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NURS 5433: Advanced Nursing Practice
Comprehensive Examination 200 Practice
Questions with Evidence-Based
Rationales
Section 1: Advanced Pathophysiology (Q1–40)
Q1. A 45-year-old male with hypertension develops left ventricular hypertrophy.
Which of the following best explains this adaptation?
A) Increased afterload leading to myocyte stretch and hypertrophy
B) Decreased preload causing apoptosis of cardiac myocytes
C) Increased contractility due to beta-1 receptor upregulation
D) Fibrosis of the interventricular septum due to inflammation
Verified Answer: A
Rationale: Chronic hypertension increases afterload (resistance the left ventricle
must pump against). Over time, myocytes undergo hypertrophy (increase in size, not
number) to compensate. Options B and D describe maladaptive changes, and beta-1
upregulation is not the primary mechanism.
Q2. Which cytokine is primarily responsible for fever in systemic inflammation?
A) Interleukin-2
B) Interleukin-6
,C) Tumor necrosis factor-alpha
D) Interferon-gamma
Verified Answer: B
Rationale: IL-6 acts on the hypothalamus to increase prostaglandin E2 synthesis,
raising the thermoregulatory set point. TNF-alpha and IL-1 also contribute, but IL-6 is
a key pyrogen.
Q3. A patient with heart failure has decreased ejection fraction. Which
compensatory mechanism initially increases but later worsens outcomes?
A) Atrial natriuretic peptide release
B) Activation of the renin-angiotensin-aldosterone system (RAAS)
C) Increased vagal tone
D) Decreased sympathetic nervous system activity
Verified Answer: B
Rationale: RAAS activation increases preload and afterload via sodium/water
retention and vasoconstriction. While initially compensatory, chronic RAAS
activation leads to remodeling, fibrosis, and worsening HF.
Q4. A patient with type 2 diabetes develops end-stage renal disease. Which finding is
most consistent with diabetic nephropathy?
A) Ketonuria
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B) Nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)
C) Hyaline arteriolosclerosis of efferent arterioles only
D) IgA deposits in mesangium
Verified Answer: B
Rationale: Nodular glomerulosclerosis is pathognomonic for diabetic nephropathy.
Option C describes benign nephrosclerosis (hypertension). IgA nephropathy presents
with hematuria.
Q5. Which acid-base disorder is most likely in a patient with salicylate overdose?
A) Metabolic acidosis with increased anion gap
B) Metabolic alkalosis
C) Respiratory acidosis
D) Mixed metabolic acidosis and respiratory alkalosis
Verified Answer: D
Rationale: Salicylates directly stimulate respiratory center → respiratory alkalosis
(early). Later, they cause uncoupling of oxidative phosphorylation → lactic acidosis
(increased anion gap metabolic acidosis). Mixed disorder is classic.
Q6. A patient with sickle cell disease presents with acute chest pain, fever, and
hypoxemia. What is the most likely diagnosis?
A) Acute myocardial infarction
, B) Acute chest syndrome
C) Pulmonary embolism
D) Pneumonia
Verified Answer: B
Rationale: Acute chest syndrome in sickle cell disease results from vaso-occlusion in
pulmonary vasculature, often triggered by infection or hypoxia. Presents similarly to
pneumonia or PE but requires exchange transfusion.
Q7. Which laboratory finding is consistent with prerenal acute kidney injury?
A) Fractional excretion of sodium (FeNa) <1%
B) Urine sodium >40 mEq/L
C) Muddy brown casts
D) Normal BUN-to-creatinine ratio
Verified Answer: A
Rationale: FeNa <1% indicates intact tubular reabsorption of sodium, seen in
prerenal states (decreased perfusion with intact tubules). Option C (muddy brown
casts) suggests acute tubular necrosis.
Q8. A patient with cirrhosis develops asterixis and confusion. What is the primary
pathogenesis?
