Saunders Comprehensive Review for the NCLEX-PN®
Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri
ANATOMY AND PHYSIOLOGY TEST BANK
1) Cardiovascular — Heart sounds and valve anatomy
A client has a systolic murmur heard best at the left lower
sternal border that increases when the client stands from a
sitting position. Which valvular or structural issue most likely
explains this finding?
A. Mitral regurgitation due to papillary muscle dysfunction
B. Aortic stenosis from calcified leaflets
C. Hypertrophic obstructive cardiomyopathy (HOCM) with
septal hypertrophy
D. Tricuspid regurgitation from right ventricular failure
Correct answer: C
Rationale — Correct (C): Hypertrophic obstructive
cardiomyopathy (HOCM) typically produces a systolic ejection
murmur that increases with maneuvers that decrease venous
return (e.g., standing). Reduced ventricular volume allows the
hypertrophied interventricular septum and anterior leaflet of
,the mitral valve to approximate more, increasing obstruction
and murmur intensity. This is a structural/mechanical issue of
septal hypertrophy.
Rationale — Incorrect:
A. Mitral regurgitation causes a holosystolic murmur best heard
at the apex and typically does not increase in intensity when
standing (often decreases when venous return is reduced).
B. Aortic stenosis produces a systolic ejection murmur best
heard at the right upper sternal border and generally decreases
in intensity with standing because output is reduced.
D. Tricuspid regurgitation murmur is best heard at the left lower
sternal border and may change with respiration (increasing with
inspiration); it is not classically intensified by standing.
2) Respiratory — V/Q mismatch and hypoxemia
A patient with a pulmonary embolus develops acute
hypoxemia. Which physiological explanation best accounts for
the hypoxemia?
A. Increased dead space ventilation leads to decreased effective
alveolar ventilation.
B. Right-to-left intracardiac shunt allows deoxygenated blood to
bypass the lungs.
C. Diffusion impairment due to thickened alveolar membrane
from edema.
D. Hypoventilation secondary to central respiratory depression.
,Correct answer: A
Rationale — Correct (A): A pulmonary embolus occludes
pulmonary arteries, creating areas of lung that are ventilated
but not perfused — physiologic dead space. This reduces
effective alveolar ventilation and impairs gas exchange, causing
hypoxemia.
Rationale — Incorrect:
B. A right-to-left intracardiac shunt causes hypoxemia but is not
the mechanism in acute pulmonary embolism.
C. Diffusion impairment occurs with interstitial lung disease or
pulmonary edema over time; while edema can cause diffusion
issues, acute PE primarily causes ventilation–perfusion
mismatch (dead space), not diffusion limitation.
D. Hypoventilation causes hypercapnia and hypoxemia, but PE
patients typically have normal or low PaCO₂ (hyperventilation)
and hypoxemia from V/Q mismatch rather than central
respiratory depression.
3) Renal — Glomerular filtration & creatinine clearance
Which statement best explains why serum creatinine is a
delayed indicator of acute changes in glomerular filtration rate
(GFR)?
A. Creatinine is actively secreted in proximal tubule at high rates
masking early GFR changes.
B. Serum creatinine rises only after significant loss of nephron
, mass because creatinine accumulates slowly.
C. Creatinine is fully reabsorbed by renal tubules, so it reflects
only filtration changes.
D. Creatinine production decreases rapidly during illness,
lowering its sensitivity.
Correct answer: B
Rationale — Correct (B): Creatinine is produced at a relatively
constant rate by muscle and is freely filtered; serum creatinine
does not rise until GFR falls substantially because remaining
nephrons compensate. Therefore serum creatinine is an
insensitive, delayed marker of early GFR decline.
Rationale — Incorrect:
A. Some creatinine is secreted by proximal tubules, but
secretion would tend to overestimate GFR; secretion is not the
main reason for delay in detecting acute GFR changes.
C. Creatinine is not reabsorbed; it is filtered and partially
secreted—so the option is false.
D. Creatinine production decreases slowly with muscle wasting
but does not typically drop rapidly during acute illness; reduced
production would actually blunt rises, not cause the delayed
increase described.
