NURS 546 EXAM 2
Comprehensive Practice Examination
Questions with Complete Solutions
Academic Year
Course NURS 546 / NUR 5461 - Advanced Pathophysiology
Exam Examination 2 - Practice Set
Total Questions 100 Multiple Choice Questions
Cognitive Mix 20% Recall | 50% Application | 30% Analysis
Question Style 75% Scenario-Based | 25% Direct Knowledge
Sections 5 (Acid-Base, Cardiovascular, Hematologic, Pulmonary, Cases)
Format 4 options (A-D) with complete rationales
Audience Graduate Nursing & Advanced Practice Students
Examination Content Overview
This comprehensive practice examination is aligned with the NURS 546 Advanced Pathophysiology
Course Syllabus and covers core topics including acid-base balance and compensation mechanisms,
cardiovascular pathophysiology (heart failure, shock, hypertension, ischemic heart disease),
hematologic pathophysiology (hemolysis, thrombosis, sepsis, anemia), and pulmonary
pathophysiology (gas exchange, V/Q matching, COPD, asthma, ARDS, pulmonary embolism). The
Page 1
,NURS 546 Exam 2 - Comprehensive Practice Examination (2026/2027)
final section integrates multiple systems in complex clinical case scenarios requiring advanced clinical
reasoning.
Page 2
,NURS 546 Exam 2 - Comprehensive Practice Examination (2026/2027)
Section 1: Acid-Base Balance, Buffers, & Compensation
25 questions covering chemical buffer systems, Henderson-Hasselbalch equation, renal and respiratory compensation,
metabolic and respiratory acidosis/alkalosis, and ABG interpretation.
Q1: A 52-year-old female presents to the emergency department with severe vomiting and diarrhea for 3 days.
ABG analysis reveals pH 7.29, PaCO2 34 mmHg, HCO3- 18 mEq/L. The body's FIRST and MOST
IMMEDIATE defense against this acid-base disturbance is mediated by which mechanism?
A. Renal excretion of hydrogen ions into the distal tubule (onset: hours to days)
B. Respiratory compensation via hyperventilation to reduce PaCO2 (onset: minutes to hours)
C. Chemical buffer systems (bicarbonate, phosphate, proteins) acting within seconds *[CORRECT]*
D. Hepatic metabolism of lactic acid to glucose via the Cori cycle (onset: minutes)
Correct Answer: C
Rationale: Chemical buffers are the body's first-line defense against acid-base imbalances, acting immediately within
seconds to minimize pH changes by binding or releasing H+ ions. The bicarbonate, phosphate, and protein buffer systems
respond instantaneously, whereas respiratory compensation requires minutes to hours and renal compensation requires
hours to days. The patient's ABG demonstrates metabolic acidosis (low pH, low HCO3-) with partial respiratory
compensation (low PaCO2), but buffers acted first to prevent lethal pH shifts.
Q2: A patient with chronic COPD has an arterial pH of 7.38, PaCO2 of 60 mmHg, and HCO3- of 34 mEq/L.
Applying the Henderson-Hasselbalch equation (pH = 6.1 + log[HCO3-]/(0.03 x PaCO2)), the
bicarbonate-to-carbonic acid ratio in this patient is approximately:
A. 10:1
B. 20:1 *[CORRECT]*
C. 30:1
D. 40:1
Correct Answer: B
Rationale: The Henderson-Hasselbalch equation defines the relationship between pH, bicarbonate, and dissolved CO2. For
this patient: HCO3-/(0.03 x PaCO2) = 34/(0.03 x 60) = 34/1.8 = approximately 19:1, which rounds to 20:1, the same ratio
that maintains a normal pH of 7.40. Despite elevated PaCO2 (chronic CO2 retention), renal compensation has elevated
HCO3- proportionally to keep the ratio near 20:1, producing the near-normal pH of 7.38.
Q3: A 68-year-old male with chronic kidney disease (stage 4) develops metabolic acidosis. The kidney's
primary compensatory mechanisms for acid-base balance include which pair of processes?
