WESTERN GOVERNORS UNIVERSITY
Pathophysiology D236
Official Practice Exam
2026/2027 Edition
Questions Minutes Passing Score Recertification
100 120 80% Required
TABLE OF CONTENTS
Section: Cellular Biology and Cellular Adaptation . . . . . . . . . . . . . . . . . . . . . Questions 1-18
Section: Immunity and Inflammation . . . . . . . . . . . . . . . . . . . . . Questions 19-35
Section: Infection and Neoplasia . . . . . . . . . . . . . . . . . . . . . Questions 36-52
Section: Fluid, Electrolyte, and Acid-Base Balance . . . . . . . . . . . . . . . . . . . . . Questions 53-68
Section: Cardiovascular and Hematologic Disorders . . . . . . . . . . . . . . . . . . . . . Questions 69-84
Section: Pulmonary, Renal, and Neurologic Disorders . . . . . . . . . . . . . . . . . . . . . Questions 85-100
INSTRUCTIONS
This practice exam contains 100 multiple-choice questions divided into 6 sections. You have 120 minutes to complete
the exam. Select the single best answer for each question. A passing score of 80% (80 correct out of 100) is required.
Each question includes a rationale explaining the correct answer and why the most common wrong answer is incorrect.
Review all rationales carefully to maximize your learning and exam readiness.
WGU Pathophysiology D236 -- 2026/2027 | Passing Score: 80% | Page 1 of 1
,Section 1: Cellular Biology and Cellular Adaptation | Questions 1-18 | 2026/2027
Q1 Question 1 of 100
A 58-year-old male factory worker with chronic exposure to carbon tetrachloride presents with
elevated liver enzymes and hepatomegaly. A biopsy reveals cells with dense, eosinophilic, glassy
cytoplasm and pyknotic nuclei. Which cellular adaptation best describes these findings?
A. Coagulative necrosis with loss of nuclear detail
B. Metaplasia of hepatocytes to squamous cells
C. Fatty degeneration with intracellular lipid accumulation
D. Apoptosis with formation of apoptotic bodies
Correct Answer: A
Rationale:
Coagulative necrosis is the classic pattern seen in toxic injury from carbon tetrachloride, where cell outlines are
preserved but nuclei become pyknotic and cytoplasm appears glassy and eosinophilic. Fatty degeneration
(choice C) involves lipid vacuoles rather than the dense eosinophilic cytoplasm described. Metaplasia (choice A)
involves replacement of one cell type by another, not necrosis.
Q2 Question 2 of 100
A 42-year-old woman with a long history of severe gastroesophageal reflux disease undergoes
endoscopy, which reveals salmon-colored mucosa in the distal esophagus replacing the normal
squamous epithelium. Biopsy confirms intestinal-type columnar cells with goblet cells. What is the
pathologic process?
A. Hyperplasia of the esophageal squamous epithelium
B. Columnar metaplasia as an adaptive response to chronic acid exposure
C. Dysplasia with atypical cellular features
D. Atrophy of the esophageal mucosal lining
Correct Answer: B
Rationale:
Barrett esophagus is a classic example of columnar metaplasia, in which chronic acid reflux causes the
squamous epithelium to be replaced by intestinal-type columnar epithelium as a protective adaptation. Dysplasia
(choice B) involves disordered cellular growth with atypia, not the organized substitution seen here. Hyperplasia
(choice A) would increase cell number without changing cell type.
,Q3 Question 3 of 100
A 67-year-old man with a 40-pack-year smoking history has a chest X-ray showing a 3-cm mass in
the right upper lobe. Bronchoscopic biopsy reveals squamous epithelium replacing the normal
bronchial columnar ciliated epithelium. What cellular adaptation preceded this finding?
A. Hyperplasia of ciliated columnar cells
B. Hypertrophy of smooth muscle in bronchial walls
C. Squamous metaplasia of bronchial epithelium
D. Atrophy of the bronchial mucous glands
Correct Answer: C
Rationale:
Squamous metaplasia is a well-documented response to chronic irritation from cigarette smoke, where the
normal ciliated columnar epithelium of the bronchi is replaced by stratified squamous epithelium. Hyperplasia
(choice B) increases the number of existing cell types without substitution. Hypertrophy (choice C) involves
enlargement of existing cells, not epithelial transformation.
Q4 Question 4 of 100
A 35-year-old male bodybuilder has been using anabolic steroids for five years. He presents with
right upper quadrant pain, and liver function tests are elevated. Imaging shows an enlarged liver.
Biopsy demonstrates hepatocytes with enlarged, hyperchromatic nuclei and increased cytoplasmic
volume. What cellular adaptation is primarily responsible for the hepatomegaly?
