NSG 527 Midterm Exam and
Final Exam
NSG 527 Midterm and Final Exam
SECTION 1: CELLULAR PATHOPHYSIOLOGY AND GENETICS (Q1–Q20)
Q1. A 58-year-old patient with a 15-year history of gastroesophageal reflux disease undergoes
endoscopy that reveals columnar epithelium replacing the normal stratified squamous epithelium in
the lower esophagus. Which cellular adaptation does this finding represent?
A. Hyperplasia
B. Metaplasia
C. Dysplasia
D. Anaplasia
Correct Answer: B. Metaplasia
Rationale: Metaplasia is the reversible replacement of one mature cell type by another in response
to chronic irritation. In GERD, chronic acid exposure causes squamous cells to be replaced by
columnar cells (Barrett's esophagus), which are more resistant to acid. Hyperplasia involves an
increase in cell number, dysplasia refers to abnormal cell growth, and anaplasia describes
undifferentiated malignant cells.
Q2. A 62-year-old male with poorly controlled hypertension presents with an ejection fraction of
40% and echocardiographic evidence of a thickened left ventricular wall. Which cellular adaptation
has occurred in the myocardial cells?
A. Atrophy
B. Hyperplasia
C. Hypertrophy
D. Metaplasia
Correct Answer: C. Hypertrophy
Rationale: Hypertrophy is an increase in the size of individual cells, leading to increased organ size. In
the heart, chronic pressure overload from hypertension causes ventricular myocytes to enlarge to
generate greater force. Myocardial cells are terminally differentiated and do not undergo
hyperplasia. Atrophy is a decrease in cell size, and metaplasia is a change from one cell type to
another.
pg. 1
,Q3. A bronchial biopsy from a 55-year-old smoker reveals ciliated columnar epithelium replaced by
stratified squamous epithelium. What is the primary clinical concern associated with this
adaptation?
A. Immediate metastatic spread
B. Progression to dysplasia and malignancy
C. Reversible return to normal within days
D. Increased susceptibility to viral infection
Correct Answer: B. Progression to dysplasia and malignancy
Rationale: Squamous metaplasia in the respiratory tract is an adaptive response to chronic smoke
exposure. However, this change places the patient at increased risk for dysplasia (pre-malignant
changes) and eventual squamous cell carcinoma. Metaplasia itself is not cancer and does not
metastasize immediately, but it serves as a precursor to malignancy.
Q4. A patient presents with a myocardial infarction. The ischemic myocardial tissue demonstrates
coagulative necrosis. Which pathophysiologic mechanism is the primary initiator of this cellular
death?
A. Rapid calcium influx leading to enzymatic digestion
B. Depletion of ATP and failure of sodium-potassium pumps
C. Activation of caspases by intrinsic apoptotic pathways
D. Lipid peroxidation by reactive oxygen species
Correct Answer: B. Depletion of ATP and failure of sodium-potassium pumps
Rationale: Coagulative necrosis results from sudden ischemia. Hypoxia leads to rapid depletion of
ATP, causing failure of the sodium-potassium pump. Sodium accumulates intracellularly, water
follows, and cellular swelling occurs, progressing to membrane damage and necrosis. Calcium influx
and reactive oxygen species contribute secondarily, while caspases mediate apoptosis, not
coagulative necrosis.
Q5. A patient with severe bacterial infection develops septic shock and multi-organ failure.
Laboratory tests show highly elevated liver enzymes. Which cellular injury mechanism is most likely
responsible for the hepatocellular damage?
A. Free radical injury from reactive oxygen species
B. Direct bacterial invasion of hepatocytes
C. ATP depletion from mitochondrial dysfunction
D. Apoptotic pathway activation by tumor necrosis factor
Correct Answer: C. ATP depletion from mitochondrial dysfunction
Rationale: In septic shock, systemic hypoperfusion and inflammatory mediators impair
mitochondrial function, leading to ATP depletion. This energy failure disrupts cellular pumps and
processes, causing necrosis. While free radicals and TNF-mediated apoptosis contribute to the
overall injury, ATP depletion from mitochondrial dysfunction is the central mechanism driving
hepatocellular damage in this setting.
Q6. A 45-year-old male with poorly controlled diabetes mellitus has a hemoglobin A1c of 9.2%.
