MARYVILLE NURS 620 ADVANCED
PATHOPHYSIOLOGY EXAM 3 2026/2027 | Complete
Solution | A+ Certified | DNP Program | Pass
Guaranteed - A+ Graded
Section 1: Cardiovascular Pathophysiology - Heart Failure, Valvular Disease &
CAD (Q1-18)
Q1. A 72-year-old female with long-standing hypertension presents with exertional
dyspnea, fatigue, and bilateral pulmonary crackles. Echocardiography reveals an
ejection fraction of 58% and markedly elevated left ventricular end-diastolic pressure
with abnormal tissue Doppler imaging. This presentation is most consistent with:
A. Heart failure with reduced ejection fraction (HFrEF)
B. Heart failure with preserved ejection fraction (HFpEF)
C. Dilated cardiomyopathy
D. Hypertrophic obstructive cardiomyopathy
Correct Answer: B. Heart failure with preserved ejection fraction (HFpEF) [CORRECT]
Rationale: HFpEF is characterized by preserved systolic function (EF ≥50%) with
impaired diastolic filling and elevated filling pressures, commonly associated with
chronic hypertension and ventricular stiffness. HFrEF (A) requires reduced EF, dilated
cardiomyopathy (C) presents with systolic dysfunction and chamber dilation, and
HOCM (D) causes dynamic outflow obstruction.
Q2. In HFrEF, sustained activation of the renin-angiotensin-aldosterone system
(RAAS) produces which pathophysiologic consequence that perpetuates cardiac
remodeling?
A. Vasodilation and natriuresis
B. Vasoconstriction, sodium retention, and myocardial fibrosis
C. Decreased sympathetic nervous system activity
D. Increased nitric oxide bioavailability
,Correct Answer: B. Vasoconstriction, sodium retention, and myocardial fibrosis
[CORRECT]
Rationale: RAAS activation in HFrEF promotes maladaptive vasoconstriction, volume
overload, and collagen deposition, worsening afterload and ventricular stiffness.
Options A, C, and D describe compensatory or therapeutic mechanisms, not the
pathophysiologic consequences of RAAS overactivity.
Q3. A 68-year-old male with HFpEF is hospitalized with acute decompensation. The
primary hemodynamic defect in this condition is:
A. Reduced contractility and increased ventricular volumes
B. Impaired ventricular relaxation and increased passive stiffness
C. Severe mitral regurgitation with volume overload
D. High-output circulatory state
Correct Answer: B. Impaired ventricular relaxation and increased passive stiffness
[CORRECT]
Rationale: HFpEF is fundamentally a disorder of diastolic dysfunction where the
ventricle cannot relax or fill properly during diastole due to increased passive
stiffness. Reduced contractility (A) defines HFrEF, severe mitral regurgitation (C) is a
separate valvular problem, and high-output states (D) are unrelated.
Q4. A 75-year-old male reports syncope with exertion, angina, and progressive
dyspnea. Physical examination reveals a harsh crescendo-decrescendo systolic
murmur at the right upper sternal border radiating to the carotids. The underlying
pathophysiology involves:
A. Volume overload with eccentric left ventricular hypertrophy
B. Pressure overload with concentric left ventricular hypertrophy
C. Left ventricular dilation and reduced wall thickness
D. Right ventricular pressure overload from pulmonary hypertension
,Correct Answer: B. Pressure overload with concentric left ventricular hypertrophy
[CORRECT]
Rationale: Aortic stenosis creates a fixed outflow obstruction, generating pressure
overload that stimulates concentric LV hypertrophy to maintain wall stress. Volume
overload (A) occurs in regurgitant lesions, LV dilation (C) occurs in dilated
cardiomyopathy, and RV pressure overload (D) occurs in pulmonary hypertension.
Q5. A patient with chronic aortic regurgitation develops bounding pulses, a wide
pulse pressure, and Austin Flint murmur. The left ventricle undergoes:
A. Concentric hypertrophy without dilation
B. Eccentric hypertrophy with chamber dilation to accommodate regurgitant volume
C. Apical ballooning and akinesis
D. Right ventricular hypertrophy from pulmonary congestion
Correct Answer: B. Eccentric hypertrophy with chamber dilation to accommodate
regurgitant volume [CORRECT]
Rationale: Chronic volume overload from aortic regurgitation triggers eccentric
hypertrophy—sarcomeres added in series—producing a dilated, compliant ventricle
that handles increased preload. Concentric hypertrophy (A) responds to pressure
overload, apical ballooning (C) describes Takotsubo cardiomyopathy, and RV
hypertrophy (D) is not the primary adaptation.
