NSG 530 Exam 2 Actual Exam V1 | NSG 530 Advanced
Pathophysiology (NSG530 Exam 2) [PDF] | Wilkes University
1. A 62-year-old male with a history of tobacco use and hypertension presents with stable
angina. Which statement best describes the underlying pathophysiology of stable angina
pectoris?
A. A sudden, complete occlusion of a coronary artery by a thrombus.
B. Vasospasm of the coronary arteries occurring primarily at rest.
C. A predictable imbalance between myocardial oxygen supply and demand due to a fixed
atherosclerotic plaque.
D. Inflammation of the pericardial sac causing chest pain during inspiration.
Answer: C
Rationale: Stable angina is characterized by chest pain that occurs with predictable levels
of exertion or emotional stress. This occurs when the coronary arteries are narrowed by
fixed atherosclerotic plaques, limiting the increase in blood flow required by the
myocardium during high demand. The pain is typically relieved by rest or nitroglycerin,
which reduces the myocardial workload and improves oxygenation.
2. Following an acute myocardial infarction, the heart undergoes a process known as
ventricular remodeling. What is the primary driving force behind this structural change?
A. Decreased production of natriuretic peptides.
B. Selective apoptosis of fibroblasts in the infarct zone.
C. Rapid regeneration of cardiac myocytes to replace necrotic tissue.
D. Myocyte hypertrophy and collagen deposition mediated by angiotensin II and
aldosterone.
Answer: D
Rationale: Ventricular remodeling involves changes in the size, shape, and function of the
heart after injury. The neurohormonal activation of the RAAS system, specifically
angiotensin II and aldosterone, stimulates myocyte hypertrophy and the deposition of
fibrous tissue. While this initially helps maintain stroke volume, it eventually leads to
increased wall stress and progressive heart failure.
3. A patient is diagnosed with Systolic Heart Failure with a Reduced Ejection Fraction (HFrEF).
Which hemodynamic change is most characteristic of this condition?
A. Increased ejection fraction due to compensatory tachycardia.
B. Increased left ventricular end-diastolic volume with decreased stroke volume.
,C. Decreased pulmonary artery wedge pressure.
D. Systemic vasodilation to improve cardiac output.
Answer: B
Rationale: In HFrEF, the left ventricle is unable to contract effectively, leading to a
decrease in stroke volume and an increase in residual blood volume at the end of diastole.
This increase in end-diastolic volume leads to chamber dilation and increased wall tension.
The body attempts to compensate via the Frank-Starling mechanism, but the failing
myocardium cannot sustain adequate output.
4. During the development of atherosclerosis, ‘foam cells’ are formed. What is the
composition of a foam cell?
A. Platelets that have aggregated around a rupture site.
B. Smooth muscle cells that have migrated to the tunica intima.
C. Macrophages that have engulfed oxidized low-density lipoproteins (LDL).
D. Endothelial cells that have undergone malignant transformation.
Answer: C
Rationale: Foam cells are a hallmark of the early atherosclerotic lesion known as the fatty
streak. They are created when circulating monocytes migrate into the subendothelial space
and transform into macrophages. These macrophages then take up oxidized LDL through
scavenger receptors, becoming bloated with lipids and taking on a foamy appearance.
5. A 50-year-old woman is evaluated for secondary hypertension. Laboratory results reveal
elevated levels of serum aldosterone and low plasma renin activity. What is the most likely
cause?
A. Primary hyperaldosteronism (Conn Syndrome).
B. Renal artery stenosis.
C. Chronic obstructive pulmonary disease.
D. Pheochromocytoma.
Answer: A
Rationale: Primary hyperaldosteronism is characterized by an autonomous
overproduction of aldosterone, usually by an adrenal adenoma. Excess aldosterone leads to
sodium and water retention and potassium excretion, which subsequently suppresses
renin production via negative feedback. This results in the classic finding of hypertension
with low renin and high aldosterone levels.
, 6. Which dysrhythmia is characterized by the absence of P waves and an irregularly irregular
ventricular rhythm, significantly increasing the risk of thromboembolic stroke?
A. Ventricular Tachycardia.
B. First-degree Atrioventricular Block.
C. Sinus Bradycardia.
D. Atrial Fibrillation.
Answer: D
Rationale: Atrial fibrillation involves rapid, disorganized electrical activity in the atria,
which prevents effective atrial contraction. This leads to blood stasis in the atria,
particularly in the left atrial appendage, which facilitates the formation of thrombi. If a
thrombus dislodges, it can travel to the brain and cause an embolic stroke.
7. In the context of valvular heart disease, which condition leads to left ventricular
hypertrophy due to increased afterload?
A. Mitral Regurgitation.
B. Tricuspid Stenosis.
C. Aortic Stenosis.
D. Mitral Valve Prolapse.
Answer: C
Rationale: Aortic stenosis creates a resistance to blood flow from the left ventricle into the
aorta during systole, thereby increasing the afterload. To maintain cardiac output against
this high pressure, the left ventricle undergoes concentric hypertrophy. Over time, this
hypertrophy increases myocardial oxygen demand and may eventually lead to heart
failure.
8. A patient presents with sudden onset of pleuritic chest pain and dyspnea. A V/Q scan
indicates a ‘mismatch’ where there is ventilation but no perfusion in certain areas of the lung.
This is diagnostic of:
A. Atelectasis.
B. Asthma.
C. Pneumonia.
D. Pulmonary Embolism.
Answer: D
Rationale: A pulmonary embolism (PE) occurs when a blood clot obstructs a pulmonary
artery, stopping blood flow to the distal lung tissue. While the alveoli in that area are still
Pathophysiology (NSG530 Exam 2) [PDF] | Wilkes University
1. A 62-year-old male with a history of tobacco use and hypertension presents with stable
angina. Which statement best describes the underlying pathophysiology of stable angina
pectoris?
