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NSG 3850/ NSG3850 Exam 2 – (New 2026/ 2027 Update) Pathophysiology for Nurses II Guide | Questions & Answers | Grade A| 100% Correct (Verified Solutions)- Galen

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NSG 3850/ NSG3850 Exam 2 – (New 2026/ 2027 Update) Pathophysiology for Nurses II Guide | Questions & Answers | Grade A| 100% Correct (Verified Solutions)- Galen

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NSG 3850/ NSG3850 Exam 2 – (New 2026/ 2027 Update)
Pathophysiology for Nurses II Guide | Questions & Answers |
Grade A| 100% Correct (Verified Solutions)- Galen


Q1. A patient with long-standing hypertension develops left ventricular hypertrophy. This adaptive
mechanism initially:
A. Decreases myocardial oxygen demand
B. Increases the force of contraction to overcome increased afterload
C. Reduces cardiac output
D. Causes ventricular dilation

Correct Answer: B
Rationale: In hypertension, the left ventricle must pump against increased systemic vascular resistance
(afterload). The ventricle hypertrophies to generate a stronger contraction. Over time, however, this
leads to increased oxygen demand and diastolic dysfunction.



Q2. A patient with heart failure has an ejection fraction of 30%. This finding is consistent with:
A. Heart failure with preserved ejection fraction (HFpEF)
B. Heart failure with reduced ejection fraction (HFrEF)
C. Cor pulmonale
D. Pericarditis

Correct Answer: B
Rationale: HFrEF is defined as an EF ≤40%. Normal EF is 55-70%. This patient's EF of 30% indicates
significant systolic dysfunction.



Q3. The primary hemodynamic consequence of mitral stenosis is:
A. Increased left ventricular afterload
B. Increased left atrial pressure and pulmonary congestion
C. Decreased right ventricular preload
D. Increased systemic vascular resistance

Correct Answer: B
Rationale: Mitral stenosis obstructs blood flow from the left atrium to the left ventricle. This causes
pressure to build in the left atrium, which is transmitted backward to the pulmonary veins, leading to
pulmonary congestion and edema.




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Q4. A patient presents with sharp, pleuritic chest pain that improves when sitting up and leaning
forward. A pericardial friction rub is auscultated. These findings are most consistent with:
A. Myocardial infarction
B. Acute pericarditis
C. Pulmonary embolism
D. Aortic dissection

Correct Answer: B
Rationale: Acute pericarditis typically presents with positional chest pain (relieved by sitting forward)
and a pericardial friction rub, caused by inflammation of the pericardial sac.



Q5. A patient with a history of rheumatic fever develops aortic regurgitation. What is the primary
hemodynamic change?
A. Pressure overload of the left ventricle
B. Volume overload of the left ventricle due to diastolic backflow of blood
C. Pressure overload of the right ventricle
D. Decreased left ventricular end-diastolic volume

Correct Answer: B
Rationale: In aortic regurgitation, the aortic valve does not close completely during diastole, allowing
blood to flow back from the aorta into the left ventricle. This causes volume overload and left
ventricular dilation.



Q6. Which of the following is a common cause of right-sided heart failure?
A. Aortic stenosis
B. Left-sided heart failure
C. Mitral regurgitation
D. Hypertension

Correct Answer: B
Rationale: The most common cause of right-sided heart failure is left-sided heart failure. When the left
ventricle fails, pressure builds in the pulmonary circulation, increasing the workload on the right
ventricle, which eventually fails.



Q7. A patient with a tension pneumothorax develops tracheal deviation and hypotension. The
underlying pathophysiology is:
A. Increased intrathoracic pressure compressing the heart and great vessels, decreasing venous return
B. Massive blood loss into the pleural space
C. Vagal nerve stimulation causing bradycardia
D. Acute right ventricular failure

Correct Answer: A
Rationale: A tension pneumothorax causes air to accumulate in the pleural space under pressure,


pg. 2

,3


shifting the mediastinum, compressing the vena cava, and severely reducing venous return and cardiac
output.



Q8. The most common cause of infective endocarditis in IV drug users is:
A. Streptococcus viridans
B. Staphylococcus aureus
C. Enterococcus faecalis
D. Pseudomonas aeruginosa

Correct Answer: B
Rationale: IV drug users are at high risk for endocarditis caused by S. aureus, which often affects the
tricuspid valve. In non-IV drug users, Streptococcus viridans is more common on damaged native valves.



Q9. A patient with chronic hypertension is at increased risk for developing which of the following?
(Select all that apply)
A. Left ventricular hypertrophy
B. Stroke
C. Chronic kidney disease
D. Aortic dissection
E. Retinopathy

Correct Answer: A, B, C, D, E
Rationale: Chronic hypertension damages the vasculature throughout the body, leading to target-organ
damage including LVH, stroke, CKD, aortic dissection, and hypertensive retinopathy.



Q10. The pathophysiologic mechanism underlying stable angina is:
A. Coronary artery vasospasm
B. A fixed atherosclerotic plaque that reduces coronary blood flow, causing ischemia when myocardial
oxygen demand increases
C. Plaque rupture with thrombus formation
D. Microvascular dysfunction without obstructive coronary disease

Correct Answer: B
Rationale: Stable angina occurs when a stable, flow-limiting atherosclerotic plaque limits coronary
perfusion. Symptoms occur when myocardial oxygen demand (e.g., with exertion) exceeds the fixed
supply.



Q11. Unstable angina and non-ST-elevation myocardial infarction (NSTEMI) share a common
pathophysiology, which is:
A. Complete, persistent coronary occlusion
B. Plaque rupture or erosion with partial, transient thrombus formation



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C. Coronary artery vasospasm
D. Ventricular hypertrophy

Correct Answer: B
Rationale: Both are part of the acute coronary syndrome spectrum. Unstable angina and NSTEMI result
from plaque disruption causing partial thrombus formation, leading to subtotal occlusion and ischemia.
STEMI involves total occlusion.



Q12. A patient with an acute ST-elevation myocardial infarction (STEMI) has a totally occluded coronary
artery. The primary goal of emergency treatment is:
A. Administer high-dose statins
B. Reperfuse the myocardium as quickly as possible via PCI or thrombolysis
C. Control pain with morphine
D. Monitor for dysrhythmias

Correct Answer: B
Rationale: In STEMI, the artery is completely occluded, and myocardial cells are dying. The priority is
rapid reperfusion (door-to-balloon time <90 minutes for PCI, or thrombolysis within 30 minutes) to
salvage as much myocardium as possible.



Q13. A patient with an inferior wall MI develops bradycardia and hypotension. This is most likely due to:
A. Cardiogenic shock
B. Increased vagal tone (Bezold-Jarisch reflex) or involvement of the right coronary artery supplying the
SA/AV nodes
C. Pericarditis
D. Ventricular septal rupture

Correct Answer: B
Rationale: Inferior MIs often involve the right coronary artery, which supplies the SA and AV nodes.
Ischemia can cause bradycardia and heart block. Increased vagal tone also contributes.



Q14. A patient who had an MI 5 days ago develops a new, loud holosystolic murmur at the left lower
sternal border and acute pulmonary edema. The most likely diagnosis is:
A. Papillary muscle rupture causing acute mitral regurgitation
B. Ventricular septal rupture
C. Pericarditis
D. Aortic dissection

Correct Answer: B
Rationale: A new holosystolic murmur at the LLSB after an MI with acute pulmonary edema suggests a
ventricular septal rupture, a mechanical complication. Papillary muscle rupture causes a murmur at the
apex.



pg. 4

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