BIOD 331 | NURS 231
Pathophysiology Final Exam
Questions and Answers
2026/2027 Update | 100% Correct
Portage Learning BIOD 331 & NURS 231 - Comprehensive Final Examination
Total Questions: 150 Multiple-Choice Questions (4 options, 1 correct)
Cognitive Mix: 30% Recall | 50% Application | 20% Analysis
Question Style: 70% Scenario-based | 30% Direct mechanism / definition
Sections: 10 sections covering the full BIOD 331 / NURS 231 scope
Rationale Format: Mechanism-based justification + distractor analysis
Verification: Each rationale cross-checked against Portage Learning BIOD 331 and NURS 231 course
materials
Examination Sections
Section Questions Topic Coverage
Cellular Structure, Function, and Adaptation
S1 Q1-Q14
Cell Biology, Adaptation, Injury, and Death
Genetics and Genetic Disorders
S2 Q15-Q28
DNA, Mutation, Inheritance, and Genetic Diseases
Inflammation, Immunity, and Infection
S3 Q29-Q46
Innate/Adaptive Immunity, Inflammation, and Immunopathology
Fluid, Electrolyte, and Acid-Base Disorders
S4 Q47-Q62
Fluid Balance, Sodium, Potassium, and Acid-Base
Cardiovascular Pathophysiology
S5 Q63-Q80
Atherosclerosis, Hypertension, Heart Failure, and Dysrhythmias
Respiratory Pathophysiology
S6 Q81-Q96
Obstructive, Restrictive, ARDS, and V/Q Mismatch
Neurological Pathophysiology
S7 Q97-Q112
Stroke, Seizures, Neurodegeneration, and CNS Disorders
Page 1
,BIOD 331 | NURS 231 Pathophysiology Final Exam | 2026/2027 Update 100% Correct - Verified Q&A
Endocrine Pathophysiology
S8 Q113-Q128
Diabetes, Thyroid, Adrenal, and Pituitary Disorders
Renal and Gastrointestinal Pathophysiology
S9 Q129-Q142
AKI, CKD, Liver Disease, and GI Disorders
Musculoskeletal, Integumentary, and Hematologic Pathophysiology
S10 Q143-Q150
Bone, Joint, Skin, and Blood Disorders
Examination Instructions: Each question has exactly ONE correct answer (A, B, C, or D). Read the stem carefully, then
evaluate each option using pathophysiological reasoning. Rationales follow every question, providing mechanism-based
justification for the correct answer and explaining why distractors are incorrect. Verification notes confirm alignment with the
Portage Learning BIOD 331 and NURS 231 course competencies.
Page 2
,BIOD 331 | NURS 231 Pathophysiology Final Exam | 2026/2027 Update 100% Correct - Verified Q&A
Section 1: Cellular Structure, Function, and Adaptation
Topics: Cell Biology, Adaptation, Injury, and Death - Questions Q1 through Q14
Q1: A 68-year-old male with longstanding essential hypertension is found on echocardiography to have a
thickened left ventricular wall with normal chamber volume. Biopsy reveals enlarged myocytes with no
increase in cell number. Which cellular adaptation BEST explains this finding?
A. Atrophy
B. Hypertrophy [CORRECT]
C. Hyperplasia
D. Metaplasia
Correct Answer: B
Rationale:
Hypertrophy is an increase in cell SIZE without an increase in cell number, classically seen in cardiac and skeletal muscle
(terminally differentiated cells that cannot undergo mitosis). The increased afterload in hypertension forces ventricular
myocytes to add sarcomeres in parallel, producing concentric hypertrophy. Atrophy is a decrease in cell size, hyperplasia
is an increase in cell number (not possible in cardiac myocytes), and metaplasia is reversible replacement of one
differentiated cell type by another. Verification: this mechanism is emphasized in BIOD 331 Module 2 and NURS 231
cellular adaptation competencies.
Q2: A 55-year-old chronic smoker undergoes bronchoscopy. Biopsy of the bronchial epithelium shows
replacement of the normal ciliated pseudostratified columnar epithelium with stratified squamous
epithelium. Which pathophysiological mechanism BEST explains this finding, and what is its clinical
significance?
A. Dysplasia; reversible upon smoking cessation with no malignant potential
B. Metaplasia; reversible adaptive substitution but a precursor lesion for squamous carcinoma
[CORRECT]
C. Hyperplasia; benign proliferative response with no premalignant implications
D. Anaplasia; irreversible malignant transformation indicating invasive carcinoma
Correct Answer: B
Rationale:
Smoking induces reversible substitution of ciliated columnar epithelium with stratified squamous epithelium, a classic
example of metaplasia—an adaptive substitution of one differentiated cell type for another better able to withstand chronic
irritation. While initially reversible with smoking cessation, persistent injury may progress to dysplasia and squamous cell
carcinoma. Dysplasia (A) implies disordered growth within the same cell type; anaplasia (D) indicates frank malignancy.
Verification: aligned with Portage Learning BIOD 331 cellular adaptation module.
Page 3
, BIOD 331 | NURS 231 Pathophysiology Final Exam | 2026/2027 Update 100% Correct - Verified Q&A
Q3: A researcher is studying a tissue exposed to sustained hypoxia. Cells demonstrate mitochondrial
swelling, blebbing of the plasma membrane, and clumping of nuclear chromatin. Intracellular calcium
rises, ATP depletion is profound, and ROS generation accelerates. Which sequence BEST describes the
irreversible point of cell injury?
