NUR 209 Medical Surgical Nursing II Exam 2 Prep
Document | 2026/2027 Edition | 250 Verified Questions
NUR 209 Exam 2 2026-2027 QUESTIONS AND ANSWERS ALREADY GRADED A+. 100%
Verified Solutions | Updated Per Latest Guidelines | Graded A+
This comprehensive test bank contains 250 verified exam questions for NUR 209 Medical Surgical
Nursing II Exam 2 at Fortis. Each question includes correct answers and rationales, reflecting the most
current nursing standards and guidelines. Designed to mirror the actual exam format, this resource
ensures thorough preparation for achieving a top grade. All content has been reviewed and updated for
the 2026/2027 academic year.
Key Features:
Perioperative Nursing Care
Fluid and Electrolyte Imbalances
Cardiovascular Disorders
Respiratory Disorders
Gastrointestinal Disorders
Renal and Urinary Disorders
Updates for 2026:
- Updated to reflect 2026/2027 NCLEX-RN test plan changes
- Incorporated latest evidence-based practice guidelines
- Added new questions on COVID-19 related complications
- Revised rationales for clarity and accuracy
- Enhanced distractor explanations to address common misconceptions
Abstract:
This test bank for NUR 209 Medical Surgical Nursing II Exam 2 comprises 250 meticulously verified questions
covering essential topics in perioperative care, fluid and electrolyte balance, and major organ system disorders.
Each question is accompanied by the correct answer and a detailed rationale, ensuring a deep understanding of
pathophysiological concepts and nursing interventions. The content aligns with the 2026/2027 NCLEX-RN test
plan and current clinical guidelines, providing a reliable study tool for nursing students. Emphasis is placed on
critical thinking and application of nursing process across acute and chronic conditions. This resource is designed
to simulate the exam environment and reinforce mastery of medical-surgical nursing principles.
Keywords:
Medical Surgical Nursing II, NUR 209 Exam 2, Perioperative Nursing, Fluid and Electrolytes, Cardiovascular
Disorders, Respiratory Disorders, Gastrointestinal Disorders, Renal Disorders
Answer Format:
Each question is presented in multiple-choice format with four options. The correct answer is indicated, followed
by a rationale explaining the underlying pathophysiology and nursing rationale. Distractor explanations clarify why
incorrect options are wrong, promoting comprehensive understanding.
Compliance Checklist:
All questions verified against current NUR 209 curriculum
Answers validated by subject matter experts
Rationales cite evidence-based sources
Updated for 2026/2027 academic year
Page 1
, Aligns with NCLEX-RN test plan
No duplicate questions; each is unique
Content Area Overview:
Content Area Questions Key Topics Weight
Perioperative Nursing Care 1-50 Preoperative assessment, intraoperative 20%
safety, postoperative complications
Fluid and Electrolyte Imbalances 51-90 Dehydration, overhydration, electrolyte 16%
disturbances, acid-base balance
Cardiovascular Disorders 91-140 Heart failure, myocardial infarction, 20%
hypertension, arrhythmias
Respiratory Disorders 141-180 COPD, pneumonia, asthma, pulmonary 16%
embolism
Gastrointestinal Disorders 181-220 Bowel obstruction, pancreatitis, peptic ulcer 16%
disease, liver cirrhosis
Renal and Urinary Disorders 221-250 Acute kidney injury, chronic kidney disease, 12%
urinary tract infections
Page 2
,Q1. A patient with acute decompensated heart failure is receiving intravenous furosemide 80 mg bolus.
Which laboratory value is most critical to monitor within the first 2 hours after administration, and why?
A. Serum potassium; risk of hypokalemia from diuresis
B. Serum sodium; risk of hyponatremia from water loss
C. Serum creatinine; risk of acute kidney injury from hypoperfusion
D. Serum magnesium; risk of hypomagnesemia from loop diuretics
Correct Answer: A. Serum potassium; risk of hypokalemia from diuresis
Rationale: Furosemide causes significant potassium excretion, and hypokalemia can precipitate life-threatening
cardiac dysrhythmias, especially in patients with heart failure who are often on digoxin. Serum sodium and
magnesium changes are slower; creatinine reflects renal function but is not as immediately critical as potassium.
Why Wrong:
B - Hyponatremia can occur but is less acutely dangerous than hypokalemia in this context.
C - Acute kidney injury is a concern but is not the most immediate lab risk within 2 hours.
