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
Multiple-Choice Questions: Robbins & Cotran Pathologic Basis
of Disease, 10th Ed. – Chapter 1
The Genome & Cellular Housekeeping
1. Chapter 1, Section: The Genome
A 45-year-old patient is diagnosed with a disorder linked to
genomic instability. The clinical report highlights mutations in
genes responsible for nucleotide excision repair. Which cellular
process is most directly compromised by this defect?
a) Correction of single-base mismatches during DNA replication
b) Repair of double-stranded DNA breaks
c) Removal of bulky DNA adducts caused by ultraviolet light
d) Repair of nucleotide errors in mitochondrial DNA
Correct Answer: C
Rationale: Nucleotide excision repair is specifically designed to
,identify and remove bulky, helix-distorting lesions in DNA,
such as those caused by UV light (pyrimidine dimers). This is a
key mechanism for maintaining genomic integrity against
environmental insults. The other options describe different
repair pathways: mismatch repair (a), nonhomologous end
joining or homologous recombination (b), and mitochondrial
DNA has its own distinct repair mechanisms (d).
Teaching Point: Nucleotide excision repair is the primary
defense against bulky DNA adducts, protecting against UV-
induced damage and certain chemical carcinogens.
2. Chapter 1, Section: The Genome
A pathology report for a patient with a specific cancer notes a
"CpG island hypermethylation" pattern in the promoter region of
a tumor suppressor gene. What is the most likely consequence of
this epigenetic change?
a) Increased stability of the tumor suppressor mRNA
b) Enhanced binding of transcription factors to the promoter
c) Transcriptional silencing of the tumor suppressor gene
d) A gain-of-function mutation in the tumor suppressor protein
Correct Answer: C
Rationale: Methylation of CpG islands in gene promoter
regions typically leads to a condensed chromatin state
(heterochromatin), which prevents the transcriptional machinery
from accessing the gene, effectively silencing it. This is a
common epigenetic mechanism for inactivating tumor
suppressor genes in cancer. This process does not directly affect
mRNA stability (a), enhance transcription (b), or alter the
protein's structure/function (d).
,Teaching Point: Promoter hypermethylation is an epigenetic
mechanism that silences genes without changing the DNA
sequence itself, commonly involved in tumor suppressor
inactivation.
3. Chapter 1, Section: Cellular Housekeeping
A patient has a rare genetic disease characterized by the
accumulation of undegraded proteins and organelles within
neurons. A defect in which fundamental cellular process is most
likely responsible for this pathology?
a) Ubiquitin-proteasome system
b) Autophagic pathway
c) DNA damage repair
d) Glycogen synthesis
Correct Answer: B
Rationale: Autophagy is the primary cellular mechanism for
degrading damaged organelles and long-lived proteins,
maintaining cellular cleanliness. A defect in this pathway leads
to the accumulation of cellular debris, which is particularly
damaging to long-lived cells like neurons. The ubiquitin-
proteasome system (a) mainly degrades short-lived and
misfolded proteins, not entire organelles.
Teaching Point: Autophagy is a vital recycling and quality-
control process that clears damaged organelles and protein
aggregates from the cell.
Cellular Metabolism and Mitochondrial Function
4. Chapter 1, Section: Cellular Metabolism and
Mitochondrial Function
, A laboratory test on cultured cells reveals a significant decrease
in ATP production despite normal oxygen levels. Further
analysis shows an accumulation of intermediates in the citric
acid cycle. Which mitochondrial component is most likely
dysfunctional?
a) The outer mitochondrial membrane porins
b) Complex II (succinate dehydrogenase) of the electron
transport chain
c) The mitochondrial matrix enzymes for beta-oxidation
d) The F1F0 ATP synthase (Complex V)
Correct Answer: B
Rationale: Complex II is unique as it is both an enzyme in the
citric acid cycle (succinate dehydrogenase) and a component of
the electron transport chain. A defect here would directly halt
the cycle (causing intermediate accumulation) and impair the
electron flow needed for ATP synthesis. A defect in ATP
synthase (d) would stop ATP production but would not cause a
backup in the TCA cycle.
Teaching Point: Complex II directly links the citric acid cycle
to the electron transport chain; its dysfunction disrupts both
metabolic processes.
