NSG 530 Exam 2 Actual Exam V1 | NSG 530 Advanced
Pathophysiology (NSG530 Exam 2) | Wilkes University
1. A 65-year-old patient with left-sided heart failure experiences worsening dyspnea and
orthopnea. Which mechanism is primarily responsible for these clinical manifestations?
A. Decreased systemic vascular resistance leading to hypotension.
B. Reduced oncotic pressure due to hepatic congestion and impaired protein synthesis.
C. Increased pulmonary capillary hydrostatic pressure causing fluid movement into the
alveoli.
D. Activation of the parasympathetic nervous system resulting in bronchoconstriction.
Answer: C
Rationale: In left-sided heart failure, the left ventricle fails to pump blood efficiently into
the systemic circulation, leading to a backup of blood into the pulmonary veins. This
increases hydrostatic pressure in the pulmonary capillaries, forcing fluid into the lung
interstitium and alveoli. Consequently, this leads to the classic symptoms of pulmonary
edema, including dyspnea and orthopnea.
2. Which compensatory mechanism is activated in response to decreased cardiac output in
heart failure but eventually contributes to cardiac remodeling and worsening failure?
A. Chronic activation of the sympathetic nervous system (SNS).
B. Increased secretion of atrial natriuretic peptide (ANP).
C. Inhibition of the renin-angiotensin-aldosterone system (RAAS).
D. Downregulation of endothelin-1 receptors.
Answer: A
Rationale: Decreased cardiac output triggers the sympathetic nervous system to increase
heart rate and contractility to maintain perfusion. However, chronic SNS activation leads to
increased myocardial oxygen demand and exposure to catecholamines, which promotes
myocyte hypertrophy and apoptosis. This process contributes significantly to the structural
remodeling and progressive decline of cardiac function seen in heart failure.
3. A patient is diagnosed with Prinzmetal (variant) angina. What is the underlying
pathophysiology of this condition?
A. Stable atherosclerotic plaque obstructing blood flow during exercise.
B. Rupture of an unstable plaque leading to transient thrombus formation.
C. Vasospasm of the coronary arteries, often occurring at rest.
,D. Increased demand for oxygen in the setting of severe aortic stenosis.
Answer: C
Rationale: Prinzmetal angina is characterized by chest pain caused by temporary
vasospasm of a coronary artery rather than fixed atherosclerotic narrowing. These spasms
often occur at rest or during sleep and are typically associated with ST-segment elevation
on an ECG. The mechanism involves hyper-reactivity of the vascular smooth muscle, often
related to altered calcium channel function or sympathetic activity.
4. In the pathogenesis of atherosclerosis, what is the significance of ‘foam cells’?
A. They are smooth muscle cells that have migrated to the adventitia.
B. They represent platelets that have aggregated at the site of endothelial injury.
C. They are macrophages that have ingested oxidized LDL cholesterol.
D. They are neutrophils that release reactive oxygen species to dissolve plaques.
Answer: C
Rationale: Foam cells are formed when macrophages migrate into the arterial wall and
ingest oxidized low-density lipoprotein (LDL) cholesterol. These cells accumulate in the
subendothelial space, forming the ‘fatty streak’ which is the earliest visible lesion of
atherosclerosis. The accumulation of foam cells triggers further inflammatory responses
and contributes to the progression of the atherosclerotic plaque.
5. Which valve disorder is most likely to result in left ventricular hypertrophy due to
increased afterload?
A. Mitral valve prolapse.
B. Aortic stenosis.
C. Tricuspid regurgitation.
D. Mitral stenosis.
Answer: B
Rationale: Aortic stenosis creates a narrow opening for blood to exit the left ventricle into
the aorta, significantly increasing the resistance or afterload the ventricle must overcome.
To maintain cardiac output against this resistance, the left ventricular myocardium
undergoes compensatory hypertrophy. Over time, this thickening of the wall decreases
ventricular compliance and can lead to heart failure.
6. A patient with chronic obstructive pulmonary disease (COPD) presents with polycythemia.
What is the physiological driver for this increase in red blood cells?
