A 35-year-old woman has been taking acetylsalicylic acid (aspirin) for ahritis for several years. Her joint pain is reduced this therapy, though the joint destruction with loss of aicular cailage still continues. However, the aspirin therapy temporarily alletes her pain. This pain reduction is primarily the result of diminishing the inflammatory response characterized by:
Prostaglandins are produced the cyclooxygenase pathway of arachidonic acid metabolism. Aspirin and nonsteroidal anti-inflammatory drugs block the synthesis of prostaglandins, which can produce pain. NSAID anti-inflammatory activity is mediated chiefly through inhibition of prostaglandin biosynthesis Ref: Furst D.E., Ulrich R.W., Prakash S. (2012). Chapter 36. Nonsteroidal Anti-Inflammatory Drugs, Disease-Modifying Antirheumatic Drugs, Nonopioid Analgesics, & Drugs Used in Gout.
Neutrophil chemotaxis by leukotriene B4
Fever resulting from interleukin-1 release
Prostaglandin mediated vasodilation
Pain resulting from bradykinin generation