CPNRE - Canadian Practical Nurse Registration Examination Pediatric and Child Health Nursing Questions and Answers Flashcards

A 4-year-old child with nephrotic syndrome is admitted with severe periorbital edema, ascites, and oliguria. Serum albumin is 1.4 g/dL. The physician orders 25% albumin infusion followed by furosemide. During the infusion, the child develops increased respiratory rate, crackles on auscultation, and oxygen saturation drops to 91%. What is the nurse's priority action?

Answer: Slow the albumin infusion rate and notify the physician immediately

The child is showing signs of pulmonary edema — a known complication of albumin infusion in nephrotic syndrome when oncotic pressure rapidly shifts fluid into the vascular space faster than it can be mobilized. The priority is to slow (not stop abruptly) the infusion and notify the physician immediately. Trendelenburg would worsen pulmonary edema. A second furosemide dose without physician direction is outside nursing scope and could cause dangerous electrolyte shifts. Stopping furosemide would remove the mechanism meant to prevent this complication.

A nurse is caring for a 7-week-old infant who underwent surgical repair of a myelomeningocele 48 hours ago. The infant is now irritable, has a bulging anterior fontanelle, and a high-pitched cry. Temperature is 37.1°C. Which complication is MOST likely developing and requires immediate escalation?

Answer: Post-operative hydrocephalus requiring shunt evaluation

Hydrocephalus is the most common and serious complication following myelomeningocele repair, often manifesting 48–72 hours post-operatively as CSF flow dynamics change after closure. Bulging fontanelle, high-pitched cry, and irritability are classic signs of increased intracranial pressure in an infant. The normal temperature makes infection less likely as the primary driver. NAS would present with tremors, poor feeding, and hypertonicity, not a bulging fontanelle. Normal post-operative pain would not cause a bulging fontanelle.

A 13-year-old with Type 1 diabetes mellitus presents to the emergency department with blood glucose of 28 mmol/L, Kussmaul respirations, and a serum potassium of 5.8 mEq/L. IV insulin and normal saline are initiated. Two hours into treatment, the repeat potassium is 3.1 mEq/L. What does this drop in potassium indicate about the patient's status?

Answer: The patient is developing hypokalemia due to excessive insulin causing cellular potassium shift

In DKA, insulin drives potassium back into cells (K+ shifts intracellularly with glucose metabolism), rapidly dropping serum potassium levels even though total body potassium was already depleted. The initial hyperkalemia in DKA is paradoxical — it reflects acidosis-driven extracellular shift, not true excess. Once insulin therapy begins and acidosis corrects, potassium rapidly moves intracellularly, revealing the true total-body deficit. Potassium replacement must be initiated before serum levels drop to dangerous levels, typically when K+ falls below 5.0 mEq/L during DKA treatment.

A nurse is assessing a 6-month-old infant brought in by parents who report the baby 'stopped breathing for a moment' during sleep. The infant is alert and feeding well now. This is the second such episode. The infant's 3-year-old sibling died suddenly at home 8 months ago with no determined cause. Which action reflects the nurse's MOST appropriate professional and ethical response?

Answer: Document the episodes thoroughly and report concerns to the charge nurse and physician without accusatory statements, following the agency's safeguarding protocol

The combination of recurrent apparent life-threatening events (ALTEs/BRUEs) in an infant and an unexplained sibling death raises significant safeguarding concerns consistent with possible non-accidental suffocation or a familial condition. The nurse's role is to document objectively and escalate through proper channels (charge nurse, physician, and safeguarding protocol) — not to accuse parents or make a diagnosis, but also not to dismiss the pattern. Discharging with an apnea monitor without investigation would be inadequate given the sibling history. Directly accusing parents is inappropriate and could impede a proper multidisciplinary investigation.

A 10-year-old child with sickle cell disease is admitted in vaso-occlusive crisis. They are receiving IV morphine via PCA and oxygen at 2 L/min by nasal cannula with SpO2 at 95%. The child's pain score remains 8/10. The parents insist staff increase the oxygen to 10 L/min because 'more oxygen will fix the sickling faster.' What is the evidence-based rationale for the nurse's response?

Answer: High-flow oxygen suppresses erythropoietin and can worsen anaemia long-term; supplemental O2 is indicated only if SpO2 is below 95% to avoid hypoxic sickling

Current evidence-based guidelines for sickle cell vaso-occlusive crisis indicate supplemental oxygen is only beneficial when SpO2 falls below 95%. At SpO2 of 95%, additional oxygen does not meaningfully reduce sickling and can suppress the natural erythropoietin response, potentially worsening chronic anaemia. The nurse should educate the parents that with SpO2 maintained at 95%, the priority interventions are adequate analgesia, IV hydration, and warmth — not escalating oxygen. This requires therapeutic communication that validates the parents' concern while providing evidence-based rationale.

A 14-year-old adolescent with anorexia nervosa is admitted for refeeding. On day 3 of nutritional rehabilitation, the patient develops muscle weakness, cardiac dysrhythmia on the monitor, and paresthesias in the extremities. Serum phosphate is 0.5 mmol/L. Which pathophysiological mechanism BEST explains this cluster of findings?

Answer: Refeeding syndrome: insulin release from carbohydrate intake drives phosphate, magnesium, and potassium intracellularly, causing severe serum depletion

Refeeding syndrome is a life-threatening metabolic complication occurring when malnourished patients receive nutrition after prolonged starvation. As carbohydrates are introduced, insulin surges and drives phosphate (along with potassium and magnesium) from the bloodstream into cells, causing severe hypophosphatemia. Phosphate is critical for ATP synthesis; without it, neuromuscular function (weakness, paresthesias), cardiac conduction (dysrhythmias), and respiratory muscle function are impaired. Prevention requires slow caloric escalation, pre-refeeding electrolyte correction, and close monitoring of phosphate, magnesium, and potassium. Thiamine deficiency is also important in refeeding but does not directly explain the hypophosphatemia cluster.