A child with nephrotic syndrome is prescribed a corticosteroid. The nurse should ensure the child is:
Taken off the medication after 1 week
Monitored closely for signs of infection
Administered the medication with milk
Given the medication at bedtime
The Correct Answer is B
Choice A reason: Discontinuing corticosteroids after one week in nephrotic syndrome is inappropriate, as treatment requires a prolonged course (weeks to months) to reduce proteinuria and edema. Abrupt cessation risks adrenal insufficiency and disease relapse due to persistent glomerular inflammation, making this an incorrect approach for managing the immune-mediated pathology effectively.
Choice B reason: Corticosteroids in nephrotic syndrome suppress the immune system, increasing infection risk due to reduced immunoglobulin production and impaired immune response. Children are particularly vulnerable to bacterial infections like peritonitis. Close monitoring for fever, leukocytosis, or other infection signs is critical to detect and treat complications early, ensuring safe management.
Choice C reason: Administering corticosteroids with milk may reduce gastrointestinal irritation but is not the priority in nephrotic syndrome. The primary concern is immunosuppression, increasing infection risk. While milk may aid tolerability, it does not address the significant risk of sepsis or other infections, making monitoring for infection the more critical nursing action.
Choice D reason: Giving corticosteroids at bedtime may align with diurnal cortisol rhythms but is not the priority in nephrotic syndrome. Timing does not mitigate the immunosuppression that increases infection risk. Monitoring for infection signs like fever or malaise is essential, as corticosteroids heighten susceptibility, making bedtime administration a less critical consideration.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is A
Explanation
Choice A reason: The Somogyi phenomenon involves rebound hyperglycemia in the morning following nocturnal hypoglycemia, triggering counter-regulatory hormones (e.g., glucagon, cortisol), causing diaphoresis and headaches. Excess insulin at night lowers glucose, prompting a hyperglycemic rebound. This explains the child’s symptoms, requiring insulin dose adjustment to prevent nocturnal hypoglycemia.
Choice B reason: The Honeymoon effect is a temporary period of improved insulin production post-diagnosis in type 1 diabetes, not causing hyperglycemia, diaphoresis, or headaches. It reflects residual beta-cell function, not a morning rebound. The Somogyi phenomenon better explains the symptoms, making this an incorrect diagnosis.
Choice C reason: Ketoacidosis causes hyperglycemia, but with fruity breath, lethargy, and dehydration, not diaphoresis or headaches alone. It results from insulin deficiency, not nocturnal hypoglycemia rebound. The Somogyi phenomenon’s counter-regulatory response better matches the morning symptoms, making ketoacidosis an incorrect suspicion for this presentation.
Choice D reason: The Dawn phenomenon causes morning hyperglycemia due to growth hormone surges, not diaphoresis or headaches, which suggest a hypoglycemic event. It lacks the rebound mechanism of the Somogyi phenomenon, which explains the combination of symptoms, making this an incorrect suspicion for the child’s condition.
Correct Answer is A
Explanation
Choice A reason: Nephrotic syndrome causes massive proteinuria, hypoalbuminemia, and edema due to reduced oncotic pressure. Steroids, like prednisone, reduce glomerular inflammation, decrease protein leakage, and restore oncotic pressure, alleviating edema. By targeting the underlying immune-mediated damage, steroids effectively reduce fluid retention, making them the primary medication class for managing edema in this condition.
Choice B reason: Antibiotics treat bacterial infections, which nephrotic syndrome patients are prone to due to immunoglobulin loss, but they do not address edema. Edema results from hypoalbuminemia, not infection. Antibiotics are used for complications like peritonitis, not for reducing fluid retention, making them ineffective for the primary management of nephrotic syndrome edema.
Choice C reason: Fungicides treat fungal infections, which are rare in nephrotic syndrome unless immunocompromised from prolonged steroid use. Edema in nephrotic syndrome stems from proteinuria and low albumin, not fungal pathology. Fungicides have no role in reducing fluid retention, making them irrelevant for addressing the primary pathophysiological mechanism of edema.
Choice D reason: Analgesics relieve pain, which is not a primary feature of nephrotic syndrome. Edema results from hypoalbuminemia, causing fluid shifts into interstitial spaces. Pain management does not address this mechanism or reduce fluid retention. Steroids target the root cause, making analgesics inappropriate for managing edema in nephrotic syndrome.
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