During a preoperative assessment for a client with a family history of malignant hyperthermia, which of the following actions should the nurse take? Select all that apply.

Choice A rationale

This antimalarial medication is a cornerstone in managing systemic lupus erythematosus by inhibiting the stimulation of toll-like receptors and reducing the production of inflammatory cytokines. It is primarily used to control skin rashes, joint pain, and fatigue while significantly reducing the frequency of disease flares. Clinical evidence suggests it also provides a long-term survival benefit and prevents organ damage accrual in patients with chronic autoimmune responses.

Choice B rationale

This monoclonal antibody specifically targets B-lymphocyte stimulator proteins to reduce the activity of B cells contributing to the autoimmune response in lupus. While it is an approved adjunct treatment for active, autoantibody-positive systemic lupus erythematosus, it is generally reserved for patients who do not respond adequately to standard therapies. It is not considered the most common first-line systemic agent compared to the widespread and foundational use of antimalarial drugs in this population.

Choice C rationale

Nonsteroidal anti-inflammatory drugs are frequently utilized in lupus management to alleviate musculoskeletal pain, pleurisy, and fever by inhibiting cyclooxygenase enzymes and prostaglandin synthesis. However, these medications only provide symptomatic relief for minor manifestations and do not modify the underlying disease course or prevent major organ exacerbations. Their use is often limited by potential side effects including gastrointestinal irritation, renal impairment, and increased cardiovascular risk in patients with systemic inflammation.

Choice D rationale

This folate antimetabolite acts as a potent immunosuppressant by interfering with DNA synthesis and cellular proliferation, particularly in rapidly dividing immune cells. It is often employed in lupus cases involving significant arthritis or skin disease that remains refractory to antimalarials. While effective for controlling inflammation, it carries a higher risk profile than first-line agents, necessitating frequent monitoring of liver function tests and complete blood counts to detect potential hepatotoxicity or bone marrow suppression.

Choice A rationale

While fatigue is a common symptom of Addison's disease due to glucocorticoid deficiency, high-sugar snacks are not a therapeutic recommendation for long-term management. Patients often experience hypoglycemia because cortisol is necessary for gluconeogenesis, but complex carbohydrates are preferred over simple sugars to maintain stable glucose levels. Rapid spikes and drops in blood sugar from high-sugar snacks can worsen the metabolic instability associated with adrenal insufficiency and lead to further energy fluctuations.

Choice B rationale

Adrenal insufficiency leads to a deficiency in aldosterone, which normally functions to excrete potassium and retain sodium. Consequently, patients with Addison's disease are at a high risk for hyperkalemia, where serum potassium levels exceed the normal range of 3.5 to 5.0 mEq/L. Increasing the intake of potassium-rich foods would be dangerous as it could lead to cardiac dysrhythmias and neuromuscular complications. Patients are typically advised to avoid salt substitutes that contain high amounts of potassium.

Choice C rationale

Reducing sodium intake is contraindicated in Addison's disease because the lack of aldosterone results in excessive renal wasting of sodium. Patients often experience hyponatremia, where serum sodium levels fall below the normal range of 135 to 145 mEq/L. Lowering sodium intake further would exacerbate fluid volume deficit and hypotension, potentially triggering an addisonian crisis. Sodium restriction is generally reserved for conditions involving fluid overload, such as heart failure or renal failure, rather than adrenal insufficiency.

Choice D rationale

In Addison's disease, the adrenal cortex fails to produce adequate mineralocorticoids, specifically aldosterone. This leads to the inability of the kidneys to retain sodium, resulting in chronic salt wasting and dehydration. Increasing dietary sodium intake helps maintain extracellular fluid volume and prevents the development of orthostatic hypotension. During periods of stress, heat, or intense exercise, the need for supplemental sodium becomes even more critical to prevent vascular collapse and maintain electrolyte homeostasis.