GNRS 515 Advanced Pathophysiology Exam
Questions and answer with rationale Top
Rated
Question 1 (Cellular Adaptation – Week 1)
A 55-year-old male smoker undergoes bronchoscopy. The biopsy shows
replacement of normal ciliated columnar epithelium with stratified squamous
epithelium. This cellular change is best described as:
A. Hypertrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Correct Answer: C
Rationale: Metaplasia is the reversible substitution of one differentiated adult cell
type for another in response to chronic irritation (here, cigarette smoke). It is an
adaptive response that allows the tissue to better withstand the stressor. If
smoking ceases, the change is usually reversible. Dysplasia involves disordered
growth with loss of uniformity and is more likely to progress to neoplasia;
hypertrophy and hyperplasia involve size or number changes, not cell-type
replacement.
Question 2 (Cellular Injury – Hypoxic Mechanism)
In hypoxic cell injury, failure of the Na+/K+ ATPase pump leads to:
A. Potassium efflux and cellular shrinkage
B. Sodium influx, osmotic water movement, and cellular swelling
C. Immediate mitochondrial calcium sequestration and ATP restoration
D. Lysosomal stabilization preventing enzyme release
,Correct Answer: B
Rationale: ATP depletion from hypoxia impairs the Na+/K+ pump, allowing Na+ to
accumulate inside the cell. This increases intracellular osmolarity, drawing water
in and causing cellular (cytotoxic) edema. Calcium influx later activates destructive
enzymes. This is a hallmark reversible stage of hypoxic/ischemic injury before
progression to necrosis.
Question 3 (Cell Death – Apoptosis vs. Necrosis)
Which statement best distinguishes apoptosis from necrosis?
A. Apoptosis triggers a robust inflammatory response due to lysosomal enzyme
release
B. Apoptosis affects contiguous groups of cells and results in caseous debris
C. Apoptosis is an energy-dependent, programmed process that produces
membrane-bound apoptotic bodies with no inflammation
D. Necrosis is genetically regulated and occurs in single scattered cells
Correct Answer: C
Rationale: Apoptosis is ATP-dependent “programmed cell death” (cell suicide) that
eliminates unwanted or damaged cells while maintaining membrane integrity.
Apoptotic bodies are phagocytosed without releasing intracellular contents, so
there is no inflammation. Necrosis is passive, unregulated cell death with
membrane rupture, enzyme leakage, and inflammation. This distinction is critical
in exams (e.g., viral hepatitis shows Councilman bodies = apoptosis).
Question 4 (Genetics – Mutation Types)
A point mutation changes a single base pair, resulting in a codon that now codes
for a different amino acid. This is classified as a:
A. Silent mutation
B. Nonsense mutation
C. Missense mutation
,D. Frameshift mutation
Correct Answer: C
Rationale: Missense mutation (base-pair substitution) alters the codon so a
different amino acid is incorporated (e.g., sickle cell – Glu → Val). Silent mutation
changes the codon but not the amino acid (due to degeneracy). Nonsense creates
a premature stop codon. Frameshift (insertion/deletion) shifts the entire reading
frame downstream. All are tested heavily in GNRS 515 genetics unit.
Question 5 (Epigenetics)
Identical twins with the same DNA sequence show different disease phenotypes
(one develops type 2 diabetes, the other does not). The most likely explanation is:
A. Germline mutation
B. Epigenetic modifications
C. Frameshift mutation in one twin
D. Chromosomal nondisjunction
Correct Answer: B
Rationale: Epigenetics involves heritable changes in gene expression without
altering the DNA sequence (DNA methylation, histone acetylation, miRNA). These
can be influenced by environment/lifestyle and explain discordant phenotypes in
monozygotic twins. This is a key concept in the GNRS 515 genetics/epigenetics
module.
Question 6 (Fluid & Electrolyte – Starling Forces)
A patient with liver failure develops generalized edema. The primary mechanism
is:
A. Increased capillary hydrostatic pressure
B. Decreased plasma oncotic pressure due to hypoalbuminemia
C. Increased interstitial hydrostatic pressure
, D. Decreased capillary permeability
Correct Answer: B
Rationale: Starling forces govern fluid movement: net filtration = (Pc – Pi) – (πc –
πi). In hypoalbuminemia (liver failure), plasma oncotic pressure (πc) drops
dramatically, allowing fluid to leave the vascular space into the interstitium →
edema. This is classic in GNRS 515 fluid/electrolyte imbalance Questions.
Question 7 (Inflammation – Acute Phase)
During the acute inflammatory response, the first cells to arrive at the site of
injury (within minutes) are:
A. Macrophages
B. Lymphocytes
C. Neutrophils
D. Eosinophils
Correct Answer: C
Rationale: Neutrophils are the hallmark of acute inflammation (first 6–24 hours).
They marginate, roll, adhere (via selectins/integrins), and diapedese in response
to chemotactic factors (IL-8, C5a, LTB4). Macrophages dominate chronic
inflammation (after 24–48 hours). This sequence is tested on every
inflammation/immunity exam.
