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McCance & Huether Pathophysiology 9th Ed. — Complete Chapter-by-Chapter Test Bank with Expert-Verified Answers & Clinical Rationales

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McCance & Huether Pathophysiology 9th Ed. — Complete Chapter-by-Chapter Test Bank with Expert-Verified Answers & Clinical Rationales Title 2 (exam-ready + conversion) The Ultimate McCance & Huether 9th Ed. Question Bank — Chapter MCQs, Detailed Rationales & Exam-Prep Toolkit (Stuvia Edition) High-converting Stuvia product description (ready to paste) Short tagline (one line): Comprehensive chapter-by-chapter MCQ bank for McCance & Huether — Pathophysiology (9th Ed.) with expert-verified answers, clinical rationales, and exam-ready teaching notes. Full description (sale-conversion focused — 3 short paragraphs + disclaimer): This test bank is a complete, chapter-by-chapter study companion aligned to McCance & Huether: Pathophysiology — The Biologic Basis for Disease in Adults and Children (9th Edition, Julia Rogers). Each chapter includes carefully written single-best-answer MCQs designed by experienced nursing/pathophysiology item-writers, clinically realistic stems, four plausible distractors, and concise, evidence-based rationales to deepen understanding — not just memorize answers. What you get: expert-validated answers and clinical rationales mapped to learning objectives; teaching points for quick review; question tags by Bloom’s level (recall, application, analysis); and a clear answer key for rapid self-assessment. Questions are optimized for classroom quizzes, NCLEX/HESI-style review, and individual mastery of each chapter’s high-yield mechanisms and clinical correlations. Why students buy: study faster with chapter-focused practice, strengthen weak areas with rationale-driven feedback, and build clinical reasoning with scenario-based items. Note: this product is an exam-prep resource designed to improve knowledge and test performance — no single resource can guarantee certification or exam success; outcomes depend on individual study and practice. One-line Stuvia meta description (for listing preview) Complete chapter-by-chapter MCQ bank for McCance & Huether 9th Ed. — expert-verified answers, clinical rationales, and exam-prep teaching notes. #PathophysiologyStudyBank #McCanceHuether9thEd #NCLEXPrep #NursingExamQuestions #ClinicalRationales #ChapterByChapterMCQs #ExamReadyResources #MedicalEducation #HESIReview #StudySmart McCance & Huether 9th edition question bank Pathophysiology MCQs chapter by chapter Nursing pathophysiology practice questions NCLEX pathophysiology review questions Clinical rationales pathophysiology questions McCance study guide 9th ed HESI pathophysiology question bank Expert-verified pathophysiology quizzes

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Subido en
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2025/2026
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McCance & Huether’s Pathophysiology
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK




McCance & Huether — Pathophysiology, 9th Ed. — Chapter 1:
Cellular Biology.
1.
Chapter Reference: Chapter 1 — Prokaryotes and Eukaryotes —
Cellular Biology
Stem: A 28-year-old transplant patient develops severe sepsis
after a central line infection. The lab report notes the infecting
organism lacks a true nucleus and has a rigid cell wall containing
peptidoglycan. Which description best fits this organism?
A. Gram-negative eukaryote with membrane-bound nucleus
B. Prokaryote with peptidoglycan cell wall
C. Eukaryote with chitin cell wall
D. Virus lacking cellular structure

,Correct Answer: B
Rationales:
• Correct (B): Prokaryotes (bacteria) lack a membrane-
bound nucleus and many have cell walls containing
peptidoglycan; this matches a typical bacterial central-line
pathogen causing sepsis.
• A: Incorrect — eukaryotes have membrane-bound nuclei;
they do not have peptidoglycan cell walls.
• C: Incorrect — chitin-based walls are typical of fungi
(eukaryotes), not bacteria.
• D: Incorrect — viruses are noncellular and do not possess
peptidoglycan cell walls.
Teaching Point: Bacteria are prokaryotic cells often
identified by peptidoglycan-containing walls.
Stem Rules: Single-sentence clinical vignette; clear,
concise, clinically relevant.


2.
Chapter Reference: Chapter 1 — Prokaryotes and Eukaryotes —
Cellular Biology
Stem: Which cellular feature differentiates eukaryotic human
cells from common bacterial pathogens in terms of therapeutic
targeting?
A. Presence of peptidoglycan in cytoplasm
B. Ribosomes of identical size to bacteria

,C. Membrane-bound organelles like mitochondria
D. Lack of genetic material
Correct Answer: C
Rationales:
• Correct (C): Eukaryotic cells have membrane-bound
organelles (e.g., mitochondria) that differ
structurally/functionally from bacterial components,
allowing selective drug targeting.
• A: Incorrect — peptidoglycan is a cell wall polymer present
in many bacteria, not in human cytoplasm.
• B: Incorrect — eukaryotic ribosomes (80S) differ in size
from bacterial (70S), which is exploited by antibiotics.
• D: Incorrect — all living cells contain genetic material;
eukaryotes certainly do.
Teaching Point: Membrane-bound organelles distinguish
eukaryotes from prokaryotes and guide selective therapy.
Stem Rules: Conceptual one-liner; avoids ambiguous
wording.


3.
Chapter Reference: Chapter 1 — Cellular Functions — Cellular
Biology
Stem: A patient with a mitochondrial disorder has fatigue and
lactic acidosis during exercise. Which primary cellular
dysfunction explains these findings?

, A. Impaired oxidative phosphorylation in mitochondria
B. Excessive ATP production via Krebs cycle
C. Increased glycolytic capacity with more ATP per glucose
D. Overactive electron transport chain causing
hypermetabolism
Correct Answer: A
Rationales:
• Correct (A): Mitochondrial oxidative phosphorylation
defect reduces ATP from aerobic metabolism, causing cells
to rely on anaerobic glycolysis and accumulate lactate.
• B: Incorrect — excessive ATP production would reduce
fatigue and lactate, not cause it.
• C: Incorrect — glycolysis yields much less ATP per glucose
and increases lactate; however, it is a compensatory
mechanism, not the primary dysfunction.
• D: Incorrect — overactive electron transport would not
typically cause lactic acidosis; dysfunction (not
overactivity) causes impaired ATP and lactate build-up.
Teaching Point: Defective mitochondrial oxidative
phosphorylation leads to anaerobic metabolism and lactic
acidosis.
Stem Rules: Short clinical vignette with lab implication;
mechanism-based.


4.
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