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 1 — Section: Prokaryotes and Eukaryotes — Title:
Differences Relevant to Antimicrobial Targets
Stem: A patient has a bacterial bloodstream infection. Which
cellular feature of bacteria most directly explains why
aminoglycoside antibiotics selectively inhibit bacterial protein
synthesis without affecting host cells?
A. Presence of circular DNA
B. Smaller, structurally distinct ribosomes
C. Lack of membrane-bound organelles
D. Peptidoglycan cell wall
Correct Answer: B
Rationales:
, • Correct (B): Bacterial ribosomes are 70S (30S + 50S) and
differ structurally from eukaryotic 80S ribosomes;
aminoglycosides bind the bacterial 30S subunit and inhibit
protein synthesis.
• A: Circular DNA is true for many bacteria but is not the
direct target of aminoglycosides.
• C: Lack of membrane-bound organelles is a general
prokaryotic trait but does not explain aminoglycoside
specificity.
• D: Peptidoglycan is targeted by β-lactams, not
aminoglycosides.
Teaching Point: Antibiotics exploit structural differences in
bacterial ribosomes to selectively inhibit protein synthesis.
Stem Rules: 1–2 sentences, clinical scenario, concise,
avoids negatives.
2. Chapter 1 — Section: Cellular Functions — Title: Energy-
Dependent Ion Homeostasis
Stem: A patient with hypoxic tissue injury shows cellular
swelling. Which failed cellular function best explains this early
change?
A. Mitochondrial DNA damage
B. Loss of Na⁺/K⁺ ATPase activity
C. Increased lysosomal enzyme release
D. Activation of caspases
,Correct Answer: B
Rationales:
• Correct (B): Na⁺/K⁺ ATPase is ATP-dependent; with hypoxia
ATP drops, pump fails, intracellular Na⁺ and water
accumulate, causing cellular swelling.
• A: Mitochondrial DNA damage may occur but is not the
immediate mechanism for swelling.
• C: Lysosomal enzyme release causes later membrane
digestion/necrosis, not early reversible swelling.
• D: Caspase activation mediates apoptosis, a different cell-
death pathway.
Teaching Point: Na⁺/K⁺ ATPase failure from ATP depletion
causes early cellular swelling in ischemia.
Stem Rules: 1–2 sentences, mechanism-based, clinically
relevant.
3. Chapter 1 — Section: Structure and Function of Cellular
Components — Title: Mitochondrial Dysfunction
Stem: A child presents with lactic acidosis and exercise
intolerance. Which mitochondrial defect best explains high
lactate with normal oxygen delivery?
A. Impaired glycolytic enzymes
B. Defective pyruvate dehydrogenase or ETC dysfunction
C. Increased activity of lactate dehydrogenase
D. Reduced hemoglobin affinity for oxygen
, Correct Answer: B
Rationales:
• Correct (B): If pyruvate cannot enter the TCA cycle (PDH
defect) or the electron transport chain is dysfunctional,
pyruvate is shunted to lactate despite adequate oxygen.
• A: Glycolytic defects would reduce lactate production, not
increase it.
• C: Increased LDH activity alone without upstream block is
unlikely to cause persistent lactic acidosis.
• D: Reduced hemoglobin O₂ affinity would cause tissue
hypoxia — the stem specifies normal oxygen delivery.
Teaching Point: Defects in PDH or ETC force anaerobic
metabolism and lactic acidosis despite normal oxygen.
Stem Rules: Short, focused on mechanism, clinical
vignette.
4. Chapter 1 — Section: Cell-to-Cell Adhesions — Title:
Desmosomes and Skin Integrity
Stem: A patient presents with flaccid epidermal blisters and
positive Nikolsky’s sign. Autoantibodies target desmoglein 3.
Which adhesion structure is primarily disrupted?