Question 8 (Immunity – HIV Pathophysiology)
The primary target cells for HIV are:
A. CD8+ cytotoxic T cells
B. CD4+ helper T cells, macrophages, and dendritic cells
C. B lymphocytes
D. Natural killer cells
Correct Answer: B
Questions and answer with rationale Top
Rated
Question 1 (Cellular Adaptation – Week 1)
A 55-year-old male smoker undergoes bronchoscopy. The biopsy shows
replacement of normal ciliated columnar epithelium with stratified squamous
epithelium. This cellular change is best described as:
A. Hypertrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Correct Answer: C
Rationale: Metaplasia is the reversible substitution of one differentiated adult cell
type for another in response to chronic irritation (here, cigarette smoke). It is an
adaptive response that allows the tissue to better withstand the stressor. If
smoking ceases, the change is usually reversible. Dysplasia involves disordered
growth with loss of uniformity and is more likely to progress to neoplasia;
hypertrophy and hyperplasia involve size or number changes, not cell-type
replacement.
Question 2 (Cellular Injury – Hypoxic Mechanism)
In hypoxic cell injury, failure of the Na+/K+ ATPase pump leads to:
A. Potassium efflux and cellular shrinkage
B. Sodium influx, osmotic water movement, and cellular swelling
C. Immediate mitochondrial calcium sequestration and ATP restoration
D. Lysosomal stabilization preventing enzyme release
,Correct Answer: B
Rationale: ATP depletion from hypoxia impairs the Na+/K+ pump, allowing Na+ to
accumulate inside the cell. This increases intracellular osmolarity, drawing water
in and causing cellular (cytotoxic) edema. Calcium influx later activates destructive
enzymes. This is a hallmark reversible stage of hypoxic/ischemic injury before
progression to necrosis.
Question 3 (Cell Death – Apoptosis vs. Necrosis)
Which statement best distinguishes apoptosis from necrosis?
A. Apoptosis triggers a robust inflammatory response due to lysosomal enzyme
release
B. Apoptosis affects contiguous groups of cells and results in caseous debris
C. Apoptosis is an energy-dependent, programmed process that produces
membrane-bound apoptotic bodies with no inflammation
D. Necrosis is genetically regulated and occurs in single scattered cells
Correct Answer: C
Rationale: Apoptosis is ATP-dependent “programmed cell death” (cell suicide) that
eliminates unwanted or damaged cells while maintaining membrane integrity.
Apoptotic bodies are phagocytosed without releasing intracellular contents, so
there is no inflammation. Necrosis is passive, unregulated cell death with
membrane rupture, enzyme leakage, and inflammation. This distinction is critical
in exams (e.g., viral hepatitis shows Councilman bodies = apoptosis).
Question 4 (Genetics – Mutation Types)
A point mutation changes a single base pair, resulting in a codon that now codes
for a different amino acid. This is classified as a:
A. Silent mutation
B. Nonsense mutation
C. Missense mutation
,D. Frameshift mutation
Correct Answer: C
Rationale: Missense mutation (base-pair substitution) alters the codon so a
different amino acid is incorporated (e.g., sickle cell – Glu → Val). Silent mutation
changes the codon but not the amino acid (due to degeneracy). Nonsense creates
a premature stop codon. Frameshift (insertion/deletion) shifts the entire reading
frame downstream. All are tested heavily in GNRS 515 genetics unit.
Question 5 (Epigenetics)
Identical twins with the same DNA sequence show different disease phenotypes
(one develops type 2 diabetes, the other does not). The most likely explanation is:
A. Germline mutation
B. Epigenetic modifications
C. Frameshift mutation in one twin
D. Chromosomal nondisjunction
Correct Answer: B
Rationale: Epigenetics involves heritable changes in gene expression without
altering the DNA sequence (DNA methylation, histone acetylation, miRNA). These
can be influenced by environment/lifestyle and explain discordant phenotypes in
monozygotic twins. This is a key concept in the GNRS 515 genetics/epigenetics
module.
Question 6 (Fluid & Electrolyte – Starling Forces)
A patient with liver failure develops generalized edema. The primary mechanism
is:
A. Increased capillary hydrostatic pressure
B. Decreased plasma oncotic pressure due to hypoalbuminemia
C. Increased interstitial hydrostatic pressure
, D. Decreased capillary permeability
Correct Answer: B
Rationale: Starling forces govern fluid movement: net filtration = (Pc – Pi) – (πc –
πi). In hypoalbuminemia (liver failure), plasma oncotic pressure (πc) drops
dramatically, allowing fluid to leave the vascular space into the interstitium →
edema. This is classic in GNRS 515 fluid/electrolyte imbalance Questions.
Question 7 (Inflammation – Acute Phase)
During the acute inflammatory response, the first cells to arrive at the site of
injury (within minutes) are:
A. Macrophages
B. Lymphocytes
C. Neutrophils
D. Eosinophils
Correct Answer: C
Rationale: Neutrophils are the hallmark of acute inflammation (first 6–24 hours).
They marginate, roll, adhere (via selectins/integrins), and diapedese in response
to chemotactic factors (IL-8, C5a, LTB4). Macrophages dominate chronic
inflammation (after 24–48 hours). This sequence is tested on every
inflammation/immunity exam.
Question 8 (Immunity – HIV Pathophysiology)
The primary target cells for HIV are:
A. CD8+ cytotoxic T cells
B. CD4+ helper T cells, macrophages, and dendritic cells
C. B lymphocytes
D. Natural killer cells
Correct Answer: B