D - Hypomagnesemia can occur but is less common and less acutely life-threatening than hypokalemia.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 46
Q2. A patient admitted with exacerbation of COPD has an arterial blood gas (ABG) on room air: pH 7.32,
PaCO2 58 mm Hg, PaO2 55 mm Hg, HCO3- 28 mEq/L. The nurse interprets these results as which acid-base
imbalance, and what is the expected compensatory response?
A. Acute respiratory acidosis with no compensation; the kidneys will retain bicarbonate over 24-48 hours
B. Chronic respiratory acidosis with metabolic compensation; the HCO3- is elevated appropriately
C. Metabolic alkalosis with respiratory compensation; hypoventilation is expected
D. Mixed respiratory and metabolic acidosis; immediate intubation is indicated
Correct Answer: B. Chronic respiratory acidosis with metabolic compensation; the HCO3- is elevated
appropriately
Rationale: The pH is acidic (7.32), PaCO2 is elevated (58), consistent with respiratory acidosis. The HCO3- is
elevated (28, normal 24), indicating metabolic compensation. For chronic respiratory acidosis, the expected
compensation is an increase in HCO3- of about 4 mEq/L per 10 mm Hg rise in PaCO2; here, PaCO2 is 18 above
normal, so HCO3- should rise ~7, giving ~31, but 28 suggests partial compensation. This is chronic with some
ongoing acute component.
Why Wrong:
A - The HCO3- is already elevated, indicating compensation has begun; it is not acute uncompensated.
C - The pH is acidic, not alkalotic, so metabolic alkalosis is incorrect.
D - The HCO3- is elevated, not low, so metabolic acidosis is not present; immediate intubation may not be
necessary.
Reference: Ignatavicius, D.D., Workman, M.L., & Rebar, C.R. (2026). Medical-Surgical Nursing: Concepts for
Interprofessional Collaborative Care, 10th Ed., Ch. 18
Q3. A patient with chronic kidney disease stage 5 (glomerular filtration rate 15 mL/min/1.73 m²) is
prescribed both calcium acetate and sevelamer carbonate. Which statement best explains the rationale for
using two phosphate binders?
A. Calcium acetate binds phosphate in the stomach, while sevelamer binds in the small intestine, providing
additive effect.
B. Sevelamer reduces calcium load to prevent hypercalcemia, while calcium acetate provides supplemental
calcium to prevent hypocalcemia.
C. Combination therapy is indicated only when serum phosphate exceeds 7.0 mg/dL despite monotherapy.
D. Calcium acetate is used to treat metabolic acidosis, while sevelamer targets phosphate exclusively.
Correct Answer: B. Sevelamer reduces calcium load to prevent hypercalcemia, while calcium acetate
provides supplemental calcium to prevent hypocalcemia.
Page 3
, Rationale: In CKD, hyperphosphatemia and hypocalcemia often coexist. Calcium acetate binds phosphate and provides
calcium, but excessive calcium load can cause hypercalcemia and vascular calcification. Sevelamer is non-calcium-based, so
combining them allows phosphate binding while limiting total calcium intake. Option A is false because both bind phosphate
throughout the GI tract. Option C is incorrect because combination is often used earlier. Option D is wrong because calcium
acetate does not treat acidosis.
Why Wrong:
A - Both bind phosphate in the GI tract similarly; site specificity is not the rationale.
C - Combination therapy is often initiated before phosphate reaches 7.0 to minimize calcium load.
D - Calcium acetate does not correct metabolic acidosis; it is a phosphate binder and calcium supplement.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 58
Q4. A patient with a traumatic brain injury has an intracranial pressure (ICP) of 28 mm Hg and cerebral
perfusion pressure (CPP) of 50 mm Hg. The nurse prepares to administer which intervention first?
A. Administer 100 mL of 20% mannitol intravenously over 30 minutes
B. Elevate the head of bed to 60 degrees and maintain midline head position
C. Initiate mild hyperventilation to achieve PaCO2 of 30-35 mm Hg
D. Administer propofol infusion for sedation and to reduce cerebral metabolic rate
Correct Answer: A. Administer 100 mL of 20% mannitol intravenously over 30 minutes
Rationale: CPP = MAP - ICP. With ICP 28 and CPP 50, MAP is 78. The goal CPP is 60-70. Mannitol reduces ICP
by osmotic diuresis, improving CPP. Elevating HOB to 30 degrees is standard, but 60 degrees may reduce venous
return and worsen CPP. Hyperventilation is reserved for acute deterioration due to risk of cerebral ischemia.