Q6. A 45-year-old immigrant from Southeast Asia presents with dyspnea on exertion
and orthopnea. Echocardiography shows thickened, immobile mitral valve leaflets
with a "hockey stick" appearance of the anterior leaflet and a mitral valve area of 1.2
cm². The most likely etiology is:
A. Degenerative calcific mitral stenosis
B. Rheumatic heart disease
C. Mitral valve prolapse with chordal rupture
D. Infective endocarditis
, Correct Answer: B. Rheumatic heart disease [CORRECT]
Rationale: The commissural fusion, leaflet thickening, and hockey-stick deformity are
pathognomonic for rheumatic mitral stenosis, still prevalent in developing regions.
Degenerative calcification (A) typically affects the annulus in elderly patients, chordal
rupture (C) causes regurgitation, and endocarditis (D) produces vegetations and
regurgitation.
Q7. In severe mitral regurgitation, the left atrium and left ventricle dilate because:
A. Systolic ejection of blood into the aorta is obstructed
B. A portion of left ventricular stroke volume regurgitates into the low-pressure left
atrium during systole
C. Diastolic filling from the pulmonary veins is obstructed
D. Right ventricular output exceeds left ventricular output
Correct Answer: B. A portion of left ventricular stroke volume regurgitates into the
low-pressure left atrium during systole [CORRECT]
Rationale: In mitral regurgitation, the LV ejects blood retrograde into the compliant
LA during systole, creating volume overload that progressively dilates both
chambers. Obstruction (A, C) describes stenotic lesions, and RV output exceeding LV
output (D) is physiologically incorrect.
Q8. A 28-year-old female with a mid-systolic click and late systolic murmur that
worsens with Valsalva maneuver is diagnosed with mitral valve prolapse. The primary
structural abnormality is:
A. Commissural fusion and chordal shortening
B. Myxomatous degeneration with thickened, redundant valve leaflets
C. Bicuspid aortic valve with calcification
D. Papillary muscle rupture from ischemia
PATHOPHYSIOLOGY EXAM 3 2026/2027 | Complete
Solution | A+ Certified | DNP Program | Pass
Guaranteed - A+ Graded
Section 1: Cardiovascular Pathophysiology - Heart Failure, Valvular Disease &
CAD (Q1-18)
Q1. A 72-year-old female with long-standing hypertension presents with exertional
dyspnea, fatigue, and bilateral pulmonary crackles. Echocardiography reveals an
ejection fraction of 58% and markedly elevated left ventricular end-diastolic pressure
with abnormal tissue Doppler imaging. This presentation is most consistent with:
A. Heart failure with reduced ejection fraction (HFrEF)
B. Heart failure with preserved ejection fraction (HFpEF)
C. Dilated cardiomyopathy
D. Hypertrophic obstructive cardiomyopathy
Correct Answer: B. Heart failure with preserved ejection fraction (HFpEF) [CORRECT]
Rationale: HFpEF is characterized by preserved systolic function (EF ≥50%) with
impaired diastolic filling and elevated filling pressures, commonly associated with
chronic hypertension and ventricular stiffness. HFrEF (A) requires reduced EF, dilated
cardiomyopathy (C) presents with systolic dysfunction and chamber dilation, and
HOCM (D) causes dynamic outflow obstruction.
Q2. In HFrEF, sustained activation of the renin-angiotensin-aldosterone system
(RAAS) produces which pathophysiologic consequence that perpetuates cardiac
remodeling?
A. Vasodilation and natriuresis
B. Vasoconstriction, sodium retention, and myocardial fibrosis
C. Decreased sympathetic nervous system activity
D. Increased nitric oxide bioavailability
,Correct Answer: B. Vasoconstriction, sodium retention, and myocardial fibrosis
[CORRECT]
Rationale: RAAS activation in HFrEF promotes maladaptive vasoconstriction, volume
overload, and collagen deposition, worsening afterload and ventricular stiffness.
Options A, C, and D describe compensatory or therapeutic mechanisms, not the
pathophysiologic consequences of RAAS overactivity.
