A patient is admitted with acute gouty arthritis. Which medication does the nurse anticipate the health care provider may prescribe to prevent and treat an acute attack of gout?

Choice A reason: Cognitive dysfunction in advanced systemic lupus erythematosus (SLE) results from immune complex deposition in cerebral vessels, causing neuropsychiatric symptoms like confusion or memory loss. This is an ominous sign, indicating central nervous system involvement, which is severe and potentially life-threatening due to its impact on brain function and difficulty in management.

Choice B reason: Proteinuria from early glomerulonephritis is common in SLE but indicates renal involvement, not necessarily advanced disease. It is manageable with immunosuppressants and less immediately life-threatening than cerebral involvement. While significant, it is not as ominous as cognitive dysfunction, which signals severe systemic progression.

Choice C reason: Dysrhythmias from atrioventricular node fibrosis are rare in SLE and typically occur in congenital lupus or late cardiac complications. They are not a hallmark of advanced disease compared to neuropsychiatric manifestations. This sign is less ominous, as it is less common and not indicative of widespread systemic damage.

Choice D reason: Anemia from autoantibodies against red blood cells is frequent in SLE, reflecting autoimmune activity. It is manageable with corticosteroids and not uniquely indicative of advanced disease. Cognitive dysfunction is more ominous, as it suggests severe, multisystem involvement with poor prognosis due to central nervous system damage.

Choice A reason: Interleukin 1 is a pro-inflammatory cytokine involved in gout’s acute inflammatory response, not directly targeted by allopurinol. Allopurinol reduces uric acid production, preventing crystal formation, not cytokine levels. This choice is incorrect, as it misaligns with the medication’s mechanism of action in chronic gout management.

Choice B reason: Allopurinol inhibits xanthine oxidase, reducing uric acid production, which is elevated in chronic tophaceous gout. Lowering uric acid levels prevents urate crystal formation in joints, reducing tophi and gout attacks. This is the correct explanation, as allopurinol directly targets hyperuricemia, the root cause of gout pathology.

Choice C reason: Potassium levels are unrelated to gout or allopurinol’s action. Allopurinol does not affect electrolyte balance but focuses on purine metabolism to lower uric acid. This choice is incorrect, as potassium is not involved in gout’s pathophysiology or the therapeutic effect of allopurinol.

Choice D reason: Chloride is an electrolyte not associated with gout or allopurinol’s mechanism. Allopurinol’s role is specific to uric acid reduction, not chloride homeostasis. This choice is irrelevant, as chloride levels do not contribute to gout or require modification in chronic tophaceous gout management.