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Salicylate poisoning. A skeletal structural formula for aspirin. Salicylate poisoning, also known as aspirin poisoning, is the acute or chronic poisoning with a salicylate such as aspirin. [1] The classic symptoms are ringing in the ears, nausea, abdominal pain, and a fast breathing rate. [1]
For pain or fever, effects typically begin within 30 minutes. [10] Aspirin works similarly to other NSAIDs but also suppresses the normal functioning of platelets. [10] One common adverse effect is an upset stomach. [10] More significant side effects include stomach ulcers, stomach bleeding, and worsening asthma. [10]
Salicylate intolerance is a form of food intolerance or of drug intolerance. Salicylate sensitivity is a pharmacological reaction, not a true IgE -mediated allergy. However, it is possible for aspirin to trigger non-allergic hypersensitivity reactions. [8][9] About 5–10% of asthmatics have aspirin hypersensitivity, but dietary salicylates ...
Salicylic acid is a phenolic phytohormone, and is found in plants with roles in plant growth and development, photosynthesis, transpiration, and ion uptake and transport. [53] Salicylic acid is involved in endogenous signaling, mediating plant defense against pathogens. [54]
History of aspirin. Aspirin (acetylsalicylic acid), an organic compound that does not occur in nature, was first synthesised in 1899. In 1897, scientists at the drug and dye firm Bayer began investigating acetylated organic compounds as possible new medicines, following the success of acetanilide ten years earlier.
Sodium salicylate is a sodium salt of salicylic acid. It can be prepared from sodium phenolate and carbon dioxide under higher temperature and pressure. Historically, it has been synthesized by refluxing methyl salicylate ( wintergreen oil) with an excess of sodium hydroxide .
Mechanism of action of aspirin. Tridimensional model of the chemical structure of aspirin. Aspirin causes several different effects in the body, mainly the reduction of inflammation, analgesia (relief of pain), the prevention of clotting, and the reduction of fever. Much of this is believed to be due to decreased production of prostaglandins ...
These differential effects are due to the different roles and tissue localisations of each COX isoenzyme. [11] By inhibiting physiological COX activity, NSAIDs may cause deleterious effects on kidney function, [12] and, perhaps as a result of water and sodium retention and decreases in renal blood flow, may lead to heart problems. [13]