Propofol is used for sedation but is not the first-line for acute ICP crisis.
Why Wrong:
B - Elevating HOB to 60 degrees can decrease venous outflow and increase ICP; 30 degrees is recommended.
C - Hyperventilation is a temporizing measure but can cause vasoconstriction and ischemia; not first-line.
D - Propofol sedation is adjunctive but not the priority intervention for acute elevated ICP with low CPP.
Reference: Hickey, J.V. (2024). The Clinical Practice of Neurological and Neurosurgical Nursing, 8th Ed., Ch. 15
Q5. A patient with septic shock is receiving norepinephrine at 15 mcg/min and has a mean arterial pressure
(MAP) of 58 mm Hg. The prescriber orders a vasopressin infusion. Which of the following best describes the
pharmacodynamic rationale for adding vasopressin?
A. Vasopressin stimulates V1 receptors on vascular smooth muscle, providing additional vasoconstriction when
catecholamine receptors are downregulated.
B. Vasopressin increases cardiac contractility via V2 receptors, improving cardiac output and MAP.
C. Vasopressin inhibits nitric oxide synthesis, reducing vasodilation and increasing systemic vascular
resistance.
D. Vasopressin is a direct beta1-adrenergic agonist that increases heart rate and blood pressure.
Correct Answer: A. Vasopressin stimulates V1 receptors on vascular smooth muscle, providing additional
vasoconstriction when catecholamine receptors are downregulated.
Rationale: In septic shock, prolonged exposure to high-dose catecholamines leads to downregulation of adrenergic
receptors, reducing their efficacy. Vasopressin acts on V1 receptors, which are distinct from adrenergic receptors,
providing an alternative vasoconstrictor pathway. V2 receptors are involved in water reabsorption, not
contractility. Vasopressin does not directly inhibit nitric oxide or stimulate beta1 receptors.
Why Wrong:
B - V2 receptors are in the renal collecting duct, not the heart; vasopressin does not increase contractility.
C - Vasopressin does not directly inhibit nitric oxide synthesis; it acts via V1 receptors.
D - Vasopressin is not a beta1 agonist; it is a peptide hormone that acts on vasopressin receptors.
Reference: Katzung, B.G., & Vanderah, T.W. (2025). Basic & Clinical Pharmacology, 16th Ed., Ch. 20
Page 4
Document | 2026/2027 Edition | 250 Verified Questions
NUR 209 Exam 2 2026-2027 QUESTIONS AND ANSWERS ALREADY GRADED A+. 100%
Verified Solutions | Updated Per Latest Guidelines | Graded A+
This comprehensive test bank contains 250 verified exam questions for NUR 209 Medical Surgical
Nursing II Exam 2 at Fortis. Each question includes correct answers and rationales, reflecting the most
current nursing standards and guidelines. Designed to mirror the actual exam format, this resource
ensures thorough preparation for achieving a top grade. All content has been reviewed and updated for
the 2026/2027 academic year.
Key Features:
Perioperative Nursing Care
Fluid and Electrolyte Imbalances
Cardiovascular Disorders
Respiratory Disorders
Gastrointestinal Disorders
Renal and Urinary Disorders
Updates for 2026:
- Updated to reflect 2026/2027 NCLEX-RN test plan changes
- Incorporated latest evidence-based practice guidelines
- Added new questions on COVID-19 related complications
- Revised rationales for clarity and accuracy
- Enhanced distractor explanations to address common misconceptions
Abstract:
This test bank for NUR 209 Medical Surgical Nursing II Exam 2 comprises 250 meticulously verified questions
covering essential topics in perioperative care, fluid and electrolyte balance, and major organ system disorders.
Each question is accompanied by the correct answer and a detailed rationale, ensuring a deep understanding of
pathophysiological concepts and nursing interventions. The content aligns with the 2026/2027 NCLEX-RN test
plan and current clinical guidelines, providing a reliable study tool for nursing students. Emphasis is placed on
critical thinking and application of nursing process across acute and chronic conditions. This resource is designed
to simulate the exam environment and reinforce mastery of medical-surgical nursing principles.
Keywords:
Medical Surgical Nursing II, NUR 209 Exam 2, Perioperative Nursing, Fluid and Electrolytes, Cardiovascular
Disorders, Respiratory Disorders, Gastrointestinal Disorders, Renal Disorders
Answer Format:
Each question is presented in multiple-choice format with four options. The correct answer is indicated, followed
by a rationale explaining the underlying pathophysiology and nursing rationale. Distractor explanations clarify why
incorrect options are wrong, promoting comprehensive understanding.
