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 pregnant woman is offered noninvasive
prenatal screening that uses cell-free fetal DNA. Which cellular
process most directly explains how fetal DNA fragments appear
in maternal plasma?
A. Exocytosis of intact fetal cells into maternal bloodstream
B. Apoptotic fragmentation of placental trophoblasts releasing
DNA
C. Active transport of fetal DNA across the placenta by
syncytiotrophoblasts
D. Horizontal gene transfer via maternal macrophages
Correct Answer: B
Rationale (correct): Robbins explains that cell-free fetal DNA in
maternal plasma mainly arises from apoptosis of placental
trophoblasts, which generates small DNA fragments that enter
,maternal circulation. This is the primary mechanism underlying
noninvasive prenatal testing.
Rationale (A): Exocytosis of intact fetal cells into maternal
blood is not the main source; intact fetal cells are rare and not
the principal basis for cell-free DNA tests.
Rationale (C): Active transport of DNA across the placenta is
not described as a mechanism; the placenta is a barrier and
trophoblast apoptosis is the primary source.
Rationale (D): Horizontal gene transfer via maternal
macrophages is not a relevant mechanism for cell-free fetal
DNA in plasma.
Teaching Point: Cell-free fetal DNA mainly reflects apoptotic
trophoblast-derived fragments.
Citation: Robbins & Cotran Pathologic Basis of Disease, 10th
Ed., Chapter 1 — The Genome / Cell Death and Apoptosis.
2 — Chapter 1: The Genome
Stem: A patient’s tumor is found to have defective mismatch
repair enzymes and microsatellite instability. Which genomic
mechanism most likely produced this phenotype?
A. Failure of base excision repair leading to point mutations
B. Defective DNA mismatch repair causing replication errors at
repetitive sequences
C. Impaired nucleotide excision repair causing bulky adduct
accumulation
D. Overactive homologous recombination increasing crossover
,events
Correct Answer: B
Rationale (correct): Robbins describes that mismatch repair
defects fail to correct replication errors, particularly in
microsatellite (repetitive) sequences, producing microsatellite
instability commonly seen in certain cancers.
Rationale (A): Base excision repair corrects small base lesions
(e.g., deamination); its failure does not characteristically
produce microsatellite instability.
Rationale (C): Nucleotide excision repair defects lead to
inability to remove bulky DNA adducts (e.g., UV-induced
thymidine dimers), not microsatellite instability.
Rationale (D): Overactive homologous recombination affects
large-scale DNA repair and chromosomal stability but is not the
canonical cause of microsatellite instability.
Teaching Point: Mismatch repair defects cause microsatellite
instability from uncorrected replication errors.
Citation: Robbins & Cotran, Chapter 1 — DNA Repair and
Genomic Instability.
3 — Chapter 1: Cellular Housekeeping
Stem: A 60-year-old man with long-standing diabetes presents
with accumulation of pigmented, cross-linked proteins
(lipofuscin) in his hepatocytes. Which cellular process best
explains lipofuscin accumulation?
A. Increased proteasomal degradation of damaged proteins
, B. Excessive autophagy leading to clearance of aggregates
C. Insufficient lysosomal degradation of oxidized organelles and
proteins
D. Enhanced exocytosis of protein aggregates
Correct Answer: C
Rationale (correct): Robbins states lipofuscin derives from
incompletely degraded, oxidized organelle and protein residues
in lysosomes; impaired lysosomal turnover and oxidative stress
promote accumulation.
Rationale (A): Proteasomal degradation handles soluble
misfolded proteins; lipofuscin is insoluble and accumulates in
lysosomes, not the proteasome.
Rationale (B): Autophagy delivers material to lysosomes for
degradation; excessive autophagy would reduce, not increase,
lipofuscin.
Rationale (D): Exocytosis of protein aggregates is not a major
pathway for removal of damaged organelles that produce
lipofuscin.
Teaching Point: Lipofuscin reflects incomplete lysosomal
degradation of oxidized cellular components.
Citation: Robbins & Cotran, Chapter 1 — Cellular Responses to
Stress: Intracellular Accumulations.