Which mechanism best explains the accumulation of advanced glycation end-products (AGEs) in this
patient?
pg. 2
, A. Increased glucose availability leads to non-enzymatic glycation of proteins
B. Enhanced renal clearance of glycated hemoglobin
C. Decreased insulin receptor sensitivity
D. Increased hepatic gluconeogenesis
Correct Answer: A. Increased glucose availability leads to non-enzymatic glycation of proteins
Rationale: Chronic hyperglycemia causes non-enzymatic glycation of proteins, forming AGEs. These
irreversible products accumulate in tissues and contribute to diabetic complications including
nephropathy, retinopathy, and neuropathy. Decreased insulin sensitivity and increased
gluconeogenesis contribute to hyperglycemia but do not directly cause AGE formation.
Q7. A child is diagnosed with Down syndrome. Which genetic mechanism is responsible for this
condition?
A. Trinucleotide repeat expansion
B. Trisomy of chromosome 21
C. Monosomy of chromosome 21
D. Point mutation in the APP gene
Correct Answer: B. Trisomy of chromosome 21
Rationale: Down syndrome results from trisomy 21, usually due to nondisjunction during meiosis.
This produces three copies of chromosome 21. Trinucleotide repeat expansion causes disorders such
as Huntington's disease, monosomy 21 is not compatible with life, and point mutations in specific
genes do not cause Down syndrome.
Q8. A 30-year-old male presents with choreiform movements, personality changes, and a family
history of a similar condition. Genetic testing reveals CAG trinucleotide repeat expansion. Which
disorder is most likely?
A. Huntington's disease
B. Myotonic dystrophy
C. Fragile X syndrome
D. Friedreich ataxia
Correct Answer: A. Huntington's disease
Rationale: Huntington's disease is an autosomal dominant disorder caused by CAG trinucleotide
repeat expansion in the HTT gene. It presents with chorea, psychiatric symptoms, and cognitive
decline. Myotonic dystrophy involves CTG repeats, Fragile X involves CGG repeats, and Friedreich
ataxia involves GAA repeats.
Q9. A patient with sickle cell disease experiences a vaso-occlusive crisis. Which pathophysiologic
mechanism is primarily responsible for this event?
A. Iron overload from chronic transfusions
B. Deoxygenation causing hemoglobin S polymerization
C. Autoimmune destruction of red blood cells
D. Bone marrow failure
Correct Answer: B. Deoxygenation causing hemoglobin S polymerization
pg. 3
Final Exam
NSG 527 Midterm and Final Exam
SECTION 1: CELLULAR PATHOPHYSIOLOGY AND GENETICS (Q1–Q20)
Q1. A 58-year-old patient with a 15-year history of gastroesophageal reflux disease undergoes
endoscopy that reveals columnar epithelium replacing the normal stratified squamous epithelium in
the lower esophagus. Which cellular adaptation does this finding represent?
A. Hyperplasia
B. Metaplasia
C. Dysplasia
D. Anaplasia
Correct Answer: B. Metaplasia
Rationale: Metaplasia is the reversible replacement of one mature cell type by another in response
to chronic irritation. In GERD, chronic acid exposure causes squamous cells to be replaced by
columnar cells (Barrett's esophagus), which are more resistant to acid. Hyperplasia involves an
increase in cell number, dysplasia refers to abnormal cell growth, and anaplasia describes
undifferentiated malignant cells.
Q2. A 62-year-old male with poorly controlled hypertension presents with an ejection fraction of
40% and echocardiographic evidence of a thickened left ventricular wall. Which cellular adaptation
has occurred in the myocardial cells?
A. Atrophy
B. Hyperplasia
C. Hypertrophy
D. Metaplasia
Correct Answer: C. Hypertrophy
Rationale: Hypertrophy is an increase in the size of individual cells, leading to increased organ size. In
the heart, chronic pressure overload from hypertension causes ventricular myocytes to enlarge to
generate greater force. Myocardial cells are terminally differentiated and do not undergo
hyperplasia. Atrophy is a decrease in cell size, and metaplasia is a change from one cell type to
another.
pg. 1
,Q3. A bronchial biopsy from a 55-year-old smoker reveals ciliated columnar epithelium replaced by
stratified squamous epithelium. What is the primary clinical concern associated with this
adaptation?
A. Immediate metastatic spread
B. Progression to dysplasia and malignancy
C. Reversible return to normal within days
D. Increased susceptibility to viral infection
Correct Answer: B. Progression to dysplasia and malignancy
Rationale: Squamous metaplasia in the respiratory tract is an adaptive response to chronic smoke
exposure. However, this change places the patient at increased risk for dysplasia (pre-malignant
changes) and eventual squamous cell carcinoma. Metaplasia itself is not cancer and does not
metastasize immediately, but it serves as a precursor to malignancy.