A. Hyperplasia of hepatocytes with increased cell number
B. Metaplasia of hepatocytes to fibrous tissue
C. Dysplasia of hepatic parenchymal cells
D. Hypertrophy of individual hepatocytes with increased cell size
Correct Answer: D
Rationale:
Anabolic steroid use causes hepatomegaly primarily through hypertrophy, where individual hepatocytes increase
in size due to stimulation of protein synthesis and cellular organelle proliferation. Hyperplasia (choice A) involves
increased cell number rather than cell size, which is less characteristic of steroid-induced hepatomegaly.
Metaplasia (choice C) involves cell-type conversion, not enlargement.
WGU Pathophysiology D236 -- 2026/2027 | Passing Score: 80% | Page 2 of 2
, Q5 Question 5 of 100
A 70-year-old woman with chronic venous stasis in her lower extremities develops brownish
pigmentation and thickened skin around her ankles. Microscopic examination reveals dermal
macrophages containing iron pigment. Which intracellular accumulation best explains the
pigmentation?
A. Hemosiderin accumulation from red blood cell breakdown
B. Lipofuscin accumulation indicating cellular aging
C. Bilirubin accumulation from hepatic dysfunction
D. Melanin overproduction by dermal melanocytes
Correct Answer: A
Rationale:
Chronic venous stasis leads to extravasation of red blood cells into the tissue, where macrophages phagocytose
the hemoglobin and convert it to hemosiderin, producing the characteristic brown pigmentation known as stasis
dermatitis. Lipofuscin (choice A) is an aging pigment not related to hemoglobin breakdown. Bilirubin (choice B)
would produce jaundice rather than localized brown discoloration.
Q6 Question 6 of 100
A 50-year-old woman with untreated hyperlipidemia develops yellowish nodules on her eyelids and
extensor tendons. Serum cholesterol is 420 mg/dL. Biopsy of a nodule shows lipid-laden
macrophages (foam cells) in the dermis. Which cellular process best accounts for these findings?
A. Glycogen storage disease affecting dermal cells
B. Intracellular accumulation of cholesterol esters in macrophages
C. Amyloid deposition in soft tissue
D. Mucopolysaccharide accumulation in fibroblasts
Correct Answer: B
Rationale:
Xanthomas result from intracellular accumulation of cholesterol esters within macrophages (foam cells) in
patients with severe hyperlipidemia, producing the characteristic yellowish skin and tendon nodules. Glycogen
storage disease (choice A) affects liver and muscle, not typically producing dermal foam cells. Amyloid (choice
C) deposits as extracellular fibrillar protein, not intracellular lipid.
WGU Pathophysiology D236 -- 2026/2027 | Passing Score: 80% | Page 3 of 3
Pathophysiology D236
Official Practice Exam
2026/2027 Edition
Questions Minutes Passing Score Recertification
100 120 80% Required
TABLE OF CONTENTS
Section: Cellular Biology and Cellular Adaptation . . . . . . . . . . . . . . . . . . . . . Questions 1-18
Section: Immunity and Inflammation . . . . . . . . . . . . . . . . . . . . . Questions 19-35
Section: Infection and Neoplasia . . . . . . . . . . . . . . . . . . . . . Questions 36-52
Section: Fluid, Electrolyte, and Acid-Base Balance . . . . . . . . . . . . . . . . . . . . . Questions 53-68
Section: Cardiovascular and Hematologic Disorders . . . . . . . . . . . . . . . . . . . . . Questions 69-84
Section: Pulmonary, Renal, and Neurologic Disorders . . . . . . . . . . . . . . . . . . . . . Questions 85-100
INSTRUCTIONS
This practice exam contains 100 multiple-choice questions divided into 6 sections. You have 120 minutes to complete
the exam. Select the single best answer for each question. A passing score of 80% (80 correct out of 100) is required.
Each question includes a rationale explaining the correct answer and why the most common wrong answer is incorrect.
Review all rationales carefully to maximize your learning and exam readiness.
WGU Pathophysiology D236 -- 2026/2027 | Passing Score: 80% | Page 1 of 1
,Section 1: Cellular Biology and Cellular Adaptation | Questions 1-18 | 2026/2027
Q1 Question 1 of 100
A 58-year-old male factory worker with chronic exposure to carbon tetrachloride presents with
elevated liver enzymes and hepatomegaly. A biopsy reveals cells with dense, eosinophilic, glassy
cytoplasm and pyknotic nuclei. Which cellular adaptation best describes these findings?
A. Coagulative necrosis with loss of nuclear detail
B. Metaplasia of hepatocytes to squamous cells
C. Fatty degeneration with intracellular lipid accumulation
D. Apoptosis with formation of apoptotic bodies
Correct Answer: A
Rationale:
Coagulative necrosis is the classic pattern seen in toxic injury from carbon tetrachloride, where cell outlines are
preserved but nuclei become pyknotic and cytoplasm appears glassy and eosinophilic. Fatty degeneration
(choice C) involves lipid vacuoles rather than the dense eosinophilic cytoplasm described. Metaplasia (choice A)
involves replacement of one cell type by another, not necrosis.
