NSG 5003 Exam 1 Questions and Answers
Course: Advanced Pathophysiology / Nursing Practice (NSG 5003)
Focus: Graduate-Level Nursing Exam Preparation & Verified Solutions
Module 1: Cellular Adaptation, Injury, Hypoxia, and Death
Q1. A 55-year-old male with a history of long-standing uncontrolled hypertension
shows left ventricular enlargement on echocardiogram. What cellular adaptation has
occurred?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Dysplasia
Answer: B. Hypertrophy
Explanation: Hypertrophy is an increase in individual cell size, leading to an increase in organ
size, commonly seen in cardiac muscle in response to increased workload (afterload) caused by
hypertension.
Q2. Which adaptive cellular change occurs when a patient with chronic GERD
exhibits columnar cell replacement of normal stratified squamous epithelium in the
lower esophagus?
A. Dysplasia
B. Hyperplasia
C. Metaplasia
D. Anaplasia
Answer: C. Metaplasia
Explanation: Metaplasia is the reversible replacement of one mature cell type by another mature
cell type. Barrett esophagus is a classic example where stratified squamous cells become
intestinal columnar cells due to chronic acid exposure.
Q3. Hypoxic cell injury leads to a loss of ATP production. Which immediate
secondary effect occurs at the membrane level?
A. Increased efflux of sodium
B. Influx of sodium and water causing cellular swelling
C. Rapid efflux of intracellular calcium
, D. Decreased lactic acid accumulation
Answer: B. Influx of sodium and water causing cellular swelling
Explanation: Lack of ATP causes failure of the Na+/K+ ATPase pump, leading to intracellular
sodium accumulation, osmotic influx of water, and hydropic degeneration (cellular swelling).
Q4. A biopsy of kidney tissue from a patient experiencing acute ischemic injury
reveals coagulative necrosis. What is the characteristic microscopic feature of
coagulative necrosis?
A. Complete enzymatic dissolution of tissue into liquid pus
B. Preserved basic cell outline with denatured structural proteins
C. Cheese-like friable tissue formation
D. Saponification of surrounding adipose tissue
Answer: B. Preserved basic cell outline with denatured structural proteins
Explanation: Coagulative necrosis typically results from ischemia/hypoxia in most solid organs
(except the brain). Denaturation of structural proteins preserves the cellular architecture for
several days.
Q5. Liquefactive necrosis is most typically seen in which of the following tissues
following ischemic stroke?
A. Myocardium
B. Brain
C. Liver
D. Skeletal muscle
Answer: B. Brain
Explanation: Brain tissue is rich in hydrolytic enzymes and lipids; ischemic injury triggers rapid
enzymatic digestion of cellular structures, resulting in liquefactive necrosis and cyst formation.
Q6. Which cellular enzyme family is directly responsible for executing apoptosis
during programmed cell death?
A. Metalloproteinases
B. Caspases
C. Kinases
D. Cyclins
Answer: B. Caspases
Explanation: Caspases (cysteine-aspartic proteases) are the central executioners of apoptosis,
cleaving specific intracellular targets to systematically disassemble the cell.
, Q7. Dystrophic calcification differs from metastatic calcification in that dystrophic
calcification occurs:
A. In normal tissue with hypercalcemia
B. In dead or dying tissues with normal systemic calcium levels
C. Primarily due to hyperparathyroidism
D. Exclusively in pulmonary alveoli
Answer: B. In dead or dying tissues with normal systemic calcium levels
Explanation: Dystrophic calcification occurs locally in injured or necrotic tissue while serum
calcium levels are normal. Metastatic calcification occurs in normal tissue due to hypercalcemia.
Q8. Free radicals damage cells primarily through which of the following mechanism?
A. Inhibition of viral protein synthesis
B. Lipid peroxidation, protein alteration, and DNA fragmenting
C. Increasing membrane stability
D. Enhancing mitochondrial oxidative phosphorylation
Answer: B. Lipid peroxidation, protein alteration, and DNA fragmenting
Explanation: Free radicals (ROS) cause oxidative stress, leading to lipid peroxidation of cellular
membranes, oxidative modification of proteins, and double-strand DNA cleavage.
Q9. Which endogenous antioxidant enzyme catalyzes the conversion of superoxide
radicals ($O_2^-$) into hydrogen peroxide ($H_2O_2$)?
A. Catalase
B. Glutathione peroxidase
C. Superoxide dismutase (SOD)
D. Myeloperoxidase
Answer: C. Superoxide dismutase (SOD)
Explanation: SOD neutralizes superoxide radicals by converting them to $H_2O_2$, which is
then converted to water by catalase or glutathione peroxidase.
Q10. Reperfusion injury following ischemic tissue rescue is largely driven by:
A. Sudden intracellular glycogen accumulation
B. Massive release of reactive oxygen species (ROS) and calcium overload
C. Rapid inhibition of neutrophil activation
D. Immediate restoration of cellular resting potential
Answer: B. Massive release of reactive oxygen species (ROS) and calcium
overload
Explanation: Re-establishing oxygen supply to previously ischemic tissue generates large
amounts of ROS and drives intracellular calcium influx, exacerbating cell membrane and organelle
damage.
