Care Final Exam – NR 571 / NR 571 –
Chamberlain University (2025/2026) |
Verified Questions and 100% Correct
Answers | Grade A
Comprehensive Study Assessment
Student ID: _________________ Date: _________________
Instructor: [Instructor Name] Course Mentor: [Mentor Name]
Time Limit: 120 minutes Total Points: 100 points
Instructions
This final exam consists of 100 advanced multiple-choice and case-based questions
(A–E format) designed to assess complex diagnosis and management skills for
Acute Care Nurse Practitioners (ACNPs) per Chamberlain University’s NR 571
curriculum. Questions cover differential diagnosis, pathophysiology,
evidence-based management, diagnostic reasoning,
pharmacologic/non-pharmacologic interventions, patient safety, ethical
decision-making, and interprofessional care. Select the single best answer for each
question. Answers are provided in blue with detailed rationales aligned with NR
571 objectives, AACN/AANP standards, and 2025/2026 clinical guidelines (e.g.,
AHA, ACC, ATS, IDSA). This exam reflects real-world acute care scenarios. Good
luck!
Section 1: Complex Differential Diagnosis and Pathophysiology (Questions 1–25)
A 62-year-old male presents with chest pain, diaphoresis, and nausea. ECG
shows ST-elevation in leads V1–V4. What is the most likely diagnosis?
,A. Pericarditis
B. Aortic dissection
C. Anterior wall myocardial infarction
D. Pulmonary embolism
E. Stable angina
C. Anterior wall myocardial infarction
1. Rationale: ST-elevation in V1–V4 indicates acute transmural ischemia of the
anterior wall, typically due to left anterior descending artery occlusion
(ACC/AHA, 2025). Competency: Diagnose acute coronary syndrome using
ECG.
What is the primary pathophysiological mechanism of septic shock?
A. Increased cardiac output
B. Vasodilation and capillary leak
C. Hypovolemia from hemorrhage
D. Cardiogenic pump failure
E. Neurogenic vasodilation
B. Vasodilation and capillary leak
2. Rationale: Sepsis triggers cytokine release, causing vasodilation, increased
vascular permeability, and distributive shock (SCCM, 2025). Competency:
Understand septic shock pathophysiology.
A 45-year-old female presents with sudden dyspnea and pleuritic chest pain.
CT pulmonary angiogram shows a saddle embolus. What is the most likely
source?
A. Left atrial thrombus
B. Deep vein thrombosis
C. Aortic aneurysm
D. Septic emboli
,E. Amniotic fluid embolus
B. Deep vein thrombosis
3. Rationale: Pulmonary embolism commonly arises from DVT dislodgement,
causing pulmonary artery occlusion (CHEST, 2025). Competency: Identify
pulmonary embolism etiology.
In a patient with diabetic ketoacidosis (DKA), what is the primary acid-base
disturbance?
A. Respiratory alkalosis
B. Metabolic acidosis with anion gap
C. Metabolic alkalosis
D. Respiratory acidosis
E. Mixed metabolic-respiratory acidosis
B. Metabolic acidosis with anion gap
4. Rationale: DKA causes ketone accumulation, leading to high anion gap
metabolic acidosis (ADA, 2025). Competency: Interpret acid-base disorders
in acute care.
A 70-year-old male with acute heart failure has an ejection fraction of 30%.
Which class of heart failure is this?
A. Heart failure with preserved EF (HFpEF)
B. Heart failure with reduced EF (HFrEF)
C. Heart failure with mid-range EF (HFmrEF)
D. Right-sided heart failure
E. High-output heart failure
B. Heart failure with reduced EF (HFrEF)
, 5. Rationale: EF <40% defines HFrEF, indicating systolic dysfunction (AHA,
2025). Competency: Classify heart failure types.
A 55-year-old female with COPD presents with acute respiratory distress.
ABG shows pH 7.28, PaCO2 60 mmHg, PaO2 55 mmHg. What is the
diagnosis?
A. Acute respiratory alkalosis
B. Chronic respiratory acidosis
C. Acute respiratory acidosis
D. Metabolic acidosis
E. Mixed acid-base disorder
C. Acute respiratory acidosis
6. Rationale: Elevated PaCO2 with low pH indicates acute hypoventilation,
common in COPD exacerbation (ATS, 2025). Competency: Interpret ABGs
in respiratory failure.
What is the primary mechanism of acute kidney injury (AKI) in
rhabdomyolysis?
A. Glomerular sclerosis
B. Myoglobin-induced tubular injury
C. Hypoperfusion from hypovolemia
D. Immune complex deposition
E. Ureteral obstruction
B. Myoglobin-induced tubular injury
7. Rationale: Myoglobin precipitates in tubules, causing direct toxicity and
obstruction (NKF, 2025). Competency: Understand AKI pathophysiology.