SOUTH UNIVERSITY -- COLLEGE OF NURSING
NSG 6330 Final Exam
Advanced Pathophysiology
Official Practice Exam . 2026/2027 Edition
100 Questions | 120 Minutes | 80% Passing Score | 6 Sections
TABLE OF CONTENTS
Section 1: Cellular Pathophysiology & Inflammation (16 Questions)
Section 2: Cardiovascular & Hemodynamic Pathophysiology (14 Questions)
Section 3: Renal & Fluid-Electrolyte Pathophysiology (14 Questions)
Section 4: Neurologic Pathophysiology (16 Questions)
Section 5: Endocrine & Metabolic Pathophysiology (10 Questions)
Section 6: Gastrointestinal & Hepatobiliary Pathophysiology (14 Questions)
Section 7: Pulmonary & Respiratory Pathophysiology (16 Questions)
EXAM INSTRUCTIONS
Read each question carefully. Select the single best answer from the four options provided. Each question includes a
rationale explaining the correct answer and why a key distractor is incorrect. A score of 80% or higher (80 of 100) is
required to pass. Manage your time to allow approximately 1.2 minutes per question. Review all answers before
submission.
NSG 6330 Final Exam -- 2026/2027 | Passing Score: 80% | Page 0 of 0
NSG 6330 Final Exam | South University | 2026/2027 Edition
,Section 1: Cellular Pathophysiology & Inflammation
Q1. Question 1 of 100
Q1. A 42-year-old male construction worker presents with progressive muscle weakness, elevated creatine
kinase, and a history of recurrent rhabdomyolysis episodes after strenuous activity. Muscle biopsy reveals
subsarcolemmal accumulations of abnormal glycogen. The nurse practitioner recognizes this disorder results
from a deficiency in which enzyme?
A. Muscle phosphorylase
B. Acid maltase (acid alpha-glucosidase)
C. Glucose-6-phosphatase
D. Galactose-1-phosphate uridyltransferase
Correct Answer: A
Rationale:
The findings describe McArdle disease, caused by deficiency of muscle phosphorylase, which impairs glycogen
breakdown in skeletal muscle. Glucose-6-phosphatase deficiency causes von Gierke disease (hepatomegaly,
hypoglycemia), not muscle-specific symptoms. Acid maltase deficiency (Pompe disease) affects lysosomal
glycogen storage in multiple tissues including cardiac muscle, presenting differently than exercise-induced
cramping and myoglobinuria.
Q2. Question 2 of 100
Q2. A 58-year-old woman with rheumatoid arthritis on long-term methotrexate therapy develops progressive
dyspnea and a nonproductive cough. High-resolution CT shows ground-glass opacities and reticular markings in
the lower lung fields. Which cellular mechanism best explains this patient's pulmonary findings?
A. Direct cytotoxic injury to type I pneumocytes leading to diffuse alveolar damage
B. Drug-induced mitochondrial dysfunction triggering pulmonary fibrosis via TGF-beta activation
C. Immune complex deposition in pulmonary capillaries causing hypersensitivity pneumonitis
D. Lysosomal storage of methotrexate in alveolar macrophages impairing surfactant clearance
Correct Answer: B
Rationale:
Methotrexate-induced pneumonitis involves mitochondrial injury in pulmonary epithelial cells and subsequent
activation of TGF-beta signaling, which drives fibroblast proliferation and collagen deposition. Direct cytotoxic
alveolar damage (choice A) is more characteristic of acute respiratory distress syndrome or bleomycin toxicity.
Hypersensitivity pneumonitis (choice C) involves a different immunologic mechanism with granuloma formation,
while lysosomal storage (choice D) is not a recognized pathway for methotrexate pulmonary toxicity.
NSG 6330 Final Exam -- 2026/2027 | Passing Score: 80% | Page 1 of 0
,Q3. Question 3 of 100
Q3. A 34-year-old man with sickle cell disease is admitted with acute chest pain, fever, and hypoxia. His
hemoglobin has dropped from 8.2 to 5.9 g/dL. A peripheral smear shows sickled cells and Howell-Jolly bodies.
The nurse practitioner understands that the pathogenesis of vaso-occlusive crisis primarily involves which
sequence?
