WGU D236 Pathophysiology
OA and PA Study Guide
──────────────────────────────────────────────────
2026/2027 Edition | 100 Practice Questions | Verified Solutions
Western Governors University | Nursing Programs
Aligned with WGU Competency Standards and AACN Essentials
Page 1 | D236 Pathophysiology Study Guide 2026
,Table of Contents
This study guide covers the following domains. Each section contains practice questions with verified
answers and detailed rationales.
1. Cellular Adaptation, Injury & Death (8 Questions)
2. Inflammation & Immunity (9 Questions)
3. Fluid, Electrolyte & Acid-Base Balance (8 Questions)
4. Neoplasia & Cancer Biology (7 Questions)
5. Hematologic Disorders (6 Questions)
6. Cardiovascular Pathophysiology (12 Questions)
7. Respiratory Pathophysiology (7 Questions)
8. Renal & Urinary Pathophysiology (6 Questions)
9. Gastrointestinal Pathophysiology (5 Questions)
10. Endocrine Pathophysiology (7 Questions)
11. Neurological Pathophysiology (7 Questions)
12. Reproductive Pathophysiology (5 Questions)
13. Musculoskeletal & Integumentary Disorders (5 Questions)
14. Shock & Multiple Organ Dysfunction (4 Questions)
15. Scenario-Based Clinical Reasoning (4 Questions)
16. Performance Assessment (PA) Preparation Guidance
17. Key Pathophysiology Concepts Quick Reference
Page 2 | D236 Pathophysiology Study Guide 2026
,Cellular Adaptation, Injury & Death
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Q1. A 68-year-old male with a left femoral fracture has been on bedrest for 3 weeks.
Physical therapy notes significant weakness and reduced muscle mass in his left leg
compared to the right. Which cellular adaptation best describes this finding?
A. Hypertrophy
B. Hyperplasia
C. Atrophy
D. Metaplasia
Rationale: Atrophy is a reduction in cell size and number due to decreased workload, disuse, or
inadequate nutrition. Disuse atrophy occurs rapidly with immobilization, as seen in this patient.
Hypertrophy (A) is an increase in cell size, not a decrease. Hyperplasia (B) is an increase in cell
number, which requires mitotic capacity. Metaplasia (D) is a reversible change from one mature
cell type to another, not a change in cell size or number. (McCance & Huether, Ch. 2)
Q2. A 52-year-old woman presents with postmenopausal bleeding. Endometrial biopsy
reveals an increased number of endometrial glands with crowded, irregular architecture.
Which cellular adaptation is the primary mechanism driving this condition?
A. Pathologic hyperplasia
B. Physiologic hypertrophy
C. Atrophy
D. Metaplasia
Rationale: Endometrial hyperplasia is caused by pathologic hyperplasia driven by prolonged
estrogen stimulation without adequate progesterone opposition. The increased glandular cell
number leads to crowded architecture and abnormal bleeding. Physiologic hypertrophy (B)
increases cell size, not number. Atrophy (C) decreases cell size. Metaplasia (D) involves
replacement of one cell type with another, which is not the mechanism here. Endometrial
hyperplasia is considered a premalignant condition requiring monitoring. (Porth, Ch. 2)
Q3. A 45-year-old smoker with a 20 pack-year history undergoes bronchoscopy. Biopsy of
the tracheal epithelium shows replacement of normal ciliated columnar epithelium with
stratified squamous epithelium. Which cellular adaptation is demonstrated?
A. Hyperplasia
B. Dysplasia
C. Metaplasia
D. Anaplasia
Rationale: Metaplasia is the reversible transformation of one differentiated cell type to another,
often in response to chronic irritation. Smoking-induced injury causes ciliated columnar epithelium
to transform into stratified squamous epithelium, which is more resistant to tobacco toxins.
Hyperplasia (A) increases cell number. Dysplasia (B) involves abnormal maturation and
disordered growth, which may develop after metaplasia. Anaplasia (D) refers to undifferentiated
cells seen in malignancy. While metaplasia is protective in the short term, persistent irritation can
progress to dysplasia and cancer. (Hammer & McPhee, Ch. 1)
Q4. A 38-year-old woman has a Pap smear showing abnormal cells with nuclear
hyperchromasia, pleomorphism, and increased nuclear-to-cytoplasmic ratio confined to
the epithelial layer. What is the most accurate interpretation of these findings?