Q2 Question 2 of 100
A 42-year-old woman with a long history of severe gastroesophageal reflux disease undergoes
endoscopy, which reveals salmon-colored mucosa in the distal esophagus replacing the normal
squamous epithelium. Biopsy confirms intestinal-type columnar cells with goblet cells. What is the
pathologic process?
A. Hyperplasia of the esophageal squamous epithelium
B. Columnar metaplasia as an adaptive response to chronic acid exposure
C. Dysplasia with atypical cellular features
D. Atrophy of the esophageal mucosal lining
Correct Answer: B
Rationale:
Barrett esophagus is a classic example of columnar metaplasia, in which chronic acid reflux causes the
squamous epithelium to be replaced by intestinal-type columnar epithelium as a protective adaptation. Dysplasia
(choice B) involves disordered cellular growth with atypia, not the organized substitution seen here. Hyperplasia
(choice A) would increase cell number without changing cell type.
,Q3 Question 3 of 100
A 67-year-old man with a 40-pack-year smoking history has a chest X-ray showing a 3-cm mass in
the right upper lobe. Bronchoscopic biopsy reveals squamous epithelium replacing the normal
bronchial columnar ciliated epithelium. What cellular adaptation preceded this finding?
A. Hyperplasia of ciliated columnar cells
B. Hypertrophy of smooth muscle in bronchial walls
C. Squamous metaplasia of bronchial epithelium
D. Atrophy of the bronchial mucous glands
Correct Answer: C
Rationale:
Squamous metaplasia is a well-documented response to chronic irritation from cigarette smoke, where the
normal ciliated columnar epithelium of the bronchi is replaced by stratified squamous epithelium. Hyperplasia
(choice B) increases the number of existing cell types without substitution. Hypertrophy (choice C) involves
enlargement of existing cells, not epithelial transformation.
Q4 Question 4 of 100
A 35-year-old male bodybuilder has been using anabolic steroids for five years. He presents with
right upper quadrant pain, and liver function tests are elevated. Imaging shows an enlarged liver.
Biopsy demonstrates hepatocytes with enlarged, hyperchromatic nuclei and increased cytoplasmic
volume. What cellular adaptation is primarily responsible for the hepatomegaly?
A. Hyperplasia of hepatocytes with increased cell number
B. Metaplasia of hepatocytes to fibrous tissue
C. Dysplasia of hepatic parenchymal cells
D. Hypertrophy of individual hepatocytes with increased cell size
Correct Answer: D
Rationale:
Anabolic steroid use causes hepatomegaly primarily through hypertrophy, where individual hepatocytes increase
in size due to stimulation of protein synthesis and cellular organelle proliferation. Hyperplasia (choice A) involves
increased cell number rather than cell size, which is less characteristic of steroid-induced hepatomegaly.
Metaplasia (choice C) involves cell-type conversion, not enlargement.
WGU Pathophysiology D236 -- 2026/2027 | Passing Score: 80% | Page 2 of 2
, Q5 Question 5 of 100
A 70-year-old woman with chronic venous stasis in her lower extremities develops brownish
pigmentation and thickened skin around her ankles. Microscopic examination reveals dermal
macrophages containing iron pigment. Which intracellular accumulation best explains the
pigmentation?
A. Hemosiderin accumulation from red blood cell breakdown
B. Lipofuscin accumulation indicating cellular aging
C. Bilirubin accumulation from hepatic dysfunction
D. Melanin overproduction by dermal melanocytes
Correct Answer: A
Rationale:
Chronic venous stasis leads to extravasation of red blood cells into the tissue, where macrophages phagocytose
the hemoglobin and convert it to hemosiderin, producing the characteristic brown pigmentation known as stasis
dermatitis. Lipofuscin (choice A) is an aging pigment not related to hemoglobin breakdown. Bilirubin (choice B)
would produce jaundice rather than localized brown discoloration.
Q6 Question 6 of 100
A 50-year-old woman with untreated hyperlipidemia develops yellowish nodules on her eyelids and
extensor tendons. Serum cholesterol is 420 mg/dL. Biopsy of a nodule shows lipid-laden
macrophages (foam cells) in the dermis. Which cellular process best accounts for these findings?
A. Glycogen storage disease affecting dermal cells
B. Intracellular accumulation of cholesterol esters in macrophages
C. Amyloid deposition in soft tissue
D. Mucopolysaccharide accumulation in fibroblasts
Correct Answer: B
Rationale:
Xanthomas result from intracellular accumulation of cholesterol esters within macrophages (foam cells) in
patients with severe hyperlipidemia, producing the characteristic yellowish skin and tendon nodules. Glycogen
storage disease (choice A) affects liver and muscle, not typically producing dermal foam cells. Amyloid (choice
C) deposits as extracellular fibrillar protein, not intracellular lipid.
WGU Pathophysiology D236 -- 2026/2027 | Passing Score: 80% | Page 3 of 3