A. Chronic hypercapnia stimulating the bone marrow.
B. Increased erythropoietin production in response to chronic hypoxemia.
, C. Decreased plasma volume leading to hemoconcentration.
D. Impaired iron metabolism due to chronic inflammation.
Answer: B
Rationale: Chronic hypoxemia, common in advanced COPD, is sensed by the kidneys,
which respond by increasing the production of erythropoietin. Erythropoietin stimulates
the bone marrow to produce more red blood cells (erythrocytes) to increase the oxygen-
carrying capacity of the blood. This secondary polycythemia is a compensatory mechanism
that increases blood viscosity and the risk of thromboembolic events.
7. During an asthma attack, the early-phase response is primarily mediated by which of the
following?
A. Eosinophil recruitment and tissue remodeling.
B. Alveolar macrophage activation and cytokine storm.
C. Increased production of surfactant by type II pneumocytes.
D. Mast cell degranulation and release of histamine.
Answer: D
Rationale: The early-phase response of asthma occurs within minutes of allergen exposure
and is driven by IgE-mediated mast cell degranulation. Mast cells release preformed
mediators like histamine and leukotrienes, which cause rapid bronchoconstriction,
increased vascular permeability, and mucus secretion. This phase explains the acute onset
of wheezing and shortness of breath in sensitized individuals.
8. What is the hallmark physiological finding in Acute Respiratory Distress Syndrome (ARDS)?
A. Refractory hypoxemia due to right-to-left shunting.
B. Hypoxemia that is highly responsive to supplemental oxygen.
C. Decreased alveolar-capillary membrane permeability.
D. Increased pulmonary compliance and hyperinflation.
Answer: A
Rationale: ARDS is characterized by severe inflammation that damages the alveolar-
capillary membrane, leading to non-cardiogenic pulmonary edema and alveolar collapse.
This results in significant ventilation-perfusion mismatching and shunting, where blood
passes through non-ventilated areas of the lung. The resulting hypoxemia is termed
‘refractory’ because it does not significantly improve with increasing concentrations of
inspired oxygen.
9. Emphysema is characterized by which of the following structural changes in the lungs?
A. Hyperplasia of goblet cells in the large airways.
Pathophysiology (NSG530 Exam 2) | Wilkes University
1. A 65-year-old patient with left-sided heart failure experiences worsening dyspnea and
orthopnea. Which mechanism is primarily responsible for these clinical manifestations?
A. Decreased systemic vascular resistance leading to hypotension.
B. Reduced oncotic pressure due to hepatic congestion and impaired protein synthesis.
C. Increased pulmonary capillary hydrostatic pressure causing fluid movement into the
alveoli.
D. Activation of the parasympathetic nervous system resulting in bronchoconstriction.
Answer: C
Rationale: In left-sided heart failure, the left ventricle fails to pump blood efficiently into
the systemic circulation, leading to a backup of blood into the pulmonary veins. This
increases hydrostatic pressure in the pulmonary capillaries, forcing fluid into the lung
interstitium and alveoli. Consequently, this leads to the classic symptoms of pulmonary
edema, including dyspnea and orthopnea.
2. Which compensatory mechanism is activated in response to decreased cardiac output in
heart failure but eventually contributes to cardiac remodeling and worsening failure?
A. Chronic activation of the sympathetic nervous system (SNS).
B. Increased secretion of atrial natriuretic peptide (ANP).
C. Inhibition of the renin-angiotensin-aldosterone system (RAAS).
D. Downregulation of endothelin-1 receptors.
Answer: A
Rationale: Decreased cardiac output triggers the sympathetic nervous system to increase
heart rate and contractility to maintain perfusion. However, chronic SNS activation leads to
increased myocardial oxygen demand and exposure to catecholamines, which promotes
myocyte hypertrophy and apoptosis. This process contributes significantly to the structural
remodeling and progressive decline of cardiac function seen in heart failure.
3. A patient is diagnosed with Prinzmetal (variant) angina. What is the underlying
pathophysiology of this condition?
A. Stable atherosclerotic plaque obstructing blood flow during exercise.
B. Rupture of an unstable plaque leading to transient thrombus formation.
C. Vasospasm of the coronary arteries, often occurring at rest.
,D. Increased demand for oxygen in the setting of severe aortic stenosis.
