NURS 6521 Exam 2 | NURS 6521 Advanced
Pathophysiology II | Actual Q&A with Rationale
(NURS 6521 Exam 2) | Walden
Exam 2 (Midterm) – Advanced Pathophysiology II
NURS 6521 – Walden University
Section A: Cardiovascular Disorders (Questions 1–20)
Q1. A patient with chronic heart failure presents with dyspnea, fatigue, and bilateral
lower extremity edema. Which pathophysiological mechanism best explains the
development of edema in this patient?
A. Increased capillary permeability due to inflammation
B. Decreased cardiac output leading to activation of the renin-angiotensin-
aldosterone system (RAAS) ✅
C. Increased lymphatic drainage
D. Decreased venous pressure
Rationale: In heart failure, decreased cardiac output triggers RAAS activation,
leading to increased angiotensin II and aldosterone levels. Aldosterone causes
sodium and water retention, increasing blood volume and venous pressure, which
results in peripheral edema and pulmonary congestion. The RAAS system also
causes vasoconstriction, which further increases afterload and worsens cardiac
function.
Q2. Which cardiac chamber undergoes hypertrophy in response to chronic
hypertension?
A. Right atrium
B. Left ventricle ✅
,C. Right ventricle
D. Left atrium
Rationale: Chronic hypertension increases systemic vascular resistance, which
creates an increased afterload that the left ventricle must pump against. To
compensate, the left ventricular myocardium undergoes concentric hypertrophy,
thickening the ventricular wall while reducing chamber size. Over time, this adaptive
mechanism can become maladaptive, leading to diastolic dysfunction and
eventually heart failure.
Q3. A patient with atrial fibrillation is at increased risk for which of the following
complications?
A. Myocardial infarction
B. Embolic stroke ✅
C. Pulmonary embolism
D. Aortic aneurysm
Rationale: In atrial fibrillation, the atria quiver rather than contract effectively,
causing blood stasis in the left atrial appendage. This stasis predisposes to
thrombus formation, which can embolize to the cerebral circulation, causing an
ischemic stroke. Anticoagulation therapy with warfarin, direct oral anticoagulants
(DOACs), or aspirin is often indicated based on stroke risk factors.
Q4. Which medication class is considered first-line therapy for reducing mortality in
patients with heart failure with reduced ejection fraction (HFrEF)?
A. Calcium channel blockers
B. Beta blockers ✅
C. Direct vasodilators
D. Class I antiarrhythmics
,Rationale: Beta blockers (e.g., metoprolol succinate, carvedilol, bisoprolol) have
been shown in multiple clinical trials to reduce mortality and hospitalizations in
patients with HFrEF. They work by blocking the chronic sympathetic activation that
is detrimental to the failing heart, reducing heart rate, improving ventricular
remodeling, and decreasing myocardial oxygen demand. ACE inhibitors/ARBs and
aldosterone antagonists are also part of guideline-directed medical therapy.
Q5. Which electrocardiographic finding is characteristic of hyperkalemia?
A. Prolonged QT interval
B. Tall, peaked T waves ✅
C. ST segment elevation
D. U waves
Rationale: Hyperkalemia causes accelerated repolarization of the ventricular
myocardium, resulting in tall, peaked, symmetrical T waves on the ECG. As
potassium levels rise further, the QRS complex widens, the P wave flattens, and
eventually sine wave patterns or ventricular fibrillation may occur. Immediate
treatment includes intravenous calcium gluconate to stabilize the cardiac
membrane, followed by measures to shift potassium into cells (insulin + glucose,
albuterol) and enhance elimination.
Q6. A patient with hypertension is started on lisinopril. Which laboratory value
should be monitored closely after initiation?
A. Serum sodium
B. Serum creatinine and potassium ✅
C. Serum calcium
D. Serum magnesium
, Rationale: ACE inhibitors like lisinopril reduce angiotensin II levels, which decreases
aldosterone secretion, leading to potassium retention and potential hyperkalemia.
They also dilate the efferent arteriole in the glomerulus, which can reduce
glomerular filtration rate and increase serum creatinine, especially in patients with
renal artery stenosis or dehydration. Monitoring renal function and electrolytes
within 1–2 weeks of initiation is standard practice.
Q7. Which type of shock is most commonly associated with anaphylaxis?
A. Cardiogenic shock
B. Hypovolemic shock
C. Distributive shock ✅
D. Obstructive shock
Rationale: Anaphylaxis causes massive vasodilation and increased capillary
permeability
Q8. A patient with acute myocardial infarction presents with ST-segment elevation
in leads V1–V4. Which coronary artery is most likely occluded?
A. Right coronary artery
B. Left anterior descending artery ✅
C. Left circumflex artery
D. Posterior descending artery
Rationale: ST-segment elevation in the anterior precordial leads (V1–V4) indicates
an anterior wall myocardial infarction, which is most commonly caused by occlusion
of the left anterior descending (LAD) artery. The LAD supplies the anterior wall of
the left ventricle and the interventricular septum. Occlusion of the LAD carries a
high risk of left ventricular dysfunction and cardiogenic shock due to the large
amount of myocardium at risk.