A. Metaplasia — reversible change with no malignant potential
B. Dysplasia — precancerous change with potential to progress to neoplasia
C. Anaplasia — fully malignant transformation has occurred
D. Hyperplasia — physiologic increase in cell number only
Page 3 | D236 Pathophysiology Study Guide 2026
, Rationale: Dysplasia is characterized by abnormal cell growth with changes in size, shape, and
organization, including nuclear hyperchromasia, pleomorphism, and loss of normal polarity. It is
considered a precancerous lesion. When confined to the epithelial layer it has not yet invaded the
basement membrane (carcinoma in situ). Metaplasia (A) is a reversible cell-type change without
nuclear atypia. Anaplasia (D) indicates fully malignant, undifferentiated cells that have invaded
beyond the basement membrane. Hyperplasia (C) is an increase in cell number without atypical
features. (McCance & Huether, Ch. 11)
Q5. A 55-year-old male presents with right upper quadrant pain and fever following an
episode of hypotension during surgery. CT shows a wedge-shaped area of coagulative
necrosis in the liver. A separate patient has a brain abscess with liquefactive necrosis.
What best explains the difference in necrosis type between these two organs?
A. The liver has a richer blood supply than the brain
B. The liver has more lysosomal enzymes that prevent liquefaction
C. The brain has high lipid and low protein content with limited regenerative capacity
D. The liver undergoes apoptosis while the brain undergoes necrosis
Rationale: The type of necrosis depends on tissue composition. Coagulative necrosis occurs in
organs with high protein and low lipid content (heart, liver, kidneys); the denatured proteins
maintain tissue architecture. Liquefactive necrosis occurs in the brain and abscesses because the
brain is rich in lipids and poor in structural proteins, and hydrolytic enzymes from neutrophils and
microglia digest the tissue into a liquid. Blood supply (A) affects infarct risk but not necrosis type.
Lysosomes (B) contribute to liquefaction rather than prevent it. Apoptosis (D) is programmed cell
death, a distinct process from necrosis. (Porth, Ch. 3)
Q6. A researcher is studying a pathway in which cytochrome c is released from
mitochondria, activating caspase-9 and subsequently caspase-3. This results in cell
shrinkage, chromatin condensation, and formation of apoptotic bodies without an
inflammatory response. Which statement best characterizes this process?
A. It is a necrotic process triggered by ATP depletion
B. It is the intrinsic (mitochondrial) pathway of apoptosis
C. It is the extrinsic (death receptor) pathway of apoptosis
D. It represents pyroptosis mediated by inflammasome activation
Rationale: The intrinsic (mitochondrial) pathway of apoptosis is triggered by intracellular stress
(DNA damage, oxidative stress) causing mitochondrial release of cytochrome c, which forms the
apoptosome with Apaf-1 and activates caspase-9, then caspase-3. This produces apoptotic bodies
phagocytosed without inflammation. Necrosis (A) causes inflammation and is not caspase-
dependent. The extrinsic pathway (C) involves death receptors (Fas, TNF-R1) activating caspase-8,
not cytochrome c. Pyroptosis (D) is inflammasome-mediated and inherently pro-inflammatory.
(McCance & Huether, Ch. 2)
Q7. A patient is exposed to a toxin that generates excessive superoxide radicals.
Antioxidant defenses including superoxide dismutase, catalase, and glutathione
peroxidase are overwhelmed. Which of the following describes the correct sequence of free
radical-mediated cellular injury?
A. Lipid peroxidation → membrane damage → calcium influx → enzyme activation →
DNA damage
B. DNA damage → protein denaturation → lipid peroxidation → membrane repair
C. Calcium influx → protein cross-linking → membrane damage → lipid peroxidation
D. Mitochondrial biogenesis → ATP depletion → reactive oxygen species generation → apoptosis
Rationale: Free radicals, particularly reactive oxygen species (ROS), cause injury through lipid
peroxidation of cell membranes, which increases membrane permeability. This allows calcium
influx, which activates intracellular enzymes (proteases, phospholipases, endonucleases) causing
further damage and DNA fragmentation. Option B reverses the typical sequence; lipid
peroxidation is an early event. Option C incorrectly sequences calcium before membrane damage.