Answer: C
Rationale: Prinzmetal angina is characterized by chest pain caused by temporary
vasospasm of a coronary artery rather than fixed atherosclerotic narrowing. These spasms
often occur at rest or during sleep and are typically associated with ST-segment elevation
on an ECG. The mechanism involves hyper-reactivity of the vascular smooth muscle, often
related to altered calcium channel function or sympathetic activity.
4. In the pathogenesis of atherosclerosis, what is the significance of ‘foam cells’?
A. They are smooth muscle cells that have migrated to the adventitia.
B. They represent platelets that have aggregated at the site of endothelial injury.
C. They are macrophages that have ingested oxidized LDL cholesterol.
D. They are neutrophils that release reactive oxygen species to dissolve plaques.
Answer: C
Rationale: Foam cells are formed when macrophages migrate into the arterial wall and
ingest oxidized low-density lipoprotein (LDL) cholesterol. These cells accumulate in the
subendothelial space, forming the ‘fatty streak’ which is the earliest visible lesion of
atherosclerosis. The accumulation of foam cells triggers further inflammatory responses
and contributes to the progression of the atherosclerotic plaque.
5. Which valve disorder is most likely to result in left ventricular hypertrophy due to
increased afterload?
A. Mitral valve prolapse.
B. Aortic stenosis.
C. Tricuspid regurgitation.
D. Mitral stenosis.
Answer: B
Rationale: Aortic stenosis creates a narrow opening for blood to exit the left ventricle into
the aorta, significantly increasing the resistance or afterload the ventricle must overcome.
To maintain cardiac output against this resistance, the left ventricular myocardium
undergoes compensatory hypertrophy. Over time, this thickening of the wall decreases
ventricular compliance and can lead to heart failure.
6. A patient with chronic obstructive pulmonary disease (COPD) presents with polycythemia.
What is the physiological driver for this increase in red blood cells?
A. Chronic hypercapnia stimulating the bone marrow.
B. Increased erythropoietin production in response to chronic hypoxemia.
, C. Decreased plasma volume leading to hemoconcentration.
D. Impaired iron metabolism due to chronic inflammation.
Answer: B
Rationale: Chronic hypoxemia, common in advanced COPD, is sensed by the kidneys,
which respond by increasing the production of erythropoietin. Erythropoietin stimulates
the bone marrow to produce more red blood cells (erythrocytes) to increase the oxygen-
carrying capacity of the blood. This secondary polycythemia is a compensatory mechanism
that increases blood viscosity and the risk of thromboembolic events.
7. During an asthma attack, the early-phase response is primarily mediated by which of the
following?
A. Eosinophil recruitment and tissue remodeling.
B. Alveolar macrophage activation and cytokine storm.
C. Increased production of surfactant by type II pneumocytes.
D. Mast cell degranulation and release of histamine.
Answer: D
Rationale: The early-phase response of asthma occurs within minutes of allergen exposure
and is driven by IgE-mediated mast cell degranulation. Mast cells release preformed
mediators like histamine and leukotrienes, which cause rapid bronchoconstriction,
increased vascular permeability, and mucus secretion. This phase explains the acute onset
of wheezing and shortness of breath in sensitized individuals.
8. What is the hallmark physiological finding in Acute Respiratory Distress Syndrome (ARDS)?
A. Refractory hypoxemia due to right-to-left shunting.
B. Hypoxemia that is highly responsive to supplemental oxygen.
C. Decreased alveolar-capillary membrane permeability.
D. Increased pulmonary compliance and hyperinflation.
Answer: A
Rationale: ARDS is characterized by severe inflammation that damages the alveolar-
capillary membrane, leading to non-cardiogenic pulmonary edema and alveolar collapse.
This results in significant ventilation-perfusion mismatching and shunting, where blood
passes through non-ventilated areas of the lung. The resulting hypoxemia is termed
‘refractory’ because it does not significantly improve with increasing concentrations of
inspired oxygen.
9. Emphysema is characterized by which of the following structural changes in the lungs?
A. Hyperplasia of goblet cells in the large airways.
