Analgesicos no esteroideos pdf

In the 1990s, researchers discovered that two different COX enzymes exist: COX-1 and COX-2. COX-1 is present in most tissues, including the stomach lining. It’s also involved in kidney function. COX-2 is the enzyme primarily present at sites of inflammation . Both COX-1 and COX-2 convert arachidonic acid to prostaglandin, resulting in pain and inflammation. The anti-inflammatory action of NSAIDs is mainly due to inhibition of COX-2, and their unwanted side effects (like bleeding ulcers) are largely due to inhibition of COX-1. ( 12 )

From Epi to Policy: Prescription Drug Overdose: State Health Department Training and Technical Assistance Meeting [PDF – 4M]
This report was prepared to summarize a meeting of health officials from 15 states funded to receive training on how to take what we know about the epidemic of Prescription Drug Overdose and turn it into effective action. The meeting sought to combine CDC’s research and epidemiology on prescription drug overdose with real-world discussions of the challenges and successes states have faced in confronting the epidemic. (Atlanta, Georgia, April 22-23, 2013)

A variety of allergic or allergic-like NSAID hypersensitivity reactions follow the ingestion of NSAIDs. These hypersensitivity reactions differ from the other adverse reactions listed here which are toxicity reactions, . unwanted reactions that result from the pharmacological action of a drug, are dose-related, and can occur in any treated individual; hypersensitivity reactions are idiosyncratic reactions to a drug. [67] Some NSAID hypersensitivity reactions are truly allergic in origin: 1) repetitive IgE -mediated urticarial skin eruptions, angioedema , and anaphylaxis following immediately to hours after ingesting one structural type of NSAID but not after ingesting structurally unrelated NSAIDs; and 2) Comparatively mild to moderately severe T cell -mediated delayed onset (usually more than 24 hour), skin reactions such as maculopapular rash , fixed drug eruptions , photosensitivity reactions , delayed urticaria , and contact dermatitis ; or 3) far more severe and potentially life-threatening t-cell-mediated delayed systemic reactions such as the DRESS syndrome , acute generalized exanthematous pustulosis , the Stevens–Johnson syndrome , and toxic epidermal necrolysis . Other NSAID hypersensitivity reactions are allergy-like symptoms but do not involve true allergic mechanisms; rather, they appear due to the ability of NSAIDs to alter the metabolism of arachidonic acid in favor of forming metabolites that promote allergic symptoms. Afflicted individuals may be abnormally sensitive to these provocative metabolites or overproduce them and typically are susceptible to a wide range of structurally dissimilar NSAIDs, particularly those that inhibit COX1. Symptoms, which develop immediately to hours after ingesting any of various NSAIDs that inhibit COX-1, are: 1) exacerbations of asthmatic and rhinitis (see aspirin-induced asthma ) symptoms in individuals with a history of asthma or rhinitis and 2) exacerbation or first-time development of wheals or angioedema in individuals with or without a history of chronic urticarial lesions or angioedema. [26]

Analgesicos no esteroideos pdf

analgesicos no esteroideos pdf

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