Medical-Surgical Nursing Flashcards

A 58-year-old male patient in a Riyadh tertiary hospital is post-operative day 2 following an open abdominal aortic aneurysm repair. His urine output drops to 18 mL/hour over 3 consecutive hours. Serum creatinine rises from 88 to 210 µmol/L. Which assessment finding would MOST specifically indicate acute tubular necrosis rather than prerenal azotemia?

Answer: Urine sodium of 45 mEq/L with fractional excretion of sodium (FeNa) of 3.2%

Acute tubular necrosis (ATN) is characterized by tubular dysfunction, evidenced by a high urine sodium (>40 mEq/L) and FeNa >2%, because damaged tubules cannot reabsorb sodium. In prerenal azotemia, kidneys are functionally intact and avidly retain sodium (urine Na <20 mEq/L, FeNa <1%). Options C and D suggest hypovolemia (prerenal cause), while option A (low urine Na, high osmolality) indicates prerenal state with concentrated urine. The FeNa of 3.2% in option B confirms intrinsic renal injury consistent with ATN.

A nurse in a Saudi MOH hospital is caring for a patient with chronic liver disease who develops hepatic encephalopathy Grade III. The physician orders lactulose 30 mL orally every 2 hours. After 6 hours, the patient has had 5 loose stools and arterial ammonia is 180 µmol/L (normal <50 µmol/L). The patient's sodium is 128 mEq/L. Which nursing intervention takes HIGHEST priority at this point?

Answer: Hold lactulose and notify physician of hyponatremia with risk of osmotic demyelination syndrome

While lactulose is first-line for hepatic encephalopathy, the patient now has significant hyponatremia (Na 128 mEq/L). Continued aggressive lactulose-induced diarrhea can worsen hyponatremia through free water and electrolyte losses. In cirrhotic patients, hyponatremia is often dilutional; rapid correction with isotonic saline risks osmotic demyelination syndrome (ODS). The nurse must hold the lactulose and escalate to the physician to reassess the regimen, potentially adding rifaximin (approved in Saudi MOH formularies) and addressing electrolyte balance before continuing. Normal saline bolus (option D) is dangerous in dilutional hyponatremia with fluid overload.

During a thoracentesis procedure at a Saudi hospital, a patient with a large pleural effusion suddenly develops acute hypotension (BP 80/50 mmHg), tachycardia (HR 128 bpm), and severe dyspnea after 900 mL of fluid has been drained. Oxygen saturation drops to 88% on room air. Which complication has MOST likely occurred, and what is the CORRECT immediate nursing response?

Answer: Re-expansion pulmonary edema — stop the procedure, apply high-flow oxygen, and position the patient upright

Re-expansion pulmonary edema (RPE) is a recognized complication when large volumes of pleural fluid (>1,000–1,500 mL) are rapidly removed. It results from rapid re-inflation of a previously collapsed lung, causing increased capillary permeability and pulmonary edema. Clinical signs include sudden dyspnea, hypotension, and desaturation occurring during or immediately after drainage. The correct response is to STOP the procedure immediately, apply high-flow oxygen (non-rebreather mask), and sit the patient upright to reduce pulmonary venous pressure. Tension pneumothorax (A) typically presents with tracheal deviation and absent breath sounds. Vasovagal (C) does not cause severe hypoxia. Saudi clinical guidelines align with international standards recommending removing no more than 1,000–1,500 mL per session.

A 44-year-old Saudi female patient with type 2 diabetes and CKD Stage 3b (eGFR 32 mL/min/1.73m²) is admitted for elective coronary angiography. She takes metformin 1 g twice daily. Serum creatinine is 168 µmol/L. As the admitting nurse, which pre-procedural action regarding her metformin is CORRECT according to current clinical practice?

Answer: Hold metformin 48 hours before the procedure and restart only after confirming stable renal function post-contrast

Iodinated contrast media used in coronary angiography can cause contrast-induced nephropathy (CIN), which may transiently reduce renal function. Metformin is renally cleared and accumulates in renal impairment; if AKI occurs post-contrast and metformin continues, lactic acidosis risk increases significantly. Current SCFHS/Saudi clinical practice guidelines (aligned with ESC/ACC) recommend withholding metformin 48 hours before intravascular iodinated contrast in patients with eGFR <45 mL/min/1.73m² (CKD Stage 3b), and restarting only after re-checking renal function at 48 hours post-procedure if stable. Option A is incorrect — the threshold for extra caution is eGFR <45, not <30. Option C (bicarbonate for lactic acid neutralization) is not indicated prophylactically. Option D's restart timing is too early.

A surgical nurse is reviewing a postoperative patient who had a Whipple procedure (pancreaticoduodenectomy) 5 days ago. The patient develops a sudden high-volume output from the Jackson-Pratt drain — 350 mL of clear watery fluid in 4 hours. Drain fluid amylase is sent and returns at 4,200 U/L (serum amylase 180 U/L). Which nursing action is MOST appropriate FIRST?

Answer: Notify the surgical team immediately — this drain amylase:serum amylase ratio indicates a postoperative pancreatic fistula

A drain amylase level more than 3× the upper limit of normal serum amylase on postoperative day 3 or beyond — or a drain:serum amylase ratio >3 — defines a Postoperative Pancreatic Fistula (POPF) per the International Study Group on Pancreatic Fistula (ISGPF) criteria, endorsed in Saudi hepatopancreaticobiliary surgery guidelines. This is a major complication of the Whipple procedure, carrying risks of delayed hemorrhage, abscess, and sepsis. The nurse must immediately notify the surgical team for assessment. Drain removal (A) is contraindicated — it can trap bile/pancreatic juice and cause peritonitis. Clamping (C) is dangerous. Fluid replacement (D) is supportive and may be needed, but the FIRST priority is escalation to the physician for urgent assessment of fistula severity grading.

A 67-year-old male patient with COPD Gold Stage III is admitted to a Saudi hospital with acute exacerbation. He is on supplemental oxygen at 2 L/min via nasal cannula. ABG results show: pH 7.32, PaCO₂ 68 mmHg, PaO₂ 56 mmHg, HCO₃⁻ 34 mEq/L, SaO₂ 87%. The nurse increases O₂ to 5 L/min. Thirty minutes later, the patient becomes drowsier and less responsive. Repeat ABG: pH 7.24, PaCO₂ 82 mmHg, PaO₂ 78 mmHg. Which physiological mechanism BEST explains this deterioration?

Answer: Supplemental oxygen suppressed the hypoxic ventilatory drive in a CO₂-retaining patient, reducing respiratory effort and worsening hypercapnia

In chronic CO₂ retainers (such as advanced COPD patients), the central chemoreceptors become blunted to chronically elevated CO₂, and ventilatory drive becomes increasingly dependent on hypoxia (peripheral chemoreceptors — the 'hypoxic drive'). Aggressively increasing FiO₂ removes this hypoxic stimulus, reducing respiratory rate and tidal volume, causing CO₂ to accumulate (hypercapnic respiratory failure). This is demonstrated by the rise in PaCO₂ from 68 to 82 mmHg with worsening acidosis. Saudi MOH and WHO guidelines recommend controlled oxygen therapy targeting SpO₂ 88–92% in known CO₂-retaining COPD patients to avoid this complication. The Haldane effect (D) does contribute modestly to rising PaCO₂ but is not the primary mechanism. Option A (absorption atelectasis) causes hypoxemia, not hypercapnia.