NSG 530 Exam 2 Actual Exam V2 | NSG 530 Advanced
Pathophysiology (NSG530 Exam 2) [PDF] | Wilkes University
1. A 62-year-old male presents to the emergency department with substernal chest pain that
radiates to his left jaw. His EKG shows ST-segment depression in leads V3-V6, and his initial
troponin I is slightly elevated at 0.08 ng/mL. Which mechanism best explains the underlying
pathophysiology of his condition?
A. Transmural infarction due to complete occlusion of a coronary artery
B. Subendocardial ischemia due to a partial occlusion of a coronary artery
C. Vasospasm of the coronary artery at rest (Prinzmetal angina)
D. Stable plaque rupture with immediate spontaneous thrombolysis
Answer: B
Rationale: The presence of ST-segment depression and elevated troponins indicates a
Non-ST Elevation Myocardial Infarction (NSTEMI). This condition typically results from a
subendocardial ischemia caused by a partially occluding thrombus. Unlike a STEMI, the
necrosis is limited to the inner layer of the myocardium rather than the full thickness of the
wall.
2. Following a large anterior wall myocardial infarction, a patient begins to show signs of left
ventricular enlargement and thinning of the infarcted wall. Which process is primarily
responsible for these structural changes?
A. Physiological hypertrophy
B. Myocardial stunning
C. Ventricular remodeling
D. Hibernating myocardium
Answer: C
Rationale: Ventricular remodeling involves structural changes in the heart’s shape, size,
and function following an injury like an MI. This process is driven by neurohumoral
activation, specifically the RAAS and sympathetic nervous system. While initially
compensatory, chronic remodeling often leads to progressive heart failure and decreased
contractility.
3. A 72-year-old female is diagnosed with aortic stenosis. During auscultation, the provider
hears a harsh systolic crescendo-decrescendo murmur at the right upper sternal border. What
is the primary hemodynamic consequence of this disorder?
A. Increased stroke volume
,B. Decreased left atrial pressure
C. Increased left ventricular afterload
D. Decreased left ventricular end-diastolic pressure
Answer: C
Rationale: Aortic stenosis narrows the valve orifice, creating a significant resistance to
blood being ejected from the left ventricle. This increased resistance represents an
elevation in afterload, forcing the ventricle to generate higher pressures to maintain
cardiac output. Over time, this leads to concentric left ventricular hypertrophy as the heart
adapts to the chronic pressure overload.
4. Which mediator is primarily responsible for the impaired vasodilation observed in patients
with chronic vascular endothelial dysfunction?
A. Nitric Oxide
B. Prostacyclin
C. Endothelin-1
D. Angiotensin II
Answer: A
Rationale: Endothelial dysfunction is characterized by a reduction in the bioavailability of
Nitric Oxide (NO), a potent vasodilator. Without adequate NO, the vessels remain in a
relatively constricted state and are more prone to inflammatory changes. This deficiency is
a hallmark of atherosclerosis and hypertension development.
5. A patient with long-standing COPD is found to have right ventricular hypertrophy on an
echocardiogram. The provider correctly identifies this as Cor Pulmonale. What is the initiating
factor for this condition?
A. Left-sided heart failure causing backflow
B. Chronic pulmonary hypertension due to alveolar hypoxia
C. Systemic hypertension increasing right-sided afterload
D. Aortic regurgitation leading to pulmonary congestion
Answer: B
Rationale: In COPD, chronic alveolar hypoxia triggers pulmonary vasoconstriction to
redirect blood flow to better-ventilated areas. Persistent vasoconstriction leads to
structural remodeling of the pulmonary vessels and elevated pulmonary artery pressures.
The right ventricle must then work harder against this high pressure, leading to
hypertrophy and eventual failure.
, 6. A 45-year-old male is admitted with a massive pulmonary embolism. His arterial blood gas
reveals a significant increase in the alveolar-arterial (A-a) gradient and hypoxemia. Which
V/Q abnormality is most likely present?
A. Shunt (Low V/Q)
B. Normal V/Q matching
C. Silent unit
D. Dead space (High V/Q)
Answer: D
Rationale: A pulmonary embolism blocks blood flow to a segment of the lung while
ventilation continues, creating ‘dead space’. This is considered a high V/Q ratio because
ventilation (V) is present but perfusion (Q) is absent. The lack of gas exchange in the
affected area contributes to overall hypoxemia and increased respiratory effort.
7. Which phase of Acute Respiratory Distress Syndrome (ARDS) is characterized by the
formation of hyaline membranes and the flooding of alveoli with protein-rich edema fluid?
A. Fibrotic phase
B. Proliferative phase
C. Exudative phase
D. Resolution phase
Answer: C
Rationale: The exudative phase occurs within the first 72 hours of the initial lung injury.
During this time, endothelial and epithelial damage leads to increased capillary
permeability and alveolar flooding. The accumulation of fibrin and cellular debris results in
the classic hyaline membranes seen on pathology.
8. In the pathogenesis of emphysema, the imbalance between which two substances leads to
the destruction of alveolar walls?
A. Histamine and Epinephrine
B. Surfactant and Mucus
C. Proteases and Anti-proteases
D. Nitric Oxide and Endothelin
Answer: C
Rationale: Emphysema involves the destruction of elastin in the alveolar walls due to an
excess of proteases (like elastase) relative to anti-proteases (like alpha-1 antitrypsin).