5. Chapter 1, Section: Cellular Metabolism and
Mitochondrial Function
A patient presents with a mitochondrial myopathy. Genetic
testing identifies a mutation in the mitochondrial DNA
(mtDNA). When considering the pattern of inheritance for this
disorder, which statement is accurate?
a) The mutation will be passed equally to children of both sexes
by-Chapter Questions & Verified Solutions
Robbins & Cotran Pathologic Basis of Disease
10th Edition
• Author(s)Vinay Kumar; Abul K. Abbas; Jon C. Aster
Multiple-Choice Questions: Robbins & Cotran Pathologic Basis
of Disease, 10th Ed. – Chapter 1
The Genome & Cellular Housekeeping
1. Chapter 1, Section: The Genome
A 45-year-old patient is diagnosed with a disorder linked to
genomic instability. The clinical report highlights mutations in
genes responsible for nucleotide excision repair. Which cellular
process is most directly compromised by this defect?
a) Correction of single-base mismatches during DNA replication
b) Repair of double-stranded DNA breaks
c) Removal of bulky DNA adducts caused by ultraviolet light
d) Repair of nucleotide errors in mitochondrial DNA
Correct Answer: C
Rationale: Nucleotide excision repair is specifically designed to
,identify and remove bulky, helix-distorting lesions in DNA,
such as those caused by UV light (pyrimidine dimers). This is a
key mechanism for maintaining genomic integrity against
environmental insults. The other options describe different
repair pathways: mismatch repair (a), nonhomologous end
joining or homologous recombination (b), and mitochondrial
DNA has its own distinct repair mechanisms (d).
Teaching Point: Nucleotide excision repair is the primary
defense against bulky DNA adducts, protecting against UV-
induced damage and certain chemical carcinogens.
2. Chapter 1, Section: The Genome
A pathology report for a patient with a specific cancer notes a
"CpG island hypermethylation" pattern in the promoter region of
a tumor suppressor gene. What is the most likely consequence of
this epigenetic change?
a) Increased stability of the tumor suppressor mRNA
b) Enhanced binding of transcription factors to the promoter
c) Transcriptional silencing of the tumor suppressor gene
d) A gain-of-function mutation in the tumor suppressor protein
Correct Answer: C
Rationale: Methylation of CpG islands in gene promoter
regions typically leads to a condensed chromatin state
(heterochromatin), which prevents the transcriptional machinery
from accessing the gene, effectively silencing it. This is a
common epigenetic mechanism for inactivating tumor
suppressor genes in cancer. This process does not directly affect
mRNA stability (a), enhance transcription (b), or alter the
protein's structure/function (d).
,Teaching Point: Promoter hypermethylation is an epigenetic
mechanism that silences genes without changing the DNA
sequence itself, commonly involved in tumor suppressor
inactivation.
3. Chapter 1, Section: Cellular Housekeeping
A patient has a rare genetic disease characterized by the
accumulation of undegraded proteins and organelles within
neurons. A defect in which fundamental cellular process is most
likely responsible for this pathology?
a) Ubiquitin-proteasome system
b) Autophagic pathway
c) DNA damage repair
d) Glycogen synthesis
Correct Answer: B
Rationale: Autophagy is the primary cellular mechanism for
degrading damaged organelles and long-lived proteins,
maintaining cellular cleanliness. A defect in this pathway leads
to the accumulation of cellular debris, which is particularly
damaging to long-lived cells like neurons. The ubiquitin-
proteasome system (a) mainly degrades short-lived and
misfolded proteins, not entire organelles.
Teaching Point: Autophagy is a vital recycling and quality-
control process that clears damaged organelles and protein
aggregates from the cell.
Cellular Metabolism and Mitochondrial Function
4. Chapter 1, Section: Cellular Metabolism and
Mitochondrial Function
, A laboratory test on cultured cells reveals a significant decrease
in ATP production despite normal oxygen levels. Further
analysis shows an accumulation of intermediates in the citric
acid cycle. Which mitochondrial component is most likely
dysfunctional?
a) The outer mitochondrial membrane porins
b) Complex II (succinate dehydrogenase) of the electron
transport chain
c) The mitochondrial matrix enzymes for beta-oxidation
d) The F1F0 ATP synthase (Complex V)
Correct Answer: B
Rationale: Complex II is unique as it is both an enzyme in the
citric acid cycle (succinate dehydrogenase) and a component of
the electron transport chain. A defect here would directly halt
the cycle (causing intermediate accumulation) and impair the
electron flow needed for ATP synthesis. A defect in ATP
synthase (d) would stop ATP production but would not cause a
backup in the TCA cycle.
Teaching Point: Complex II directly links the citric acid cycle
to the electron transport chain; its dysfunction disrupts both
metabolic processes.
5. Chapter 1, Section: Cellular Metabolism and
Mitochondrial Function
A patient presents with a mitochondrial myopathy. Genetic
testing identifies a mutation in the mitochondrial DNA
(mtDNA). When considering the pattern of inheritance for this
disorder, which statement is accurate?
a) The mutation will be passed equally to children of both sexes
