MARYVILLE NURS 620 EXAM 4 ACTUAL EXAM 2026/2027 |
Questions and Answers with Complete Solutions |
Graduate-Level Nursing Review | Verified Answers | Pass
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Course Context and Exam 4 Coverage
Based on Maryville University's graduate nursing curriculum structure, NURS 620
typically represents an Advanced Pathophysiology course in the MSN/DNP program.
Exam 4 generally covers the final course modules, which commonly include:
● Renal/Genitourinary Pathophysiology
● Gastrointestinal Pathophysiology
● Hematologic/Oncologic Pathophysiology
● Multisystem Disorders & Critical Care Concepts
● Integrated Complex Case Studies
The following 100 questions align with graduate-level advanced practice nursing
competencies, emphasizing clinical reasoning, diagnostic accuracy, and
evidence-based management.
Unit 1: Renal and Genitourinary Pathophysiology (25 Questions)
Q1: A 58-year-old male with type 2 diabetes presents with serum creatinine 2.8 mg/dL
(baseline 1.1), BUN 48 mg/dL, and urine output 400 mL/24 hours. He recently started
,NSAIDs for back pain. Which pathophysiological mechanism best explains his acute
kidney injury?
A. Prerenal azotemia from decreased renal perfusion due to afferent arteriolar
constriction
B. Intrarenal injury from direct tubular toxicity and medullary ischemia [CORRECT]
C. Postrenal obstruction from prostatic hypertrophy
D. Chronic diabetic nephropathy progression without acute component
Correct Answer: B
Rationale: NSAIDs cause acute kidney injury through intrarenal mechanisms: inhibition
of prostaglandin synthesis reduces afferent arteriolar vasodilation (compensatory
mechanism in chronic kidney disease), causing renal hypoperfusion; additionally, direct
tubular toxicity and interstitial nephritis may occur. The elevated creatinine with recent
NSAID use, low urine output, and diabetic background (compromised autoregulation)
support intrarenal injury. NSAIDs are contraindicated in CKD due to this
pathophysiology.
● Distractor A: While decreased perfusion occurs, NSAIDs primarily affect
intrarenal hemodynamics (afferent constriction) and have direct toxic effects,
making "prerenal" incomplete. Prerenal azotemia typically shows BUN:Cr ratio
>20:1 and responds to volume; this patient's intrinsic damage may not.
● Distractor C: No obstructive symptoms (hesitancy, dribbling, flank pain) are
described; postrenal AKI requires mechanical obstruction evidence.
● Distractor D: While diabetic nephropathy is present, the acute elevation
(creatinine 1.1→2.8) with temporal NSAID relationship indicates superimposed
AKI, not just chronic progression.
,Q2: Which of the following are risk factors for contrast-induced nephropathy? (Select all
that apply)
A. Pre-existing chronic kidney disease [CORRECT]
B. Diabetes mellitus [CORRECT]
C. Volume depletion [CORRECT]
D. Young age (under 30)
E. Use of iso-osmolar contrast agents [CORRECT]
F. Concurrent metformin use
Correct Answers: A, B, C, E
Rationale: Contrast-induced nephropathy (CIN) risk factors include: pre-existing CKD
(eGFR <60, strongest predictor), diabetes (especially with CKD), volume depletion
(reduces renal perfusion reserve), and high-osmolar contrast (though iso-osmolar is
safer, it's still nephrotoxic in vulnerable patients). Prevention includes hydration,
minimizing contrast volume, and using lowest osmolar contrast.
● Distractor D (Young age): Advanced age is a risk factor; youth is protective due to
greater renal reserve.
● Distractor F (Metformin): Metformin is contraindicated in severe renal
impairment due to lactic acidosis risk, but it doesn't cause CIN. The interaction is
that contrast-induced AKI increases metformin toxicity risk, requiring temporary
discontinuation.
Q3: A patient with chronic kidney disease stage 4 (eGFR 22 mL/min/1.73m²) develops
metabolic acidosis. Which compensatory mechanism is most likely to be impaired?
, A. Hyperventilation to decrease PaCO₂
B. Renal bicarbonate regeneration and hydrogen ion excretion [CORRECT]
C. Bone buffering of excess hydrogen ions
D. Cellular shift of hydrogen into tissues
Correct Answer: B
Rationale: The kidneys provide the only sustained compensation for metabolic acidosis
through: (1) bicarbonate regeneration (reclaiming filtered bicarbonate and generating
new bicarbonate), and (2) active hydrogen ion secretion (titratable acidity and
ammonium excretion). In CKD stage 4, nephron mass loss impairs these mechanisms,
leading to chronic metabolic acidosis, bone demineralization, and protein catabolism.
● Distractor A: Respiratory compensation (hyperventilation) occurs rapidly and
remains intact unless pulmonary complications exist; it's not renal
compensation.
● Distractor C: Bone buffering occurs with chronic acidosis but is pathological
(osteopenia/osteoporosis), not a primary compensatory mechanism, and is
impaired by renal osteodystrophy in CKD.
● Distractor D: Cellular buffering is immediate but limited capacity; it's not the
sustained mechanism impaired in CKD.
Q4: The progression of diabetic nephropathy from microalbuminuria to overt proteinuria
involves which key pathophysiological changes?
