A patient with arthritis takes a COX-2 selective inhibitor. Why does this drug regimen reduce inflammation and pain?

💡 Explanation

COX-2 selective inhibitors block the cyclooxygenase-2 enzyme, preventing the conversion of arachidonic acid into prostaglandins that mediate inflammation and pain. Therefore, prostaglandin synthesis is inhibited, rather than leukotriene production, because COX-1 inhibition increases gastric mucus production.

• Why does plaque buildup in arteries (atherosclerosis) preferentially occur at branch points rather than straight sections of a vessel?
• Why does drug dosage adjustments based on patient weight fail when treating a highly lipophilic drug exhibiting extensive tissue binding?
• Why does trabecular bone fracture more readily under torsional stress than cortical bone, despite both experiencing similar applied torque?
• Why does uncontrolled growth result from mutations affecting growth factor receptor tyrosine kinases in cancer cells?
• A patient with hypertension has increased arterial stiffness and reduced baroreceptor sensitivity. If the RAAS system is chronically overactive, which outcome is most likely?
• If a pulmonary embolism blocks blood flow to a portion of the lung, what distinguishes the observed hypoxemia from hypoxemia due to high altitude?