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 nursing student returns from a mission trip
with a persistent cough and low-grade fever. A sputum Gram
stain shows small, pleomorphic organisms lacking a true nuclear
membrane. The student’s vitals are stable but CXR shows a focal
lobar consolidation. Which statement best explains the
organism’s cellular structure and clinical implications?
A. The organism’s lack of membrane-bound organelles suggests
it depends on host cells for ATP, making intracellular antibiotics
necessary.
B. The organism’s simple cell wall and absence of a nucleus
make it prokaryotic; cell wall–targeting antibiotics are likely
effective.
C. The presence of mitochondria-like organelles indicates a
eukaryotic pathogen requiring antifungal therapy.
D. The organism’s Gram stain pattern indicates a toxin-mediated
illness rather than direct infection; antibiotics are unnecessary.
,Correct Answer: B
Rationales
Correct (B): The organism lacks a true nucleus and membrane-
bound organelles, consistent with prokaryotes. Prokaryotic cell
walls (peptidoglycan) are common antibiotic targets (e.g., beta-
lactams), aligning with McCance’s description of prokaryotic
structure and therapeutic implications. Choosing cell wall–
targeting antibiotics is the safest, mechanism-based
interpretation.
A: While some intracellular bacteria rely on host processes, not
all prokaryotes are obligate intracellular pathogens; the
statement overgeneralizes and is inconsistent with focal
consolidation typical of extracellular bacteria.
C: Mitochondria-containing organisms are eukaryotes (fungi,
protozoa); the Gram stain and lack of nucleus point away from
this.
D: Gram stain indicating presence of organisms with structural
features is more consistent with direct infection; dismissing
antibiotics risks undertreatment.
Teaching Point: Prokaryotes lack nuclei and membrane-bound
organelles; cell wall targets enable effective antibiotics.
Citation: Rogers, J., et al. (2023). Pathophysiology: The Biologic
Basis for Disease in Adults and Children (9th ed.). Ch. 1.
,Q2
Reference: Ch. 2 — Cellular Functions
Stem: A 65-year-old with long-standing type 2 diabetes reports
numbness and a burning sensation in both feet. Exam shows
reduced ankle reflexes and patchy decreased pinprick. Nerve
conduction studies reveal slowed velocities. Which cellular
functional impairment best explains these peripheral
neuropathy findings?
A. Impaired mitochondrial ATP production in neurons causing
failure of axonal transport.
B. Loss of neuronal nucleus leading to demyelination and
conduction block.
C. Increased lysosomal activity causing excessive myelin
turnover.
D. Enhanced sodium channel expression producing
hyperexcitability.
Correct Answer: A
Rationales
Correct (A): Chronic hyperglycemia causes mitochondrial
dysfunction and oxidative stress in neurons and Schwann cells,
impairing ATP-dependent axonal transport and leading to distal
symmetric polyneuropathy. McCance links metabolic
derangements with impaired cellular energy production and
organelle dysfunction, explaining slowed conduction and
sensory loss.
B: Neuronal cell bodies generally remain intact early; loss of
, nucleus (karyolysis) is necrosis, not a typical mechanism for
chronic diabetic neuropathy.
C: Increased lysosomal activity causing myelin loss is not the
primary mechanism in diabetic neuropathy; demyelination is
secondary to metabolic injury, not lysosomal hyperactivity.
D: Enhanced sodium channel expression would cause
hyperexcitability (painful neuropathies), but slowed conduction
and reduced reflexes point to impaired axonal transport/energy
failure.
Teaching Point: Chronic hyperglycemia → mitochondrial
dysfunction → impaired ATP and axonal transport → distal
neuropathy.
Citation: Rogers, J., et al. (2023). Pathophysiology: The Biologic
Basis for Disease in Adults and Children (9th ed.). Ch. 2.
Q3
Reference: Ch. 3 — Structure and Function of Cellular
Components — Mitochondria
Stem: A 42-year-old woman with progressive muscle weakness
after a viral illness has lactic acidosis and exercise intolerance.
Muscle biopsy shows ragged-red fibers and abnormal electron-
dense mitochondrial inclusions. Which mechanism best
accounts for her clinical picture?
A. Defective oxidative phosphorylation due to mitochondrial
DNA mutation causing impaired ATP generation.
