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NURS 617 Test 1 Comprehensive Review | Questions and Answers | 2026 Updated | 100% Correct - McNeese State University GRADE A+

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NURS 617 Test 1 Comprehensive Review | Questions and Answers | 2026 Updated | 100% Correct - McNeese State University GRADE A+

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NURS 617 TEST 1 COMPREHENSIVE REVIEW |
QUESTIONS AND ANSWERS | 2026 UPDATED |
100% CORRECT - MCNEESE STATE UNIVERSITY.
145 Questions with Answers and Detailed Rationales


100 PERCENT GUARANTEED PASS


INSTANT DOWNLOAD ANSWERS INCLUDED



IMPORTANCE OF THIS DOCUMENT
This comprehensive examination preparation guide has been meticulously developed to help you succeed in the
NURS 617 TEST 1 COMPREHENSIVE REVIEW | QUESTIONS AND ANSWERS | 2026 UPDATED | 100%
CORRECT - MCNEESE STATE UNIVERSITY.. It contains 145 carefully selected questions that reflect the most
current exam content and testing strategies. Each question is accompanied by a correct answer and a detailed
rationale that explains the underlying pathophysiology, pharmacology, or clinical reasoning.

Self-Assessment – Test your knowledge and Exam Preparation – Familiarize yourself with the
identify areas requiring further question format and content
study areas

Concept Reinforcement – Deepen your Confidence Building – Develop test-taking
understanding through strategies and reduce
evidence-based exam anxiety
rationales
Time Management – Practice answering
questions under simulated
exam conditions




Review Summary 145 Questions


Foundations - Application - NURS 617 1 Comprehensive Review AND 2026 Updated 100 Correct -
Mcneese State University Advanced Pathophysiology Pharmacology AND Health Assessment FOR
Advanced Nursing Graduate Master OF Science IN Nursing / Advanced
All answers with rationales

,Table of Contents

Content Area Questions Key Topics

Professional Nursing Roles 1-25 Prescribed, Finding, Medication, Therapy, Warfarin
AND Scope OF

Nursing Process AND 26-50 Medication, Understanding, Indicates, Finding, Warfarin
Clinical Judgment

Health Assessment AND 51-75 Medication, Prescribed, Laboratory, Effect, Finding
Physical Examination

Pharmacology AND 76-100 Finding, Receiving, Medication, Teaching, Therapy
Medication Administration

Infection Control AND Safety 101-125 Prescribed, Indicates, Teaching, Receiving, Laboratory
IN Nursing

Patient Education AND 126-145 Receiving, Indicates, Prescribed, Finding, Therapeutic
Health Promotion

TOTAL 145 All questions include answers and detailed rationales

,Section A - Professional Nursing Roles AND Scope OF

Q1.
A patient presents with sudden onset of severe, tearing chest pain radiating to the back,
with a blood pressure differential of 28 mm Hg between arms. Which pathophysiologic
mechanism best explains this presentation?


A. Rupture of an atherosclerotic plaque B. Cystic medial degeneration leading to an
within the left anterior descending coronary intimal tear and false lumen formation in the
artery aorta

C. Acute inflammation of the pericardial sac D. Embolization of a left atrial thrombus into
causing friction rub and positional pain the systemic circulation
Correct: B - Cystic medial degeneration leading to an intimal tear and false lumen
formation in the aorta


Rationale:The presentation is classic for aortic dissection, which results from cystic medial
degeneration (often associated with hypertension or connective tissue disorders) that
weakens the aortic wall, allowing an intimal tear and creation of a false lumen. The blood
pressure differential between arms and tearing pain radiating to the back are hallmark
features. Coronary artery plaque rupture causes MI, pericarditis causes positional pain, and
systemic embolization causes stroke or peripheral ischemia, not this constellation.
Why the other answers are wrong:
A. Coronary plaque rupture leads to myocardial infarction, typically with substernal pressure
and no marked interarm BP differential.
C. Pericarditis causes sharp, positional chest pain with a friction rub, not tearing pain with
interarm BP differential.
D. Systemic embolization causes focal ischemic deficits (e.g., stroke, limb ischemia), not
tearing chest pain with interarm BP differential.
Reference: Hammer, G.D. & McPhee, S.J. (2024). Pathophysiology of Disease: An Introduction to
Clinical Medicine, 9th Ed., Ch. 11


Q2.
A patient is prescribed warfarin for atrial fibrillation. Which concurrent medication would
most significantly increase the risk of bleeding by inhibiting warfarin metabolism via
CYP2C9?


A. Rifampin B. Carbamazepine

C. Fluconazole D. Phenobarbital
Correct: C - Fluconazole




Page 3

, Section A - Professional Nursing Roles AND Scope OF



Rationale: Fluconazole is a potent inhibitor of CYP2C9, the primary enzyme responsible for

metabolizing S-warfarin, leading to increased warfarin levels and elevated INR/bleeding risk.

Rifampin, carbamazepine, and phenobarbital are CYP enzyme inducers that would decrease

warfarin levels and reduce its anticoagulant effect.

Why the other answers are wrong:
A. Rifampin is a strong CYP inducer that decreases warfarin effect and increases risk of
thrombosis.
B. Carbamazepine induces CYP enzymes and reduces warfarin levels, decreasing
anticoagulant effect.
D. Phenobarbital induces CYP enzymes and reduces warfarin levels, decreasing anticoagulant
effect.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 52


Q3.
Which laboratory finding is most consistent with primary hyperaldosteronism (Conn
syndrome) in a patient with resistant hypertension and unexplained hypokalemia?


A. Low plasma aldosterone and low plasma B. Elevated plasma aldosterone and
renin activity suppressed plasma renin activity

C. Elevated plasma renin activity and D. Low plasma aldosterone and elevated
normal aldosterone plasma renin activity
Correct: B - Elevated plasma aldosterone and suppressed plasma renin activity


Rationale:Primary hyperaldosteronism is characterized by autonomous aldosterone
secretion, leading to sodium retention, potassium excretion, and hypertension. The elevated
aldosterone suppresses renin via negative feedback, so renin activity is low. This combination
(high aldosterone, low renin) distinguishes primary from secondary hyperaldosteronism (e.g.,
renal artery stenosis), where renin is elevated.
Why the other answers are wrong:
A. Low aldosterone with low renin is not consistent with hyperaldosteronism; this pattern
suggests a low-renin state without aldosterone excess.
C. Elevated renin with normal aldosterone suggests secondary hypertension (e.g., renal artery
stenosis) rather than primary hyperaldosteronism.
D. Low aldosterone with high renin is seen in conditions like adrenal insufficiency or diuretic
use, not Conn syndrome.
Reference: Fauci, A.S. et al. (2024). Harrison's Principles of Internal Medicine, 22nd Ed., Ch. 386


Q4.
A patient with type 2 diabetes on metformin and empagliflozin presents with nausea,
vomiting, and Kussmaul respirations. Labs: glucose 210 mg/dL, pH 7.28, HCO3- 14 mEq/L,
anion gap 22, and ketones positive. Which diagnosis is most likely?




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