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MSNC 505 WEEK 4: ADVANCED PATHOPHYSIOLOGY OF CARDIOVASCULAR AND RESPIRATORY SYSTEMS. QUESTIONS AND DETAILED SOLUTIONS JUST RELEASED

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MSNC 505 WEEK 4: ADVANCED PATHOPHYSIOLOGY OF CARDIOVASCULAR AND RESPIRATORY SYSTEMS. QUESTIONS AND DETAILED SOLUTIONS JUST RELEASED

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MSNC 505 WEEK 4: ADVANCED
PATHOPHYSIOLOGY OF
CARDIOVASCULAR AND
RESPIRATORY SYSTEMS. QUESTIONS
AND DETAILED SOLUTIONS JUST
RELEASED


1. Which cellular adaptation is most characteristic of the heart’s response to chronic

hypertension?

A. Hyperplasia of cardiac myocytes


B. Metaplasia of the endocardial lining


C. Eccentric hypertrophy of the right atrium


D. Concentric hypertrophy of the left ventricle


Answer: D


Conceptual Explanation: Chronic hypertension increases afterload, leading to concentric

hypertrophy of the left ventricle as myocytes increase in thickness to handle the increased

pressure work.


2. In the pathophysiology of atherosclerosis, what is the primary role of oxidized LDL?

A. It triggers macrophage recruitment and transformation into foam cells

,B. It promotes the secretion of nitric oxide by endothelial cells


C. It stabilizes the fibrous cap of the plaque


D. It prevents smooth muscle cell proliferation


Answer: A


Conceptual Explanation: Oxidized LDL is proinflammatory and toxic to endothelial cells;

it is engulfed by macrophages, which then become lipid-laden foam cells, a hallmark of

early atherosclerotic lesions.


3. Which mechanism best describes the development of Cardiogenic Shock following an

extensive myocardial infarction?

A. Decreased systemic vascular resistance due to vasodilation


B. Severe decrease in cardiac output despite adequate intravascular volume


C. Fluid shift from the intravascular to the interstitial space


D. Impaired oxygen delivery due to hemoglobin dysfunction


Answer: B


Conceptual Explanation: Cardiogenic shock results from the heart’s inability to pump

effectively, leading to low cardiac output and tissue hypoxia despite normal filling

pressures.

, 4. A patient with Systolic Heart Failure (HFrEF) exhibits an activation of the Renin-

Angiotensin-Aldosterone System (RAAS). What is a detrimental long-term effect of this

activation?

A. Decreased cardiac afterload


B. Promotion of ventricular remodeling and fibrosis


C. Improved myocardial oxygen supply-demand ratio


D. Increased renal perfusion and diuresis


Answer: B


Conceptual Explanation: Chronic RAAS activation leads to Angiotensin II and Aldosterone

mediated cardiac remodeling, including collagen deposition and fibrosis, which worsens

heart failure.


5. Which of the following describes the Frank-Starling law in the context of compensated

heart failure?

A. Increased contractility due to catecholamine release


B. Increased stroke volume as a result of increased end-diastolic volume


C. Decreased heart rate to allow for better filling


D. Decreased peripheral resistance to enhance flow


Answer: B

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