A. Reabsorption of hydrogen ions and excretion of bicarbonate in the proximal tubule
B. Excretion of hydrogen ions (as titratable acid and NH4+) and reabsorption/regeneration of bicarbonate
*[CORRECT]*
C. Secretion of bicarbonate into the distal tubule and reabsorption of chloride
D. Conversion of CO2 to carbonic acid in the glomerulus and passive diffusion of H+ into urine
Correct Answer: B
Rationale: The kidney maintains acid-base balance by excreting hydrogen ions (as titratable acid buffered by phosphate and
as ammonium (NH4+)) while simultaneously reabsorbing filtered bicarbonate and generating new bicarbonate. In chronic
kidney disease, reduced nephron mass impairs both NH4+ excretion and HCO3- regeneration, leading to metabolic acidosis.
Renal compensation is slow (hours to days) but sustained, unlike the rapid but limited respiratory compensation.
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, NURS 546 Exam 2 - Comprehensive Practice Examination (2026/2027)
Q4: A 19-year-old patient with type 1 diabetes presents with DKA. ABG: pH 7.20, PaCO2 24 mmHg, HCO3-
9 mEq/L. Which compensatory mechanism is MOST responsible for the reduced PaCO2?
A. Decreased renal bicarbonate excretion
B. Kussmaul respirations (hyperventilation) to expel CO2 *[CORRECT]*
C. Hypoventilation to retain CO2 and lower pH further
D. Increased chloride shift in erythrocytes
Correct Answer: B
Rationale: In metabolic acidosis, the primary compensatory mechanism is increased respiratory rate (hyperventilation,
termed Kussmaul respirations when severe) to expel CO2 and lower PaCO2, thereby raising pH back toward normal. The
patient's PaCO2 of 24 mmHg reflects appropriate respiratory compensation for severe metabolic acidosis. Renal
compensation (choice A) is too slow to be effective in acute DKA, and choice C would worsen acidemia.
Q5: A 24-year-old with new-onset type 1 diabetes is admitted with DKA (glucose 612 mg/dL, pH 7.18, HCO3-
8 mEq/L). The PRIMARY pathophysiologic mechanism producing the metabolic acidosis is:
A. Lactic acid accumulation from tissue hypoperfusion alone
B. Hepatic ketone body production (beta-hydroxybutyrate, acetoacetate) from unrestrained lipolysis
*[CORRECT]*
C. Renal bicarbonate wasting from osmotic diuresis
D. Accumulation of sulfates and phosphates from catabolism
Correct Answer: B
Rationale: DKA produces metabolic acidosis primarily through hepatic ketogenesis: insulin deficiency and
counter-regulatory hormone excess (glucagon, cortisol, catecholamines) drive unrestrained lipolysis, releasing free fatty
acids that the liver converts to ketoacids (beta-hydroxybutyrate and acetoacetate). These strong acids consume bicarbonate,
producing a high-anion-gap metabolic acidosis. While lactic acidosis and renal bicarbonate wasting may coexist, ketone
production is the dominant mechanism in DKA.
Q6: A 72-year-old male with stage 5 CKD has pH 7.28, PaCO2 32 mmHg, HCO3- 14 mEq/L. The metabolic
acidosis in renal failure is BEST explained by:
A. Excessive GI bicarbonate loss from diarrhea
B. Inability to excrete daily acid load (NH4+ production impaired) and reabsorb/generate HCO3-
*[CORRECT]*
C. Accumulation of ketones from impaired glucose metabolism
D. Hypoventilation causing primary CO2 retention
Correct Answer: B
Rationale: Renal failure causes metabolic acidosis primarily through the kidney's inability to excrete the daily acid load
(impaired NH4+ excretion) and to regenerate/reabsorb bicarbonate. This produces a high-anion-gap metabolic acidosis from
accumulation of sulfates, phosphates, and organic acids, combined with a hyperchloremic component from reduced HCO3-
reabsorption. Choice D would produce respiratory acidosis, and choices A and C describe different etiologies.