A) Accumulation of ammonia crossing blood-brain barrier
NURS 5433: Advanced Nursing Practice
Comprehensive Examination 200 Practice
Questions with Evidence-Based
Rationales
Section 1: Advanced Pathophysiology (Q1–40)
Q1. A 45-year-old male with hypertension develops left ventricular hypertrophy.
Which of the following best explains this adaptation?
A) Increased afterload leading to myocyte stretch and hypertrophy
B) Decreased preload causing apoptosis of cardiac myocytes
C) Increased contractility due to beta-1 receptor upregulation
D) Fibrosis of the interventricular septum due to inflammation
Verified Answer: A
Rationale: Chronic hypertension increases afterload (resistance the left ventricle
must pump against). Over time, myocytes undergo hypertrophy (increase in size, not
number) to compensate. Options B and D describe maladaptive changes, and beta-1
upregulation is not the primary mechanism.
Q2. Which cytokine is primarily responsible for fever in systemic inflammation?
A) Interleukin-2
B) Interleukin-6
,C) Tumor necrosis factor-alpha
D) Interferon-gamma
Verified Answer: B
Rationale: IL-6 acts on the hypothalamus to increase prostaglandin E2 synthesis,
raising the thermoregulatory set point. TNF-alpha and IL-1 also contribute, but IL-6 is
a key pyrogen.
Q3. A patient with heart failure has decreased ejection fraction. Which
compensatory mechanism initially increases but later worsens outcomes?
A) Atrial natriuretic peptide release
B) Activation of the renin-angiotensin-aldosterone system (RAAS)
C) Increased vagal tone
D) Decreased sympathetic nervous system activity
Verified Answer: B
Rationale: RAAS activation increases preload and afterload via sodium/water
retention and vasoconstriction. While initially compensatory, chronic RAAS
activation leads to remodeling, fibrosis, and worsening HF.
Q4. A patient with type 2 diabetes develops end-stage renal disease. Which finding is
most consistent with diabetic nephropathy?
A) Ketonuria
,3
B) Nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)
C) Hyaline arteriolosclerosis of efferent arterioles only
D) IgA deposits in mesangium
Verified Answer: B
Rationale: Nodular glomerulosclerosis is pathognomonic for diabetic nephropathy.
Option C describes benign nephrosclerosis (hypertension). IgA nephropathy presents
with hematuria.
Q5. Which acid-base disorder is most likely in a patient with salicylate overdose?
A) Metabolic acidosis with increased anion gap
B) Metabolic alkalosis
C) Respiratory acidosis
D) Mixed metabolic acidosis and respiratory alkalosis
Verified Answer: D
Rationale: Salicylates directly stimulate respiratory center → respiratory alkalosis
(early). Later, they cause uncoupling of oxidative phosphorylation → lactic acidosis
(increased anion gap metabolic acidosis). Mixed disorder is classic.
Q6. A patient with sickle cell disease presents with acute chest pain, fever, and
hypoxemia. What is the most likely diagnosis?
A) Acute myocardial infarction
, B) Acute chest syndrome
C) Pulmonary embolism
D) Pneumonia
Verified Answer: B
Rationale: Acute chest syndrome in sickle cell disease results from vaso-occlusion in
pulmonary vasculature, often triggered by infection or hypoxia. Presents similarly to
pneumonia or PE but requires exchange transfusion.
Q7. Which laboratory finding is consistent with prerenal acute kidney injury?
A) Fractional excretion of sodium (FeNa) <1%
B) Urine sodium >40 mEq/L
C) Muddy brown casts
D) Normal BUN-to-creatinine ratio
Verified Answer: A
Rationale: FeNa <1% indicates intact tubular reabsorption of sodium, seen in
prerenal states (decreased perfusion with intact tubules). Option C (muddy brown
casts) suggests acute tubular necrosis.
Q8. A patient with cirrhosis develops asterixis and confusion. What is the primary
pathogenesis?
A) Accumulation of ammonia crossing blood-brain barrier
