McCance & Huether’s Pathophysiology
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
Q1
Reference
Ch. 1 — Prokaryotes and Eukaryotes
Stem
A 28-year-old nurse presents after a needlestick injury from a
patient known to have an encapsulated, gram-negative
organism. She is asymptomatic but anxious. Initial rapid lab
shows a clear distinction between organisms on a slide: some
cells lack membrane-bound organelles and have a single circular
chromosome. Which cellular feature best explains why certain
pathogens are targeted by antibiotics that inhibit peptidoglycan
synthesis while host cells are spared?
Options
A. Presence of membrane-bound organelles in host cells.
,B. Presence of a rigid peptidoglycan cell wall in prokaryotes.
C. Use of linear chromosomes in eukaryotic cells.
D. Presence of 80S ribosomes in eukaryotic cells.
Correct Answer
B
Rationales
Correct (B): Prokaryotes (bacteria) possess a rigid peptidoglycan
cell wall that is absent in eukaryotic host cells; many antibiotics
(e.g., beta-lactams) inhibit enzymes involved in peptidoglycan
synthesis, producing selective toxicity. This mechanism aligns
with McCance’s distinction of prokaryotic cell walls versus
eukaryotic membranes and explains the therapeutic window.
Clinically, targeting peptidoglycan spares human cells because
human cells lack that structure.
Incorrect (A): Membrane-bound organelles distinguish
eukaryotes but do not directly account for antibiotic selectivity
toward peptidoglycan synthesis.
Incorrect (C): Chromosome structure (circular vs linear) is a
difference but is not the direct target of most peptidoglycan-
inhibiting antibiotics.
Incorrect (D): Ribosome size differences (70S vs 80S) are
exploited by some antibiotics, but peptidoglycan inhibition
specifically depends on the bacterial cell wall, so this distractor
is less accurate.
,Teaching Point
Peptidoglycan cell walls in bacteria enable selective antibiotic
targeting.
Citation
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 1.
Q2
Reference
Ch. 1 — Cellular Functions
Stem
A 65-year-old man with chronic ischemic heart disease reports
increasing exercise intolerance. Cardiac biopsy shows reduced
ATP production and impaired contractility despite preserved
myofibril structure. Which primary cellular function failure best
accounts for decreased contractility in viable but energy-
depleted myocytes?
Options
A. Impaired membrane transport due to ATP depletion affecting
Na⁺/K⁺-ATPase.
B. Loss of structural proteins of the sarcomere.
C. Increased apoptosis from death receptor activation.
D. Overexpression of growth factors causing hypertrophy.
Correct Answer
A
, Rationales
Correct (A): Myocyte contractility depends on ATP-driven ion
pumps (especially Na⁺/K⁺-ATPase and Ca²⁺-ATPases); ATP
depletion impairs ion gradients and calcium reuptake, reducing
contractile force despite preserved sarcomere structure
(McCance: energy failure → pump dysfunction → functional
impairment). This explains reversible contractile dysfunction
seen in ischemic but viable myocardium.
Incorrect (B): Structural sarcomere loss would cause permanent
dysfunction and histologic changes; biopsy shows preserved
myofibrils, making this unlikely.
Incorrect (C): Apoptosis would reduce cell numbers and cause
different histologic features; ATP depletion more directly
explains pump failure and contractility loss.
Incorrect (D): Growth factor–mediated hypertrophy is a chronic
adaptation and would not acutely reduce ATP production to
explain current findings.
Teaching Point
ATP depletion impairs ion pumps → abnormal Ca²⁺ handling →
reduced contractility without structural loss.
Citation
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 1.
Q3
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
Q1
Reference
Ch. 1 — Prokaryotes and Eukaryotes
Stem
A 28-year-old nurse presents after a needlestick injury from a
patient known to have an encapsulated, gram-negative
organism. She is asymptomatic but anxious. Initial rapid lab
shows a clear distinction between organisms on a slide: some
cells lack membrane-bound organelles and have a single circular
chromosome. Which cellular feature best explains why certain
pathogens are targeted by antibiotics that inhibit peptidoglycan
synthesis while host cells are spared?
Options
A. Presence of membrane-bound organelles in host cells.
,B. Presence of a rigid peptidoglycan cell wall in prokaryotes.
C. Use of linear chromosomes in eukaryotic cells.
D. Presence of 80S ribosomes in eukaryotic cells.
Correct Answer
B
Rationales
Correct (B): Prokaryotes (bacteria) possess a rigid peptidoglycan
cell wall that is absent in eukaryotic host cells; many antibiotics
(e.g., beta-lactams) inhibit enzymes involved in peptidoglycan
synthesis, producing selective toxicity. This mechanism aligns
with McCance’s distinction of prokaryotic cell walls versus
eukaryotic membranes and explains the therapeutic window.
Clinically, targeting peptidoglycan spares human cells because
human cells lack that structure.
Incorrect (A): Membrane-bound organelles distinguish
eukaryotes but do not directly account for antibiotic selectivity
toward peptidoglycan synthesis.
Incorrect (C): Chromosome structure (circular vs linear) is a
difference but is not the direct target of most peptidoglycan-
inhibiting antibiotics.
Incorrect (D): Ribosome size differences (70S vs 80S) are
exploited by some antibiotics, but peptidoglycan inhibition
specifically depends on the bacterial cell wall, so this distractor
is less accurate.
,Teaching Point
Peptidoglycan cell walls in bacteria enable selective antibiotic
targeting.
Citation
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 1.
Q2
Reference
Ch. 1 — Cellular Functions
Stem
A 65-year-old man with chronic ischemic heart disease reports
increasing exercise intolerance. Cardiac biopsy shows reduced
ATP production and impaired contractility despite preserved
myofibril structure. Which primary cellular function failure best
accounts for decreased contractility in viable but energy-
depleted myocytes?
Options
A. Impaired membrane transport due to ATP depletion affecting
Na⁺/K⁺-ATPase.
B. Loss of structural proteins of the sarcomere.
C. Increased apoptosis from death receptor activation.
D. Overexpression of growth factors causing hypertrophy.
Correct Answer
A
, Rationales
Correct (A): Myocyte contractility depends on ATP-driven ion
pumps (especially Na⁺/K⁺-ATPase and Ca²⁺-ATPases); ATP
depletion impairs ion gradients and calcium reuptake, reducing
contractile force despite preserved sarcomere structure
(McCance: energy failure → pump dysfunction → functional
impairment). This explains reversible contractile dysfunction
seen in ischemic but viable myocardium.
Incorrect (B): Structural sarcomere loss would cause permanent
dysfunction and histologic changes; biopsy shows preserved
myofibrils, making this unlikely.
Incorrect (C): Apoptosis would reduce cell numbers and cause
different histologic features; ATP depletion more directly
explains pump failure and contractility loss.
Incorrect (D): Growth factor–mediated hypertrophy is a chronic
adaptation and would not acutely reduce ATP production to
explain current findings.
Teaching Point
ATP depletion impairs ion pumps → abnormal Ca²⁺ handling →
reduced contractility without structural loss.
Citation
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 1.
Q3