A. Autoimmune hemolysis triggered by cold agglutinins producing intravascular clotting in pulmonary
vessels
B. Oxidative membrane damage from G6PD deficiency creating rigid cells that obstruct capillary beds
C. Deoxygenation leading to HbS polymerization, causing rigid sickled erythrocytes that obstruct
microvasculature
D. Megaloblastic transformation of erythroid precursors releasing immature nucleated red cells into
circulation
Correct Answer: C
Rationale:
In sickle cell disease, deoxygenation causes hemoglobin S to polymerize, distorting red blood cells into rigid sickle
shapes that obstruct the microvasculature and trigger vaso-occlusive crisis. Cold agglutinin hemolysis (choice B)
is unrelated to sickle cell pathophysiology. G6PD deficiency (choice C) is a separate X-linked disorder causing
oxidative hemolysis, not vaso-occlusion. Megaloblastic transformation (choice D) describes B12 or folate
deficiency, not sickle cell crisis.
Q4. Question 4 of 100
Q4. A 67-year-old woman with a 30-pack-year smoking history presents with chronic cough, wheezing, and
exertional dyspnea. Pulmonary function tests show FEV1/FVC of 0.58 and reduced diffusing capacity. Which
pathophysiologic process best accounts for the reduced DLCO in this patient?
A. Hyperinflation of alveoli compressing the pulmonary capillary bed
B. Mucus plugging of small airways reducing gas mixing efficiency
C. Hypertrophy of bronchial smooth muscle increasing airway resistance
D. Destruction of alveolar walls and loss of pulmonary capillary surface area
Correct Answer: D
Rationale:
The patient has emphysema, characterized by destruction of alveolar septa and loss of capillary surface area,
which directly reduces DLCO. Hyperinflation (choice A) contributes to symptoms but does not primarily reduce
DLCO. Mucus plugging (choice C) and smooth muscle hypertrophy (choice D) are features of chronic bronchitis
and may reduce FEV1/FVC but do not destroy the alveolar-capillary interface necessary for diffusion.
NSG 6330 Final Exam -- 2026/2027 | Passing Score: 80% | Page 2 of 0
, Q5. Question 5 of 100
Q5. A 28-year-old woman presents with a butterfly rash across her cheeks and nose, joint pain in her hands, and
oral ulcers. Laboratory testing reveals positive ANA and anti-dsDNA antibodies with a low complement C3 level.
The underlying pathogenesis of her condition involves which primary mechanism?
A. Defective apoptosis allowing persistence of autoreactive lymphocytes and immune complex
deposition
B. Viral integration into the genome producing continuously expressed foreign antigens
C. Inherited deficiency of early complement components causing impaired immune complex clearance
D. B-cell lymphoproliferative disorder producing monoclonal autoantibodies against nuclear antigens
Correct Answer: A
Rationale:
Systemic lupus erythematosus results from defective apoptosis that allows nuclear antigens to persist and
stimulate autoreactive B and T cells, leading to immune complex formation and tissue injury. Viral integration
(choice B) is not the primary mechanism. Complement deficiency (choice C) is a risk factor but not the central
pathogenesis. SLE produces polyclonal, not monoclonal, autoantibodies (choice D).
Q6. Question 6 of 100
Q6. A 55-year-old man with long-standing GERD develops dysphagia for solid foods and unintentional weight
loss. Endoscopy reveals salmon-colored mucosa extending 4 cm proximal to the gastroesophageal junction with
biopsy confirming intestinal metaplasia. The sequence of cellular changes in this condition follows which
pathway?
A. Squamous epithelium to acute gastritis to chronic atrophic gastritis to intestinal metaplasia to
adenocarcinoma
B. Squamous epithelium to intestinal metaplasia to low-grade dysplasia to high-grade dysplasia to
adenocarcinoma
C. Columnar epithelium to squamous metaplasia to dysplasia to invasive squamous cell carcinoma
D. Glandular epithelium to fundic gland metaplasia to hyperplastic polyps to tubular adenoma to
adenocarcinoma
Correct Answer: B
Rationale:
Barrett esophagus follows the metaplasia-dysplasia-carcinoma sequence: chronic reflux damages squamous
epithelium, which is replaced by intestinal metaplasia (columnar with goblet cells), then may progress through
low-grade and high-grade dysplasia to adenocarcinoma. Chronic atrophic gastritis (choice B) describes the gastric
pathway for intestinal-type gastric cancer. Squamous metaplasia (choice C) and fundic gland metaplasia (choice
D) do not describe the Barrett sequence.
