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 Reference – Chapter 1: The Cell as a Unit of Health
and Disease — The Genome
Stem: A 32-year-old woman’s tumor DNA sequencing shows a
single base change that converts a codon for glycine into a stop
codon, producing a truncated protein. Which mutation type best
describes this change?
A. Missense mutation
B. Nonsense mutation
C. Silent mutation
D. Frameshift mutation
Correct Answer — B. Nonsense mutation
Rationale (correct): A nonsense mutation converts a codon
specifying an amino acid into a stop codon, producing truncated
proteins with likely loss of function. This explains the tumor’s
,truncated protein product.
Rationale (A): Missense mutations change one amino acid to
another; they do not introduce a premature stop codon.
Rationale (C): Silent mutations change the DNA without
altering the encoded amino acid, so they would not truncate the
protein.
Rationale (D): Frameshift mutations are insertions or deletions
that shift the reading frame; they typically alter many
downstream amino acids rather than a single stop codon
substitution.
Teaching Point: Nonsense mutations create premature stop
codons, producing truncated, often nonfunctional proteins.
2
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — The Genome
Stem: A patient with suspected Lynch syndrome has tumors
showing microsatellite instability. Which DNA repair pathway
is most likely defective?
A. Base excision repair (BER)
B. Nucleotide excision repair (NER)
C. Mismatch repair (MMR)
D. Homologous recombination (HR)
Correct Answer — C. Mismatch repair (MMR)
,Rationale (correct): MMR corrects replication errors,
particularly insertion–deletion loops at microsatellite repeats;
defects produce microsatellite instability seen in Lynch
syndrome.
Rationale (A): BER removes single damaged bases (e.g.,
deaminated bases), not replication-induced microsatellite errors.
Rationale (B): NER repairs bulky helix-distorting lesions like
UV-induced pyrimidine dimers, not microsatellite instability.
Rationale (D): HR repairs double-strand breaks, not replication
slippage at microsatellites.
Teaching Point: Mismatch repair defects cause microsatellite
instability and predispose to Lynch syndrome.
3
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — Cellular Housekeeping
Stem: A hepatocyte exposed to prolonged nutrient deprivation
upregulates autophagosome formation marked by LC3-II.
Which molecular event most directly triggers autophagy in
starvation?
A. Activation of mTORC1
B. Inhibition of AMPK
C. Inhibition of mTORC1
D. Increased insulin signaling
Correct Answer — C. Inhibition of mTORC1
, Rationale (correct): Starvation inhibits mTORC1, which
relieves suppression of the ULK1 complex and initiates
autophagy and autophagosome formation (LC3 lipidation).
Rationale (A): Activation of mTORC1 suppresses autophagy,
not induces it.
Rationale (B): AMPK activation (not inhibition) promotes
autophagy by inhibiting mTORC1 and activating ULK1.
Rationale (D): Insulin signaling activates mTORC1 and
suppresses autophagy, opposite to starvation response.
Teaching Point: Starvation induces autophagy primarily via
mTORC1 inhibition.
4
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — Cellular Housekeeping
Stem: A neurodegenerative disease biopsy shows accumulation
of ubiquitin-positive protein aggregates in neurons. Which
intracellular system most likely failed to clear the misfolded
proteins?
A. Lysosomal pathway (autophagy) only
B. Ubiquitin-proteasome system (UPS)
C. Mitochondrial matrix proteases
D. Endoplasmic reticulum-associated degradation (ERAD) only
Correct Answer — B. Ubiquitin-proteasome system (UPS)
by-Chapter Questions & Verified Solutions
Robbins & Cotran Pathologic Basis of Disease
10th Edition
• Author(s)Vinay Kumar; Abul K. Abbas; Jon C. Aster
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — The Genome
Stem: A 32-year-old woman’s tumor DNA sequencing shows a
single base change that converts a codon for glycine into a stop
codon, producing a truncated protein. Which mutation type best
describes this change?
A. Missense mutation
B. Nonsense mutation
C. Silent mutation
D. Frameshift mutation
Correct Answer — B. Nonsense mutation
Rationale (correct): A nonsense mutation converts a codon
specifying an amino acid into a stop codon, producing truncated
proteins with likely loss of function. This explains the tumor’s
,truncated protein product.
Rationale (A): Missense mutations change one amino acid to
another; they do not introduce a premature stop codon.
Rationale (C): Silent mutations change the DNA without
altering the encoded amino acid, so they would not truncate the
protein.
Rationale (D): Frameshift mutations are insertions or deletions
that shift the reading frame; they typically alter many
downstream amino acids rather than a single stop codon
substitution.
Teaching Point: Nonsense mutations create premature stop
codons, producing truncated, often nonfunctional proteins.
2
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — The Genome
Stem: A patient with suspected Lynch syndrome has tumors
showing microsatellite instability. Which DNA repair pathway
is most likely defective?
A. Base excision repair (BER)
B. Nucleotide excision repair (NER)
C. Mismatch repair (MMR)
D. Homologous recombination (HR)
Correct Answer — C. Mismatch repair (MMR)
,Rationale (correct): MMR corrects replication errors,
particularly insertion–deletion loops at microsatellite repeats;
defects produce microsatellite instability seen in Lynch
syndrome.
Rationale (A): BER removes single damaged bases (e.g.,
deaminated bases), not replication-induced microsatellite errors.
Rationale (B): NER repairs bulky helix-distorting lesions like
UV-induced pyrimidine dimers, not microsatellite instability.
Rationale (D): HR repairs double-strand breaks, not replication
slippage at microsatellites.
Teaching Point: Mismatch repair defects cause microsatellite
instability and predispose to Lynch syndrome.
3
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — Cellular Housekeeping
Stem: A hepatocyte exposed to prolonged nutrient deprivation
upregulates autophagosome formation marked by LC3-II.
Which molecular event most directly triggers autophagy in
starvation?
A. Activation of mTORC1
B. Inhibition of AMPK
C. Inhibition of mTORC1
D. Increased insulin signaling
Correct Answer — C. Inhibition of mTORC1
, Rationale (correct): Starvation inhibits mTORC1, which
relieves suppression of the ULK1 complex and initiates
autophagy and autophagosome formation (LC3 lipidation).
Rationale (A): Activation of mTORC1 suppresses autophagy,
not induces it.
Rationale (B): AMPK activation (not inhibition) promotes
autophagy by inhibiting mTORC1 and activating ULK1.
Rationale (D): Insulin signaling activates mTORC1 and
suppresses autophagy, opposite to starvation response.
Teaching Point: Starvation induces autophagy primarily via
mTORC1 inhibition.
4
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — Cellular Housekeeping
Stem: A neurodegenerative disease biopsy shows accumulation
of ubiquitin-positive protein aggregates in neurons. Which
intracellular system most likely failed to clear the misfolded
proteins?
A. Lysosomal pathway (autophagy) only
B. Ubiquitin-proteasome system (UPS)
C. Mitochondrial matrix proteases
D. Endoplasmic reticulum-associated degradation (ERAD) only
Correct Answer — B. Ubiquitin-proteasome system (UPS)
