NRNP 6566 ADVANCED CARE OF ADULTS IN ACUTE
SETTINGS I WEEK 6 KNOWLEDGE CHECK 2026/2027 |
Questions and Verified Answers | Pass Guaranteed - A+
Graded
Domain 1: Renal & Fluid/Electrolyte Management (15 Questions)
Q1: A 68-year-old male with a history of heart failure and chronic kidney disease
(baseline creatinine 1.8 mg/dL) is admitted with acute decompensated heart failure. He
received IV furosemide 80 mg daily for 3 days. Current vitals: BP 92/58 mmHg, HR 112
bpm, RR 24/min. Labs: Creatinine 3.2 mg/dL (increased from 1.8), BUN 68 mg/dL, urine
sodium 12 mEq/L, FeNa 0.8%. Urinalysis shows hyaline casts. Which classification of
acute kidney injury does this patient have, and what is the most appropriate immediate
intervention?
A. Intrarenal AKI; initiate nephrotoxic medication avoidance and renal dose dopamine
B. Postrenal AKI; obtain urgent renal ultrasound and consider catheterization
C. Prerenal azotemia; discontinue diuretics and initiate cautious fluid resuscitation with
balanced crystalloids [CORRECT]
D. Intrinsic renal AKI; initiate high-dose loop diuretics to "flush" the kidneys
Correct Answer: C
,Rationale: This patient demonstrates classic prerenal azotemia secondary to
over-diuresis in the setting of hypoperfusion. The FeNa <1% (specifically 0.8%) indicates
sodium avidity by the kidneys, consistent with prerenal physiology. The hyaline casts
(rather than muddy brown casts or cellular casts) support this diagnosis. The
BUN:creatinine ratio is approximately 21:1 (68:3.2), also suggesting prerenal physiology.
The patient is hypotensive (92/58 mmHg) with tachycardia, indicating intravascular
volume depletion.
Option A is incorrect because renal dose dopamine is not recommended based on
current evidence (NEJM 1994; 2000 studies showed no benefit and potential harm). The
FeNa argues against intrarenal AKI, which would typically show FeNa >2% with tubular
damage.
Option B is incorrect because there is no evidence of obstructive uropathy (no anuria, no
flank pain, no palpable bladder, normal baseline urinalysis without hematuria). Postrenal
AKI would not explain the low FeNa.
Option D is incorrect because high-dose diuretics would worsen the prerenal state.
"Renal dose" or high-dose diuretics do not prevent or treat AKI; they may worsen it by
further reducing renal perfusion.
The correct management involves discontinuing the offending agent (furosemide),
cautious fluid resuscitation with balanced crystalloids (Plasma-Lyte or Lactated Ringer's
preferred over normal saline to prevent hyperchloremic metabolic acidosis), and
hemodynamic monitoring. The patient requires careful fluid management given his
heart failure history—likely needing invasive hemodynamic monitoring or bedside
ultrasound to guide resuscitation without precipitating pulmonary edema.
,Q2: A 54-year-old female with septic shock from pneumonia develops oliguric AKI (urine
output <0.5 mL/kg/hr for 12 hours). Her creatinine has risen from 1.0 to 2.8 mg/dL over
48 hours. According to the KDIGO AKI staging criteria, what stage of AKI does she have,
and what is the most appropriate next step in management?
A. Stage 1 AKI; continue current management with monitoring
B. Stage 2 AKI; initiate loop diuretics to convert oliguria to non-oliguria
C. Stage 3 AKI; immediate preparation for renal replacement therapy
D. Stage 2 AKI; continue sepsis resuscitation with avoidance of nephrotoxins and
hemodynamic optimization [CORRECT]
Correct Answer: D
Rationale: According to KDIGO 2012 criteria, AKI staging is defined as: Stage 1
(creatinine increase 1.5-1.9x baseline OR ≥0.3 mg/dL increase OR urine output <0.5
mL/kg/hr for 6-12 hours); Stage 2 (creatinine increase 2.0-2.9x baseline OR urine output
<0.5 mL/kg/hr for ≥12 hours); Stage 3 (creatinine increase 3.0x baseline OR ≥4.0 mg/dL
OR urine output <0.3 mL/kg/hr for ≥24 hours OR anuria ≥12 hours OR need for RRT).
