Which of the following individuals is at increased risk for developing Guillain-Barre syndrome?

Choice A rationale

Tumor lysis syndrome is an oncologic emergency characterized by the rapid release of intracellular contents, including potassium, phosphate, and nucleic acids, into the bloodstream. These nucleic acids are metabolized into uric acid, which can precipitate in the renal tubules, leading to obstructive uropathy and acute kidney injury. Aggressive hydration, typically 3 liters or more daily, is the primary intervention to increase urine flow, dilute the concentration of these substances, and promote their renal excretion.

Choice B rationale

The semi-Fowler's position is primarily utilized to improve lung expansion and decrease the work of breathing in patients with respiratory distress or to prevent aspiration. While comfortable, it does not directly address the underlying pathophysiology of tumor lysis syndrome or the prevention of acute kidney injury. The priority in this metabolic emergency is maintaining high intravascular volume and renal perfusion to clear the excessive load of electrolytes and uric acid produced by the rapidly lysing malignant cells.

Choice C rationale

Obtaining blood cultures is a standard intervention for suspected sepsis or systemic infection but is not a primary treatment for tumor lysis syndrome. While oncology patients are often immunocompromised and at risk for infection, the immediate threat in tumor lysis syndrome is metabolic derangement and renal failure. Nurses should focus on monitoring electrolyte levels, such as potassium (normal 3.5 to 5.0 mEq/L) and phosphorus (normal 2.5 to 4.5 mg/dL), and ensuring aggressive fluid resuscitation rather than diagnostic tests for infection.

Choice D rationale

High-dose intravenous corticosteroids are not the standard treatment for preventing acute kidney injury in the context of tumor lysis syndrome. While steroids may be part of the chemotherapy regimen that initially triggered the cell lysis, the management of the resulting syndrome involves hydration, allopurinol or rasburicase to lower uric acid levels, and the management of electrolyte imbalances. Corticosteroids do not assist in the clearance of uric acid or the protection of renal tubules from metabolic crystalline deposits. .

Choice A rationale

Adrenal tumors represent only one specific cause of hypercortisolism. This statement is scientifically inaccurate because it fails to account for pituitary adenomas, ectopic ACTH production, or exogenous steroid administration. While adrenal adenomas or carcinomas can lead to Cushing's syndrome by autonomously secreting cortisol, they do not define Cushing's disease. Pathophysiologically, the term syndrome encompasses all etiologies of high cortisol, whereas the disease is specifically linked to the pituitary gland's overproduction of adrenocorticotropic hormone.

Choice B rationale

Cushing's disease is a specific subset of Cushing's syndrome caused by a pituitary adenoma secreting excess adrenocorticotropic hormone. This hormone stimulates the adrenal cortex to produce cortisol. Conversely, Cushing's syndrome is an umbrella term for any condition resulting in prolonged exposure to high cortisol levels, whether endogenous or exogenous. Common causes include long-term glucocorticoid therapy, adrenal tumors, or ectopic ACTH from small cell lung cancer. Normal serum cortisol ranges are 5 to 23 mcg/dL.

Choice C rationale

This choice incorrectly identifies the primary cause of Cushing's disease. Long-term glucocorticoid use is actually the most common cause of exogenous Cushing's syndrome, not the disease itself. Cushing's disease involves a primary internal pathology of the pituitary gland. Furthermore, claiming the syndrome is caused only by adrenal tumors is scientifically false, as it ignores the massive clinical population receiving therapeutic steroids for autoimmune or inflammatory conditions. The underlying molecular mechanism involves the disruption of the hypothalamic-pituitary-adrenal axis.

Choice D rationale

This statement reverses the clinical definitions and causes confusion regarding the terminology. Cushing's disease is never defined by external glucocorticoid administration; that is a hallmark of iatrogenic Cushing's syndrome. The disease refers specifically to the pituitary-driven process. While both involve high cortisol, the diagnostic differentiation is critical because treatment for the disease usually involves transsphenoidal surgery, while treatment for the syndrome depends entirely on the specific underlying trigger, such as tapering off prednisone or removing an adrenal mass.