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 – Chapter 1: The Cell as a Unit of Health
and Disease — The Genome
Stem: A 45-year-old man is found to have a heterozygous
germline mutation in the TP53 gene. Which cellular defect best
explains his increased lifetime cancer risk?
A. Increased telomerase activity in somatic cells
B. Loss of a key DNA damage checkpoint and impaired
apoptosis
C. Constitutive activation of repair by homologous
recombination
D. Overexpression of mismatch repair proteins leading to
hypermutation
Correct Answer: B
,Rationale:
Correct: TP53 encodes p53, a central DNA damage checkpoint
protein that induces cell-cycle arrest and apoptosis when damage
is irreparable; loss impairs these safeguards and increases
malignant transformation.
Incorrect A: Increased telomerase promotes immortalization
but is not the principal defect in TP53 loss.
Incorrect C: Constitutive homologous recombination would not
promote cancer risk via TP53 mutation; defective, not
overactive, repair is the usual issue.
Incorrect D: Overexpression of mismatch repair proteins would
not cause hypermutation; loss of mismatch repair causes
microsatellite instability.
Teaching Point: p53 loss removes cell-cycle checkpoints and
apoptosis, promoting tumorigenesis.
2.
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — The Genome
Stem: A cell exposed to ionizing radiation accumulates double-
strand DNA breaks. Which pathway is most critical for accurate
repair during S/G2 phases?
A. Nonhomologous end joining (NHEJ)
B. Base excision repair (BER)
C. Homologous recombination (HR)
D. Nucleotide excision repair (NER)
Correct Answer: C
,Rationale:
Correct: Homologous recombination uses the sister chromatid
as a template and is the high-fidelity mechanism active in S/G2
for double-strand break repair.
Incorrect A: NHEJ is active throughout the cell cycle and is
quicker but error-prone compared with HR.
Incorrect B: BER fixes small base lesions and single-strand
breaks, not double-strand breaks.
Incorrect D: NER removes bulky helix-distorting lesions like
thymine dimers, not DSBs.
Teaching Point: Homologous recombination repairs double-
strand breaks accurately using sister chromatids.
3.
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — The Genome
Stem: A patient with defective telomerase has early hair
greying, bone marrow failure, and pulmonary fibrosis. Which
cellular process directly explains tissue failure?
A. Uncontrolled cell proliferation
B. Premature cellular senescence due to telomere shortening
C. Excessive autophagy of stem cells
D. Constitutive activation of Wnt signaling
Correct Answer: B
Rationale:
Correct: Telomerase deficiency causes accelerated telomere
, shortening with each division, triggering replicative senescence
and exhaustion of renewing stem cell populations, leading to
organ failure.
Incorrect A: Defective telomerase causes reduced replicative
capacity, not uncontrolled proliferation.
Incorrect C: Autophagy is not the primary mechanism linking
telomerase defects to stem cell exhaustion.
Incorrect D: Wnt activation is unrelated to telomerase
deficiency in this context.
Teaching Point: Telomere shortening induces replicative
senescence and stem cell exhaustion.
4.
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — Cellular Housekeeping
Stem: A biopsy of liver from a patient with chronic alcohol use
shows cytoplasmic inclusions (Mallory bodies) composed
mainly of misfolded intermediate filaments. Which cellular
system normally degrades such abnormal proteins?
A. Lysosomal hydrolases via autophagy only
B. Ubiquitin-proteasome system (UPS)
C. Mitochondrial proteases
D. Extracellular proteases secreted by the cell
Correct Answer: B
Rationale:
Correct: The ubiquitin-proteasome system tags misfolded
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 – Chapter 1: The Cell as a Unit of Health
and Disease — The Genome
Stem: A 45-year-old man is found to have a heterozygous
germline mutation in the TP53 gene. Which cellular defect best
explains his increased lifetime cancer risk?
A. Increased telomerase activity in somatic cells
B. Loss of a key DNA damage checkpoint and impaired
apoptosis
C. Constitutive activation of repair by homologous
recombination
D. Overexpression of mismatch repair proteins leading to
hypermutation
Correct Answer: B
,Rationale:
Correct: TP53 encodes p53, a central DNA damage checkpoint
protein that induces cell-cycle arrest and apoptosis when damage
is irreparable; loss impairs these safeguards and increases
malignant transformation.
Incorrect A: Increased telomerase promotes immortalization
but is not the principal defect in TP53 loss.
Incorrect C: Constitutive homologous recombination would not
promote cancer risk via TP53 mutation; defective, not
overactive, repair is the usual issue.
Incorrect D: Overexpression of mismatch repair proteins would
not cause hypermutation; loss of mismatch repair causes
microsatellite instability.
Teaching Point: p53 loss removes cell-cycle checkpoints and
apoptosis, promoting tumorigenesis.
2.
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — The Genome
Stem: A cell exposed to ionizing radiation accumulates double-
strand DNA breaks. Which pathway is most critical for accurate
repair during S/G2 phases?
A. Nonhomologous end joining (NHEJ)
B. Base excision repair (BER)
C. Homologous recombination (HR)
D. Nucleotide excision repair (NER)
Correct Answer: C
,Rationale:
Correct: Homologous recombination uses the sister chromatid
as a template and is the high-fidelity mechanism active in S/G2
for double-strand break repair.
Incorrect A: NHEJ is active throughout the cell cycle and is
quicker but error-prone compared with HR.
Incorrect B: BER fixes small base lesions and single-strand
breaks, not double-strand breaks.
Incorrect D: NER removes bulky helix-distorting lesions like
thymine dimers, not DSBs.
Teaching Point: Homologous recombination repairs double-
strand breaks accurately using sister chromatids.
3.
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — The Genome
Stem: A patient with defective telomerase has early hair
greying, bone marrow failure, and pulmonary fibrosis. Which
cellular process directly explains tissue failure?
A. Uncontrolled cell proliferation
B. Premature cellular senescence due to telomere shortening
C. Excessive autophagy of stem cells
D. Constitutive activation of Wnt signaling
Correct Answer: B
Rationale:
Correct: Telomerase deficiency causes accelerated telomere
, shortening with each division, triggering replicative senescence
and exhaustion of renewing stem cell populations, leading to
organ failure.
Incorrect A: Defective telomerase causes reduced replicative
capacity, not uncontrolled proliferation.
Incorrect C: Autophagy is not the primary mechanism linking
telomerase defects to stem cell exhaustion.
Incorrect D: Wnt activation is unrelated to telomerase
deficiency in this context.
Teaching Point: Telomere shortening induces replicative
senescence and stem cell exhaustion.
4.
Chapter Reference – Chapter 1: The Cell as a Unit of Health
and Disease — Cellular Housekeeping
Stem: A biopsy of liver from a patient with chronic alcohol use
shows cytoplasmic inclusions (Mallory bodies) composed
mainly of misfolded intermediate filaments. Which cellular
system normally degrades such abnormal proteins?
A. Lysosomal hydrolases via autophagy only
B. Ubiquitin-proteasome system (UPS)
C. Mitochondrial proteases
D. Extracellular proteases secreted by the cell
Correct Answer: B
Rationale:
Correct: The ubiquitin-proteasome system tags misfolded
