NUR 265
Exam 1 Review: Advanced Med-Surg
Key Points, Clinical Rationale & Lab Summary
KEY LABORATORY VALUES REFERENCE
Normal Creatinine: 0.6–1.2 mg/dL | AKI: rises 1–2 mg/dL every 24–48 hrs
Normal Urine Output: ≥30 mL/hr | Oliguria: ≤400 mL/day
Normal Potassium (K): 3.5–5.0 mEq/L
Normal Sodium (Na): 135–145 mEq/L
Normal Troponin: <0.5 ng/mL | Elevated = myocardial injury
GFR Staging (CKD): Stage 1: GFR ≥90 · Stage 5 (Failure): GFR ≤15 mL/min
HOW TO USE THIS STUDY GUIDE
Each question (Q) is followed immediately by its Answer (ANS). A Clinical Rationale explains the physiological
or pharmacological reasoning behind the answer — essential for NCLEX-style application questions. Cover the
ANS row to self-quiz before reading.
SECTION 1: ACUTE KIDNEY INJURY (AKI)
Pathophysiology · Phases · Nursing Management
Q1 What are the classic signs and symptoms of Acute Kidney Injury (AKI)?
ANSWER
• Oliguria / decreased urine output
• Azotemia (buildup of nitrogenous waste)
ANS • Fluid overload: crackles, edema, confusion, SpO₂ <88%, tachycardia
• Mean arterial pressure (MAP) below 65 mmHg
Clinical Rationale: Oliguria (<400 mL/day) and azotemia are hallmarks of AKI. MAP <65
indicates shock-level perfusion failure requiring immediate intervention.
Q2 What does a chest X-ray typically reveal in a patient with AKI?
ANSWER
Pulmonary infiltration — fluid accumulation in the lungs.
ANS
Clinical Rationale: Fluid overload from impaired renal clearance causes fluid to shift into the
pulmonary interstitium, visible as infiltrates on X-ray.
,Q3 What ABG finding is commonly seen in AKI?
ANSWER
Respiratory alkalosis when SpO₂ drops below 88%.
ANS
Clinical Rationale: Hypoxia triggers compensatory hyperventilation, causing CO₂ to drop,
resulting in respiratory alkalosis.
Q4 List examples of PRE-RENAL causes of AKI.
ANSWER
• Dehydration
• Blood loss (hemorrhage)
• Decreased cardiac output / Heart failure
ANS • Sepsis / Infection
• NG suction
• Vomiting / Diarrhea
Clinical Rationale: Pre-renal AKI results from decreased blood flow TO the kidneys. Restoring
perfusion (fluids, treating infection) typically reverses it.
Q5 List examples of INTRA-RENAL (intrinsic) causes of AKI.
ANSWER
• Myoglobinuria (muscle breakdown)
• Benign prostatic hyperplasia (BPH)
• Acute tubular necrosis (ATN)
ANS
• Nephrotoxicity (drugs, contrast)
• Acute glomerulonephritis
Clinical Rationale: Intra-renal causes involve direct damage to kidney parenchyma. Tubular
necrosis is the most common intrinsic cause in hospitalized patients.
Q6 List examples of POST-RENAL causes of AKI.
ANSWER
• Bladder neck obstruction
• Bladder cancer
ANS • Renal calculi (kidney stones)
• Tumor
Clinical Rationale: Post-renal AKI is caused by obstruction distal to the kidneys. Relieving the
obstruction (e.g., Foley catheter for BPH) often restores function.
Q7 What are the nursing priorities during the DIURETIC PHASE (Phase 3) of AKI?
ANS ANSWER
• Administer 3–6 liters of IV fluid per day
• Insert a Foley catheter and monitor I&O (expected output: 1,000–2,000 mL/day)
• Replace fluids and closely monitor electrolytes
, • Prepare for possible dialysis
Clinical Rationale: The diuretic phase brings large volumes of urine, risking dehydration and
electrolyte imbalances (especially hypokalemia). Vigilant monitoring is essential.
What is the single best laboratory indicator of kidney function in both AKI and
Q8
CKD?
ANSWER
• Creatinine — Normal: 0.6–1.2 mg/dL.
ANS • In AKI, creatinine rises 1–2 mg/dL every 24–48 hours.
Clinical Rationale: Creatinine is freely filtered and not reabsorbed, making it the most reliable
serum indicator of GFR and renal clearance.
Q9 What is the normal urine output per hour, and how is oliguria defined?
ANSWER
• Normal urine output: ≥30 mL/hr
ANS • Oliguria: decreased urine production — 400 mL/day or less (< ~17 mL/hr)
Clinical Rationale: Output <30 mL/hr signals compromised renal perfusion and must be
reported immediately.
Q 10 What are the nephrotoxic agents the nurse must monitor for in AKI patients?
ANSWER
• IV contrast dye
• Aminoglycoside antibiotics (e.g., gentamicin, tobramycin) — monitor peak and
ANS trough levels
• NSAIDs: celecoxib, ibuprofen, ketorolac, naproxen
Clinical Rationale: These agents damage renal tubules directly. Peak and trough levels for
aminoglycosides guide dosing to avoid toxicity.
Q 11 What diet modifications are recommended for AKI patients?
ANSWER
• General AKI: moderate protein, high carbohydrate
• AKI with dialysis: protein 40 g/day
ANS • AKI without dialysis: protein 1–1.5 g/kg/day; sodium 60–90 mEq/day; potassium
restriction 60–70 mEq/day
Clinical Rationale: Protein is restricted to reduce nitrogenous waste buildup. High
carbohydrates spare protein for essential body functions.
Q 12 What is a serious complication of AKI?
ANS ANSWER
Pericarditis — inflammation of the pericardium caused by uremic toxin accumulation.