NSG 6330 Final Exam -- 2026/2027 | Passing Score: 80% | Page 3 of 0
NSG 6330 Final Exam
Advanced Pathophysiology
Official Practice Exam . 2026/2027 Edition
100 Questions | 120 Minutes | 80% Passing Score | 6 Sections
TABLE OF CONTENTS
Section 1: Cellular Pathophysiology & Inflammation (16 Questions)
Section 2: Cardiovascular & Hemodynamic Pathophysiology (14 Questions)
Section 3: Renal & Fluid-Electrolyte Pathophysiology (14 Questions)
Section 4: Neurologic Pathophysiology (16 Questions)
Section 5: Endocrine & Metabolic Pathophysiology (10 Questions)
Section 6: Gastrointestinal & Hepatobiliary Pathophysiology (14 Questions)
Section 7: Pulmonary & Respiratory Pathophysiology (16 Questions)
EXAM INSTRUCTIONS
Read each question carefully. Select the single best answer from the four options provided. Each question includes a
rationale explaining the correct answer and why a key distractor is incorrect. A score of 80% or higher (80 of 100) is
required to pass. Manage your time to allow approximately 1.2 minutes per question. Review all answers before
submission.
NSG 6330 Final Exam -- 2026/2027 | Passing Score: 80% | Page 0 of 0
NSG 6330 Final Exam | South University | 2026/2027 Edition
,Section 1: Cellular Pathophysiology & Inflammation
Q1. Question 1 of 100
Q1. A 42-year-old male construction worker presents with progressive muscle weakness, elevated creatine
kinase, and a history of recurrent rhabdomyolysis episodes after strenuous activity. Muscle biopsy reveals
subsarcolemmal accumulations of abnormal glycogen. The nurse practitioner recognizes this disorder results
from a deficiency in which enzyme?
A. Muscle phosphorylase
B. Acid maltase (acid alpha-glucosidase)
C. Glucose-6-phosphatase
D. Galactose-1-phosphate uridyltransferase
Correct Answer: A
Rationale:
The findings describe McArdle disease, caused by deficiency of muscle phosphorylase, which impairs glycogen
breakdown in skeletal muscle. Glucose-6-phosphatase deficiency causes von Gierke disease (hepatomegaly,
hypoglycemia), not muscle-specific symptoms. Acid maltase deficiency (Pompe disease) affects lysosomal
glycogen storage in multiple tissues including cardiac muscle, presenting differently than exercise-induced
cramping and myoglobinuria.
Q2. Question 2 of 100
Q2. A 58-year-old woman with rheumatoid arthritis on long-term methotrexate therapy develops progressive
dyspnea and a nonproductive cough. High-resolution CT shows ground-glass opacities and reticular markings in
the lower lung fields. Which cellular mechanism best explains this patient's pulmonary findings?
A. Direct cytotoxic injury to type I pneumocytes leading to diffuse alveolar damage
B. Drug-induced mitochondrial dysfunction triggering pulmonary fibrosis via TGF-beta activation
C. Immune complex deposition in pulmonary capillaries causing hypersensitivity pneumonitis
D. Lysosomal storage of methotrexate in alveolar macrophages impairing surfactant clearance
Correct Answer: B
Rationale:
Methotrexate-induced pneumonitis involves mitochondrial injury in pulmonary epithelial cells and subsequent
activation of TGF-beta signaling, which drives fibroblast proliferation and collagen deposition. Direct cytotoxic
alveolar damage (choice A) is more characteristic of acute respiratory distress syndrome or bleomycin toxicity.
Hypersensitivity pneumonitis (choice C) involves a different immunologic mechanism with granuloma formation,
while lysosomal storage (choice D) is not a recognized pathway for methotrexate pulmonary toxicity.
NSG 6330 Final Exam -- 2026/2027 | Passing Score: 80% | Page 1 of 0
,Q3. Question 3 of 100
Q3. A 34-year-old man with sickle cell disease is admitted with acute chest pain, fever, and hypoxia. His
hemoglobin has dropped from 8.2 to 5.9 g/dL. A peripheral smear shows sickled cells and Howell-Jolly bodies.
The nurse practitioner understands that the pathogenesis of vaso-occlusive crisis primarily involves which
sequence?