4 — Chapter 1: Cellular Metabolism and Mitochondrial
Function
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 pregnant woman is offered noninvasive
prenatal screening that uses cell-free fetal DNA. Which cellular
process most directly explains how fetal DNA fragments appear
in maternal plasma?
A. Exocytosis of intact fetal cells into maternal bloodstream
B. Apoptotic fragmentation of placental trophoblasts releasing
DNA
C. Active transport of fetal DNA across the placenta by
syncytiotrophoblasts
D. Horizontal gene transfer via maternal macrophages
Correct Answer: B
Rationale (correct): Robbins explains that cell-free fetal DNA in
maternal plasma mainly arises from apoptosis of placental
trophoblasts, which generates small DNA fragments that enter
,maternal circulation. This is the primary mechanism underlying
noninvasive prenatal testing.
Rationale (A): Exocytosis of intact fetal cells into maternal
blood is not the main source; intact fetal cells are rare and not
the principal basis for cell-free DNA tests.
Rationale (C): Active transport of DNA across the placenta is
not described as a mechanism; the placenta is a barrier and
trophoblast apoptosis is the primary source.
Rationale (D): Horizontal gene transfer via maternal
macrophages is not a relevant mechanism for cell-free fetal
DNA in plasma.
Teaching Point: Cell-free fetal DNA mainly reflects apoptotic
trophoblast-derived fragments.
Citation: Robbins & Cotran Pathologic Basis of Disease, 10th
Ed., Chapter 1 — The Genome / Cell Death and Apoptosis.
2 — Chapter 1: The Genome
Stem: A patient’s tumor is found to have defective mismatch
repair enzymes and microsatellite instability. Which genomic
mechanism most likely produced this phenotype?
A. Failure of base excision repair leading to point mutations
B. Defective DNA mismatch repair causing replication errors at
repetitive sequences
C. Impaired nucleotide excision repair causing bulky adduct
accumulation
D. Overactive homologous recombination increasing crossover
,events
Correct Answer: B
Rationale (correct): Robbins describes that mismatch repair
defects fail to correct replication errors, particularly in
microsatellite (repetitive) sequences, producing microsatellite
instability commonly seen in certain cancers.
Rationale (A): Base excision repair corrects small base lesions
(e.g., deamination); its failure does not characteristically
produce microsatellite instability.
Rationale (C): Nucleotide excision repair defects lead to
inability to remove bulky DNA adducts (e.g., UV-induced
thymidine dimers), not microsatellite instability.
Rationale (D): Overactive homologous recombination affects
large-scale DNA repair and chromosomal stability but is not the
canonical cause of microsatellite instability.
Teaching Point: Mismatch repair defects cause microsatellite
instability from uncorrected replication errors.
Citation: Robbins & Cotran, Chapter 1 — DNA Repair and
Genomic Instability.
3 — Chapter 1: Cellular Housekeeping
Stem: A 60-year-old man with long-standing diabetes presents
with accumulation of pigmented, cross-linked proteins
(lipofuscin) in his hepatocytes. Which cellular process best
explains lipofuscin accumulation?
A. Increased proteasomal degradation of damaged proteins
, B. Excessive autophagy leading to clearance of aggregates
C. Insufficient lysosomal degradation of oxidized organelles and
proteins
D. Enhanced exocytosis of protein aggregates
Correct Answer: C
Rationale (correct): Robbins states lipofuscin derives from
incompletely degraded, oxidized organelle and protein residues
in lysosomes; impaired lysosomal turnover and oxidative stress
promote accumulation.
Rationale (A): Proteasomal degradation handles soluble
misfolded proteins; lipofuscin is insoluble and accumulates in
lysosomes, not the proteasome.
Rationale (B): Autophagy delivers material to lysosomes for
degradation; excessive autophagy would reduce, not increase,
lipofuscin.
Rationale (D): Exocytosis of protein aggregates is not a major
pathway for removal of damaged organelles that produce
lipofuscin.
Teaching Point: Lipofuscin reflects incomplete lysosomal
degradation of oxidized cellular components.
Citation: Robbins & Cotran, Chapter 1 — Cellular Responses to
Stress: Intracellular Accumulations.
4 — Chapter 1: Cellular Metabolism and Mitochondrial
Function