Q4. A patient presents with a myocardial infarction. The ischemic myocardial tissue demonstrates
coagulative necrosis. Which pathophysiologic mechanism is the primary initiator of this cellular
death?
A. Rapid calcium influx leading to enzymatic digestion
B. Depletion of ATP and failure of sodium-potassium pumps
C. Activation of caspases by intrinsic apoptotic pathways
D. Lipid peroxidation by reactive oxygen species
Correct Answer: B. Depletion of ATP and failure of sodium-potassium pumps
Rationale: Coagulative necrosis results from sudden ischemia. Hypoxia leads to rapid depletion of
ATP, causing failure of the sodium-potassium pump. Sodium accumulates intracellularly, water
follows, and cellular swelling occurs, progressing to membrane damage and necrosis. Calcium influx
and reactive oxygen species contribute secondarily, while caspases mediate apoptosis, not
coagulative necrosis.
Q5. A patient with severe bacterial infection develops septic shock and multi-organ failure.
Laboratory tests show highly elevated liver enzymes. Which cellular injury mechanism is most likely
responsible for the hepatocellular damage?
A. Free radical injury from reactive oxygen species
B. Direct bacterial invasion of hepatocytes
C. ATP depletion from mitochondrial dysfunction
D. Apoptotic pathway activation by tumor necrosis factor
Correct Answer: C. ATP depletion from mitochondrial dysfunction
Rationale: In septic shock, systemic hypoperfusion and inflammatory mediators impair
mitochondrial function, leading to ATP depletion. This energy failure disrupts cellular pumps and
processes, causing necrosis. While free radicals and TNF-mediated apoptosis contribute to the
overall injury, ATP depletion from mitochondrial dysfunction is the central mechanism driving
hepatocellular damage in this setting.
Q6. A 45-year-old male with poorly controlled diabetes mellitus has a hemoglobin A1c of 9.2%.
Which mechanism best explains the accumulation of advanced glycation end-products (AGEs) in this
patient?
pg. 2
, A. Increased glucose availability leads to non-enzymatic glycation of proteins
B. Enhanced renal clearance of glycated hemoglobin
C. Decreased insulin receptor sensitivity
D. Increased hepatic gluconeogenesis
Correct Answer: A. Increased glucose availability leads to non-enzymatic glycation of proteins
Rationale: Chronic hyperglycemia causes non-enzymatic glycation of proteins, forming AGEs. These
irreversible products accumulate in tissues and contribute to diabetic complications including
nephropathy, retinopathy, and neuropathy. Decreased insulin sensitivity and increased
gluconeogenesis contribute to hyperglycemia but do not directly cause AGE formation.
Q7. A child is diagnosed with Down syndrome. Which genetic mechanism is responsible for this
condition?
A. Trinucleotide repeat expansion
B. Trisomy of chromosome 21
C. Monosomy of chromosome 21
D. Point mutation in the APP gene
Correct Answer: B. Trisomy of chromosome 21
Rationale: Down syndrome results from trisomy 21, usually due to nondisjunction during meiosis.
This produces three copies of chromosome 21. Trinucleotide repeat expansion causes disorders such
as Huntington's disease, monosomy 21 is not compatible with life, and point mutations in specific
genes do not cause Down syndrome.
Q8. A 30-year-old male presents with choreiform movements, personality changes, and a family
history of a similar condition. Genetic testing reveals CAG trinucleotide repeat expansion. Which
disorder is most likely?
A. Huntington's disease
B. Myotonic dystrophy
C. Fragile X syndrome
D. Friedreich ataxia
Correct Answer: A. Huntington's disease
Rationale: Huntington's disease is an autosomal dominant disorder caused by CAG trinucleotide
repeat expansion in the HTT gene. It presents with chorea, psychiatric symptoms, and cognitive
decline. Myotonic dystrophy involves CTG repeats, Fragile X involves CGG repeats, and Friedreich
ataxia involves GAA repeats.
Q9. A patient with sickle cell disease experiences a vaso-occlusive crisis. Which pathophysiologic
mechanism is primarily responsible for this event?
A. Iron overload from chronic transfusions
B. Deoxygenation causing hemoglobin S polymerization
C. Autoimmune destruction of red blood cells
D. Bone marrow failure
Correct Answer: B. Deoxygenation causing hemoglobin S polymerization
pg. 3
