Exam 3: NUR 209/ NUR 209 (Latest 2026/ 2027 Update) Medical Surgical Nursing II: Med-Surg Review| Questions and Answers| Grade A| 100% Correct (Verified Solutions) – Fortis

INSTANT PDF DOWNLOAD — This comprehensive exam preparation resource for NUR 209 Exam 3 Medical Surgical Nursing II at Fortis College covers all content for the 2026/2027 academic year third examination. It features verified questions and answers with detailed rationales in multiple-choice, select-all-that-apply (SATA), ordered response, and clinical scenario formats aligned with nursing program standards. RENAL AND URINARY SYSTEM DISORDERS (EXAM 3 FOCUS) ACUTE KIDNEY INJURY (AKI) Definition – Sudden (hours to days) decrease in kidney function resulting in accumulation of nitrogenous wastes (BUN, creatinine) and dysregulation of fluid, electrolyte, and acid-base balance. Diagnostic criteria: increase in serum creatinine by ≥0.3 mg/dL within 48 hours OR increase in creatinine to ≥1.5x baseline within prior 7 days OR urine output 0.5 mL/kg/hour for 6 hours. Phases of AKI – Initiation phase (onset of injury, lasts hours to days, early intervention may prevent progression). Oliguric phase (most common presentation – urine output 400 mL/day or 0.5 mL/kg/hour for 6+ hours, lasts 1-3 weeks, BUN/Cr rise daily, electrolyte imbalances, fluid overload, metabolic acidosis). Diuretic phase (gradual increase in urine output up to 1-3 L/day or more, lasts 1-3 weeks, monitor for dehydration, hyponatremia, hypokalemia, hypotension). Recovery phase (renal function gradually returns to baseline, may take 3-12 months, some may have permanent kidney damage). Prerenal AKI (Most Common – 40-60%) – Caused by decreased renal perfusion (hypovolemia, hypotension, decreased cardiac output, renal artery stenosis). Laboratory findings: BUN/Cr ratio 20:1 (normal ratio 12-20), FeNa 1% (fractional excretion of sodium – indicates sodium retention due to decreased perfusion), urine osmolality 500, urine sodium 20 mEq/L. Example: BUN 58, Cr 2.3 → ratio 25 suggests prerenal etiology. Intrinsic AKI (30-40%) – Caused by damage to kidney tissue itself. Acute tubular necrosis (ATN) – most common cause of intrinsic AKI (ischemic or nephrotoxic – contrast dye, aminoglycosides, NSAIDs, heavy metals, myoglobin, hemoglobin). Laboratory findings: BUN/Cr ratio 15:1, FeNa 2%, urine osmolality 350, urine sodium 40 mEq/L, muddy brown casts, renal tubular epithelial cells. Other intrinsic causes: glomerulonephritis, interstitial nephritis (medications: NSAIDs, antibiotics, PPIs), vasculitis. Postrenal AKI (5-10%) – Caused by obstruction of urine flow (BPH, stones, tumors, strictures, neurogenic bladder). Laboratory findings: variable BUN/Cr ratio, anuria (complete obstruction) or oliguria (partial obstruction), hydronephrosis on imaging (renal ultrasound). Relief of obstruction (foley catheter, nephrostomy tube, surgery) leads to post-obstructive diuresis (monitor for fluid/electrolyte losses). AKI Management – Identify and treat underlying cause, correct fluid volume (IV fluids for prerenal, avoid overhydration), manage electrolytes (hyperkalemia: calcium gluconate stabilizes myocardium, insulin+glucose shifts K+ into cells, albuterol nebulizer, sodium polystyrene sulfonate Kayexalate, dialysis if severe), monitor acid-base status (metabolic acidosis), adjust medication doses (renal excretion), renal replacement therapy (hemodialysis, CRRT) indications: severe hyperkalemia (6.5), severe metabolic acidosis (pH 7.1), volume overload (pulmonary edema), uremic complications (pericarditis, encephalopathy, bleeding), BUN 100, Cr 10.