Page 4 | D236 Pathophysiology Study Guide 2026
OA and PA Study Guide
──────────────────────────────────────────────────
2026/2027 Edition | 100 Practice Questions | Verified Solutions
Western Governors University | Nursing Programs
Aligned with WGU Competency Standards and AACN Essentials
Page 1 | D236 Pathophysiology Study Guide 2026
,Table of Contents
This study guide covers the following domains. Each section contains practice questions with verified
answers and detailed rationales.
1. Cellular Adaptation, Injury & Death (8 Questions)
2. Inflammation & Immunity (9 Questions)
3. Fluid, Electrolyte & Acid-Base Balance (8 Questions)
4. Neoplasia & Cancer Biology (7 Questions)
5. Hematologic Disorders (6 Questions)
6. Cardiovascular Pathophysiology (12 Questions)
7. Respiratory Pathophysiology (7 Questions)
8. Renal & Urinary Pathophysiology (6 Questions)
9. Gastrointestinal Pathophysiology (5 Questions)
10. Endocrine Pathophysiology (7 Questions)
11. Neurological Pathophysiology (7 Questions)
12. Reproductive Pathophysiology (5 Questions)
13. Musculoskeletal & Integumentary Disorders (5 Questions)
14. Shock & Multiple Organ Dysfunction (4 Questions)
15. Scenario-Based Clinical Reasoning (4 Questions)
16. Performance Assessment (PA) Preparation Guidance
17. Key Pathophysiology Concepts Quick Reference
Page 2 | D236 Pathophysiology Study Guide 2026
,Cellular Adaptation, Injury & Death
──────────────────────────────────────────────────────────────────
────
Q1. A 68-year-old male with a left femoral fracture has been on bedrest for 3 weeks.
Physical therapy notes significant weakness and reduced muscle mass in his left leg
compared to the right. Which cellular adaptation best describes this finding?
A. Hypertrophy
B. Hyperplasia
C. Atrophy
D. Metaplasia
Rationale: Atrophy is a reduction in cell size and number due to decreased workload, disuse, or
inadequate nutrition. Disuse atrophy occurs rapidly with immobilization, as seen in this patient.
Hypertrophy (A) is an increase in cell size, not a decrease. Hyperplasia (B) is an increase in cell
number, which requires mitotic capacity. Metaplasia (D) is a reversible change from one mature
cell type to another, not a change in cell size or number. (McCance & Huether, Ch. 2)
Q2. A 52-year-old woman presents with postmenopausal bleeding. Endometrial biopsy
reveals an increased number of endometrial glands with crowded, irregular architecture.
Which cellular adaptation is the primary mechanism driving this condition?
A. Pathologic hyperplasia
B. Physiologic hypertrophy
C. Atrophy
D. Metaplasia
Rationale: Endometrial hyperplasia is caused by pathologic hyperplasia driven by prolonged
estrogen stimulation without adequate progesterone opposition. The increased glandular cell
number leads to crowded architecture and abnormal bleeding. Physiologic hypertrophy (B)
increases cell size, not number. Atrophy (C) decreases cell size. Metaplasia (D) involves
replacement of one cell type with another, which is not the mechanism here. Endometrial
hyperplasia is considered a premalignant condition requiring monitoring. (Porth, Ch. 2)
Q3. A 45-year-old smoker with a 20 pack-year history undergoes bronchoscopy. Biopsy of
the tracheal epithelium shows replacement of normal ciliated columnar epithelium with
stratified squamous epithelium. Which cellular adaptation is demonstrated?
A. Hyperplasia
B. Dysplasia
C. Metaplasia
D. Anaplasia
Rationale: Metaplasia is the reversible transformation of one differentiated cell type to another,
often in response to chronic irritation. Smoking-induced injury causes ciliated columnar epithelium
to transform into stratified squamous epithelium, which is more resistant to tobacco toxins.
Hyperplasia (A) increases cell number. Dysplasia (B) involves abnormal maturation and
disordered growth, which may develop after metaplasia. Anaplasia (D) refers to undifferentiated
cells seen in malignancy. While metaplasia is protective in the short term, persistent irritation can
progress to dysplasia and cancer. (Hammer & McPhee, Ch. 1)
Q4. A 38-year-old woman has a Pap smear showing abnormal cells with nuclear
hyperchromasia, pleomorphism, and increased nuclear-to-cytoplasmic ratio confined to
the epithelial layer. What is the most accurate interpretation of these findings?