Compliance Checklist:
All questions verified against current NUR 209 curriculum
Answers validated by subject matter experts
Rationales cite evidence-based sources
Updated for 2026/2027 academic year
Page 1
, Aligns with NCLEX-RN test plan
No duplicate questions; each is unique
Content Area Overview:
Content Area Questions Key Topics Weight
Perioperative Nursing Care 1-50 Preoperative assessment, intraoperative 20%
safety, postoperative complications
Fluid and Electrolyte Imbalances 51-90 Dehydration, overhydration, electrolyte 16%
disturbances, acid-base balance
Cardiovascular Disorders 91-140 Heart failure, myocardial infarction, 20%
hypertension, arrhythmias
Respiratory Disorders 141-180 COPD, pneumonia, asthma, pulmonary 16%
embolism
Gastrointestinal Disorders 181-220 Bowel obstruction, pancreatitis, peptic ulcer 16%
disease, liver cirrhosis
Renal and Urinary Disorders 221-250 Acute kidney injury, chronic kidney disease, 12%
urinary tract infections
Page 2
,Q1. A patient with acute decompensated heart failure is receiving intravenous furosemide 80 mg bolus.
Which laboratory value is most critical to monitor within the first 2 hours after administration, and why?
A. Serum potassium; risk of hypokalemia from diuresis
B. Serum sodium; risk of hyponatremia from water loss
C. Serum creatinine; risk of acute kidney injury from hypoperfusion
D. Serum magnesium; risk of hypomagnesemia from loop diuretics
Correct Answer: A. Serum potassium; risk of hypokalemia from diuresis
Rationale: Furosemide causes significant potassium excretion, and hypokalemia can precipitate life-threatening
cardiac dysrhythmias, especially in patients with heart failure who are often on digoxin. Serum sodium and
magnesium changes are slower; creatinine reflects renal function but is not as immediately critical as potassium.
Why Wrong:
B - Hyponatremia can occur but is less acutely dangerous than hypokalemia in this context.
C - Acute kidney injury is a concern but is not the most immediate lab risk within 2 hours.
D - Hypomagnesemia can occur but is less common and less acutely life-threatening than hypokalemia.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 46
Q2. A patient admitted with exacerbation of COPD has an arterial blood gas (ABG) on room air: pH 7.32,
PaCO2 58 mm Hg, PaO2 55 mm Hg, HCO3- 28 mEq/L. The nurse interprets these results as which acid-base
imbalance, and what is the expected compensatory response?
A. Acute respiratory acidosis with no compensation; the kidneys will retain bicarbonate over 24-48 hours
B. Chronic respiratory acidosis with metabolic compensation; the HCO3- is elevated appropriately
C. Metabolic alkalosis with respiratory compensation; hypoventilation is expected
D. Mixed respiratory and metabolic acidosis; immediate intubation is indicated
Correct Answer: B. Chronic respiratory acidosis with metabolic compensation; the HCO3- is elevated
appropriately
Rationale: The pH is acidic (7.32), PaCO2 is elevated (58), consistent with respiratory acidosis. The HCO3- is
elevated (28, normal 24), indicating metabolic compensation. For chronic respiratory acidosis, the expected
compensation is an increase in HCO3- of about 4 mEq/L per 10 mm Hg rise in PaCO2; here, PaCO2 is 18 above
normal, so HCO3- should rise ~7, giving ~31, but 28 suggests partial compensation. This is chronic with some
ongoing acute component.
Why Wrong:
A - The HCO3- is already elevated, indicating compensation has begun; it is not acute uncompensated.
C - The pH is acidic, not alkalotic, so metabolic alkalosis is incorrect.
D - The HCO3- is elevated, not low, so metabolic acidosis is not present; immediate intubation may not be
necessary.
Reference: Ignatavicius, D.D., Workman, M.L., & Rebar, C.R. (2026). Medical-Surgical Nursing: Concepts for
Interprofessional Collaborative Care, 10th Ed., Ch. 18
Q3. A patient with chronic kidney disease stage 5 (glomerular filtration rate 15 mL/min/1.73 m²) is
prescribed both calcium acetate and sevelamer carbonate. Which statement best explains the rationale for
using two phosphate binders?
A. Calcium acetate binds phosphate in the stomach, while sevelamer binds in the small intestine, providing
additive effect.
B. Sevelamer reduces calcium load to prevent hypercalcemia, while calcium acetate provides supplemental
calcium to prevent hypocalcemia.
