NSG 5140 Advanced Pathophysiology Final
Exam
200 Questions & Answers with Rationales
South College | 2026-2027 Academic Year
SECTION 1: CELLULAR ADAPTATION, INJURY, AND DEATH
(Questions 1-25)
Q1. A patient with chronic hypertension develops left ventricular wall
thickening. Which mechanism best explains this adaptation?
A. Increased myocyte number due to cell division
B. Increased myocyte size due to increased workload
C. Replacement of cardiac cells with fibrous tissue
D. Transformation of cardiac cells into smooth muscle
Correct Answer: B
Rationale: Cardiac myocytes are terminally differentiated and cannot undergo
hyperplasia (increase in cell number). They respond to chronic pressure overload
through hypertrophy—an increase in individual cell size to generate greater
contractile force. This is an adaptive response to increased afterload. Fibrous tissue
replacement and metaplasia are not adaptive mechanisms in this scenario .
Q2. During ischemic injury, loss of adenosine triphosphate (ATP) most
directly leads to:
A. Increased oxidative phosphorylation
B. Failure of the sodium-potassium pump
C. Increased protein synthesis
D. Mitochondrial membrane stabilization
Correct Answer: B
,Rationale: ATP is required for the function of the Na⁺/K⁺ ATPase pump. Its
depletion causes this pump to fail, leading to an influx of sodium and water into
the cell, which results in cellular swelling and is a key event in the pathway to cell
death. ATP depletion is the primary initiating mechanism in hypoxia .
Q3. A patient's biopsy reveals an increase in the number of breast glandular
cells due to hormonal stimulation. What is this cellular adaptation called?
A. Hypertrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Correct Answer: B
Rationale: Hyperplasia is an increase in the number of cells in an organ or tissue,
typically in response to hormonal stimulation or increased functional demand.
Breast glandular cells proliferate in response to estrogen stimulation during
pregnancy. Unlike hypertrophy (increase in cell size), hyperplasia involves cell
division in tissues capable of mitotic activity .
Q4. A patient with chronic GERD develops a change in the esophageal
epithelium from stratified squamous to columnar epithelium with goblet cells.
This adaptation is termed:
A. Hypertrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Correct Answer: C
Rationale: Metaplasia is a reversible change in which one differentiated cell type
is replaced by another cell type. In Barrett's esophagus, chronic acid exposure
causes the normal stratified squamous epithelium to transform into columnar
,epithelium with goblet cells as an adaptive response to chronic irritation. This
change is adaptive but can increase cancer risk .
Q5. Following a hypoxic event like a stroke, brain tissue often softens and
liquefies. Which type of necrosis is this?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Fat necrosis
Correct Answer: B
Rationale: Liquefactive necrosis is characteristic of the central nervous system
(brain). It is caused by the release of hydrolytic enzymes from dead cells and
inflammatory cells, which dissolve the tissue into a liquid, viscous mass.
Coagulative necrosis is typical of myocardial infarction; caseous necrosis is seen in
tuberculosis .
Q6. Which organ is most susceptible to irreversible damage from ischemia?
A. Kidney
B. Liver
C. Brain
D. Skeletal muscle
Correct Answer: C
Rationale: Neurons rely almost exclusively on aerobic metabolism and have
minimal energy stores. They can suffer irreversible injury within just 4–6 minutes
of complete ischemia, making the brain the most vulnerable organ. The kidney and
liver have greater ischemic tolerance, and skeletal muscle can withstand longer
periods of ischemia .
, Q7. Which type of cell death is a programmed, energy-dependent process that
k k k k k k k k k k k
does not trigger inflammation?
k k k k
A. Necrosis
B. Apoptosis
C. Autolysis
D. Gangrene
CorrectAnswer: B k k
Rationale: Apoptosis, or "programmed cell death," is an ATP-dependent, tightly
k k k k k k k k k
regulated process. It eliminates unwanted or damaged cells without releasing
k k k k k k k k k k
cellular contents, thus avoiding an inflammatory response. Necrosis, conversely,
k k k k k k k k k
releases intracellular contents, triggering inflammation .
k k k k k k
Q8. A patient has a mutation where one DNA base pair is substituted for another,
k k k k k k k k k k k k k k
resulting in a codon for a different amino acid. What type of mutation is this?
k k k k k k k k k k k k k k k
A. Silent mutation k
B. Missense mutation k
C. Nonsense mutation k
D. Frameshift mutation k
CorrectAnswer: B k k
Rationale: A missense mutation is a point mutation where a single nucleotide change
k k k k k k k k k k k k
results in a codon coding for a different amino acid. This can alter protein function, as
k k k k k k k k k k k k k k k k
seen in sickle cell disease (glutamic acid → valine substitution). Silent mutations do
k k k k k k k k k k k k k
not change amino acids; nonsense mutations create premature stop codons;
k k k k k k k k k k
frameshift mutations alter the reading frame .
k k k k k k k
Q9. Which of the following best describes free radical injury?
k k k k k k k k k
A. Damage caused by protein misfolding k k k k
B. Cellular injury caused by unpaired electrons reacting with lipids, proteins, and
k k k k k k k k k k
DNA
k
Exam
200 Questions & Answers with Rationales
South College | 2026-2027 Academic Year
SECTION 1: CELLULAR ADAPTATION, INJURY, AND DEATH
(Questions 1-25)
Q1. A patient with chronic hypertension develops left ventricular wall
thickening. Which mechanism best explains this adaptation?
