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Examen

Saunders NCLEX-RN Anatomy & Physiology Test Bank 2025 | 200+ Original Practice Questions & Rationales | Master Major Body Systems & Exam Success

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Saunders NCLEX-RN Anatomy & Physiology Test Bank 2025 | 200+ Original Practice Questions & Rationales | Master Major Body Systems & Exam Success Meta Description (≈175 characters) Boost your NCLEX-RN confidence with 200+ original Anatomy & Physiology test bank questions, detailed rationales, and full 2025 NCLEX alignment for nursing mastery. Long-Form Product Description (≈540 words)

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Subido en
19 de octubre de 2025
Número de páginas
866
Escrito en
2025/2026
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Examen
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Saunders Comprehensive Review for the NCLEX-PN®
Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri


ANATOMY AND PHYSIOLOGY TEST BANK


1. (Cardiovascular)
A nurse observes a patient with aortic stenosis who reports
chest pain on exertion. Which physiological mechanism best
explains the chest pain?
A. Increased coronary perfusion because of valve obstruction.
B. Reduced coronary perfusion due to increased left ventricular
pressure and wall tension.
C. Coronary vasospasm secondary to decreased afterload.
D. Enhanced myocardial oxygen delivery from collateral
formation.
Correct answer: B
Rationale:
• Correct (B): Aortic stenosis increases left ventricular (LV)
systolic pressure and wall tension (Laplace’s law). The
hypertrophied LV demands more oxygen while high LV
end-diastolic pressure reduces subendocardial coronary

, perfusion during diastole → myocardial ischemia and
exertional chest pain.
• A (incorrect): Coronary perfusion is not increased;
obstruction raises LV pressure and decreases effective
perfusion gradient.
• C (incorrect): Afterload is increased, not decreased;
vasospasm is not the primary mechanism in aortic
stenosis.
• D (incorrect): Collateral formation may occur over time but
does not acutely prevent ischemia with increased LV
demand.


2. (Cardiovascular — Hemodynamics)
Which clinical finding best correlates with left-sided heart
failure resulting from myocardial infarction?
A. Peripheral pitting edema and jugular venous distention.
B. Hepatomegaly and ascites.
C. Pulmonary crackles and orthopnea.
D. Splenomegaly and peripheral cyanosis.
Correct answer: C
Rationale:
• Correct (C): Left-sided pump failure causes elevated left
atrial pressure and pulmonary venous congestion →

, interstitial and alveolar edema leading to crackles and
orthopnea.
• A (incorrect): Peripheral edema and JVD are more
characteristic of right-sided failure.
• B (incorrect): Hepatomegaly/ascites reflect chronic right-
sided congestion.
• D (incorrect): Splenomegaly is not a primary sign of
isolated LV failure; peripheral cyanosis is nonspecific.


3. (Cardiovascular — Conduction)
A patient has a new third-degree (complete) AV block. Which
physiological consequence is expected?
A. Ventricular rate matches atrial rate and P waves conducted
normally.
B. Atrial and ventricular contractions are independent;
ventricular escape rhythm is slower.
C. Rapid ventricular rate due to increased sympathetic tone.
D. PR interval gradually lengthens until a beat is dropped.
Correct answer: B
Rationale:
• Correct (B): In complete AV block there's no conduction
from atria to ventricles; ventricles produce an escape
rhythm (junctional or ventricular) at an intrinsically slower
rate, so atria and ventricles beat independently.

, • A (incorrect): Ventricular rate does not match atrial rate;
conduction is absent.
• C (incorrect): Sympathetic tone may increase but does not
create a rapid ventricular rate when the conduction block
is distal.
• D (incorrect): Gradual PR lengthening until a dropped beat
describes Mobitz I (Wenckebach), not third-degree block.


4. (Respiratory — Structure/Function)
A nurse notes a patient with emphysema has a barrel chest and
decreased breath sounds. Which structural change explains
these findings?
A. Thickening of bronchial smooth muscle causing airflow
obstruction.
B. Destruction of alveolar walls with loss of elastic recoil and air
trapping.
C. Accumulation of fibrous tissue in alveolar walls increasing
diffusion.
D. Increased surfactant production causing alveolar
overdistension.
Correct answer: B
Rationale:
• Correct (B): Emphysema destroys alveolar septa and elastic
fibers → loss of elastic recoil and airway collapse on
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