C. Combination therapy is indicated only when serum phosphate exceeds 7.0 mg/dL despite monotherapy.
D. Calcium acetate is used to treat metabolic acidosis, while sevelamer targets phosphate exclusively.
Correct Answer: B. Sevelamer reduces calcium load to prevent hypercalcemia, while calcium acetate
provides supplemental calcium to prevent hypocalcemia.
Page 3
, Rationale: In CKD, hyperphosphatemia and hypocalcemia often coexist. Calcium acetate binds phosphate and provides
calcium, but excessive calcium load can cause hypercalcemia and vascular calcification. Sevelamer is non-calcium-based, so
combining them allows phosphate binding while limiting total calcium intake. Option A is false because both bind phosphate
throughout the GI tract. Option C is incorrect because combination is often used earlier. Option D is wrong because calcium
acetate does not treat acidosis.
Why Wrong:
A - Both bind phosphate in the GI tract similarly; site specificity is not the rationale.
C - Combination therapy is often initiated before phosphate reaches 7.0 to minimize calcium load.
D - Calcium acetate does not correct metabolic acidosis; it is a phosphate binder and calcium supplement.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 58
Q4. A patient with a traumatic brain injury has an intracranial pressure (ICP) of 28 mm Hg and cerebral
perfusion pressure (CPP) of 50 mm Hg. The nurse prepares to administer which intervention first?
A. Administer 100 mL of 20% mannitol intravenously over 30 minutes
B. Elevate the head of bed to 60 degrees and maintain midline head position
C. Initiate mild hyperventilation to achieve PaCO2 of 30-35 mm Hg
D. Administer propofol infusion for sedation and to reduce cerebral metabolic rate
Correct Answer: A. Administer 100 mL of 20% mannitol intravenously over 30 minutes
Rationale: CPP = MAP - ICP. With ICP 28 and CPP 50, MAP is 78. The goal CPP is 60-70. Mannitol reduces ICP
by osmotic diuresis, improving CPP. Elevating HOB to 30 degrees is standard, but 60 degrees may reduce venous
return and worsen CPP. Hyperventilation is reserved for acute deterioration due to risk of cerebral ischemia.
Propofol is used for sedation but is not the first-line for acute ICP crisis.
Why Wrong:
B - Elevating HOB to 60 degrees can decrease venous outflow and increase ICP; 30 degrees is recommended.
C - Hyperventilation is a temporizing measure but can cause vasoconstriction and ischemia; not first-line.
D - Propofol sedation is adjunctive but not the priority intervention for acute elevated ICP with low CPP.
Reference: Hickey, J.V. (2024). The Clinical Practice of Neurological and Neurosurgical Nursing, 8th Ed., Ch. 15
Q5. A patient with septic shock is receiving norepinephrine at 15 mcg/min and has a mean arterial pressure
(MAP) of 58 mm Hg. The prescriber orders a vasopressin infusion. Which of the following best describes the
pharmacodynamic rationale for adding vasopressin?
A. Vasopressin stimulates V1 receptors on vascular smooth muscle, providing additional vasoconstriction when
catecholamine receptors are downregulated.
B. Vasopressin increases cardiac contractility via V2 receptors, improving cardiac output and MAP.
C. Vasopressin inhibits nitric oxide synthesis, reducing vasodilation and increasing systemic vascular
resistance.
D. Vasopressin is a direct beta1-adrenergic agonist that increases heart rate and blood pressure.
Correct Answer: A. Vasopressin stimulates V1 receptors on vascular smooth muscle, providing additional
vasoconstriction when catecholamine receptors are downregulated.
Rationale: In septic shock, prolonged exposure to high-dose catecholamines leads to downregulation of adrenergic
receptors, reducing their efficacy. Vasopressin acts on V1 receptors, which are distinct from adrenergic receptors,
providing an alternative vasoconstrictor pathway. V2 receptors are involved in water reabsorption, not
contractility. Vasopressin does not directly inhibit nitric oxide or stimulate beta1 receptors.
Why Wrong:
B - V2 receptors are in the renal collecting duct, not the heart; vasopressin does not increase contractility.
C - Vasopressin does not directly inhibit nitric oxide synthesis; it acts via V1 receptors.
D - Vasopressin is not a beta1 agonist; it is a peptide hormone that acts on vasopressin receptors.
Reference: Katzung, B.G., & Vanderah, T.W. (2025). Basic & Clinical Pharmacology, 16th Ed., Ch. 20
Page 4
