NURS 611 Exam 2 V1 | NURS 611
Advanced Pathophysiology | Maryville
University of St. Louis | 2026 Q&A with
Rationale (Maryville NURS611 Exam 2
2026)
1. A patient is diagnosed with secondary hypertension. Which of the following conditions is a
known cause of this type of hypertension?
A. Sedentary lifestyle
B. High sodium intake
C. Genetic predisposition
D. Primary hyperaldosteronism
Correct Answer: D
Rationale: Secondary hypertension is caused by an underlying systemic disease or
medication that raises peripheral vascular resistance or cardiac output. Primary
hyperaldosteronism causes excessive sodium and water retention, leading to increased
blood volume and blood pressure. In contrast, factors like high sodium intake and lifestyle
are associated with primary or essential hypertension.
2. Which cellular change is most characteristic of the progression from stable angina to
unstable angina?
A. Transmural myocardial infarction
,B. Stable fibrous plaque formation
C. Plaque rupture with subsequent thrombus formation
D. Temporary vasospasm of coronary arteries
Correct Answer: C
Rationale: Unstable angina occurs when a previously stable atherosclerotic plaque
becomes complicated by rupture or erosion. This leads to the formation of a labile
thrombus that periodically occludes the vessel lumen, causing ischemia at rest. Stable
angina usually involves a fixed obstruction, whereas unstable angina is part of the acute
coronary syndrome spectrum.
3. A 65-year-old patient presents with shortness of breath, orthopnea, and paroxysmal
nocturnal dyspnea. Which pathophysiological mechanism explains these symptoms?
A. Right-to-left shunting in the heart
B. Decreased systemic vascular resistance
C. Increased oncotic pressure in the capillaries
D. Increased pulmonary capillary hydrostatic pressure
Correct Answer: D
Rationale: Left-sided heart failure leads to the backup of blood into the pulmonary
circulation. This elevates the pulmonary capillary hydrostatic pressure, forcing fluid into
the interstitial and alveolar spaces, causing pulmonary edema. The resulting symptoms of
, orthopnea and dyspnea are direct consequences of impaired gas exchange and fluid
accumulation in the lungs.
4. Which of the following describes the role of BNP (B-type Natriuretic Peptide) in the
management of heart failure?
A. It is secreted by the ventricles in response to increased wall stretch
B. It promotes vasoconstriction and sodium retention
C. It serves as a primary marker for myocardial necrosis
D. It increases the activity of the RAAS system
Correct Answer: A
Rationale: BNP is synthesized and released by the ventricular myocardium in response to
increased pressure or volume overload. It acts to promote diuresis, natriuresis, and
vasodilation to counteract the effects of the RAAS and sympathetic nervous systems.
Clinical measurement of BNP levels helps clinicians differentiate between cardiac and non-
cardiac causes of dyspnea.
5. In the development of atherosclerosis, which step occurs immediately after endothelial
injury?
A. Formation of a fibrous plaque
B. Oxidation of LDL and recruitment of macrophages
C. Rupture of the lipid core
Advanced Pathophysiology | Maryville
University of St. Louis | 2026 Q&A with
Rationale (Maryville NURS611 Exam 2
2026)
1. A patient is diagnosed with secondary hypertension. Which of the following conditions is a
known cause of this type of hypertension?
A. Sedentary lifestyle
B. High sodium intake
C. Genetic predisposition
D. Primary hyperaldosteronism
Correct Answer: D
Rationale: Secondary hypertension is caused by an underlying systemic disease or
medication that raises peripheral vascular resistance or cardiac output. Primary
hyperaldosteronism causes excessive sodium and water retention, leading to increased
blood volume and blood pressure. In contrast, factors like high sodium intake and lifestyle
are associated with primary or essential hypertension.
2. Which cellular change is most characteristic of the progression from stable angina to
unstable angina?
A. Transmural myocardial infarction
,B. Stable fibrous plaque formation
C. Plaque rupture with subsequent thrombus formation
D. Temporary vasospasm of coronary arteries
Correct Answer: C
Rationale: Unstable angina occurs when a previously stable atherosclerotic plaque
becomes complicated by rupture or erosion. This leads to the formation of a labile
thrombus that periodically occludes the vessel lumen, causing ischemia at rest. Stable
angina usually involves a fixed obstruction, whereas unstable angina is part of the acute
coronary syndrome spectrum.
3. A 65-year-old patient presents with shortness of breath, orthopnea, and paroxysmal
nocturnal dyspnea. Which pathophysiological mechanism explains these symptoms?
A. Right-to-left shunting in the heart
B. Decreased systemic vascular resistance
C. Increased oncotic pressure in the capillaries
D. Increased pulmonary capillary hydrostatic pressure
Correct Answer: D
Rationale: Left-sided heart failure leads to the backup of blood into the pulmonary
circulation. This elevates the pulmonary capillary hydrostatic pressure, forcing fluid into
the interstitial and alveolar spaces, causing pulmonary edema. The resulting symptoms of
, orthopnea and dyspnea are direct consequences of impaired gas exchange and fluid
accumulation in the lungs.
4. Which of the following describes the role of BNP (B-type Natriuretic Peptide) in the
management of heart failure?
A. It is secreted by the ventricles in response to increased wall stretch
B. It promotes vasoconstriction and sodium retention
C. It serves as a primary marker for myocardial necrosis
D. It increases the activity of the RAAS system
Correct Answer: A
Rationale: BNP is synthesized and released by the ventricular myocardium in response to
increased pressure or volume overload. It acts to promote diuresis, natriuresis, and
vasodilation to counteract the effects of the RAAS and sympathetic nervous systems.
Clinical measurement of BNP levels helps clinicians differentiate between cardiac and non-
cardiac causes of dyspnea.
5. In the development of atherosclerosis, which step occurs immediately after endothelial
injury?
A. Formation of a fibrous plaque
B. Oxidation of LDL and recruitment of macrophages
C. Rupture of the lipid core
