GI bleeding is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost and avoidance of GI bleeding will further define populations that will most benefit from COX-2 inhibitors.
Primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme; it is induced by pain and inflammatory stimuli. The inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, the incidence of GI toxicity, such as endoscopic peptic ulcers, bleeding ulcers, perforations, and obstructions, may be decreased in comparison with nonselective NSAIDs. Seek the lowest dose for each patient.
COX-2 neutralizes circulating myelin antibodies through anti-idiotypic antibodies; down-regulates pro-inflammatory cytokines, including INF-gamma; blocks Fc receptors on macrophages; suppresses inducer T and B cells and augments suppressor T cells; blocks complement cascade; promotes remyelination; and may increase CSF IgG (10%).
COX-2 has a sulfonamide chain and is primarily dependent on cytochrome P450 enzymes (hepatic enzymes) for metabolism.
Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience pain.
Ensures patient comfort, promotes pulmonary toilet, and has sedating properties
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