McCance & Huether’s Pathophysiology
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
1
Reference
Ch. X — Cellular Biology — Structure and Function of Cellular
Components
Stem
A 68-year-old man is admitted with progressive muscle
weakness and fatigue. Lab results show hypokalemia (K⁺ 2.8
mEq/L) and a prolonged QT interval on ECG. He reports recent
use of a herbal supplement. Which cellular structure’s
dysfunction best explains his muscle weakness and cardiac
conduction changes?
Options
A. Mitochondrial oxidative phosphorylation failure
B. Na⁺/K⁺-ATPase pump inhibition
C. Increased membrane permeability from lipid peroxidation
D. Defective sarcoplasmic reticulum Ca²⁺ release channels
Correct Answer
B
,Rationales
• Correct (B): Inhibition of the Na⁺/K⁺-ATPase disrupts the
transmembrane ionic gradients that maintain resting
membrane potential. Hypokalemia combined with pump
inhibition increases membrane hyperpolarization
variability, reducing muscle fiber excitability and
prolonging cardiac repolarization (QT). Mechanistically this
aligns with McCance’s discussion of membrane pumps
maintaining electrochemical gradients and excitability. This
interpretation prioritizes ionic gradient failure as the
primary, reversible cause.
• A: Mitochondrial failure causes energy deficit and muscle
fatigue but would not directly explain acute hypokalemia
with QT prolongation as the primary mechanism.
• C: Lipid peroxidation increases nonspecific permeability
and causes cell injury, but it produces diffuse cellular
dysfunction rather than an acute pattern tied to
extracellular K⁺ and membrane excitability.
• D: SR Ca²⁺ channel defects alter excitation–contraction
coupling, typically causing cramping or weakness but not
the specific ECG QT-prolongation pattern linked to altered
extracellular K⁺ and Na⁺/K⁺ pump activity.
Teaching Point
Na⁺/K⁺-ATPase maintains resting potential—its inhibition plus
hypokalemia disrupts excitability and repolarization.
,Citation
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. X.
2
Reference
Ch. X — Cellular Biology — Membrane Transport: Cellular Intake
and Output
Stem
A 45-year-old woman presents with confusion and rapid
shallow breathing. Labs: serum sodium 158 mEq/L, serum
osmolality elevated. Her history includes excessive intake of
concentrated sports supplements. At the cellular level, which
transport phenomenon most directly explains the neuronal
shrinkage causing her neurologic signs?
Options
A. Osmosis causing water efflux from neurons
B. Facilitated diffusion of Na⁺ into neurons
C. Endocytosis of aquaporin channels
D. Active Ca²⁺ extrusion via Ca²⁺-ATPase
Correct Answer
A
Rationales
, • Correct (A): Hypernatremia elevates extracellular
osmolarity, drawing water out of neurons by osmosis,
causing cellular dehydration and shrinkage that manifest as
confusion and respiratory pattern changes. This directly
follows McCance’s membrane transport principles where
water movement across semipermeable membranes
follows osmotic gradients.
• B: Facilitated diffusion of Na⁺ into neurons would increase
intracellular osmolarity and draw water in, opposing
shrinkage; it does not explain water efflux in
hypernatremia.
• C: Endocytosis of aquaporins is not an acute mechanism
for widespread neuronal dehydration in hypernatremia;
changes in aquaporin expression are slower and less
immediately explanatory.
• D: Active Ca²⁺ extrusion affects intracellular signaling and
excitability but does not account for cell volume loss due
to extracellular hyperosmolarity.
Teaching Point
Extracellular hyperosmolarity → osmotic water efflux →
neuronal shrinkage and neurologic dysfunction.
Citation
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. X.
The Biologic Basis for Disease in Adults and Children
9th Edition
• Author(s)Julia Rogers
TEST BANK
1
Reference
Ch. X — Cellular Biology — Structure and Function of Cellular
Components
Stem
A 68-year-old man is admitted with progressive muscle
weakness and fatigue. Lab results show hypokalemia (K⁺ 2.8
mEq/L) and a prolonged QT interval on ECG. He reports recent
use of a herbal supplement. Which cellular structure’s
dysfunction best explains his muscle weakness and cardiac
conduction changes?
Options
A. Mitochondrial oxidative phosphorylation failure
B. Na⁺/K⁺-ATPase pump inhibition
C. Increased membrane permeability from lipid peroxidation
D. Defective sarcoplasmic reticulum Ca²⁺ release channels
Correct Answer
B
,Rationales
• Correct (B): Inhibition of the Na⁺/K⁺-ATPase disrupts the
transmembrane ionic gradients that maintain resting
membrane potential. Hypokalemia combined with pump
inhibition increases membrane hyperpolarization
variability, reducing muscle fiber excitability and
prolonging cardiac repolarization (QT). Mechanistically this
aligns with McCance’s discussion of membrane pumps
maintaining electrochemical gradients and excitability. This
interpretation prioritizes ionic gradient failure as the
primary, reversible cause.
• A: Mitochondrial failure causes energy deficit and muscle
fatigue but would not directly explain acute hypokalemia
with QT prolongation as the primary mechanism.
• C: Lipid peroxidation increases nonspecific permeability
and causes cell injury, but it produces diffuse cellular
dysfunction rather than an acute pattern tied to
extracellular K⁺ and membrane excitability.
• D: SR Ca²⁺ channel defects alter excitation–contraction
coupling, typically causing cramping or weakness but not
the specific ECG QT-prolongation pattern linked to altered
extracellular K⁺ and Na⁺/K⁺ pump activity.
Teaching Point
Na⁺/K⁺-ATPase maintains resting potential—its inhibition plus
hypokalemia disrupts excitability and repolarization.
,Citation
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. X.
2
Reference
Ch. X — Cellular Biology — Membrane Transport: Cellular Intake
and Output
Stem
A 45-year-old woman presents with confusion and rapid
shallow breathing. Labs: serum sodium 158 mEq/L, serum
osmolality elevated. Her history includes excessive intake of
concentrated sports supplements. At the cellular level, which
transport phenomenon most directly explains the neuronal
shrinkage causing her neurologic signs?
Options
A. Osmosis causing water efflux from neurons
B. Facilitated diffusion of Na⁺ into neurons
C. Endocytosis of aquaporin channels
D. Active Ca²⁺ extrusion via Ca²⁺-ATPase
Correct Answer
A
Rationales
, • Correct (A): Hypernatremia elevates extracellular
osmolarity, drawing water out of neurons by osmosis,
causing cellular dehydration and shrinkage that manifest as
confusion and respiratory pattern changes. This directly
follows McCance’s membrane transport principles where
water movement across semipermeable membranes
follows osmotic gradients.
• B: Facilitated diffusion of Na⁺ into neurons would increase
intracellular osmolarity and draw water in, opposing
shrinkage; it does not explain water efflux in
hypernatremia.
• C: Endocytosis of aquaporins is not an acute mechanism
for widespread neuronal dehydration in hypernatremia;
changes in aquaporin expression are slower and less
immediately explanatory.
• D: Active Ca²⁺ extrusion affects intracellular signaling and
excitability but does not account for cell volume loss due
to extracellular hyperosmolarity.
Teaching Point
Extracellular hyperosmolarity → osmotic water efflux →
neuronal shrinkage and neurologic dysfunction.
Citation
Rogers, J., et al. (2023). Pathophysiology: The Biologic Basis for
Disease in Adults and Children (9th ed.). Ch. X.