4) Endocrine — Thyroid hormone physiology & clinical signs
A client presents with weight loss, heat intolerance, and a fine
tremor. Which physiologic mechanism produced by excess
Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri
ANATOMY AND PHYSIOLOGY TEST BANK
1) Cardiovascular — Heart sounds and valve anatomy
A client has a systolic murmur heard best at the left lower
sternal border that increases when the client stands from a
sitting position. Which valvular or structural issue most likely
explains this finding?
A. Mitral regurgitation due to papillary muscle dysfunction
B. Aortic stenosis from calcified leaflets
C. Hypertrophic obstructive cardiomyopathy (HOCM) with
septal hypertrophy
D. Tricuspid regurgitation from right ventricular failure
Correct answer: C
Rationale — Correct (C): Hypertrophic obstructive
cardiomyopathy (HOCM) typically produces a systolic ejection
murmur that increases with maneuvers that decrease venous
return (e.g., standing). Reduced ventricular volume allows the
hypertrophied interventricular septum and anterior leaflet of
,the mitral valve to approximate more, increasing obstruction
and murmur intensity. This is a structural/mechanical issue of
septal hypertrophy.
Rationale — Incorrect:
A. Mitral regurgitation causes a holosystolic murmur best heard
at the apex and typically does not increase in intensity when
standing (often decreases when venous return is reduced).
B. Aortic stenosis produces a systolic ejection murmur best
heard at the right upper sternal border and generally decreases
in intensity with standing because output is reduced.
D. Tricuspid regurgitation murmur is best heard at the left lower
sternal border and may change with respiration (increasing with
inspiration); it is not classically intensified by standing.
2) Respiratory — V/Q mismatch and hypoxemia
A patient with a pulmonary embolus develops acute
hypoxemia. Which physiological explanation best accounts for
the hypoxemia?
A. Increased dead space ventilation leads to decreased effective
alveolar ventilation.
B. Right-to-left intracardiac shunt allows deoxygenated blood to
bypass the lungs.
C. Diffusion impairment due to thickened alveolar membrane
from edema.
D. Hypoventilation secondary to central respiratory depression.
,Correct answer: A
Rationale — Correct (A): A pulmonary embolus occludes
pulmonary arteries, creating areas of lung that are ventilated
but not perfused — physiologic dead space. This reduces
effective alveolar ventilation and impairs gas exchange, causing
hypoxemia.
Rationale — Incorrect:
B. A right-to-left intracardiac shunt causes hypoxemia but is not
the mechanism in acute pulmonary embolism.
C. Diffusion impairment occurs with interstitial lung disease or
pulmonary edema over time; while edema can cause diffusion
issues, acute PE primarily causes ventilation–perfusion
mismatch (dead space), not diffusion limitation.
D. Hypoventilation causes hypercapnia and hypoxemia, but PE
patients typically have normal or low PaCO₂ (hyperventilation)
and hypoxemia from V/Q mismatch rather than central
respiratory depression.
3) Renal — Glomerular filtration & creatinine clearance
Which statement best explains why serum creatinine is a
delayed indicator of acute changes in glomerular filtration rate
(GFR)?
A. Creatinine is actively secreted in proximal tubule at high rates
masking early GFR changes.
B. Serum creatinine rises only after significant loss of nephron
, mass because creatinine accumulates slowly.
C. Creatinine is fully reabsorbed by renal tubules, so it reflects
only filtration changes.
D. Creatinine production decreases rapidly during illness,
lowering its sensitivity.
Correct answer: B
Rationale — Correct (B): Creatinine is produced at a relatively
constant rate by muscle and is freely filtered; serum creatinine
does not rise until GFR falls substantially because remaining
nephrons compensate. Therefore serum creatinine is an
insensitive, delayed marker of early GFR decline.
Rationale — Incorrect:
A. Some creatinine is secreted by proximal tubules, but
secretion would tend to overestimate GFR; secretion is not the
main reason for delay in detecting acute GFR changes.
C. Creatinine is not reabsorbed; it is filtered and partially
secreted—so the option is false.
D. Creatinine production decreases slowly with muscle wasting
but does not typically drop rapidly during acute illness; reduced
production would actually blunt rises, not cause the delayed
increase described.
4) Endocrine — Thyroid hormone physiology & clinical signs
A client presents with weight loss, heat intolerance, and a fine
tremor. Which physiologic mechanism produced by excess