Page 4
Comprehensive Practice Examination
Questions with Complete Solutions
Academic Year
Course NURS 546 / NUR 5461 - Advanced Pathophysiology
Exam Examination 2 - Practice Set
Total Questions 100 Multiple Choice Questions
Cognitive Mix 20% Recall | 50% Application | 30% Analysis
Question Style 75% Scenario-Based | 25% Direct Knowledge
Sections 5 (Acid-Base, Cardiovascular, Hematologic, Pulmonary, Cases)
Format 4 options (A-D) with complete rationales
Audience Graduate Nursing & Advanced Practice Students
Examination Content Overview
This comprehensive practice examination is aligned with the NURS 546 Advanced Pathophysiology
Course Syllabus and covers core topics including acid-base balance and compensation mechanisms,
cardiovascular pathophysiology (heart failure, shock, hypertension, ischemic heart disease),
hematologic pathophysiology (hemolysis, thrombosis, sepsis, anemia), and pulmonary
pathophysiology (gas exchange, V/Q matching, COPD, asthma, ARDS, pulmonary embolism). The
Page 1
,NURS 546 Exam 2 - Comprehensive Practice Examination (2026/2027)
final section integrates multiple systems in complex clinical case scenarios requiring advanced clinical
reasoning.
Page 2
,NURS 546 Exam 2 - Comprehensive Practice Examination (2026/2027)
Section 1: Acid-Base Balance, Buffers, & Compensation
25 questions covering chemical buffer systems, Henderson-Hasselbalch equation, renal and respiratory compensation,
metabolic and respiratory acidosis/alkalosis, and ABG interpretation.
Q1: A 52-year-old female presents to the emergency department with severe vomiting and diarrhea for 3 days.
ABG analysis reveals pH 7.29, PaCO2 34 mmHg, HCO3- 18 mEq/L. The body's FIRST and MOST
IMMEDIATE defense against this acid-base disturbance is mediated by which mechanism?
A. Renal excretion of hydrogen ions into the distal tubule (onset: hours to days)
B. Respiratory compensation via hyperventilation to reduce PaCO2 (onset: minutes to hours)
C. Chemical buffer systems (bicarbonate, phosphate, proteins) acting within seconds *[CORRECT]*
D. Hepatic metabolism of lactic acid to glucose via the Cori cycle (onset: minutes)
Correct Answer: C
Rationale: Chemical buffers are the body's first-line defense against acid-base imbalances, acting immediately within
seconds to minimize pH changes by binding or releasing H+ ions. The bicarbonate, phosphate, and protein buffer systems
respond instantaneously, whereas respiratory compensation requires minutes to hours and renal compensation requires
hours to days. The patient's ABG demonstrates metabolic acidosis (low pH, low HCO3-) with partial respiratory
compensation (low PaCO2), but buffers acted first to prevent lethal pH shifts.
Q2: A patient with chronic COPD has an arterial pH of 7.38, PaCO2 of 60 mmHg, and HCO3- of 34 mEq/L.
Applying the Henderson-Hasselbalch equation (pH = 6.1 + log[HCO3-]/(0.03 x PaCO2)), the
bicarbonate-to-carbonic acid ratio in this patient is approximately:
A. 10:1
B. 20:1 *[CORRECT]*
C. 30:1
D. 40:1
Correct Answer: B
Rationale: The Henderson-Hasselbalch equation defines the relationship between pH, bicarbonate, and dissolved CO2. For
this patient: HCO3-/(0.03 x PaCO2) = 34/(0.03 x 60) = 34/1.8 = approximately 19:1, which rounds to 20:1, the same ratio
that maintains a normal pH of 7.40. Despite elevated PaCO2 (chronic CO2 retention), renal compensation has elevated
HCO3- proportionally to keep the ratio near 20:1, producing the near-normal pH of 7.38.
Q3: A 68-year-old male with chronic kidney disease (stage 4) develops metabolic acidosis. The kidney's
primary compensatory mechanisms for acid-base balance include which pair of processes?