Smoking increases the recruitment of neutrophils that release these proteases while
Pathophysiology (NSG530 Exam 2) [PDF] | Wilkes University
1. A 62-year-old male presents to the emergency department with substernal chest pain that
radiates to his left jaw. His EKG shows ST-segment depression in leads V3-V6, and his initial
troponin I is slightly elevated at 0.08 ng/mL. Which mechanism best explains the underlying
pathophysiology of his condition?
A. Transmural infarction due to complete occlusion of a coronary artery
B. Subendocardial ischemia due to a partial occlusion of a coronary artery
C. Vasospasm of the coronary artery at rest (Prinzmetal angina)
D. Stable plaque rupture with immediate spontaneous thrombolysis
Answer: B
Rationale: The presence of ST-segment depression and elevated troponins indicates a
Non-ST Elevation Myocardial Infarction (NSTEMI). This condition typically results from a
subendocardial ischemia caused by a partially occluding thrombus. Unlike a STEMI, the
necrosis is limited to the inner layer of the myocardium rather than the full thickness of the
wall.
2. Following a large anterior wall myocardial infarction, a patient begins to show signs of left
ventricular enlargement and thinning of the infarcted wall. Which process is primarily
responsible for these structural changes?
A. Physiological hypertrophy
B. Myocardial stunning
C. Ventricular remodeling
D. Hibernating myocardium
Answer: C
Rationale: Ventricular remodeling involves structural changes in the heart’s shape, size,
and function following an injury like an MI. This process is driven by neurohumoral
activation, specifically the RAAS and sympathetic nervous system. While initially
compensatory, chronic remodeling often leads to progressive heart failure and decreased
contractility.
3. A 72-year-old female is diagnosed with aortic stenosis. During auscultation, the provider
hears a harsh systolic crescendo-decrescendo murmur at the right upper sternal border. What
is the primary hemodynamic consequence of this disorder?
A. Increased stroke volume
,B. Decreased left atrial pressure
C. Increased left ventricular afterload
D. Decreased left ventricular end-diastolic pressure
Answer: C
Rationale: Aortic stenosis narrows the valve orifice, creating a significant resistance to
blood being ejected from the left ventricle. This increased resistance represents an
elevation in afterload, forcing the ventricle to generate higher pressures to maintain
cardiac output. Over time, this leads to concentric left ventricular hypertrophy as the heart
adapts to the chronic pressure overload.
4. Which mediator is primarily responsible for the impaired vasodilation observed in patients
with chronic vascular endothelial dysfunction?
A. Nitric Oxide
B. Prostacyclin
C. Endothelin-1
D. Angiotensin II
Answer: A
Rationale: Endothelial dysfunction is characterized by a reduction in the bioavailability of
Nitric Oxide (NO), a potent vasodilator. Without adequate NO, the vessels remain in a
relatively constricted state and are more prone to inflammatory changes. This deficiency is
a hallmark of atherosclerosis and hypertension development.
5. A patient with long-standing COPD is found to have right ventricular hypertrophy on an
echocardiogram. The provider correctly identifies this as Cor Pulmonale. What is the initiating
factor for this condition?
A. Left-sided heart failure causing backflow
B. Chronic pulmonary hypertension due to alveolar hypoxia
C. Systemic hypertension increasing right-sided afterload
D. Aortic regurgitation leading to pulmonary congestion
Answer: B
Rationale: In COPD, chronic alveolar hypoxia triggers pulmonary vasoconstriction to
redirect blood flow to better-ventilated areas. Persistent vasoconstriction leads to
structural remodeling of the pulmonary vessels and elevated pulmonary artery pressures.
The right ventricle must then work harder against this high pressure, leading to
hypertrophy and eventual failure.
, 6. A 45-year-old male is admitted with a massive pulmonary embolism. His arterial blood gas
reveals a significant increase in the alveolar-arterial (A-a) gradient and hypoxemia. Which
V/Q abnormality is most likely present?
A. Shunt (Low V/Q)
B. Normal V/Q matching
C. Silent unit
D. Dead space (High V/Q)
Answer: D
Rationale: A pulmonary embolism blocks blood flow to a segment of the lung while
ventilation continues, creating ‘dead space’. This is considered a high V/Q ratio because
ventilation (V) is present but perfusion (Q) is absent. The lack of gas exchange in the
affected area contributes to overall hypoxemia and increased respiratory effort.
7. Which phase of Acute Respiratory Distress Syndrome (ARDS) is characterized by the
formation of hyaline membranes and the flooding of alveoli with protein-rich edema fluid?
A. Fibrotic phase
B. Proliferative phase
C. Exudative phase
D. Resolution phase
Answer: C
Rationale: The exudative phase occurs within the first 72 hours of the initial lung injury.
During this time, endothelial and epithelial damage leads to increased capillary
permeability and alveolar flooding. The accumulation of fibrin and cellular debris results in
the classic hyaline membranes seen on pathology.
8. In the pathogenesis of emphysema, the imbalance between which two substances leads to
the destruction of alveolar walls?
A. Histamine and Epinephrine
B. Surfactant and Mucus
C. Proteases and Anti-proteases
D. Nitric Oxide and Endothelin
Answer: C
Rationale: Emphysema involves the destruction of elastin in the alveolar walls due to an
excess of proteases (like elastase) relative to anti-proteases (like alpha-1 antitrypsin).
Smoking increases the recruitment of neutrophils that release these proteases while
