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
Chapter 1 — The Genome
Stem: A 28-year-old woman presents after exposure to a
known mutagen. Her cells rapidly activate a DNA repair
pathway that recognizes single-strand mismatches during
replication. Which DNA repair mechanism is most likely
responsible?
A. Nonhomologous end-joining
B. Base excision repair
C. Nucleotide excision repair
D. Mismatch repair
Correct Answer: D
Rationales:
• Correct (D): Mismatch repair corrects base–base
mismatches and insertion–deletion loops that escape
, proofreading during DNA replication; it is rapidly activated
in proliferating cells exposed to replication-associated
mutagens. (Robbins Ch.1, "The Genome").
• A: Nonhomologous end-joining repairs double-strand
breaks and is error-prone; it’s not specific for replication
mismatches.
• B: Base excision repair fixes small base lesions (e.g.,
oxidized or deaminated bases), not replication
mismatches.
• C: Nucleotide excision repair removes bulky helix-
distorting adducts (e.g., UV photoproducts), not typical
replication mismatches.
Teaching Point: Mismatch repair corrects replication errors;
different pathways handle distinct DNA lesions.
Citation: Robbins & Cotran, 10th Ed., Chapter 1 — The Genome.
2. Chapter 1 — The Genome
Stem: A patient with hereditary nonpolyposis colorectal cancer
(Lynch syndrome) has a germline defect in one component of a
DNA repair system. Which consequence best explains the
tumor predisposition?
A. Increased double-strand break accumulation due to
defective homologous recombination
B. Microsatellite instability from mismatch repair failure
C. Failure to remove bulky adducts leading to transcription
,blockage
D. Excessive base excision repair causing point mutations
Correct Answer: B
Rationales:
• Correct (B): Lynch syndrome results from inherited defects
in mismatch repair genes (e.g., MLH1, MSH2), causing
microsatellite instability and increased mutation rates in
target genes. (Robbins Ch.1, "The Genome").
• A: Homologous recombination defects (e.g., BRCA) cause
double-strand break repair problems, not Lynch syndrome.
• C: Failure to remove bulky adducts implicates nucleotide
excision repair defects (e.g., xeroderma pigmentosum).
• D: Overactive base excision repair does not drive the
characteristic microsatellite instability seen in Lynch
syndrome.
Teaching Point: Defective mismatch repair → microsatellite
instability → cancer risk.
Citation: Robbins & Cotran, 10th Ed., Chapter 1 — The Genome.
3. Chapter 1 — Cellular Housekeeping
Stem: A clinician suspects a lysosomal storage disorder in an
infant with neurodegeneration and hepatosplenomegaly.
Which cellular defect best explains accumulation of
undegraded macromolecules in these cells?
, A. Impaired ubiquitin–proteasome system
B. Defective autophagosome–lysosome fusion or lysosomal
enzyme deficiency
C. Mitochondrial ATP shortage preventing cellular transport
D. Abnormal extracellular matrix deposition blocking
degradation
Correct Answer: B
Rationales:
• Correct (B): Lysosomal storage diseases arise from
deficient lysosomal hydrolases or defects in
autophagosome–lysosome fusion, leading to accumulation
of undegraded substrates within lysosomes. (Robbins Ch.1,
"Cellular Housekeeping").
• A: The ubiquitin–proteasome system degrades short-lived
cytosolic proteins; its failure causes different protein
accumulations, not characteristic lysosomal substrate
storage.
• C: ATP shortage can impair many processes but does not
specifically cause lysosomal substrate accumulation seen
in storage disorders.
• D: ECM deposition is extracellular and unrelated to
intracellular lysosomal substrate build-up.
Teaching Point: Lysosomal enzyme or fusion defects cause
intracellular storage of macromolecules.
by-Chapter Questions & Verified Solutions
Robbins & Cotran Pathologic Basis of Disease
10th Edition
• Author(s)Vinay Kumar; Abul K. Abbas; Jon C. Aster
Chapter 1 — The Genome
Stem: A 28-year-old woman presents after exposure to a
known mutagen. Her cells rapidly activate a DNA repair
pathway that recognizes single-strand mismatches during
replication. Which DNA repair mechanism is most likely
responsible?
A. Nonhomologous end-joining
B. Base excision repair
C. Nucleotide excision repair
D. Mismatch repair
Correct Answer: D
Rationales:
• Correct (D): Mismatch repair corrects base–base
mismatches and insertion–deletion loops that escape
, proofreading during DNA replication; it is rapidly activated
in proliferating cells exposed to replication-associated
mutagens. (Robbins Ch.1, "The Genome").
• A: Nonhomologous end-joining repairs double-strand
breaks and is error-prone; it’s not specific for replication
mismatches.
• B: Base excision repair fixes small base lesions (e.g.,
oxidized or deaminated bases), not replication
mismatches.
• C: Nucleotide excision repair removes bulky helix-
distorting adducts (e.g., UV photoproducts), not typical
replication mismatches.
Teaching Point: Mismatch repair corrects replication errors;
different pathways handle distinct DNA lesions.
Citation: Robbins & Cotran, 10th Ed., Chapter 1 — The Genome.
2. Chapter 1 — The Genome
Stem: A patient with hereditary nonpolyposis colorectal cancer
(Lynch syndrome) has a germline defect in one component of a
DNA repair system. Which consequence best explains the
tumor predisposition?
A. Increased double-strand break accumulation due to
defective homologous recombination
B. Microsatellite instability from mismatch repair failure
C. Failure to remove bulky adducts leading to transcription
,blockage
D. Excessive base excision repair causing point mutations
Correct Answer: B
Rationales:
• Correct (B): Lynch syndrome results from inherited defects
in mismatch repair genes (e.g., MLH1, MSH2), causing
microsatellite instability and increased mutation rates in
target genes. (Robbins Ch.1, "The Genome").
• A: Homologous recombination defects (e.g., BRCA) cause
double-strand break repair problems, not Lynch syndrome.
• C: Failure to remove bulky adducts implicates nucleotide
excision repair defects (e.g., xeroderma pigmentosum).
• D: Overactive base excision repair does not drive the
characteristic microsatellite instability seen in Lynch
syndrome.
Teaching Point: Defective mismatch repair → microsatellite
instability → cancer risk.
Citation: Robbins & Cotran, 10th Ed., Chapter 1 — The Genome.
3. Chapter 1 — Cellular Housekeeping
Stem: A clinician suspects a lysosomal storage disorder in an
infant with neurodegeneration and hepatosplenomegaly.
Which cellular defect best explains accumulation of
undegraded macromolecules in these cells?
, A. Impaired ubiquitin–proteasome system
B. Defective autophagosome–lysosome fusion or lysosomal
enzyme deficiency
C. Mitochondrial ATP shortage preventing cellular transport
D. Abnormal extracellular matrix deposition blocking
degradation
Correct Answer: B
Rationales:
• Correct (B): Lysosomal storage diseases arise from
deficient lysosomal hydrolases or defects in
autophagosome–lysosome fusion, leading to accumulation
of undegraded substrates within lysosomes. (Robbins Ch.1,
"Cellular Housekeeping").
• A: The ubiquitin–proteasome system degrades short-lived
cytosolic proteins; its failure causes different protein
accumulations, not characteristic lysosomal substrate
storage.
• C: ATP shortage can impair many processes but does not
specifically cause lysosomal substrate accumulation seen
in storage disorders.
• D: ECM deposition is extracellular and unrelated to
intracellular lysosomal substrate build-up.
Teaching Point: Lysosomal enzyme or fusion defects cause
intracellular storage of macromolecules.