Course: Advanced Pathophysiology / Nursing Practice (NSG 5003)
Focus: Graduate-Level Nursing Exam Preparation & Verified Solutions
Module 1: Cellular Adaptation, Injury, Hypoxia, and Death
Q1. A 55-year-old male with a history of long-standing uncontrolled hypertension
shows left ventricular enlargement on echocardiogram. What cellular adaptation has
occurred?
A. Hyperplasia
B. Hypertrophy
C. Metaplasia
D. Dysplasia
Answer: B. Hypertrophy
Explanation: Hypertrophy is an increase in individual cell size, leading to an increase in organ
size, commonly seen in cardiac muscle in response to increased workload (afterload) caused by
hypertension.
Q2. Which adaptive cellular change occurs when a patient with chronic GERD
exhibits columnar cell replacement of normal stratified squamous epithelium in the
lower esophagus?
A. Dysplasia
B. Hyperplasia
C. Metaplasia
D. Anaplasia
Answer: C. Metaplasia
Explanation: Metaplasia is the reversible replacement of one mature cell type by another mature
cell type. Barrett esophagus is a classic example where stratified squamous cells become
intestinal columnar cells due to chronic acid exposure.
Q3. Hypoxic cell injury leads to a loss of ATP production. Which immediate
secondary effect occurs at the membrane level?
A. Increased efflux of sodium
B. Influx of sodium and water causing cellular swelling
C. Rapid efflux of intracellular calcium
, D. Decreased lactic acid accumulation
Answer: B. Influx of sodium and water causing cellular swelling
Explanation: Lack of ATP causes failure of the Na+/K+ ATPase pump, leading to intracellular
sodium accumulation, osmotic influx of water, and hydropic degeneration (cellular swelling).
Q4. A biopsy of kidney tissue from a patient experiencing acute ischemic injury
reveals coagulative necrosis. What is the characteristic microscopic feature of
coagulative necrosis?
A. Complete enzymatic dissolution of tissue into liquid pus
B. Preserved basic cell outline with denatured structural proteins
C. Cheese-like friable tissue formation
D. Saponification of surrounding adipose tissue
Answer: B. Preserved basic cell outline with denatured structural proteins
Explanation: Coagulative necrosis typically results from ischemia/hypoxia in most solid organs
(except the brain). Denaturation of structural proteins preserves the cellular architecture for
several days.
Q5. Liquefactive necrosis is most typically seen in which of the following tissues
following ischemic stroke?
A. Myocardium
B. Brain
C. Liver
D. Skeletal muscle
Answer: B. Brain
Explanation: Brain tissue is rich in hydrolytic enzymes and lipids; ischemic injury triggers rapid
enzymatic digestion of cellular structures, resulting in liquefactive necrosis and cyst formation.
Q6. Which cellular enzyme family is directly responsible for executing apoptosis
during programmed cell death?
A. Metalloproteinases
B. Caspases
C. Kinases
D. Cyclins
Answer: B. Caspases
Explanation: Caspases (cysteine-aspartic proteases) are the central executioners of apoptosis,
cleaving specific intracellular targets to systematically disassemble the cell.
, Q7. Dystrophic calcification differs from metastatic calcification in that dystrophic
calcification occurs:
A. In normal tissue with hypercalcemia
B. In dead or dying tissues with normal systemic calcium levels
C. Primarily due to hyperparathyroidism
D. Exclusively in pulmonary alveoli
Answer: B. In dead or dying tissues with normal systemic calcium levels
Explanation: Dystrophic calcification occurs locally in injured or necrotic tissue while serum
calcium levels are normal. Metastatic calcification occurs in normal tissue due to hypercalcemia.
Q8. Free radicals damage cells primarily through which of the following mechanism?
A. Inhibition of viral protein synthesis
B. Lipid peroxidation, protein alteration, and DNA fragmenting
C. Increasing membrane stability
D. Enhancing mitochondrial oxidative phosphorylation
Answer: B. Lipid peroxidation, protein alteration, and DNA fragmenting
Explanation: Free radicals (ROS) cause oxidative stress, leading to lipid peroxidation of cellular
membranes, oxidative modification of proteins, and double-strand DNA cleavage.
Q9. Which endogenous antioxidant enzyme catalyzes the conversion of superoxide
radicals ($O_2^-$) into hydrogen peroxide ($H_2O_2$)?
A. Catalase
B. Glutathione peroxidase
C. Superoxide dismutase (SOD)
D. Myeloperoxidase
Answer: C. Superoxide dismutase (SOD)
Explanation: SOD neutralizes superoxide radicals by converting them to $H_2O_2$, which is
then converted to water by catalase or glutathione peroxidase.
Q10. Reperfusion injury following ischemic tissue rescue is largely driven by:
A. Sudden intracellular glycogen accumulation
B. Massive release of reactive oxygen species (ROS) and calcium overload
C. Rapid inhibition of neutrophil activation
D. Immediate restoration of cellular resting potential
Answer: B. Massive release of reactive oxygen species (ROS) and calcium
overload
Explanation: Re-establishing oxygen supply to previously ischemic tissue generates large
amounts of ROS and drives intracellular calcium influx, exacerbating cell membrane and organelle
damage.
