McCance & Huether’s Pathophysiology
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
1)
Reference
Ch. 1 — Cellular Functions: Adaptive Responses (Hyperplasia,
Hypertrophy, Atrophy, Metaplasia)
Stem
A 62-year-old man with long-standing gastroesophageal reflux
reports progressive dysphagia and intermittent heartburn.
Endoscopy shows areas of columnar epithelium replacing
normal stratified squamous mucosa of the distal esophagus.
Biopsy shows intestinal goblet cells. Vitals stable; he has no
acute distress. Which pathophysiologic process best explains
this finding and its clinical significance?
Options
A. Hyperplasia — chronic acid exposure increases cell number
causing carcinoma risk.
B. Metaplasia — chronic irritation causes phenotypic change to
a more protective cell type with malignant potential.
C. Dysplasia — reversible adaptive enlargement of existing
,squamous cells due to acid exposure.
D. Atrophy — loss of squamous cells from reduced perfusion
leading to columnar replacement.
Correct Answer
B
Rationales
Correct (B): Metaplasia is the replacement of one differentiated
cell type by another better suited to withstand chronic stress
(columnar epithelium replacing squamous in Barrett
esophagus). McCance links chronic irritation-induced
reprogramming of stem cells/precursors to metaplasia and
highlights increased risk of progression to dysplasia and
adenocarcinoma. This interpretation prioritizes recognition of a
premalignant adaptation requiring surveillance.
Incorrect (A): Hyperplasia is increased cell number (e.g.,
hormonal stimuli). The finding is a cell-type change, not simply
proliferation.
Incorrect (C): Dysplasia implies disordered growth and atypia —
biopsy indicates organized intestinal-type cells (metaplasia), not
dysplastic atypia.
Incorrect (D): Atrophy is shrinkage and loss of cells, not
replacement by a different epithelial type; ischemia is not the
mechanism here.
Teaching Point
Metaplasia = reversible cell-type switch from chronic irritation;
watch for dysplastic progression.
,Citation (APA)
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 1.
2)
Reference
Ch. 1 — Cellular Components: Plasma Membrane Structure &
Function
Stem
A 45-year-old woman presents with acute confusion and muscle
cramps. Labs show serum sodium 122 mEq/L and serum
osmolality low. She reports chronic use of an over-the-counter
drug that increases ADH-like effect. On a cellular level, which
membrane change most directly produces cerebral edema in
hyponatremia?
Options
A. Increased aquaporin insertion in neuronal membranes
causing water influx.
B. Up-regulation of Na⁺/K⁺-ATPase causing intracellular sodium
accumulation.
C. Decreased tight junction integrity increasing extracellular
water shift into brain.
D. Activation of voltage-gated sodium channels increasing
neuronal depolarization and swelling.
, Correct Answer
A
Rationales
Correct (A): In acutely low extracellular osmolarity, water
moves into cells where aquaporin channels (and membrane
permeability to water) allow rapid intracellular water influx,
producing cytotoxic cerebral edema. McCance emphasizes
membrane water channels and osmotic gradients as primary
drivers of cell swelling in hypoosmolar states. Clinically, this
explains neurologic symptoms and the urgency to correct
sodium safely.
Incorrect (B): Na⁺/K⁺-ATPase pumps keep intracellular sodium
low; up-regulation would reduce intracellular sodium and
oppose swelling.
Incorrect (C): Tight junctions affect paracellular movement in
barriers like BBB, but acute hyponatremic edema is cellular
(cytotoxic) rather than from BBB disruption.
Incorrect (D): Voltage-gated Na⁺ channels mediate action
potentials; their activation doesn’t directly cause sustained
osmotic water influx and cell swelling.
Teaching Point
Acute hyponatremia → osmotic water influx via aquaporins →
cytotoxic brain swelling; correct sodium cautiously.
Citation (APA)
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 1.
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
1)
Reference
Ch. 1 — Cellular Functions: Adaptive Responses (Hyperplasia,
Hypertrophy, Atrophy, Metaplasia)
Stem
A 62-year-old man with long-standing gastroesophageal reflux
reports progressive dysphagia and intermittent heartburn.
Endoscopy shows areas of columnar epithelium replacing
normal stratified squamous mucosa of the distal esophagus.
Biopsy shows intestinal goblet cells. Vitals stable; he has no
acute distress. Which pathophysiologic process best explains
this finding and its clinical significance?
Options
A. Hyperplasia — chronic acid exposure increases cell number
causing carcinoma risk.
B. Metaplasia — chronic irritation causes phenotypic change to
a more protective cell type with malignant potential.
C. Dysplasia — reversible adaptive enlargement of existing
,squamous cells due to acid exposure.
D. Atrophy — loss of squamous cells from reduced perfusion
leading to columnar replacement.
Correct Answer
B
Rationales
Correct (B): Metaplasia is the replacement of one differentiated
cell type by another better suited to withstand chronic stress
(columnar epithelium replacing squamous in Barrett
esophagus). McCance links chronic irritation-induced
reprogramming of stem cells/precursors to metaplasia and
highlights increased risk of progression to dysplasia and
adenocarcinoma. This interpretation prioritizes recognition of a
premalignant adaptation requiring surveillance.
Incorrect (A): Hyperplasia is increased cell number (e.g.,
hormonal stimuli). The finding is a cell-type change, not simply
proliferation.
Incorrect (C): Dysplasia implies disordered growth and atypia —
biopsy indicates organized intestinal-type cells (metaplasia), not
dysplastic atypia.
Incorrect (D): Atrophy is shrinkage and loss of cells, not
replacement by a different epithelial type; ischemia is not the
mechanism here.
Teaching Point
Metaplasia = reversible cell-type switch from chronic irritation;
watch for dysplastic progression.
,Citation (APA)
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 1.
2)
Reference
Ch. 1 — Cellular Components: Plasma Membrane Structure &
Function
Stem
A 45-year-old woman presents with acute confusion and muscle
cramps. Labs show serum sodium 122 mEq/L and serum
osmolality low. She reports chronic use of an over-the-counter
drug that increases ADH-like effect. On a cellular level, which
membrane change most directly produces cerebral edema in
hyponatremia?
Options
A. Increased aquaporin insertion in neuronal membranes
causing water influx.
B. Up-regulation of Na⁺/K⁺-ATPase causing intracellular sodium
accumulation.
C. Decreased tight junction integrity increasing extracellular
water shift into brain.
D. Activation of voltage-gated sodium channels increasing
neuronal depolarization and swelling.
, Correct Answer
A
Rationales
Correct (A): In acutely low extracellular osmolarity, water
moves into cells where aquaporin channels (and membrane
permeability to water) allow rapid intracellular water influx,
producing cytotoxic cerebral edema. McCance emphasizes
membrane water channels and osmotic gradients as primary
drivers of cell swelling in hypoosmolar states. Clinically, this
explains neurologic symptoms and the urgency to correct
sodium safely.
Incorrect (B): Na⁺/K⁺-ATPase pumps keep intracellular sodium
low; up-regulation would reduce intracellular sodium and
oppose swelling.
Incorrect (C): Tight junctions affect paracellular movement in
barriers like BBB, but acute hyponatremic edema is cellular
(cytotoxic) rather than from BBB disruption.
Incorrect (D): Voltage-gated Na⁺ channels mediate action
potentials; their activation doesn’t directly cause sustained
osmotic water influx and cell swelling.
Teaching Point
Acute hyponatremia → osmotic water influx via aquaporins →
cytotoxic brain swelling; correct sodium cautiously.
Citation (APA)
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. 1.