Pathophysiology II | Actual Q&A with Rationale
(NURS 6521 Exam 2) | Walden
Exam 2 (Midterm) – Advanced Pathophysiology II
NURS 6521 – Walden University
Section A: Cardiovascular Disorders (Questions 1–20)
Q1. A patient with chronic heart failure presents with dyspnea, fatigue, and bilateral
lower extremity edema. Which pathophysiological mechanism best explains the
development of edema in this patient?
A. Increased capillary permeability due to inflammation
B. Decreased cardiac output leading to activation of the renin-angiotensin-
aldosterone system (RAAS) ✅
C. Increased lymphatic drainage
D. Decreased venous pressure
Rationale: In heart failure, decreased cardiac output triggers RAAS activation,
leading to increased angiotensin II and aldosterone levels. Aldosterone causes
sodium and water retention, increasing blood volume and venous pressure, which
results in peripheral edema and pulmonary congestion. The RAAS system also
causes vasoconstriction, which further increases afterload and worsens cardiac
function.
Q2. Which cardiac chamber undergoes hypertrophy in response to chronic
hypertension?
A. Right atrium
B. Left ventricle ✅
,C. Right ventricle
D. Left atrium
Rationale: Chronic hypertension increases systemic vascular resistance, which
creates an increased afterload that the left ventricle must pump against. To
compensate, the left ventricular myocardium undergoes concentric hypertrophy,
thickening the ventricular wall while reducing chamber size. Over time, this adaptive
mechanism can become maladaptive, leading to diastolic dysfunction and
eventually heart failure.
Q3. A patient with atrial fibrillation is at increased risk for which of the following
complications?
A. Myocardial infarction
B. Embolic stroke ✅
C. Pulmonary embolism
D. Aortic aneurysm
Rationale: In atrial fibrillation, the atria quiver rather than contract effectively,
causing blood stasis in the left atrial appendage. This stasis predisposes to
thrombus formation, which can embolize to the cerebral circulation, causing an
ischemic stroke. Anticoagulation therapy with warfarin, direct oral anticoagulants
(DOACs), or aspirin is often indicated based on stroke risk factors.
Q4. Which medication class is considered first-line therapy for reducing mortality in
patients with heart failure with reduced ejection fraction (HFrEF)?
A. Calcium channel blockers
B. Beta blockers ✅
C. Direct vasodilators
D. Class I antiarrhythmics
,Rationale: Beta blockers (e.g., metoprolol succinate, carvedilol, bisoprolol) have
been shown in multiple clinical trials to reduce mortality and hospitalizations in
patients with HFrEF. They work by blocking the chronic sympathetic activation that
is detrimental to the failing heart, reducing heart rate, improving ventricular
remodeling, and decreasing myocardial oxygen demand. ACE inhibitors/ARBs and
aldosterone antagonists are also part of guideline-directed medical therapy.
Q5. Which electrocardiographic finding is characteristic of hyperkalemia?
A. Prolonged QT interval
B. Tall, peaked T waves ✅
C. ST segment elevation
D. U waves
Rationale: Hyperkalemia causes accelerated repolarization of the ventricular
myocardium, resulting in tall, peaked, symmetrical T waves on the ECG. As
potassium levels rise further, the QRS complex widens, the P wave flattens, and
eventually sine wave patterns or ventricular fibrillation may occur. Immediate
treatment includes intravenous calcium gluconate to stabilize the cardiac
membrane, followed by measures to shift potassium into cells (insulin + glucose,
albuterol) and enhance elimination.
Q6. A patient with hypertension is started on lisinopril. Which laboratory value
should be monitored closely after initiation?
A. Serum sodium
B. Serum creatinine and potassium ✅
C. Serum calcium
D. Serum magnesium
, Rationale: ACE inhibitors like lisinopril reduce angiotensin II levels, which decreases
aldosterone secretion, leading to potassium retention and potential hyperkalemia.
They also dilate the efferent arteriole in the glomerulus, which can reduce
glomerular filtration rate and increase serum creatinine, especially in patients with
renal artery stenosis or dehydration. Monitoring renal function and electrolytes
within 1–2 weeks of initiation is standard practice.
Q7. Which type of shock is most commonly associated with anaphylaxis?
A. Cardiogenic shock
B. Hypovolemic shock
C. Distributive shock ✅
D. Obstructive shock
Rationale: Anaphylaxis causes massive vasodilation and increased capillary
permeability
Q8. A patient with acute myocardial infarction presents with ST-segment elevation
in leads V1–V4. Which coronary artery is most likely occluded?
A. Right coronary artery
B. Left anterior descending artery ✅
C. Left circumflex artery
D. Posterior descending artery
Rationale: ST-segment elevation in the anterior precordial leads (V1–V4) indicates
an anterior wall myocardial infarction, which is most commonly caused by occlusion
of the left anterior descending (LAD) artery. The LAD supplies the anterior wall of
the left ventricle and the interventricular septum. Occlusion of the LAD carries a
high risk of left ventricular dysfunction and cardiogenic shock due to the large
amount of myocardium at risk.
