10th Edition
Author(s)Vinay Kumar; Abul K. Abbas;
Jon C. Aster
TEST BANK
1
Reference
Ch. 1 — The Genome
Question Stem
A 45-year-old patient’s tumor sequencing shows loss-of-
function variants in genes that repair double-strand DNA
breaks. Which cellular consequence best explains the patient’s
increased risk of tumor progression?
Options
A. Increased error-prone nonhomologous end-joining leading to
,chromosomal rearrangements
B. Heightened base-excision repair increasing point mutation
rate
C. Upregulated mismatch repair leading to microsatellite
stability
D. Enhanced nucleotide excision repair reducing UV-induced
lesions
Correct Answer
A
Rationales
• A (Correct): Loss of accurate double-strand break repair
forces cells to rely on error-prone nonhomologous end-
joining, producing chromosomal translocations and
genomic instability that promote tumor progression.
• B (Incorrect): Base-excision repair deals primarily with
single-base lesions; its hyperactivity would not explain
double-strand break–related chromosomal
rearrangements.
• C (Incorrect): Mismatch repair affects replication errors
and microsatellites; increased mismatch repair would
reduce instability rather than increase tumor progression.
• D (Incorrect): Nucleotide excision repair corrects bulky
DNA adducts (e.g., UV damage); enhanced activity would
not cause the described chromosomal instability.
,Teaching Point
Defective double-strand break repair → reliance on error-prone
repair → chromosomal instability.
Citation
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.). Ch. 1.
2
Reference
Ch. 1 — Cellular Housekeeping
Question Stem
A patient has peripheral neuropathy caused by accumulation of
misfolded proteins in neurons. Which impaired cellular process
most likely explains the accumulation?
Options
A. Impaired ubiquitin–proteasome system decreasing
degradation of short-lived proteins
B. Increased autophagic flux leading to excessive protein
clearance
C. Enhanced lysosomal enzyme activity causing premature
protein turnover
D. Upregulated chaperone-mediated folding correcting
misfolded proteins
Correct Answer
A
, Rationales
• A (Correct): The ubiquitin–proteasome pathway clears
many misfolded and short-lived proteins; impairment leads
to intracellular accumulation and proteotoxic stress in
neurons.
• B (Incorrect): Increased autophagy would reduce, not
increase, intracellular protein accumulation.
• C (Incorrect): Enhanced lysosomal activity would promote
degradation and would not cause accumulation.
• D (Incorrect): Upregulated chaperones help refold proteins
and would reduce misfolded protein buildup, not cause it.
Teaching Point
Ubiquitin–proteasome dysfunction → accumulation of
misfolded proteins and cell injury.
Citation
Kumar et al. (2021). Robbins Basic Pathology (10th Ed.). Ch. 1.
3
Reference
Ch. 1 — Cellular Metabolism and Mitochondrial Function
Question Stem
A patient with ischemic limb injury shows rapidly swelling cells
and loss of membrane integrity. Which metabolic failure most
directly produced these early reversible/irreversible changes?