A nurse is assessing a client who has a prescription for oral albuterol for the long-term management of asthma.
For which of the following adverse effects should the nurse monitor?

Choice A rationale

Documenting the client's refusal and the stated reason in the nurses' notes is crucial for legal and ethical reasons. It provides a clear record of the event, ensures continuity of care by informing other healthcare providers, and allows for follow-up interventions to address the client's concerns or alternative medication strategies. It upholds the client's right to refuse treatment.

Choice B rationale

Delegating medication administration to an assistive personnel (AP) is inappropriate as medication administration is a complex nursing function requiring assessment, judgment, and patient education, which are outside the scope of practice for an AP. An AP's role is typically limited to basic care activities, and they are not trained or authorized to administer medications.

Choice C rationale

Notifying the pharmacist is not the immediate or primary action when a client refuses medication. While the pharmacist may offer insights into alternative formulations or administration routes, the nurse's initial responsibility is to understand the client's refusal, document it, and then notify the prescribing provider for a revised plan of care.

Choice D rationale

Mixing medication in juice without the client's explicit consent is considered a breach of the client's autonomy and can be construed as coercive or deceptive. It violates the client's right to self-determination and informed consent regarding their treatment. Medications should only be administered with the client's knowledge and cooperation.

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.