This patient's creatinine increased 2.8x baseline (2.8/1.0), meeting Stage 2 criteria. The
oliguria duration (12 hours) also meets Stage 2 criteria.
Option A is incorrect because the creatinine increase exceeds Stage 1 parameters
(1.5-1.9x or ≥0.3 mg/dL increase).
Option B is incorrect because loop diuretics do not prevent AKI progression, reduce
mortality, or facilitate renal recovery. The FACTT trial and subsequent studies have
, shown no benefit to diuretic therapy in AKI. Diuretics may be used for volume
management once the patient is hemodynamically stable, but not to "convert" oliguric to
non-oliguric AKI.
Option C is incorrect because while she has Stage 2 AKI, there are no immediate
indications for RRT (no refractory hyperkalemia, severe metabolic acidosis, fluid
overload with pulmonary edema, uremic complications, or certain toxin ingestions). RRT
should not be initiated solely based on creatinine level or AKI stage.
Option D is correct because the primary management of septic AKI involves treating the
underlying cause (source control, appropriate antibiotics), hemodynamic optimization
(avoiding hypotension, maintaining MAP >65 mmHg), avoiding nephrotoxins (contrast,
aminoglycosides, NSAIDs), and close monitoring. The KDIGO guidelines emphasize
these supportive measures rather than specific "kidney-protective" pharmacologic
interventions.
Q3: A 72-year-old male with ESRD on hemodialysis presents with weakness and
palpitations. ECG shows peaked T waves, widened QRS complexes (0.14 seconds), and
sine wave pattern. Serum potassium is 7.8 mEq/L. Which intervention sequence
represents the most appropriate immediate management?
A. Initiate hemodialysis immediately; no other interventions needed
B. Calcium gluconate 1g IV, insulin 10 units + glucose 50g IV, albuterol nebulizer, sodium
polystyrene sulfonate 15g PO, then hemodialysis [CORRECT]
C. Sodium polystyrene sulfonate 30g PO immediately, followed by insulin/glucose
D. Calcium chloride 1g rapid IV push, furosemide 80mg IV, then observation
SETTINGS I WEEK 6 KNOWLEDGE CHECK 2026/2027 |
Questions and Verified Answers | Pass Guaranteed - A+
Graded
Domain 1: Renal & Fluid/Electrolyte Management (15 Questions)
Q1: A 68-year-old male with a history of heart failure and chronic kidney disease
(baseline creatinine 1.8 mg/dL) is admitted with acute decompensated heart failure. He
received IV furosemide 80 mg daily for 3 days. Current vitals: BP 92/58 mmHg, HR 112
bpm, RR 24/min. Labs: Creatinine 3.2 mg/dL (increased from 1.8), BUN 68 mg/dL, urine
sodium 12 mEq/L, FeNa 0.8%. Urinalysis shows hyaline casts. Which classification of
acute kidney injury does this patient have, and what is the most appropriate immediate
intervention?
A. Intrarenal AKI; initiate nephrotoxic medication avoidance and renal dose dopamine
B. Postrenal AKI; obtain urgent renal ultrasound and consider catheterization
C. Prerenal azotemia; discontinue diuretics and initiate cautious fluid resuscitation with
balanced crystalloids [CORRECT]
D. Intrinsic renal AKI; initiate high-dose loop diuretics to "flush" the kidneys
Correct Answer: C
,Rationale: This patient demonstrates classic prerenal azotemia secondary to
over-diuresis in the setting of hypoperfusion. The FeNa <1% (specifically 0.8%) indicates
sodium avidity by the kidneys, consistent with prerenal physiology. The hyaline casts
(rather than muddy brown casts or cellular casts) support this diagnosis. The
BUN:creatinine ratio is approximately 21:1 (68:3.2), also suggesting prerenal physiology.
The patient is hypotensive (92/58 mmHg) with tachycardia, indicating intravascular
volume depletion.
Option A is incorrect because renal dose dopamine is not recommended based on
current evidence (NEJM 1994; 2000 studies showed no benefit and potential harm). The
FeNa argues against intrarenal AKI, which would typically show FeNa >2% with tubular
damage.
