A nurse in the emergency department is caring for a client who accidentally doubled their last dose of diazepam.
After assessing the client, which of the following medications should the nurse plan to administer?

Choice A rationale

Magnesium levels within the normal range (1.3 to 2.1 mEq/L) are important for overall electrolyte balance, but sodium polystyrene sulfonate specifically targets potassium. While hyperkalemia can sometimes be associated with other electrolyte imbalances, a normal magnesium level does not directly indicate a therapeutic response to sodium polystyrene sulfonate, as its primary action is not on magnesium.

Choice B rationale

Calcium levels within the normal range (9 to 10.5 mg/dL) are essential for various physiological functions. Sodium polystyrene sulfonate primarily exchanges sodium ions for potassium ions, not calcium. Therefore, a normal calcium level does not reflect a therapeutic response to the medication, which is specifically aimed at reducing elevated potassium levels.

Choice C rationale

Sodium levels within the normal range (136 to 145 mEq/L) are crucial for fluid balance and neurological function. Sodium polystyrene sulfonate exchanges sodium for potassium, meaning it increases the body's sodium load. While a normal sodium level is desirable, it does not directly indicate the therapeutic efficacy of the medication in reducing potassium.

Choice D rationale

Potassium 4.8 mEq/L (3.5 to 5 mEq/L) indicates a therapeutic response. Sodium polystyrene sulfonate is an ion-exchange resin used to treat hyperkalemia by exchanging potassium ions for sodium ions in the gastrointestinal tract. A potassium level returning to within the normal range, from a previously elevated state, signifies that the medication has effectively lowered the excess potassium.

Choice A rationale

Allopurinol is a xanthine oxidase inhibitor. This enzyme is crucial in the purine catabolism pathway, converting xanthine and hypoxanthine into uric acid. By inhibiting xanthine oxidase, allopurinol effectively decreases the de novo synthesis of uric acid, thereby lowering serum uric acid levels. This reduction prevents the formation of uric acid crystals in joints and tissues, which are responsible for the painful manifestations of gout.

Choice B rationale

Tophus formation is a direct consequence of chronic hyperuricemia, where uric acid crystals accumulate in soft tissues, leading to palpable nodules. Allopurinol's primary mechanism of action is to reduce uric acid levels. By achieving this, it prevents further crystal deposition and can even lead to the regression of existing tophi over time. Therefore, it does not increase tophus formation.

Choice C rationale

Allopurinol's mechanism of action is specifically related to uric acid metabolism. It does not directly influence calcium homeostasis in the body. Calcium levels are primarily regulated by parathyroid hormone, calcitonin, and vitamin D, which are distinct physiological pathways unrelated to xanthine oxidase inhibition. Therefore, it does not lower calcium levels.

Choice D rationale

While allopurinol ultimately helps relieve joint inflammation in gout, it does so indirectly. Its primary action is to reduce uric acid production, which then prevents the formation of inflammatory uric acid crystals. The direct reduction of inflammation is typically achieved by anti-inflammatory drugs like NSAIDs or colchicine, which act on inflammatory mediators or pathways, not directly by allopurinol.