A. A sudden, complete occlusion of a coronary artery by a thrombus.
B. Vasospasm of the coronary arteries occurring primarily at rest.
C. A predictable imbalance between myocardial oxygen supply and demand due to a fixed
atherosclerotic plaque.
D. Inflammation of the pericardial sac causing chest pain during inspiration.
Answer: C
Rationale: Stable angina is characterized by chest pain that occurs with predictable levels
of exertion or emotional stress. This occurs when the coronary arteries are narrowed by
fixed atherosclerotic plaques, limiting the increase in blood flow required by the
myocardium during high demand. The pain is typically relieved by rest or nitroglycerin,
which reduces the myocardial workload and improves oxygenation.
2. Following an acute myocardial infarction, the heart undergoes a process known as
ventricular remodeling. What is the primary driving force behind this structural change?
A. Decreased production of natriuretic peptides.
B. Selective apoptosis of fibroblasts in the infarct zone.
C. Rapid regeneration of cardiac myocytes to replace necrotic tissue.
D. Myocyte hypertrophy and collagen deposition mediated by angiotensin II and
aldosterone.
Answer: D
Rationale: Ventricular remodeling involves changes in the size, shape, and function of the
heart after injury. The neurohormonal activation of the RAAS system, specifically
angiotensin II and aldosterone, stimulates myocyte hypertrophy and the deposition of
fibrous tissue. While this initially helps maintain stroke volume, it eventually leads to
increased wall stress and progressive heart failure.
3. A patient is diagnosed with Systolic Heart Failure with a Reduced Ejection Fraction (HFrEF).
Which hemodynamic change is most characteristic of this condition?
A. Increased ejection fraction due to compensatory tachycardia.
B. Increased left ventricular end-diastolic volume with decreased stroke volume.
,C. Decreased pulmonary artery wedge pressure.
D. Systemic vasodilation to improve cardiac output.
Answer: B
Rationale: In HFrEF, the left ventricle is unable to contract effectively, leading to a
decrease in stroke volume and an increase in residual blood volume at the end of diastole.
This increase in end-diastolic volume leads to chamber dilation and increased wall tension.
The body attempts to compensate via the Frank-Starling mechanism, but the failing
myocardium cannot sustain adequate output.
4. During the development of atherosclerosis, ‘foam cells’ are formed. What is the
composition of a foam cell?
A. Platelets that have aggregated around a rupture site.
B. Smooth muscle cells that have migrated to the tunica intima.
C. Macrophages that have engulfed oxidized low-density lipoproteins (LDL).
D. Endothelial cells that have undergone malignant transformation.
Answer: C
Rationale: Foam cells are a hallmark of the early atherosclerotic lesion known as the fatty
streak. They are created when circulating monocytes migrate into the subendothelial space
and transform into macrophages. These macrophages then take up oxidized LDL through
scavenger receptors, becoming bloated with lipids and taking on a foamy appearance.
5. A 50-year-old woman is evaluated for secondary hypertension. Laboratory results reveal
elevated levels of serum aldosterone and low plasma renin activity. What is the most likely
cause?
A. Primary hyperaldosteronism (Conn Syndrome).
B. Renal artery stenosis.
C. Chronic obstructive pulmonary disease.
D. Pheochromocytoma.
Answer: A
Rationale: Primary hyperaldosteronism is characterized by an autonomous
overproduction of aldosterone, usually by an adrenal adenoma. Excess aldosterone leads to
sodium and water retention and potassium excretion, which subsequently suppresses
renin production via negative feedback. This results in the classic finding of hypertension
with low renin and high aldosterone levels.
, 6. Which dysrhythmia is characterized by the absence of P waves and an irregularly irregular
ventricular rhythm, significantly increasing the risk of thromboembolic stroke?
A. Ventricular Tachycardia.
B. First-degree Atrioventricular Block.
C. Sinus Bradycardia.
D. Atrial Fibrillation.
Answer: D
Rationale: Atrial fibrillation involves rapid, disorganized electrical activity in the atria,
which prevents effective atrial contraction. This leads to blood stasis in the atria,
particularly in the left atrial appendage, which facilitates the formation of thrombi. If a
thrombus dislodges, it can travel to the brain and cause an embolic stroke.
7. In the context of valvular heart disease, which condition leads to left ventricular
hypertrophy due to increased afterload?
A. Mitral Regurgitation.
B. Tricuspid Stenosis.
C. Aortic Stenosis.
D. Mitral Valve Prolapse.
Answer: C
Rationale: Aortic stenosis creates a resistance to blood flow from the left ventricle into the
aorta during systole, thereby increasing the afterload. To maintain cardiac output against
this high pressure, the left ventricle undergoes concentric hypertrophy. Over time, this
hypertrophy increases myocardial oxygen demand and may eventually lead to heart
failure.
8. A patient presents with sudden onset of pleuritic chest pain and dyspnea. A V/Q scan
indicates a ‘mismatch’ where there is ventilation but no perfusion in certain areas of the lung.
This is diagnostic of:
A. Atelectasis.
B. Asthma.
C. Pneumonia.
D. Pulmonary Embolism.
Answer: D
Rationale: A pulmonary embolism (PE) occurs when a blood clot obstructs a pulmonary
artery, stopping blood flow to the distal lung tissue. While the alveoli in that area are still
