NR 507 Exam 2 Actual Exam V1 | NR 507 Advanced Pathophysiology
(NR507 Exam 2) [PDF] | Chamberlain University
1. A 62-year-old patient with chronic hypertension presents with left ventricular hypertrophy.
What is the primary pathophysiological driver for this adaptation?
A. Decreased peripheral vascular resistance
B. Increased afterload resulting in increased myocyte workload
C. Reduced renin-angiotensin-aldosterone system activation
D. Increased myocardial compliance and relaxation
Answer: B
Rationale: Chronic hypertension increases the resistance against which the left ventricle
must pump, known as afterload. To maintain cardiac output, the myocytes undergo
hypertrophy to generate more force. Over time, this adaptation can lead to decreased
chamber volume and eventual heart failure.
2. Which process occurs first in the development of atherosclerosis after endothelial injury?
A. Formation of a fibrous plaque
B. Accumulation of oxidized LDL in the tunica intima
C. Calcification of the vessel wall
D. Rupture of the lipid core
Answer: B
Rationale: Endothelial injury allows low-density lipoproteins (LDL) to enter the
subendothelial space where they become oxidized. These oxidized LDLs then trigger an
inflammatory response by attracting monocytes. This is considered the initiating step
before the formation of foam cells and fatty streaks.
3. A patient with stable angina experiences chest pain during exercise but finds relief with
rest. What is the underlying mechanism of this pain?
A. Myocardial oxygen demand exceeding the available supply
B. Vasospasm of the coronary arteries at rest
C. Permanent occlusion of a coronary artery by a thrombus
D. Inflammation of the pericardial sac
Answer: A
,Rationale: Stable angina occurs when fixed atherosclerotic plaques narrow the coronary
arteries, limiting blood flow. During physical exertion, the heart’s demand for oxygen
increases, but the narrowed vessels cannot provide adequate supply, leading to ischemia.
Resting reduces the heart’s workload, allowing the oxygen supply-demand balance to
return to normal.
4. In the early stages of a myocardial infarction, which cellular change is responsible for the
release of cardiac biomarkers like Troponin?
A. Increased ATP production via anaerobic metabolism
B. Stabilization of the lysosomal membranes
C. Cellular shrinkage and dehydration
D. Cell membrane rupture due to lack of energy for ion pumps
Answer: D
Rationale: Severe ischemia depletes ATP, which causes the failure of the sodium-
potassium pump and leads to cellular swelling. Eventually, the cell membrane loses its
integrity and ruptures, releasing intracellular contents into the bloodstream. These
contents, including Troponin and CK-MB, are then used as diagnostic markers for
myocardial necrosis.
5. A patient is diagnosed with Left Heart Failure (HFrEF). Which finding is a direct result of
increased pulmonary hydrostatic pressure?
A. Peripheral edema in the lower extremities
B. Jugular venous distention
C. Hepatomegaly and ascites
D. Crackles or rales upon lung auscultation
Answer: D
Rationale: In left-sided heart failure, the left ventricle cannot effectively eject blood,
causing a backup into the left atrium and pulmonary veins. This increases hydrostatic
pressure in the pulmonary capillaries, forcing fluid into the alveoli. This fluid accumulation
manifests clinically as crackles or pulmonary edema.
6. What is the compensatory role of Brain Natriuretic Peptide (BNP) in a patient with heart
failure?
A. To increase systemic vascular resistance
B. To promote sodium and water retention
C. To stimulate the release of aldosterone
D. To promote vasodilation and diuresis
, Answer: D
Rationale: BNP is released by the ventricles in response to increased wall stretch and
volume overload. It acts to counteract the RAAS system by promoting the excretion of
sodium and water by the kidneys. Additionally, it induces vasodilation to help reduce both
preload and afterload on the failing heart.
7. A patient presents with a sudden onset of sharp chest pain that worsens with deep
inspiration and is relieved by sitting forward. What is the most likely diagnosis?
A. Acute pericarditis
B. Acute myocardial infarction
C. Stable angina pectoris
D. Aortic dissection
Answer: A
Rationale: The description of pleuritic chest pain that is position-dependent is a hallmark
sign of pericarditis. Inflammation of the pericardial layers causes friction, which is heard as
a rub and felt more intensely during inspiration. Sitting forward pulls the heart away from
the pleura, often providing symptomatic relief.
8. Which dysrhythmia is characterized by the total absence of P waves and an irregularly
irregular ventricular rhythm?
A. First-degree AV block
B. Ventricular tachycardia
C. Atrial fibrillation
D. Sinus bradycardia
Answer: C
Rationale: Atrial fibrillation involves rapid, disorganized electrical activity in the atria,
which prevents coordinated atrial contraction. Because the AV node is bombarded with
impulses, the ventricular response is irregular. This condition significantly increases the
risk of thromboembolic events such as stroke.
9. A 55-year-old male with a history of smoking presents with a ‘barrel chest’ and productive
cough. Which pathophysiological change is characteristic of emphysema?