A. Thickening of the glomerular basement membrane and mesangial expansion leading
to decreased filtration surface area [CORRECT]
B. Primary tubular atrophy without glomerular changes
C. Acute inflammatory infiltration of the interstitium
Questions and Answers with Complete Solutions |
Graduate-Level Nursing Review | Verified Answers | Pass
Guaranteed - A+ Graded
Course Context and Exam 4 Coverage
Based on Maryville University's graduate nursing curriculum structure, NURS 620
typically represents an Advanced Pathophysiology course in the MSN/DNP program.
Exam 4 generally covers the final course modules, which commonly include:
● Renal/Genitourinary Pathophysiology
● Gastrointestinal Pathophysiology
● Hematologic/Oncologic Pathophysiology
● Multisystem Disorders & Critical Care Concepts
● Integrated Complex Case Studies
The following 100 questions align with graduate-level advanced practice nursing
competencies, emphasizing clinical reasoning, diagnostic accuracy, and
evidence-based management.
Unit 1: Renal and Genitourinary Pathophysiology (25 Questions)
Q1: A 58-year-old male with type 2 diabetes presents with serum creatinine 2.8 mg/dL
(baseline 1.1), BUN 48 mg/dL, and urine output 400 mL/24 hours. He recently started
,NSAIDs for back pain. Which pathophysiological mechanism best explains his acute
kidney injury?
A. Prerenal azotemia from decreased renal perfusion due to afferent arteriolar
constriction
B. Intrarenal injury from direct tubular toxicity and medullary ischemia [CORRECT]
C. Postrenal obstruction from prostatic hypertrophy
D. Chronic diabetic nephropathy progression without acute component
Correct Answer: B
Rationale: NSAIDs cause acute kidney injury through intrarenal mechanisms: inhibition
of prostaglandin synthesis reduces afferent arteriolar vasodilation (compensatory
mechanism in chronic kidney disease), causing renal hypoperfusion; additionally, direct
tubular toxicity and interstitial nephritis may occur. The elevated creatinine with recent
NSAID use, low urine output, and diabetic background (compromised autoregulation)
support intrarenal injury. NSAIDs are contraindicated in CKD due to this
pathophysiology.
● Distractor A: While decreased perfusion occurs, NSAIDs primarily affect
intrarenal hemodynamics (afferent constriction) and have direct toxic effects,
making "prerenal" incomplete. Prerenal azotemia typically shows BUN:Cr ratio
>20:1 and responds to volume; this patient's intrinsic damage may not.
● Distractor C: No obstructive symptoms (hesitancy, dribbling, flank pain) are
described; postrenal AKI requires mechanical obstruction evidence.
● Distractor D: While diabetic nephropathy is present, the acute elevation
(creatinine 1.1→2.8) with temporal NSAID relationship indicates superimposed
AKI, not just chronic progression.
,Q2: Which of the following are risk factors for contrast-induced nephropathy? (Select all
that apply)
A. Pre-existing chronic kidney disease [CORRECT]
B. Diabetes mellitus [CORRECT]
C. Volume depletion [CORRECT]
D. Young age (under 30)
E. Use of iso-osmolar contrast agents [CORRECT]
F. Concurrent metformin use
Correct Answers: A, B, C, E
Rationale: Contrast-induced nephropathy (CIN) risk factors include: pre-existing CKD
(eGFR <60, strongest predictor), diabetes (especially with CKD), volume depletion
(reduces renal perfusion reserve), and high-osmolar contrast (though iso-osmolar is
safer, it's still nephrotoxic in vulnerable patients). Prevention includes hydration,
minimizing contrast volume, and using lowest osmolar contrast.
● Distractor D (Young age): Advanced age is a risk factor; youth is protective due to
greater renal reserve.
● Distractor F (Metformin): Metformin is contraindicated in severe renal
impairment due to lactic acidosis risk, but it doesn't cause CIN. The interaction is
that contrast-induced AKI increases metformin toxicity risk, requiring temporary
discontinuation.
Q3: A patient with chronic kidney disease stage 4 (eGFR 22 mL/min/1.73m²) develops
metabolic acidosis. Which compensatory mechanism is most likely to be impaired?
, A. Hyperventilation to decrease PaCO₂
B. Renal bicarbonate regeneration and hydrogen ion excretion [CORRECT]
C. Bone buffering of excess hydrogen ions
D. Cellular shift of hydrogen into tissues
Correct Answer: B
Rationale: The kidneys provide the only sustained compensation for metabolic acidosis
through: (1) bicarbonate regeneration (reclaiming filtered bicarbonate and generating
new bicarbonate), and (2) active hydrogen ion secretion (titratable acidity and
ammonium excretion). In CKD stage 4, nephron mass loss impairs these mechanisms,
leading to chronic metabolic acidosis, bone demineralization, and protein catabolism.
● Distractor A: Respiratory compensation (hyperventilation) occurs rapidly and
remains intact unless pulmonary complications exist; it's not renal
compensation.
● Distractor C: Bone buffering occurs with chronic acidosis but is pathological
(osteopenia/osteoporosis), not a primary compensatory mechanism, and is
impaired by renal osteodystrophy in CKD.
● Distractor D: Cellular buffering is immediate but limited capacity; it's not the
sustained mechanism impaired in CKD.
Q4: The progression of diabetic nephropathy from microalbuminuria to overt proteinuria
involves which key pathophysiological changes?
A. Thickening of the glomerular basement membrane and mesangial expansion leading
to decreased filtration surface area [CORRECT]
B. Primary tubular atrophy without glomerular changes
C. Acute inflammatory infiltration of the interstitium
