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NURS 683 Exam 2 Study Guide Review | Questions and Answers | 2026 Updated - McNeese State University GRADE A+

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NURS 683 Exam 2 Study Guide Review | Questions and Answers | 2026 Updated - McNeese State University GRADE A+

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NURS 683 EXAM 2 STUDY GUIDE REVIEW |
QUESTIONS AND ANSWERS | 2026
UPDATED - MCNEESE STATE UNIVERSITY
144 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 683 EXAM 2 STUDY GUIDE REVIEW | QUESTIONS AND ANSWERS | 2026 UPDATED - MCNEESE
STATE UNIVERSITY. It contains 144 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 144 Questions


Foundations - Application - NURS 683 2 Study Guide Review AND 2026 Updated - Mcneese State
University Advanced Nursing Pharmacology AND Pathophysiology Graduate Msn/dnp-level Nursing
All answers with rationales

,Table of Contents

Content Area Questions Key Topics

Advanced Health 1-24 Prescribed, Therapy, Mechanism, Disorder, Parameter
Assessment AND Diagnostic
Reasoning

Pathophysiology OF Acute 25-48 Finding, Prescribed, Indicates, Reports, Laboratory
AND Chronic Conditions

Pharmacological 49-72 Prescribed, Receiving, Therapy, Indicates, Laboratory
Management AND
Prescriptive Authority

Primary CARE Management 73-96 Prescribed, Effect, Finding, Receiving, Adverse
OF Common Health
Problems

Health Promotion AND 97-120 Prescribed, Receiving, Therapy, Laboratory, First
Disease Prevention Across
THE Lifespan

Management OF Chronic 121-144 Prescribed, Medication, Teaching, Finding, Receiving
Diseases E G Diabetes
Hypertension COPD

TOTAL 144 All questions include answers and detailed rationales

,Section A - Advanced Health Assessment AND Diagnostic
Reasoning

Q1.
A patient with heart failure and reduced ejection fraction is prescribed sacubitril/valsartan.
Which parameter requires the most careful monitoring after initiation?


A. Serum potassium and renal function B. Serum sodium and osmolality

C. Liver enzymes and bilirubin D. Platelet count and coagulation studies
Correct: A - Serum potassium and renal function


Rationale:Sacubitril/valsartan can cause hyperkalemia and renal impairment, especially
when combined with other RAAS inhibitors. Monitoring potassium and renal function is critical
to prevent complications. Sodium, liver enzymes, and coagulation parameters are not primary
concerns with this drug.
Why the other answers are wrong:
B. Sodium and osmolality are not the primary parameters affected by sacubitril/valsartan;
hyponatremia is more associated with diuretics.
C. Hepatotoxicity is not a major adverse effect of sacubitril/valsartan; liver enzymes are not
routinely monitored.
D. Platelet and coagulation studies are not relevant to sacubitril/valsartan; bleeding risk is not a
primary concern.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 44


Q2.
Which pathophysiologic mechanism best explains the development of diabetic
ketoacidosis in a patient with type 1 diabetes?


A. Excessive insulin secretion leading to B. Absolute insulin deficiency causing
hypoglycemia lipolysis and ketone production

C. Increased peripheral glucose uptake due D. Renal failure causing decreased ketone
to insulin resistance excretion
Correct: B - Absolute insulin deficiency causing lipolysis and ketone production


Rationale:DKA results from absolute insulin deficiency, which leads to unrestrained lipolysis
and ketogenesis. This produces metabolic acidosis and hyperglycemia. The other options do
not describe the primary mechanism of DKA.
Why the other answers are wrong:
A. Excessive insulin secretion causes hypoglycemia, not DKA.
C. Insulin resistance is more characteristic of type 2 diabetes and does not typically cause




Page 3

, Section A - Advanced Health Assessment AND Diagnostic Reasoning

DKA.

D. Renal failure is not the primary cause of DKA; ketone production is driven by insulin deficiency.

Reference: McCance, K.L. & Huether, S.E. (2024). Pathophysiology: The Biologic Basis for Disease, 9th
Ed., Ch. 41


Q3.
A patient on warfarin therapy has an INR of 5.8 and is not bleeding. Which intervention is
most appropriate?


A. Administer vitamin K 10 mg IV B. Hold warfarin and give fresh frozen
plasma

C. Hold warfarin and administer oral vitamin D. Continue warfarin and recheck INR in 24
K 2.5 mg hours
Correct: C - Hold warfarin and administer oral vitamin K 2.5 mg


Rationale:For an INR of 5.8 without bleeding, guidelines recommend holding warfarin and
giving low-dose oral vitamin K (2.5 mg) to reverse anticoagulation gradually. IV vitamin K and
FFP are reserved for serious bleeding. Continuing warfarin would increase bleeding risk.
Why the other answers are wrong:
A. IV vitamin K is typically reserved for major bleeding or very high INR with bleeding; it can
cause anaphylactoid reactions.
B. Fresh frozen plasma is not indicated without active bleeding; it carries transfusion risks.
D. Continuing warfarin at this INR is unsafe and could lead to hemorrhage.
Reference: Lehne, R.A. (2026). Pharmacology for Nursing Care, 12th Ed., Ch. 52


Q4.
Which statement best describes the mechanism of action of metformin in managing type 2
diabetes?


A. It stimulates insulin release from B. It decreases hepatic glucose production
pancreatic beta cells. and improves insulin sensitivity.

C. It inhibits alpha-glucosidase in the small D. It increases urinary glucose excretion by
intestine. inhibiting SGLT2.
Correct: B - It decreases hepatic glucose production and improves insulin sensitivity.


Rationale:Metformin primarily reduces hepatic gluconeogenesis and enhances peripheral
insulin sensitivity. It does not directly stimulate insulin secretion or inhibit SGLT2.
Alpha-glucosidase inhibition is the mechanism of acarbose.
Why the other answers are wrong:
A. Stimulation of insulin release is the mechanism of sulfonylureas, not metformin.
C. Alpha-glucosidase inhibition is characteristic of acarbose, not metformin.




Page 4

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