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 nursing student returns from a mission trip
with a persistent cough and low-grade fever. A sputum Gram
stain shows small, pleomorphic organisms lacking a true nuclear
membrane. The student’s vitals are stable but CXR shows a focal
lobar consolidation. Which statement best explains the
organism’s cellular structure and clinical implications?
A. The organism’s lack of membrane-bound organelles suggests
it depends on host cells for ATP, making intracellular antibiotics
necessary.
B. The organism’s simple cell wall and absence of a nucleus
make it prokaryotic; cell wall–targeting antibiotics are likely
effective.
C. The presence of mitochondria-like organelles indicates a
eukaryotic pathogen requiring antifungal therapy.
D. The organism’s Gram stain pattern indicates a toxin-mediated
illness rather than direct infection; antibiotics are unnecessary.
,Correct Answer: B
Rationales
Correct (B): The organism lacks a true nucleus and membrane-
bound organelles, consistent with prokaryotes. Prokaryotic cell
walls (peptidoglycan) are common antibiotic targets (e.g., beta-
lactams), aligning with McCance’s description of prokaryotic
structure and therapeutic implications. Choosing cell wall–
targeting antibiotics is the safest, mechanism-based
interpretation.
A: While some intracellular bacteria rely on host processes, not
all prokaryotes are obligate intracellular pathogens; the
statement overgeneralizes and is inconsistent with focal
consolidation typical of extracellular bacteria.
C: Mitochondria-containing organisms are eukaryotes (fungi,
protozoa); the Gram stain and lack of nucleus point away from
this.
D: Gram stain indicating presence of organisms with structural
features is more consistent with direct infection; dismissing
antibiotics risks undertreatment.
Teaching Point: Prokaryotes lack nuclei and membrane-bound
organelles; cell wall targets enable effective antibiotics.
Citation: Rogers, J., et al. (2023). Pathophysiology: The Biologic
Basis for Disease in Adults and Children (9th ed.). Ch. 1.
,Q2
Reference: Ch. 2 — Cellular Functions
Stem: A 65-year-old with long-standing type 2 diabetes reports
numbness and a burning sensation in both feet. Exam shows
reduced ankle reflexes and patchy decreased pinprick. Nerve
conduction studies reveal slowed velocities. Which cellular
functional impairment best explains these peripheral
neuropathy findings?
A. Impaired mitochondrial ATP production in neurons causing
failure of axonal transport.
B. Loss of neuronal nucleus leading to demyelination and
conduction block.
C. Increased lysosomal activity causing excessive myelin
turnover.
D. Enhanced sodium channel expression producing
hyperexcitability.
Correct Answer: A
Rationales
Correct (A): Chronic hyperglycemia causes mitochondrial
dysfunction and oxidative stress in neurons and Schwann cells,
impairing ATP-dependent axonal transport and leading to distal
symmetric polyneuropathy. McCance links metabolic
derangements with impaired cellular energy production and
organelle dysfunction, explaining slowed conduction and
sensory loss.
B: Neuronal cell bodies generally remain intact early; loss of
, nucleus (karyolysis) is necrosis, not a typical mechanism for
chronic diabetic neuropathy.
C: Increased lysosomal activity causing myelin loss is not the
primary mechanism in diabetic neuropathy; demyelination is
secondary to metabolic injury, not lysosomal hyperactivity.
D: Enhanced sodium channel expression would cause
hyperexcitability (painful neuropathies), but slowed conduction
and reduced reflexes point to impaired axonal transport/energy
failure.
Teaching Point: Chronic hyperglycemia → mitochondrial
dysfunction → impaired ATP and axonal transport → distal
neuropathy.
Citation: Rogers, J., et al. (2023). Pathophysiology: The Biologic
Basis for Disease in Adults and Children (9th ed.). Ch. 2.
Q3
Reference: Ch. 3 — Structure and Function of Cellular
Components — Mitochondria
Stem: A 42-year-old woman with progressive muscle weakness
after a viral illness has lactic acidosis and exercise intolerance.
Muscle biopsy shows ragged-red fibers and abnormal electron-
dense mitochondrial inclusions. Which mechanism best
accounts for her clinical picture?
A. Defective oxidative phosphorylation due to mitochondrial
DNA mutation causing impaired ATP generation.
