<prompt> Please answer with one of the option in the bracket. Write reasoning in between . Write answer in between .Q:A 52-year-old woman with hypertension and type 2 diabetes mellitus comes to the physician because of a 1-day history of severe pain and swelling of her left great toe. She has had similar episodes sporadically over the past 3 years. She drinks 6 beers daily. She does not smoke or use illicit drugs. She is allergic to hydrochlorothiazide and glipizide. Her current medications are amlodipine and metformin. Examination shows erythema, warmth, and tenderness of the left first metatarsophalangeal joint and a nodule over the right elbow. The most appropriate next step in treatment is the administration of a drug that has which of the following mechanisms of action?? A: Reversible inhibition of prostaglandin synthesis, B: Irreversible inhibition of cyclooxygenase, C: Selective inhibition of cyclooxygenase-2, D: Increased renal excretion of uric acid, E: Irreversible inhibition of xanthine oxidase,  <response>: This is a clinical vignette describing a 52-year-old woman with a history of hypertension, type 2 diabetes mellitus, and recurrent gouty arthritis flare-ups who now presents with an acute gout attack affecting her left great toe. Key findings include erythema, warmth, tenderness of the left 1st MTP joint, and a tophus over her right elbow. She has several risk factors for gout including alcohol use, hypertension, and diabetes. The question asks about the most appropriate pharmacologic treatment to administer next, with the choices listing different mechanisms of action for gout medications. Based on the acute gouty arthritis flare, NSAIDs or colchicine would be appropriate choices to treat the inflammation and pain. NSAIDs like ibuprofen reversibly inhibit prostaglandin synthesis to reduce inflammation. Colchicine binds to tubulin and inhibits microtubule function, reducing neutrophil migration and inflammation. The other choices do not address the acute attack. Allopurinol or febuxostat decrease uric acid production and probenecid increases uric acid excretion, but these are used for long-term management to prevent attacks and are not appropriate for treating an acute flare. A: Reversible inhibition of prostaglandin synthesis 