A. Destruction of alveolar walls and loss of elastic recoil
B. Hypertrophy of mucus-secreting glands
C. Reversible airway bronchospasm
D. Permanent dilation of the bronchi
(NR507 Exam 2) [PDF] | Chamberlain University
1. A 62-year-old patient with chronic hypertension presents with left ventricular hypertrophy.
What is the primary pathophysiological driver for this adaptation?
A. Decreased peripheral vascular resistance
B. Increased afterload resulting in increased myocyte workload
C. Reduced renin-angiotensin-aldosterone system activation
D. Increased myocardial compliance and relaxation
Answer: B
Rationale: Chronic hypertension increases the resistance against which the left ventricle
must pump, known as afterload. To maintain cardiac output, the myocytes undergo
hypertrophy to generate more force. Over time, this adaptation can lead to decreased
chamber volume and eventual heart failure.
2. Which process occurs first in the development of atherosclerosis after endothelial injury?
A. Formation of a fibrous plaque
B. Accumulation of oxidized LDL in the tunica intima
C. Calcification of the vessel wall
D. Rupture of the lipid core
Answer: B
Rationale: Endothelial injury allows low-density lipoproteins (LDL) to enter the
subendothelial space where they become oxidized. These oxidized LDLs then trigger an
inflammatory response by attracting monocytes. This is considered the initiating step
before the formation of foam cells and fatty streaks.
3. A patient with stable angina experiences chest pain during exercise but finds relief with
rest. What is the underlying mechanism of this pain?
A. Myocardial oxygen demand exceeding the available supply
B. Vasospasm of the coronary arteries at rest
C. Permanent occlusion of a coronary artery by a thrombus
D. Inflammation of the pericardial sac
Answer: A
,Rationale: Stable angina occurs when fixed atherosclerotic plaques narrow the coronary
arteries, limiting blood flow. During physical exertion, the heart’s demand for oxygen
increases, but the narrowed vessels cannot provide adequate supply, leading to ischemia.
Resting reduces the heart’s workload, allowing the oxygen supply-demand balance to
return to normal.
4. In the early stages of a myocardial infarction, which cellular change is responsible for the
release of cardiac biomarkers like Troponin?
A. Increased ATP production via anaerobic metabolism
B. Stabilization of the lysosomal membranes
C. Cellular shrinkage and dehydration
D. Cell membrane rupture due to lack of energy for ion pumps
Answer: D
Rationale: Severe ischemia depletes ATP, which causes the failure of the sodium-
potassium pump and leads to cellular swelling. Eventually, the cell membrane loses its
integrity and ruptures, releasing intracellular contents into the bloodstream. These
contents, including Troponin and CK-MB, are then used as diagnostic markers for
myocardial necrosis.
5. A patient is diagnosed with Left Heart Failure (HFrEF). Which finding is a direct result of
increased pulmonary hydrostatic pressure?
A. Peripheral edema in the lower extremities
B. Jugular venous distention
C. Hepatomegaly and ascites
D. Crackles or rales upon lung auscultation
Answer: D
Rationale: In left-sided heart failure, the left ventricle cannot effectively eject blood,
causing a backup into the left atrium and pulmonary veins. This increases hydrostatic
pressure in the pulmonary capillaries, forcing fluid into the alveoli. This fluid accumulation
manifests clinically as crackles or pulmonary edema.
6. What is the compensatory role of Brain Natriuretic Peptide (BNP) in a patient with heart
failure?
A. To increase systemic vascular resistance
B. To promote sodium and water retention
C. To stimulate the release of aldosterone
D. To promote vasodilation and diuresis
, Answer: D
Rationale: BNP is released by the ventricles in response to increased wall stretch and
volume overload. It acts to counteract the RAAS system by promoting the excretion of
sodium and water by the kidneys. Additionally, it induces vasodilation to help reduce both
preload and afterload on the failing heart.
7. A patient presents with a sudden onset of sharp chest pain that worsens with deep
inspiration and is relieved by sitting forward. What is the most likely diagnosis?
A. Acute pericarditis
B. Acute myocardial infarction
C. Stable angina pectoris
D. Aortic dissection
Answer: A
Rationale: The description of pleuritic chest pain that is position-dependent is a hallmark
sign of pericarditis. Inflammation of the pericardial layers causes friction, which is heard as
a rub and felt more intensely during inspiration. Sitting forward pulls the heart away from
the pleura, often providing symptomatic relief.
8. Which dysrhythmia is characterized by the total absence of P waves and an irregularly
irregular ventricular rhythm?
A. First-degree AV block
B. Ventricular tachycardia
C. Atrial fibrillation
D. Sinus bradycardia
Answer: C
Rationale: Atrial fibrillation involves rapid, disorganized electrical activity in the atria,
which prevents coordinated atrial contraction. Because the AV node is bombarded with
impulses, the ventricular response is irregular. This condition significantly increases the
risk of thromboembolic events such as stroke.
9. A 55-year-old male with a history of smoking presents with a ‘barrel chest’ and productive
cough. Which pathophysiological change is characteristic of emphysema?
A. Destruction of alveolar walls and loss of elastic recoil
B. Hypertrophy of mucus-secreting glands
C. Reversible airway bronchospasm
D. Permanent dilation of the bronchi