Exam 1 Review: Advanced Med-Surg
Key Points, Clinical Rationale & Lab Summary
KEY LABORATORY VALUES REFERENCE
Normal Creatinine: 0.6–1.2 mg/dL | AKI: rises 1–2 mg/dL every 24–48 hrs
Normal Urine Output: ≥30 mL/hr | Oliguria: ≤400 mL/day
Normal Potassium (K): 3.5–5.0 mEq/L
Normal Sodium (Na): 135–145 mEq/L
Normal Troponin: <0.5 ng/mL | Elevated = myocardial injury
GFR Staging (CKD): Stage 1: GFR ≥90 · Stage 5 (Failure): GFR ≤15 mL/min
HOW TO USE THIS STUDY GUIDE
Each question (Q) is followed immediately by its Answer (ANS). A Clinical Rationale explains the physiological
or pharmacological reasoning behind the answer — essential for NCLEX-style application questions. Cover the
ANS row to self-quiz before reading.
SECTION 1: ACUTE KIDNEY INJURY (AKI)
Pathophysiology · Phases · Nursing Management
Q1 What are the classic signs and symptoms of Acute Kidney Injury (AKI)?
ANSWER
• Oliguria / decreased urine output
• Azotemia (buildup of nitrogenous waste)
ANS • Fluid overload: crackles, edema, confusion, SpO₂ <88%, tachycardia
• Mean arterial pressure (MAP) below 65 mmHg
Clinical Rationale: Oliguria (<400 mL/day) and azotemia are hallmarks of AKI. MAP <65
indicates shock-level perfusion failure requiring immediate intervention.
Q2 What does a chest X-ray typically reveal in a patient with AKI?
ANSWER
Pulmonary infiltration — fluid accumulation in the lungs.
ANS
Clinical Rationale: Fluid overload from impaired renal clearance causes fluid to shift into the
pulmonary interstitium, visible as infiltrates on X-ray.
,Q3 What ABG finding is commonly seen in AKI?
ANSWER
Respiratory alkalosis when SpO₂ drops below 88%.
ANS
Clinical Rationale: Hypoxia triggers compensatory hyperventilation, causing CO₂ to drop,
resulting in respiratory alkalosis.
Q4 List examples of PRE-RENAL causes of AKI.
ANSWER
• Dehydration
• Blood loss (hemorrhage)
• Decreased cardiac output / Heart failure
ANS • Sepsis / Infection
• NG suction
• Vomiting / Diarrhea
Clinical Rationale: Pre-renal AKI results from decreased blood flow TO the kidneys. Restoring
perfusion (fluids, treating infection) typically reverses it.
Q5 List examples of INTRA-RENAL (intrinsic) causes of AKI.
ANSWER
• Myoglobinuria (muscle breakdown)
• Benign prostatic hyperplasia (BPH)
• Acute tubular necrosis (ATN)
ANS
• Nephrotoxicity (drugs, contrast)
• Acute glomerulonephritis
Clinical Rationale: Intra-renal causes involve direct damage to kidney parenchyma. Tubular
necrosis is the most common intrinsic cause in hospitalized patients.
Q6 List examples of POST-RENAL causes of AKI.
ANSWER
• Bladder neck obstruction
• Bladder cancer
ANS • Renal calculi (kidney stones)
• Tumor
Clinical Rationale: Post-renal AKI is caused by obstruction distal to the kidneys. Relieving the
obstruction (e.g., Foley catheter for BPH) often restores function.
Q7 What are the nursing priorities during the DIURETIC PHASE (Phase 3) of AKI?
ANS ANSWER
• Administer 3–6 liters of IV fluid per day
• Insert a Foley catheter and monitor I&O (expected output: 1,000–2,000 mL/day)
• Replace fluids and closely monitor electrolytes
, • Prepare for possible dialysis
Clinical Rationale: The diuretic phase brings large volumes of urine, risking dehydration and
electrolyte imbalances (especially hypokalemia). Vigilant monitoring is essential.
What is the single best laboratory indicator of kidney function in both AKI and
Q8
CKD?
ANSWER
• Creatinine — Normal: 0.6–1.2 mg/dL.
ANS • In AKI, creatinine rises 1–2 mg/dL every 24–48 hours.
Clinical Rationale: Creatinine is freely filtered and not reabsorbed, making it the most reliable
serum indicator of GFR and renal clearance.
Q9 What is the normal urine output per hour, and how is oliguria defined?
ANSWER
• Normal urine output: ≥30 mL/hr
ANS • Oliguria: decreased urine production — 400 mL/day or less (< ~17 mL/hr)
Clinical Rationale: Output <30 mL/hr signals compromised renal perfusion and must be
reported immediately.
Q 10 What are the nephrotoxic agents the nurse must monitor for in AKI patients?
ANSWER
• IV contrast dye
• Aminoglycoside antibiotics (e.g., gentamicin, tobramycin) — monitor peak and
ANS trough levels
• NSAIDs: celecoxib, ibuprofen, ketorolac, naproxen
Clinical Rationale: These agents damage renal tubules directly. Peak and trough levels for
aminoglycosides guide dosing to avoid toxicity.
Q 11 What diet modifications are recommended for AKI patients?
ANSWER
• General AKI: moderate protein, high carbohydrate
• AKI with dialysis: protein 40 g/day
ANS • AKI without dialysis: protein 1–1.5 g/kg/day; sodium 60–90 mEq/day; potassium
restriction 60–70 mEq/day
Clinical Rationale: Protein is restricted to reduce nitrogenous waste buildup. High
carbohydrates spare protein for essential body functions.
Q 12 What is a serious complication of AKI?
ANS ANSWER
Pericarditis — inflammation of the pericardium caused by uremic toxin accumulation.