Q3. A 68-year-old male with HFpEF is hospitalized with acute decompensation. The
primary hemodynamic defect in this condition is:
A. Reduced contractility and increased ventricular volumes
B. Impaired ventricular relaxation and increased passive stiffness
C. Severe mitral regurgitation with volume overload
D. High-output circulatory state
Correct Answer: B. Impaired ventricular relaxation and increased passive stiffness
[CORRECT]
Rationale: HFpEF is fundamentally a disorder of diastolic dysfunction where the
ventricle cannot relax or fill properly during diastole due to increased passive
stiffness. Reduced contractility (A) defines HFrEF, severe mitral regurgitation (C) is a
separate valvular problem, and high-output states (D) are unrelated.
Q4. A 75-year-old male reports syncope with exertion, angina, and progressive
dyspnea. Physical examination reveals a harsh crescendo-decrescendo systolic
murmur at the right upper sternal border radiating to the carotids. The underlying
pathophysiology involves:
A. Volume overload with eccentric left ventricular hypertrophy
B. Pressure overload with concentric left ventricular hypertrophy
C. Left ventricular dilation and reduced wall thickness
D. Right ventricular pressure overload from pulmonary hypertension
,Correct Answer: B. Pressure overload with concentric left ventricular hypertrophy
[CORRECT]
Rationale: Aortic stenosis creates a fixed outflow obstruction, generating pressure
overload that stimulates concentric LV hypertrophy to maintain wall stress. Volume
overload (A) occurs in regurgitant lesions, LV dilation (C) occurs in dilated
cardiomyopathy, and RV pressure overload (D) occurs in pulmonary hypertension.
Q5. A patient with chronic aortic regurgitation develops bounding pulses, a wide
pulse pressure, and Austin Flint murmur. The left ventricle undergoes:
A. Concentric hypertrophy without dilation
B. Eccentric hypertrophy with chamber dilation to accommodate regurgitant volume
C. Apical ballooning and akinesis
D. Right ventricular hypertrophy from pulmonary congestion
Correct Answer: B. Eccentric hypertrophy with chamber dilation to accommodate
regurgitant volume [CORRECT]
Rationale: Chronic volume overload from aortic regurgitation triggers eccentric
hypertrophy—sarcomeres added in series—producing a dilated, compliant ventricle
that handles increased preload. Concentric hypertrophy (A) responds to pressure
overload, apical ballooning (C) describes Takotsubo cardiomyopathy, and RV
hypertrophy (D) is not the primary adaptation.
Q6. A 45-year-old immigrant from Southeast Asia presents with dyspnea on exertion
and orthopnea. Echocardiography shows thickened, immobile mitral valve leaflets
with a "hockey stick" appearance of the anterior leaflet and a mitral valve area of 1.2
cm². The most likely etiology is:
A. Degenerative calcific mitral stenosis
B. Rheumatic heart disease
C. Mitral valve prolapse with chordal rupture
D. Infective endocarditis
, Correct Answer: B. Rheumatic heart disease [CORRECT]
Rationale: The commissural fusion, leaflet thickening, and hockey-stick deformity are
pathognomonic for rheumatic mitral stenosis, still prevalent in developing regions.
Degenerative calcification (A) typically affects the annulus in elderly patients, chordal
rupture (C) causes regurgitation, and endocarditis (D) produces vegetations and
regurgitation.
Q7. In severe mitral regurgitation, the left atrium and left ventricle dilate because:
A. Systolic ejection of blood into the aorta is obstructed
B. A portion of left ventricular stroke volume regurgitates into the low-pressure left
atrium during systole
C. Diastolic filling from the pulmonary veins is obstructed
D. Right ventricular output exceeds left ventricular output
Correct Answer: B. A portion of left ventricular stroke volume regurgitates into the
low-pressure left atrium during systole [CORRECT]
Rationale: In mitral regurgitation, the LV ejects blood retrograde into the compliant
LA during systole, creating volume overload that progressively dilates both
chambers. Obstruction (A, C) describes stenotic lesions, and RV output exceeding LV
output (D) is physiologically incorrect.
Q8. A 28-year-old female with a mid-systolic click and late systolic murmur that
worsens with Valsalva maneuver is diagnosed with mitral valve prolapse. The primary
structural abnormality is:
A. Commissural fusion and chordal shortening
B. Myxomatous degeneration with thickened, redundant valve leaflets
C. Bicuspid aortic valve with calcification
D. Papillary muscle rupture from ischemia
