NSG 5003 Week 3 Exam Questions and
Answers
Course: NSG 5003 Advanced Pathophysiology
Focus Area: Cardiovascular, Renal/Electrolyte, Respiratory, and Neurological/Endocrine
Pathophysiology
Section 1: Cardiovascular Pathophysiology
Question 1: What is the primary pathophysiological mechanism underlying primary
(essential) hypertension?
Answer: Primary hypertension results from a complex interaction between genetic factors
and environmental influences that lead to increased systemic vascular resistance (SVR)
and/or increased intravascular volume. Key mechanisms include overactivity of the
Sympathetic Nervous System (SNS), dysfunction of the Renin-Angiotensin-Aldosterone
System (RAAS), endothelial dysfunction with decreased nitric oxide availability, and
impaired renal sodium excretion.
Question 2: How does chronic, untreated hypertension cause left ventricular hypertrophy
(LVH)?
Answer: High systemic vascular resistance increases the afterload against which the left
ventricle must pump to eject blood into the aorta. In response to this chronic wall stress,
cardiomyocytes undergo concentric hypertrophy (adding sarcomeres in parallel) to generate
greater contractile force, resulting in left ventricular wall thickening and reduced ventricular
compliance.
Question 3: Differentiate between stable angina, unstable angina, and Non-ST-Segment
Elevation Myocardial Infarction (NSTEMI).
Answer:
● Stable Angina: Predictable chest pain caused by fixed atherosclerotic plaque stenosis,
occurring during exertional stress and relieved by rest or nitroglycerin. No myocardial
necrosis (normal troponin).
● Unstable Angina: Unpredictable chest pain occurring at rest or with decreasing
exertion due to unstable plaque disruption and transient ischemia without cell necrosis
(normal troponin).
● NSTEMI: Partial occlusion of a coronary artery leading to myocardial ischemia severe
, enough to cause subendocardial tissue necrosis, resulting in elevated serum cardiac
biomarkers (troponin) without ST-segment elevation on ECG.
Question 4: What electrocardiographic (ECG) change indicates transmural myocardial
infarction?
Answer: Acute ST-segment elevation in anatomically contiguous leads indicates
transmural myocardial ischemia and injury (STEMI). Pathologic Q waves subsequently
develop as full-thickness necrosis occurs.
Question 5: What compensatory neurohormonal mechanisms are activated in Heart
Failure with Reduced Ejection Fraction (HFrEF), and what are their long-term
consequences?
Answer: Decreased cardiac output activates the SNS (increasing heart rate and
contractility) and the RAAS (causing vasoconstriction and sodium/water retention). While
initially compensatory, sustained neurohormonal activation leads to adverse ventricular
remodeling, increased preload/afterload, progressive cardiac fibrosis, and worsening heart
failure.
Question 6: What is the diagnostic significance of Brain Natriuretic Peptide (BNP)?
Answer: BNP is synthesized and secreted by ventricular cardiomyocytes in response to
increased ventricular wall stretch and fluid overload. Elevated plasma BNP levels help
differentiate heart failure from primary pulmonary causes of dyspnea and correlate with the
severity of heart failure.
Question 7: Describe the early cellular pathogenesis of atherosclerosis.
Answer: Endothelial injury (induced by hypertension, smoking, hyperlipidemia, or
hyperglycemia) increases permeability and leukocyte adhesion. Low-density lipoprotein
(LDL) enters the subendothelial space, undergoes oxidation, and attracts monocytes.
Monocytes differentiate into macrophages, engulf oxidized LDL, and transform into foam
cells, forming the fatty streak.
Question 8: What is the hallmark clinical triad of aortic valve stenosis?
Answer: The classic clinical triad of severe aortic stenosis includes exertional dyspnea,
angina pectoris, and syncope (SAD), caused by left ventricular outflow tract obstruction and
fixed cardiac output.
Answers
Course: NSG 5003 Advanced Pathophysiology
Focus Area: Cardiovascular, Renal/Electrolyte, Respiratory, and Neurological/Endocrine
Pathophysiology
Section 1: Cardiovascular Pathophysiology
Question 1: What is the primary pathophysiological mechanism underlying primary
(essential) hypertension?
Answer: Primary hypertension results from a complex interaction between genetic factors
and environmental influences that lead to increased systemic vascular resistance (SVR)
and/or increased intravascular volume. Key mechanisms include overactivity of the
Sympathetic Nervous System (SNS), dysfunction of the Renin-Angiotensin-Aldosterone
System (RAAS), endothelial dysfunction with decreased nitric oxide availability, and
impaired renal sodium excretion.
Question 2: How does chronic, untreated hypertension cause left ventricular hypertrophy
(LVH)?
Answer: High systemic vascular resistance increases the afterload against which the left
ventricle must pump to eject blood into the aorta. In response to this chronic wall stress,
cardiomyocytes undergo concentric hypertrophy (adding sarcomeres in parallel) to generate
greater contractile force, resulting in left ventricular wall thickening and reduced ventricular
compliance.
Question 3: Differentiate between stable angina, unstable angina, and Non-ST-Segment
Elevation Myocardial Infarction (NSTEMI).
Answer:
● Stable Angina: Predictable chest pain caused by fixed atherosclerotic plaque stenosis,
occurring during exertional stress and relieved by rest or nitroglycerin. No myocardial
necrosis (normal troponin).
● Unstable Angina: Unpredictable chest pain occurring at rest or with decreasing
exertion due to unstable plaque disruption and transient ischemia without cell necrosis
(normal troponin).
● NSTEMI: Partial occlusion of a coronary artery leading to myocardial ischemia severe
, enough to cause subendocardial tissue necrosis, resulting in elevated serum cardiac
biomarkers (troponin) without ST-segment elevation on ECG.
Question 4: What electrocardiographic (ECG) change indicates transmural myocardial
infarction?
Answer: Acute ST-segment elevation in anatomically contiguous leads indicates
transmural myocardial ischemia and injury (STEMI). Pathologic Q waves subsequently
develop as full-thickness necrosis occurs.
Question 5: What compensatory neurohormonal mechanisms are activated in Heart
Failure with Reduced Ejection Fraction (HFrEF), and what are their long-term
consequences?
Answer: Decreased cardiac output activates the SNS (increasing heart rate and
contractility) and the RAAS (causing vasoconstriction and sodium/water retention). While
initially compensatory, sustained neurohormonal activation leads to adverse ventricular
remodeling, increased preload/afterload, progressive cardiac fibrosis, and worsening heart
failure.
Question 6: What is the diagnostic significance of Brain Natriuretic Peptide (BNP)?
Answer: BNP is synthesized and secreted by ventricular cardiomyocytes in response to
increased ventricular wall stretch and fluid overload. Elevated plasma BNP levels help
differentiate heart failure from primary pulmonary causes of dyspnea and correlate with the
severity of heart failure.
Question 7: Describe the early cellular pathogenesis of atherosclerosis.
Answer: Endothelial injury (induced by hypertension, smoking, hyperlipidemia, or
hyperglycemia) increases permeability and leukocyte adhesion. Low-density lipoprotein
(LDL) enters the subendothelial space, undergoes oxidation, and attracts monocytes.
Monocytes differentiate into macrophages, engulf oxidized LDL, and transform into foam
cells, forming the fatty streak.
Question 8: What is the hallmark clinical triad of aortic valve stenosis?
Answer: The classic clinical triad of severe aortic stenosis includes exertional dyspnea,
angina pectoris, and syncope (SAD), caused by left ventricular outflow tract obstruction and
fixed cardiac output.