A. Reabsorption of hydrogen ions and excretion of bicarbonate in the proximal tubule
B. Excretion of hydrogen ions (as titratable acid and NH4+) and reabsorption/regeneration of bicarbonate
*[CORRECT]*
C. Secretion of bicarbonate into the distal tubule and reabsorption of chloride
D. Conversion of CO2 to carbonic acid in the glomerulus and passive diffusion of H+ into urine
Correct Answer: B
Rationale: The kidney maintains acid-base balance by excreting hydrogen ions (as titratable acid buffered by phosphate and
as ammonium (NH4+)) while simultaneously reabsorbing filtered bicarbonate and generating new bicarbonate. In chronic
kidney disease, reduced nephron mass impairs both NH4+ excretion and HCO3- regeneration, leading to metabolic acidosis.
Renal compensation is slow (hours to days) but sustained, unlike the rapid but limited respiratory compensation.
Page 3
, NURS 546 Exam 2 - Comprehensive Practice Examination (2026/2027)
Q4: A 19-year-old patient with type 1 diabetes presents with DKA. ABG: pH 7.20, PaCO2 24 mmHg, HCO3-
9 mEq/L. Which compensatory mechanism is MOST responsible for the reduced PaCO2?
A. Decreased renal bicarbonate excretion
B. Kussmaul respirations (hyperventilation) to expel CO2 *[CORRECT]*
C. Hypoventilation to retain CO2 and lower pH further
D. Increased chloride shift in erythrocytes
Correct Answer: B
Rationale: In metabolic acidosis, the primary compensatory mechanism is increased respiratory rate (hyperventilation,
termed Kussmaul respirations when severe) to expel CO2 and lower PaCO2, thereby raising pH back toward normal. The
patient's PaCO2 of 24 mmHg reflects appropriate respiratory compensation for severe metabolic acidosis. Renal
compensation (choice A) is too slow to be effective in acute DKA, and choice C would worsen acidemia.
Q5: A 24-year-old with new-onset type 1 diabetes is admitted with DKA (glucose 612 mg/dL, pH 7.18, HCO3-
8 mEq/L). The PRIMARY pathophysiologic mechanism producing the metabolic acidosis is:
A. Lactic acid accumulation from tissue hypoperfusion alone
B. Hepatic ketone body production (beta-hydroxybutyrate, acetoacetate) from unrestrained lipolysis
*[CORRECT]*
C. Renal bicarbonate wasting from osmotic diuresis
D. Accumulation of sulfates and phosphates from catabolism
Correct Answer: B
Rationale: DKA produces metabolic acidosis primarily through hepatic ketogenesis: insulin deficiency and
counter-regulatory hormone excess (glucagon, cortisol, catecholamines) drive unrestrained lipolysis, releasing free fatty
acids that the liver converts to ketoacids (beta-hydroxybutyrate and acetoacetate). These strong acids consume bicarbonate,
producing a high-anion-gap metabolic acidosis. While lactic acidosis and renal bicarbonate wasting may coexist, ketone
production is the dominant mechanism in DKA.
Q6: A 72-year-old male with stage 5 CKD has pH 7.28, PaCO2 32 mmHg, HCO3- 14 mEq/L. The metabolic
acidosis in renal failure is BEST explained by:
A. Excessive GI bicarbonate loss from diarrhea
B. Inability to excrete daily acid load (NH4+ production impaired) and reabsorb/generate HCO3-
*[CORRECT]*
C. Accumulation of ketones from impaired glucose metabolism
D. Hypoventilation causing primary CO2 retention
Correct Answer: B
Rationale: Renal failure causes metabolic acidosis primarily through the kidney's inability to excrete the daily acid load
(impaired NH4+ excretion) and to regenerate/reabsorb bicarbonate. This produces a high-anion-gap metabolic acidosis from
accumulation of sulfates, phosphates, and organic acids, combined with a hyperchloremic component from reduced HCO3-
reabsorption. Choice D would produce respiratory acidosis, and choices A and C describe different etiologies.
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