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 – The Genome
Stem: A 42-year-old man has a family history of colon cancer.
Tumor testing reveals microsatellite instability. Which DNA
repair defect most likely explains this pattern?
A. Base excision repair deficiency
B. Mismatch repair deficiency
C. Nucleotide excision repair deficiency
D. Homologous recombination deficiency
Answer: B
,Rationale (Correct): Mismatch repair corrects base–base
mismatches and insertion–deletion loops, particularly in
repetitive microsatellite regions; defects cause microsatellite
instability leading to increased mutation rates.
Rationale (A): Base excision repair removes small, non-helix-
distorting base lesions (e.g., deaminated cytosine); its defect
does not produce classic microsatellite instability.
Rationale (C): Nucleotide excision repair removes bulky helix-
distorting lesions (e.g., UV-induced thymine dimers), not
microsatellite mismatches.
Rationale (D): Homologous recombination repairs double-
strand breaks; defects produce chromosomal instability rather
than microsatellite instability.
Teaching Point: Mismatch repair defects produce microsatellite
instability and predispose to certain cancers.
2.
Chapter Reference – The Genome
Stem: A tumor shows amplification of the HER2 gene. Which
class of gene is HER2 most appropriately classified as?
A. Tumor suppressor gene
B. Proto-oncogene (activated by amplification)
C. DNA repair gene
D. MicroRNA regulator
Answer: B
,Rationale (Correct): HER2 is a proto-oncogene encoding a
receptor tyrosine kinase; gene amplification increases its
expression and activates oncogenic signaling.
Rationale (A): Tumor suppressor genes are typically inactivated
by loss-of-function mutations or deletions, not amplified to
drive cancer.
Rationale (C): DNA repair genes maintain genomic integrity;
HER2 is a signaling receptor, not involved primarily in DNA
repair.
Rationale (D): MicroRNAs regulate gene expression post-
transcriptionally; HER2 is a protein-coding receptor gene.
Teaching Point: Proto-oncogene amplification increases protein
activity and can drive tumorigenesis.
3.
Chapter Reference – Cellular Housekeeping
Stem: A muscle biopsy from a patient with a metabolic
myopathy shows accumulation of autophagic vacuoles and
ubiquitinated protein aggregates. Which pathway defect best
explains these findings?
A. Impaired lysosomal degradation (autophagy)
B. Excessive mitochondrial biogenesis
C. Overactive necroptosis
D. Hyperfunctional proteasome activity
Answer: A
, Rationale (Correct): Autophagy delivers cytoplasmic contents to
lysosomes for degradation; impaired autophagy or lysosomal
function causes accumulation of autophagic vacuoles and
protein aggregates.
Rationale (B): Increased mitochondrial biogenesis would
increase mitochondria, not cause accumulation of autophagic
vacuoles and ubiquitinated aggregates.
Rationale (C): Necroptosis is a regulated necrosis pathway
causing cell death, not selective accumulation of autophagic
vacuoles.
Rationale (D): Hyperfunctional proteasome activity would
decrease ubiquitinated aggregates, not increase them.
Teaching Point: Defective autophagy/lysosomal degradation
leads to intracellular aggregate accumulation.
4.
Chapter Reference – Cellular Housekeeping
Stem: A patient receives a drug that inhibits the ubiquitin–
proteasome system. Which cellular process will be most directly
impaired?
A. Autophagosome formation
B. Degradation of short-lived regulatory proteins
C. DNA replication initiation
D. Mitochondrial ATP synthesis
Answer: B
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 – The Genome
Stem: A 42-year-old man has a family history of colon cancer.
Tumor testing reveals microsatellite instability. Which DNA
repair defect most likely explains this pattern?
A. Base excision repair deficiency
B. Mismatch repair deficiency
C. Nucleotide excision repair deficiency
D. Homologous recombination deficiency
Answer: B
,Rationale (Correct): Mismatch repair corrects base–base
mismatches and insertion–deletion loops, particularly in
repetitive microsatellite regions; defects cause microsatellite
instability leading to increased mutation rates.
Rationale (A): Base excision repair removes small, non-helix-
distorting base lesions (e.g., deaminated cytosine); its defect
does not produce classic microsatellite instability.
Rationale (C): Nucleotide excision repair removes bulky helix-
distorting lesions (e.g., UV-induced thymine dimers), not
microsatellite mismatches.
Rationale (D): Homologous recombination repairs double-
strand breaks; defects produce chromosomal instability rather
than microsatellite instability.
Teaching Point: Mismatch repair defects produce microsatellite
instability and predispose to certain cancers.
2.
Chapter Reference – The Genome
Stem: A tumor shows amplification of the HER2 gene. Which
class of gene is HER2 most appropriately classified as?
A. Tumor suppressor gene
B. Proto-oncogene (activated by amplification)
C. DNA repair gene
D. MicroRNA regulator
Answer: B
,Rationale (Correct): HER2 is a proto-oncogene encoding a
receptor tyrosine kinase; gene amplification increases its
expression and activates oncogenic signaling.
Rationale (A): Tumor suppressor genes are typically inactivated
by loss-of-function mutations or deletions, not amplified to
drive cancer.
Rationale (C): DNA repair genes maintain genomic integrity;
HER2 is a signaling receptor, not involved primarily in DNA
repair.
Rationale (D): MicroRNAs regulate gene expression post-
transcriptionally; HER2 is a protein-coding receptor gene.
Teaching Point: Proto-oncogene amplification increases protein
activity and can drive tumorigenesis.
3.
Chapter Reference – Cellular Housekeeping
Stem: A muscle biopsy from a patient with a metabolic
myopathy shows accumulation of autophagic vacuoles and
ubiquitinated protein aggregates. Which pathway defect best
explains these findings?
A. Impaired lysosomal degradation (autophagy)
B. Excessive mitochondrial biogenesis
C. Overactive necroptosis
D. Hyperfunctional proteasome activity
Answer: A
, Rationale (Correct): Autophagy delivers cytoplasmic contents to
lysosomes for degradation; impaired autophagy or lysosomal
function causes accumulation of autophagic vacuoles and
protein aggregates.
Rationale (B): Increased mitochondrial biogenesis would
increase mitochondria, not cause accumulation of autophagic
vacuoles and ubiquitinated aggregates.
Rationale (C): Necroptosis is a regulated necrosis pathway
causing cell death, not selective accumulation of autophagic
vacuoles.
Rationale (D): Hyperfunctional proteasome activity would
decrease ubiquitinated aggregates, not increase them.
Teaching Point: Defective autophagy/lysosomal degradation
leads to intracellular aggregate accumulation.
4.
Chapter Reference – Cellular Housekeeping
Stem: A patient receives a drug that inhibits the ubiquitin–
proteasome system. Which cellular process will be most directly
impaired?
A. Autophagosome formation
B. Degradation of short-lived regulatory proteins
C. DNA replication initiation
D. Mitochondrial ATP synthesis
Answer: B