A. Metaplasia — reversible change with no malignant potential
B. Dysplasia — precancerous change with potential to progress to neoplasia
C. Anaplasia — fully malignant transformation has occurred
D. Hyperplasia — physiologic increase in cell number only
Page 3 | D236 Pathophysiology Study Guide 2026
, Rationale: Dysplasia is characterized by abnormal cell growth with changes in size, shape, and
organization, including nuclear hyperchromasia, pleomorphism, and loss of normal polarity. It is
considered a precancerous lesion. When confined to the epithelial layer it has not yet invaded the
basement membrane (carcinoma in situ). Metaplasia (A) is a reversible cell-type change without
nuclear atypia. Anaplasia (D) indicates fully malignant, undifferentiated cells that have invaded
beyond the basement membrane. Hyperplasia (C) is an increase in cell number without atypical
features. (McCance & Huether, Ch. 11)
Q5. A 55-year-old male presents with right upper quadrant pain and fever following an
episode of hypotension during surgery. CT shows a wedge-shaped area of coagulative
necrosis in the liver. A separate patient has a brain abscess with liquefactive necrosis.
What best explains the difference in necrosis type between these two organs?
A. The liver has a richer blood supply than the brain
B. The liver has more lysosomal enzymes that prevent liquefaction
C. The brain has high lipid and low protein content with limited regenerative capacity
D. The liver undergoes apoptosis while the brain undergoes necrosis
Rationale: The type of necrosis depends on tissue composition. Coagulative necrosis occurs in
organs with high protein and low lipid content (heart, liver, kidneys); the denatured proteins
maintain tissue architecture. Liquefactive necrosis occurs in the brain and abscesses because the
brain is rich in lipids and poor in structural proteins, and hydrolytic enzymes from neutrophils and
microglia digest the tissue into a liquid. Blood supply (A) affects infarct risk but not necrosis type.
Lysosomes (B) contribute to liquefaction rather than prevent it. Apoptosis (D) is programmed cell
death, a distinct process from necrosis. (Porth, Ch. 3)
Q6. A researcher is studying a pathway in which cytochrome c is released from
mitochondria, activating caspase-9 and subsequently caspase-3. This results in cell
shrinkage, chromatin condensation, and formation of apoptotic bodies without an
inflammatory response. Which statement best characterizes this process?
A. It is a necrotic process triggered by ATP depletion
B. It is the intrinsic (mitochondrial) pathway of apoptosis
C. It is the extrinsic (death receptor) pathway of apoptosis
D. It represents pyroptosis mediated by inflammasome activation
Rationale: The intrinsic (mitochondrial) pathway of apoptosis is triggered by intracellular stress
(DNA damage, oxidative stress) causing mitochondrial release of cytochrome c, which forms the
apoptosome with Apaf-1 and activates caspase-9, then caspase-3. This produces apoptotic bodies
phagocytosed without inflammation. Necrosis (A) causes inflammation and is not caspase-
dependent. The extrinsic pathway (C) involves death receptors (Fas, TNF-R1) activating caspase-8,
not cytochrome c. Pyroptosis (D) is inflammasome-mediated and inherently pro-inflammatory.
(McCance & Huether, Ch. 2)
Q7. A patient is exposed to a toxin that generates excessive superoxide radicals.
Antioxidant defenses including superoxide dismutase, catalase, and glutathione
peroxidase are overwhelmed. Which of the following describes the correct sequence of free
radical-mediated cellular injury?
A. Lipid peroxidation → membrane damage → calcium influx → enzyme activation →
DNA damage
B. DNA damage → protein denaturation → lipid peroxidation → membrane repair
C. Calcium influx → protein cross-linking → membrane damage → lipid peroxidation
D. Mitochondrial biogenesis → ATP depletion → reactive oxygen species generation → apoptosis
Rationale: Free radicals, particularly reactive oxygen species (ROS), cause injury through lipid
peroxidation of cell membranes, which increases membrane permeability. This allows calcium
influx, which activates intracellular enzymes (proteases, phospholipases, endonucleases) causing
further damage and DNA fragmentation. Option B reverses the typical sequence; lipid
peroxidation is an early event. Option C incorrectly sequences calcium before membrane damage.
Page 4 | D236 Pathophysiology Study Guide 2026