Option B is incorrect because there is no evidence of obstructive uropathy (no anuria, no
flank pain, no palpable bladder, normal baseline urinalysis without hematuria). Postrenal
AKI would not explain the low FeNa.
Option D is incorrect because high-dose diuretics would worsen the prerenal state.
"Renal dose" or high-dose diuretics do not prevent or treat AKI; they may worsen it by
further reducing renal perfusion.
The correct management involves discontinuing the offending agent (furosemide),
cautious fluid resuscitation with balanced crystalloids (Plasma-Lyte or Lactated Ringer's
preferred over normal saline to prevent hyperchloremic metabolic acidosis), and
hemodynamic monitoring. The patient requires careful fluid management given his
heart failure history—likely needing invasive hemodynamic monitoring or bedside
ultrasound to guide resuscitation without precipitating pulmonary edema.
,Q2: A 54-year-old female with septic shock from pneumonia develops oliguric AKI (urine
output <0.5 mL/kg/hr for 12 hours). Her creatinine has risen from 1.0 to 2.8 mg/dL over
48 hours. According to the KDIGO AKI staging criteria, what stage of AKI does she have,
and what is the most appropriate next step in management?
A. Stage 1 AKI; continue current management with monitoring
B. Stage 2 AKI; initiate loop diuretics to convert oliguria to non-oliguria
C. Stage 3 AKI; immediate preparation for renal replacement therapy
D. Stage 2 AKI; continue sepsis resuscitation with avoidance of nephrotoxins and
hemodynamic optimization [CORRECT]
Correct Answer: D
Rationale: According to KDIGO 2012 criteria, AKI staging is defined as: Stage 1
(creatinine increase 1.5-1.9x baseline OR ≥0.3 mg/dL increase OR urine output <0.5
mL/kg/hr for 6-12 hours); Stage 2 (creatinine increase 2.0-2.9x baseline OR urine output
<0.5 mL/kg/hr for ≥12 hours); Stage 3 (creatinine increase 3.0x baseline OR ≥4.0 mg/dL
OR urine output <0.3 mL/kg/hr for ≥24 hours OR anuria ≥12 hours OR need for RRT).
This patient's creatinine increased 2.8x baseline (2.8/1.0), meeting Stage 2 criteria. The
oliguria duration (12 hours) also meets Stage 2 criteria.
Option A is incorrect because the creatinine increase exceeds Stage 1 parameters
(1.5-1.9x or ≥0.3 mg/dL increase).
Option B is incorrect because loop diuretics do not prevent AKI progression, reduce
mortality, or facilitate renal recovery. The FACTT trial and subsequent studies have
, shown no benefit to diuretic therapy in AKI. Diuretics may be used for volume
management once the patient is hemodynamically stable, but not to "convert" oliguric to
non-oliguric AKI.
Option C is incorrect because while she has Stage 2 AKI, there are no immediate
indications for RRT (no refractory hyperkalemia, severe metabolic acidosis, fluid
overload with pulmonary edema, uremic complications, or certain toxin ingestions). RRT
should not be initiated solely based on creatinine level or AKI stage.
Option D is correct because the primary management of septic AKI involves treating the
underlying cause (source control, appropriate antibiotics), hemodynamic optimization
(avoiding hypotension, maintaining MAP >65 mmHg), avoiding nephrotoxins (contrast,
aminoglycosides, NSAIDs), and close monitoring. The KDIGO guidelines emphasize
these supportive measures rather than specific "kidney-protective" pharmacologic
interventions.
Q3: A 72-year-old male with ESRD on hemodialysis presents with weakness and
palpitations. ECG shows peaked T waves, widened QRS complexes (0.14 seconds), and
sine wave pattern. Serum potassium is 7.8 mEq/L. Which intervention sequence
represents the most appropriate immediate management?
A. Initiate hemodialysis immediately; no other interventions needed
B. Calcium gluconate 1g IV, insulin 10 units + glucose 50g IV, albuterol nebulizer, sodium
polystyrene sulfonate 15g PO, then hemodialysis [CORRECT]
C. Sodium polystyrene sulfonate 30g PO immediately, followed by insulin/glucose
D. Calcium chloride 1g rapid IV push, furosemide 80mg IV, then observation
