Robbins & Cotran 10th Ed. Pathology Test Bank | Chapter-
by-Chapter Questions & Verified Solutions
Robbins & Cotran Pathologic Basis of Disease
10th Edition
• Author(s)Vinay Kumar; Abul K. Abbas; Jon C. Aster
1.
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease; The Genome; Cellular Housekeeping; Cellular
Metabolism and Mitochondrial Function; Cellular Activation;
Growth Factors and Receptors; Extracellular Matrix;
Maintaining Cell Populations
Stem: A 6-year-old boy presents with recurrent infections and
failure to thrive. Genetic testing shows a frameshift mutation in
a DNA repair gene involved in non-homologous end joining.
Which cellular consequence most directly results from defective
DNA double-strand break repair?
A. Increased point mutations due to defective mismatch repair
B. Chromosomal translocations and genome instability
C. Accumulation of single-stranded DNA nicks leading to
,progeria
D. Impaired base excision repair causing uracil incorporation
Answer: B
Rationale (correct): Defective repair of double-strand breaks
(e.g., impaired non-homologous end joining) leads to misjoining
of DNA ends, creating chromosomal translocations and large-
scale genome instability, which predisposes to malignancy and
cell dysfunction.
Incorrect A: Mismatch repair defects cause microsatellite
instability and point/frame-shift mutations, not primarily double-
strand break–associated translocations.
Incorrect C: Single-stranded nicks are typically processed
differently; progeria links to nuclear lamina defects rather than
simple double-strand break repair failure.
Incorrect D: Base excision repair defects handle small base
lesions (e.g., uracil from cytosine deamination), not double-
strand break repair.
Teaching Point: Double-strand break repair defects produce
chromosomal instability and translocations.
2.
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease; The Genome; Cellular Housekeeping; Cellular
Metabolism and Mitochondrial Function; Cellular Activation;
Growth Factors and Receptors; Extracellular Matrix;
Maintaining Cell Populations
,Stem: A pathologist sees cells with abundant autophagic
vacuoles after prolonged nutrient deprivation. Which
intracellular process is primarily responsible for delivering
cytoplasmic organelles to lysosomes during starvation?
A. Ubiquitin–proteasome system
B. Macroautophagy (autophagosome formation)
C. Endocytosis via clathrin-coated pits
D. Chaperone-mediated proteolysis
Answer: B
Rationale (correct): Macroautophagy (commonly called
autophagy) sequesters portions of cytoplasm and organelles into
double-membrane autophagosomes that fuse with lysosomes for
degradation during nutrient deprivation.
Incorrect A: The ubiquitin–proteasome system degrades short-
lived and misfolded proteins, not large organelles.
Incorrect C: Endocytosis internalizes extracellular material and
membrane proteins, not bulk cytoplasmic organelles.
Incorrect D: Chaperone-mediated autophagy selectively
translocates individual proteins into lysosomes, not organelles.
Teaching Point: Macroautophagy removes organelles during
starvation via autophagosomes that fuse with lysosomes.
3.
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease; The Genome; Cellular Housekeeping; Cellular
Metabolism and Mitochondrial Function; Cellular Activation;
, Growth Factors and Receptors; Extracellular Matrix;
Maintaining Cell Populations
Stem: A patient with mitochondrial myopathy has exercise
intolerance. Which mitochondrial defect most directly reduces
ATP generation by oxidative phosphorylation?
A. Impaired glycolytic enzyme hexokinase activity
B. Increased outer mitochondrial membrane permeability to
protons
C. Defect in electron transport chain complex IV (cytochrome c
oxidase)
D. Loss of mitochondrial DNA-encoded ribosomal RNAs only
Answer: C
Rationale (correct): A defect in complex IV impairs electron
transfer to oxygen, reducing proton gradient formation and ATP
synthesis by ATP synthase, directly lowering oxidative
phosphorylation capacity.
Incorrect A: Hexokinase functions in glycolysis (cytosolic), not
oxidative phosphorylation within mitochondria.
Incorrect B: Increased proton permeability would collapse the
proton gradient and reduce ATP, but this describes uncoupling
rather than a specific defect seen in mitochondrial myopathies—
less specific than complex IV dysfunction.
Incorrect D: Loss of mitochondrial rRNAs would impair
mitochondrial protein synthesis broadly, but the most direct
cause reducing electron transport chain activity is a specific
complex defect like complex IV.
