Which medications in the drug class Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) are used in the treatment of Frostbite?

Updated: Jul 29, 2019
  • Author: Bobak Zonnoor , MD; Chief Editor: Dirk M Elston, MD  more...
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Answer

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

Pain control is essential to quality patient care. Analgesics ensure patient comfort and may have sedating properties, which are beneficial for patients who have sustained trauma or injuries.

Nonsteroidal anti-inflammatory drugs (NSAIDs) have analgesic and antipyretic activities. Their mechanism of action is not known, but these agents may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil and platelet aggregation, and various cell-membrane functions.

Ibuprofen (Ibuprin, Advil, Motrin, Caldolor)

Ibuprofen inhibits inflammatory reactions and pain by blocking synthesis of thromboxane and prostaglandins to reduce reperfusion injury. It prevents platelet aggregation. Ibuprofen is preferable to aspirin, which irreversibly blocks synthesis of the prostaglandins needed for normal cell function and integrity, because it is not associated with Reye syndrome.

Naproxen (Aleve, Anaprox, Naprosyn, Naprelan)

Naproxen is a member of the propionic acid group of NSAIDs. It is available in low-dose form as an over-the-counter (OTC) medication. It is highly protein-bound, is metabolized in the liver, and is eliminated primarily in the urine. Naproxen may reversibly inhibit platelet function.

Sulindac (Clinoril)

Sulindac decreases COX activity and, in turn, inhibits prostaglandin synthesis. This results in decreased formation of inflammatory mediators.

Celecoxib (Celebrex)

Celecoxib primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID gastrointestinal (GI) toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited; thus, GI toxicity may be decreased. Seek the lowest dose of celecoxib for each patient.

Meloxicam (Mobic)

Meloxicam decreases COX activity, and this, in turn, inhibits prostaglandin synthesis. These effects decrease the formation of inflammatory mediators.

Flurbiprofen

Flurbiprofen may inhibit COX, thereby, in turn, inhibiting prostaglandin biosynthesis. These effects may result in analgesic, antipyretic, and anti-inflammatory activities.


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