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 6-year-old child presents with extreme sensitivity to
sunlight and multiple early-onset skin cancers. Genetic testing
shows defective excision of UV-induced pyrimidine dimers.
Which DNA repair pathway is most likely defective?
A. Base excision repair
B. Mismatch repair
C. Nucleotide excision repair
D. Homologous recombination
Correct Answer: C. Nucleotide excision repair
Rationales:
• Correct (C): Nucleotide excision repair (NER) removes
bulky helix-distorting lesions such as UV-induced
thymidine dimers; defects cause xeroderma pigmentosum
, with photosensitivity and skin cancers. (Robbins Chapter 1:
The Genome)
• A: Base excision repair corrects small, non-helix-distorting
base lesions (e.g., deaminated bases), not bulky UV
dimers.
• B: Mismatch repair fixes replication errors (mispaired
bases/loops), typical in microsatellite instability, not UV
dimers.
• D: Homologous recombination repairs double-strand
breaks using a sister chromatid, not bulky pyrimidine
dimers.
Teaching Point: NER removes bulky, helix-distorting DNA
lesions like UV dimers.
Citation: Robbins & Cotran, 10th Ed., Chapter 1 — The Genome
2. Chapter 1 — The Genome
Stem: In primary human fibroblast cultures, cells undergo a
finite number of divisions before entering senescence. Which
mechanism primarily explains this replicative limit?
A. Increased telomerase activity with each division
B. Telomere shortening triggering cell-cycle checkpoints
C. Accumulation of mitochondrial DNA mutations only
D. Progressive activation of death receptors on the surface
,Correct Answer: B. Telomere shortening triggering cell-cycle
checkpoints
Rationales:
• Correct (B): Replicative senescence is driven largely by
telomere attrition; critically short telomeres activate
p53/p21 pathways and arrest proliferation. (Robbins
Chapter 1: The Genome)
• A: Increased telomerase prevents telomere shortening; it
is characteristic of germline and many cancer cells, not
normal fibroblasts.
• C: mtDNA mutations can impair function but are not the
primary cause of the Hayflick limit.
• D: Death receptor activation mediates apoptosis, not the
gradual telomere-dependent senescence of replicative
exhaustion.
Teaching Point: Telomere shortening limits somatic cell
replication and induces senescence.
Citation: Robbins & Cotran, 10th Ed., Chapter 1 — The Genome
3. Chapter 1 — Cellular Housekeeping
Stem: During short-term nutrient deprivation, a hepatocyte
reduces protein synthesis and degrades intracellular organelles
to supply amino acids. Which process primarily mediates this
adaptation?
, A. Ubiquitin-proteasome degradation of long-lived proteins
B. Macroautophagy (autophagy) of organelles and proteins
C. Extracellular proteolysis by matrix metalloproteinases
D. Apoptotic caspase-mediated cleavage
Correct Answer: B. Macroautophagy (autophagy) of organelles
and proteins
Rationales:
• Correct (B): Autophagy sequesters and degrades
cytoplasmic components and organelles in lysosomes to
recycle nutrients during starvation. (Robbins Chapter 1:
Cellular Housekeeping)
• A: The ubiquitin-proteasome system mainly degrades
short-lived and misfolded proteins, not bulk organelle
turnover during starvation.
• C: MMPs act extracellularly to remodel ECM, not to supply
intracellular nutrients.
• D: Apoptosis is a programmed cell-death pathway, not a
reversible nutrient-recycling response.
Teaching Point: Autophagy recycles intracellular components
during nutrient deprivation.
Citation: Robbins & Cotran, 10th Ed., Chapter 1 — Cellular
Housekeeping
4. Chapter 1 — Cellular Housekeeping
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 6-year-old child presents with extreme sensitivity to
sunlight and multiple early-onset skin cancers. Genetic testing
shows defective excision of UV-induced pyrimidine dimers.
Which DNA repair pathway is most likely defective?
A. Base excision repair
B. Mismatch repair
C. Nucleotide excision repair
D. Homologous recombination
Correct Answer: C. Nucleotide excision repair
Rationales:
• Correct (C): Nucleotide excision repair (NER) removes
bulky helix-distorting lesions such as UV-induced
thymidine dimers; defects cause xeroderma pigmentosum
, with photosensitivity and skin cancers. (Robbins Chapter 1:
The Genome)
• A: Base excision repair corrects small, non-helix-distorting
base lesions (e.g., deaminated bases), not bulky UV
dimers.
• B: Mismatch repair fixes replication errors (mispaired
bases/loops), typical in microsatellite instability, not UV
dimers.
• D: Homologous recombination repairs double-strand
breaks using a sister chromatid, not bulky pyrimidine
dimers.
Teaching Point: NER removes bulky, helix-distorting DNA
lesions like UV dimers.
Citation: Robbins & Cotran, 10th Ed., Chapter 1 — The Genome
2. Chapter 1 — The Genome
Stem: In primary human fibroblast cultures, cells undergo a
finite number of divisions before entering senescence. Which
mechanism primarily explains this replicative limit?
A. Increased telomerase activity with each division
B. Telomere shortening triggering cell-cycle checkpoints
C. Accumulation of mitochondrial DNA mutations only
D. Progressive activation of death receptors on the surface
,Correct Answer: B. Telomere shortening triggering cell-cycle
checkpoints
Rationales:
• Correct (B): Replicative senescence is driven largely by
telomere attrition; critically short telomeres activate
p53/p21 pathways and arrest proliferation. (Robbins
Chapter 1: The Genome)
• A: Increased telomerase prevents telomere shortening; it
is characteristic of germline and many cancer cells, not
normal fibroblasts.
• C: mtDNA mutations can impair function but are not the
primary cause of the Hayflick limit.
• D: Death receptor activation mediates apoptosis, not the
gradual telomere-dependent senescence of replicative
exhaustion.
Teaching Point: Telomere shortening limits somatic cell
replication and induces senescence.
Citation: Robbins & Cotran, 10th Ed., Chapter 1 — The Genome
3. Chapter 1 — Cellular Housekeeping
Stem: During short-term nutrient deprivation, a hepatocyte
reduces protein synthesis and degrades intracellular organelles
to supply amino acids. Which process primarily mediates this
adaptation?
, A. Ubiquitin-proteasome degradation of long-lived proteins
B. Macroautophagy (autophagy) of organelles and proteins
C. Extracellular proteolysis by matrix metalloproteinases
D. Apoptotic caspase-mediated cleavage
Correct Answer: B. Macroautophagy (autophagy) of organelles
and proteins
Rationales:
• Correct (B): Autophagy sequesters and degrades
cytoplasmic components and organelles in lysosomes to
recycle nutrients during starvation. (Robbins Chapter 1:
Cellular Housekeeping)
• A: The ubiquitin-proteasome system mainly degrades
short-lived and misfolded proteins, not bulk organelle
turnover during starvation.
• C: MMPs act extracellularly to remodel ECM, not to supply
intracellular nutrients.
• D: Apoptosis is a programmed cell-death pathway, not a
reversible nutrient-recycling response.
Teaching Point: Autophagy recycles intracellular components
during nutrient deprivation.
Citation: Robbins & Cotran, 10th Ed., Chapter 1 — Cellular
Housekeeping
4. Chapter 1 — Cellular Housekeeping