Teaching Point: Electron transport chain complex defects
directly impair oxidative phosphorylation and ATP production.
by-Chapter Questions & Verified Solutions
Robbins & Cotran Pathologic Basis of Disease
10th Edition
• Author(s)Vinay Kumar; Abul K. Abbas; Jon C. Aster
1.
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease; The Genome; Cellular Housekeeping; Cellular
Metabolism and Mitochondrial Function; Cellular Activation;
Growth Factors and Receptors; Extracellular Matrix;
Maintaining Cell Populations
Stem: A 6-year-old boy presents with recurrent infections and
failure to thrive. Genetic testing shows a frameshift mutation in
a DNA repair gene involved in non-homologous end joining.
Which cellular consequence most directly results from defective
DNA double-strand break repair?
A. Increased point mutations due to defective mismatch repair
B. Chromosomal translocations and genome instability
C. Accumulation of single-stranded DNA nicks leading to
,progeria
D. Impaired base excision repair causing uracil incorporation
Answer: B
Rationale (correct): Defective repair of double-strand breaks
(e.g., impaired non-homologous end joining) leads to misjoining
of DNA ends, creating chromosomal translocations and large-
scale genome instability, which predisposes to malignancy and
cell dysfunction.
Incorrect A: Mismatch repair defects cause microsatellite
instability and point/frame-shift mutations, not primarily double-
strand break–associated translocations.
Incorrect C: Single-stranded nicks are typically processed
differently; progeria links to nuclear lamina defects rather than
simple double-strand break repair failure.
Incorrect D: Base excision repair defects handle small base
lesions (e.g., uracil from cytosine deamination), not double-
strand break repair.
Teaching Point: Double-strand break repair defects produce
chromosomal instability and translocations.
2.
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease; The Genome; Cellular Housekeeping; Cellular
Metabolism and Mitochondrial Function; Cellular Activation;
Growth Factors and Receptors; Extracellular Matrix;
Maintaining Cell Populations
,Stem: A pathologist sees cells with abundant autophagic
vacuoles after prolonged nutrient deprivation. Which
intracellular process is primarily responsible for delivering
cytoplasmic organelles to lysosomes during starvation?
A. Ubiquitin–proteasome system
B. Macroautophagy (autophagosome formation)
C. Endocytosis via clathrin-coated pits
D. Chaperone-mediated proteolysis
Answer: B
Rationale (correct): Macroautophagy (commonly called
autophagy) sequesters portions of cytoplasm and organelles into
double-membrane autophagosomes that fuse with lysosomes for
degradation during nutrient deprivation.
Incorrect A: The ubiquitin–proteasome system degrades short-
lived and misfolded proteins, not large organelles.
Incorrect C: Endocytosis internalizes extracellular material and
membrane proteins, not bulk cytoplasmic organelles.
Incorrect D: Chaperone-mediated autophagy selectively
translocates individual proteins into lysosomes, not organelles.
Teaching Point: Macroautophagy removes organelles during
starvation via autophagosomes that fuse with lysosomes.
3.
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease; The Genome; Cellular Housekeeping; Cellular
Metabolism and Mitochondrial Function; Cellular Activation;
, Growth Factors and Receptors; Extracellular Matrix;
Maintaining Cell Populations
Stem: A patient with mitochondrial myopathy has exercise
intolerance. Which mitochondrial defect most directly reduces
ATP generation by oxidative phosphorylation?
A. Impaired glycolytic enzyme hexokinase activity
B. Increased outer mitochondrial membrane permeability to
protons
C. Defect in electron transport chain complex IV (cytochrome c
oxidase)
D. Loss of mitochondrial DNA-encoded ribosomal RNAs only
Answer: C
Rationale (correct): A defect in complex IV impairs electron
transfer to oxygen, reducing proton gradient formation and ATP
synthesis by ATP synthase, directly lowering oxidative
phosphorylation capacity.
Incorrect A: Hexokinase functions in glycolysis (cytosolic), not
oxidative phosphorylation within mitochondria.
Incorrect B: Increased proton permeability would collapse the
proton gradient and reduce ATP, but this describes uncoupling
rather than a specific defect seen in mitochondrial myopathies—
less specific than complex IV dysfunction.
Incorrect D: Loss of mitochondrial rRNAs would impair
mitochondrial protein synthesis broadly, but the most direct
cause reducing electron transport chain activity is a specific
complex defect like complex IV.
Teaching Point: Electron transport chain complex defects
directly impair oxidative phosphorylation and ATP production.