A. Tight junctions
B. Gap junctions
C. Desmosomes
D. Hemidesmosomes
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 1 — Section: Prokaryotes and Eukaryotes — Title:
Differences Relevant to Antimicrobial Targets
Stem: A patient has a bacterial bloodstream infection. Which
cellular feature of bacteria most directly explains why
aminoglycoside antibiotics selectively inhibit bacterial protein
synthesis without affecting host cells?
A. Presence of circular DNA
B. Smaller, structurally distinct ribosomes
C. Lack of membrane-bound organelles
D. Peptidoglycan cell wall
Correct Answer: B
Rationales:
, • Correct (B): Bacterial ribosomes are 70S (30S + 50S) and
differ structurally from eukaryotic 80S ribosomes;
aminoglycosides bind the bacterial 30S subunit and inhibit
protein synthesis.
• A: Circular DNA is true for many bacteria but is not the
direct target of aminoglycosides.
• C: Lack of membrane-bound organelles is a general
prokaryotic trait but does not explain aminoglycoside
specificity.
• D: Peptidoglycan is targeted by β-lactams, not
aminoglycosides.
Teaching Point: Antibiotics exploit structural differences in
bacterial ribosomes to selectively inhibit protein synthesis.
Stem Rules: 1–2 sentences, clinical scenario, concise,
avoids negatives.
2. Chapter 1 — Section: Cellular Functions — Title: Energy-
Dependent Ion Homeostasis
Stem: A patient with hypoxic tissue injury shows cellular
swelling. Which failed cellular function best explains this early
change?
A. Mitochondrial DNA damage
B. Loss of Na⁺/K⁺ ATPase activity
C. Increased lysosomal enzyme release
D. Activation of caspases
,Correct Answer: B
Rationales:
• Correct (B): Na⁺/K⁺ ATPase is ATP-dependent; with hypoxia
ATP drops, pump fails, intracellular Na⁺ and water
accumulate, causing cellular swelling.
• A: Mitochondrial DNA damage may occur but is not the
immediate mechanism for swelling.
• C: Lysosomal enzyme release causes later membrane
digestion/necrosis, not early reversible swelling.
• D: Caspase activation mediates apoptosis, a different cell-
death pathway.
Teaching Point: Na⁺/K⁺ ATPase failure from ATP depletion
causes early cellular swelling in ischemia.
Stem Rules: 1–2 sentences, mechanism-based, clinically
relevant.
3. Chapter 1 — Section: Structure and Function of Cellular
Components — Title: Mitochondrial Dysfunction
Stem: A child presents with lactic acidosis and exercise
intolerance. Which mitochondrial defect best explains high
lactate with normal oxygen delivery?
A. Impaired glycolytic enzymes
B. Defective pyruvate dehydrogenase or ETC dysfunction
C. Increased activity of lactate dehydrogenase
D. Reduced hemoglobin affinity for oxygen
, Correct Answer: B
Rationales:
• Correct (B): If pyruvate cannot enter the TCA cycle (PDH
defect) or the electron transport chain is dysfunctional,
pyruvate is shunted to lactate despite adequate oxygen.
• A: Glycolytic defects would reduce lactate production, not
increase it.
• C: Increased LDH activity alone without upstream block is
unlikely to cause persistent lactic acidosis.
• D: Reduced hemoglobin O₂ affinity would cause tissue
hypoxia — the stem specifies normal oxygen delivery.
Teaching Point: Defects in PDH or ETC force anaerobic
metabolism and lactic acidosis despite normal oxygen.
Stem Rules: Short, focused on mechanism, clinical
vignette.
4. Chapter 1 — Section: Cell-to-Cell Adhesions — Title:
Desmosomes and Skin Integrity
Stem: A patient presents with flaccid epidermal blisters and
positive Nikolsky’s sign. Autoantibodies target desmoglein 3.
Which adhesion structure is primarily disrupted?
A. Tight junctions
B. Gap junctions
C. Desmosomes
D. Hemidesmosomes