A. Autoimmune hemolysis triggered by cold agglutinins producing intravascular clotting in pulmonary
vessels
B. Oxidative membrane damage from G6PD deficiency creating rigid cells that obstruct capillary beds
C. Deoxygenation leading to HbS polymerization, causing rigid sickled erythrocytes that obstruct
microvasculature
D. Megaloblastic transformation of erythroid precursors releasing immature nucleated red cells into
circulation
Correct Answer: C
Rationale:
In sickle cell disease, deoxygenation causes hemoglobin S to polymerize, distorting red blood cells into rigid sickle
shapes that obstruct the microvasculature and trigger vaso-occlusive crisis. Cold agglutinin hemolysis (choice B)
is unrelated to sickle cell pathophysiology. G6PD deficiency (choice C) is a separate X-linked disorder causing
oxidative hemolysis, not vaso-occlusion. Megaloblastic transformation (choice D) describes B12 or folate
deficiency, not sickle cell crisis.
Q4. Question 4 of 100
Q4. A 67-year-old woman with a 30-pack-year smoking history presents with chronic cough, wheezing, and
exertional dyspnea. Pulmonary function tests show FEV1/FVC of 0.58 and reduced diffusing capacity. Which
pathophysiologic process best accounts for the reduced DLCO in this patient?
A. Hyperinflation of alveoli compressing the pulmonary capillary bed
B. Mucus plugging of small airways reducing gas mixing efficiency
C. Hypertrophy of bronchial smooth muscle increasing airway resistance
D. Destruction of alveolar walls and loss of pulmonary capillary surface area
Correct Answer: D
Rationale:
The patient has emphysema, characterized by destruction of alveolar septa and loss of capillary surface area,
which directly reduces DLCO. Hyperinflation (choice A) contributes to symptoms but does not primarily reduce
DLCO. Mucus plugging (choice C) and smooth muscle hypertrophy (choice D) are features of chronic bronchitis
and may reduce FEV1/FVC but do not destroy the alveolar-capillary interface necessary for diffusion.
NSG 6330 Final Exam -- 2026/2027 | Passing Score: 80% | Page 2 of 0
, Q5. Question 5 of 100
Q5. A 28-year-old woman presents with a butterfly rash across her cheeks and nose, joint pain in her hands, and
oral ulcers. Laboratory testing reveals positive ANA and anti-dsDNA antibodies with a low complement C3 level.
The underlying pathogenesis of her condition involves which primary mechanism?
A. Defective apoptosis allowing persistence of autoreactive lymphocytes and immune complex
deposition
B. Viral integration into the genome producing continuously expressed foreign antigens
C. Inherited deficiency of early complement components causing impaired immune complex clearance
D. B-cell lymphoproliferative disorder producing monoclonal autoantibodies against nuclear antigens
Correct Answer: A
Rationale:
Systemic lupus erythematosus results from defective apoptosis that allows nuclear antigens to persist and
stimulate autoreactive B and T cells, leading to immune complex formation and tissue injury. Viral integration
(choice B) is not the primary mechanism. Complement deficiency (choice C) is a risk factor but not the central
pathogenesis. SLE produces polyclonal, not monoclonal, autoantibodies (choice D).
Q6. Question 6 of 100
Q6. A 55-year-old man with long-standing GERD develops dysphagia for solid foods and unintentional weight
loss. Endoscopy reveals salmon-colored mucosa extending 4 cm proximal to the gastroesophageal junction with
biopsy confirming intestinal metaplasia. The sequence of cellular changes in this condition follows which
pathway?
A. Squamous epithelium to acute gastritis to chronic atrophic gastritis to intestinal metaplasia to
adenocarcinoma
B. Squamous epithelium to intestinal metaplasia to low-grade dysplasia to high-grade dysplasia to
adenocarcinoma
C. Columnar epithelium to squamous metaplasia to dysplasia to invasive squamous cell carcinoma
D. Glandular epithelium to fundic gland metaplasia to hyperplastic polyps to tubular adenoma to
adenocarcinoma
Correct Answer: B
Rationale:
Barrett esophagus follows the metaplasia-dysplasia-carcinoma sequence: chronic reflux damages squamous
epithelium, which is replaced by intestinal metaplasia (columnar with goblet cells), then may progress through
low-grade and high-grade dysplasia to adenocarcinoma. Chronic atrophic gastritis (choice B) describes the gastric
pathway for intestinal-type gastric cancer. Squamous metaplasia (choice C) and fundic gland metaplasia (choice
D) do not describe the Barrett sequence.
NSG 6330 Final Exam -- 2026/2027 | Passing Score: 80% | Page 3 of 0