A. Increased myocyte number due to cell division
B. Increased myocyte size due to increased workload
C. Replacement of cardiac cells with fibrous tissue
D. Transformation of cardiac cells into smooth muscle
Correct Answer: B
Rationale: Cardiac myocytes are terminally differentiated and cannot undergo
hyperplasia (increase in cell number). They respond to chronic pressure overload
through hypertrophy—an increase in individual cell size to generate greater
contractile force. This is an adaptive response to increased afterload. Fibrous tissue
replacement and metaplasia are not adaptive mechanisms in this scenario .
Q2. During ischemic injury, loss of adenosine triphosphate (ATP) most
directly leads to:
A. Increased oxidative phosphorylation
B. Failure of the sodium-potassium pump
C. Increased protein synthesis
D. Mitochondrial membrane stabilization
Correct Answer: B
,Rationale: ATP is required for the function of the Na⁺/K⁺ ATPase pump. Its
depletion causes this pump to fail, leading to an influx of sodium and water into
the cell, which results in cellular swelling and is a key event in the pathway to cell
death. ATP depletion is the primary initiating mechanism in hypoxia .
Q3. A patient's biopsy reveals an increase in the number of breast glandular
cells due to hormonal stimulation. What is this cellular adaptation called?
A. Hypertrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Correct Answer: B
Rationale: Hyperplasia is an increase in the number of cells in an organ or tissue,
typically in response to hormonal stimulation or increased functional demand.
Breast glandular cells proliferate in response to estrogen stimulation during
pregnancy. Unlike hypertrophy (increase in cell size), hyperplasia involves cell
division in tissues capable of mitotic activity .
Q4. A patient with chronic GERD develops a change in the esophageal
epithelium from stratified squamous to columnar epithelium with goblet cells.
This adaptation is termed:
A. Hypertrophy
B. Hyperplasia
C. Metaplasia
D. Dysplasia
Correct Answer: C
Rationale: Metaplasia is a reversible change in which one differentiated cell type
is replaced by another cell type. In Barrett's esophagus, chronic acid exposure
causes the normal stratified squamous epithelium to transform into columnar
,epithelium with goblet cells as an adaptive response to chronic irritation. This
change is adaptive but can increase cancer risk .
Q5. Following a hypoxic event like a stroke, brain tissue often softens and
liquefies. Which type of necrosis is this?
A. Coagulative necrosis
B. Liquefactive necrosis
C. Caseous necrosis
D. Fat necrosis
Correct Answer: B
Rationale: Liquefactive necrosis is characteristic of the central nervous system
(brain). It is caused by the release of hydrolytic enzymes from dead cells and
inflammatory cells, which dissolve the tissue into a liquid, viscous mass.
Coagulative necrosis is typical of myocardial infarction; caseous necrosis is seen in
tuberculosis .
Q6. Which organ is most susceptible to irreversible damage from ischemia?
A. Kidney
B. Liver
C. Brain
D. Skeletal muscle
Correct Answer: C
Rationale: Neurons rely almost exclusively on aerobic metabolism and have
minimal energy stores. They can suffer irreversible injury within just 4–6 minutes
of complete ischemia, making the brain the most vulnerable organ. The kidney and
liver have greater ischemic tolerance, and skeletal muscle can withstand longer
periods of ischemia .
, Q7. Which type of cell death is a programmed, energy-dependent process that
k k k k k k k k k k k
does not trigger inflammation?
k k k k
A. Necrosis
B. Apoptosis
C. Autolysis
D. Gangrene
CorrectAnswer: B k k
Rationale: Apoptosis, or "programmed cell death," is an ATP-dependent, tightly
k k k k k k k k k
regulated process. It eliminates unwanted or damaged cells without releasing
k k k k k k k k k k
cellular contents, thus avoiding an inflammatory response. Necrosis, conversely,
k k k k k k k k k
releases intracellular contents, triggering inflammation .
k k k k k k
Q8. A patient has a mutation where one DNA base pair is substituted for another,
k k k k k k k k k k k k k k
resulting in a codon for a different amino acid. What type of mutation is this?
k k k k k k k k k k k k k k k
A. Silent mutation k
B. Missense mutation k
C. Nonsense mutation k
D. Frameshift mutation k
CorrectAnswer: B k k
Rationale: A missense mutation is a point mutation where a single nucleotide change
k k k k k k k k k k k k
results in a codon coding for a different amino acid. This can alter protein function, as
k k k k k k k k k k k k k k k k
seen in sickle cell disease (glutamic acid → valine substitution). Silent mutations do
k k k k k k k k k k k k k
not change amino acids; nonsense mutations create premature stop codons;
k k k k k k k k k k
frameshift mutations alter the reading frame .
k k k k k k k
Q9. Which of the following best describes free radical injury?
k k k k k k k k k
A. Damage caused by protein misfolding k k k k
B. Cellular injury caused by unpaired electrons reacting with lipids, proteins, and
k k k k k k k k k k
DNA
k