A. Depletion of glycogen stores and onset of anaerobic glycolysis
B. Severe ATP depletion leading to Na+/K+ pump failure and massive mitochondrial calcium overload
with membrane permeability transition [CORRECT]
C. Activation of caspase-3 followed by orderly chromatin laddering
D. Rupture of lysosomes with autophagy and adaptive upregulation of HIF-1α
Correct Answer: B
Rationale:
Irreversible injury is defined by severe ATP depletion causing failure of the Na+/K+-ATPase, massive calcium influx, and
opening of the mitochondrial permeability transition pore (mPTP). Calcium activates phospholipases, proteases, and
endonucleases that destroy membranes and chromatin. Option A describes early reversible injury; option C describes
apoptosis (programmed, orderly); option D describes a mixed autophagic response that is generally adaptive. The mPTP
opening and mitochondrial calcium overload mark the point of no return. Verification: consistent with NURS 231 cell
injury pathophysiology objectives.
Q4: A 6-hour-old neonate develops severe seizures. Laboratory testing reveals hyperammonemia,
metabolic acidosis, and elevated orotic acid. The defect is traced to a mitochondrial enzyme. Which
organelle is PRIMARILY implicated, and what is the underlying mechanism?
A. Rough endoplasmic reticulum; defective post-translational protein folding
B. Mitochondrion; defective oxidative phosphorylation and urea cycle enzyme mislocalization
[CORRECT]
C. Golgi apparatus; defective glycosylation of carrier proteins
D. Peroxisome; defective β-oxidation of very-long-chain fatty acids
Correct Answer: B
Rationale:
The combination of hyperammonemia, metabolic acidosis, and elevated orotic acid suggests a mitochondrial urea cycle
disorder (e.g., ornithine transcarbamylase deficiency, which is mitochondrial). Mitochondria generate ATP via oxidative
phosphorylation and house several metabolic enzymes, including OTC and carbamoyl-phosphate synthetase I. Defective
mitochondrial function disrupts the urea cycle and energy production. The rough ER (A) is for protein synthesis/secretion;
Golgi (C) for glycosylation/sorting; peroxisomes (D) for VLCFA β-oxidation. Verification: aligns with BIOD 331
organelle function content.
Page 4
Pathophysiology Final Exam
Questions and Answers
2026/2027 Update | 100% Correct
Portage Learning BIOD 331 & NURS 231 - Comprehensive Final Examination
Total Questions: 150 Multiple-Choice Questions (4 options, 1 correct)
Cognitive Mix: 30% Recall | 50% Application | 20% Analysis
Question Style: 70% Scenario-based | 30% Direct mechanism / definition
Sections: 10 sections covering the full BIOD 331 / NURS 231 scope
Rationale Format: Mechanism-based justification + distractor analysis
Verification: Each rationale cross-checked against Portage Learning BIOD 331 and NURS 231 course
materials
Examination Sections
Section Questions Topic Coverage
Cellular Structure, Function, and Adaptation
S1 Q1-Q14
Cell Biology, Adaptation, Injury, and Death
Genetics and Genetic Disorders
S2 Q15-Q28
DNA, Mutation, Inheritance, and Genetic Diseases
Inflammation, Immunity, and Infection
S3 Q29-Q46
Innate/Adaptive Immunity, Inflammation, and Immunopathology
Fluid, Electrolyte, and Acid-Base Disorders
S4 Q47-Q62
Fluid Balance, Sodium, Potassium, and Acid-Base
Cardiovascular Pathophysiology
S5 Q63-Q80
Atherosclerosis, Hypertension, Heart Failure, and Dysrhythmias
Respiratory Pathophysiology
S6 Q81-Q96
Obstructive, Restrictive, ARDS, and V/Q Mismatch
Neurological Pathophysiology
S7 Q97-Q112
Stroke, Seizures, Neurodegeneration, and CNS Disorders
Page 1
,BIOD 331 | NURS 231 Pathophysiology Final Exam | 2026/2027 Update 100% Correct - Verified Q&A
Endocrine Pathophysiology
S8 Q113-Q128
Diabetes, Thyroid, Adrenal, and Pituitary Disorders
Renal and Gastrointestinal Pathophysiology
S9 Q129-Q142
AKI, CKD, Liver Disease, and GI Disorders
Musculoskeletal, Integumentary, and Hematologic Pathophysiology
S10 Q143-Q150
Bone, Joint, Skin, and Blood Disorders
Examination Instructions: Each question has exactly ONE correct answer (A, B, C, or D). Read the stem carefully, then
evaluate each option using pathophysiological reasoning. Rationales follow every question, providing mechanism-based
justification for the correct answer and explaining why distractors are incorrect. Verification notes confirm alignment with the
Portage Learning BIOD 331 and NURS 231 course competencies.
Page 2
,BIOD 331 | NURS 231 Pathophysiology Final Exam | 2026/2027 Update 100% Correct - Verified Q&A
Section 1: Cellular Structure, Function, and Adaptation
Topics: Cell Biology, Adaptation, Injury, and Death - Questions Q1 through Q14
Q1: A 68-year-old male with longstanding essential hypertension is found on echocardiography to have a
thickened left ventricular wall with normal chamber volume. Biopsy reveals enlarged myocytes with no
increase in cell number. Which cellular adaptation BEST explains this finding?
A. Atrophy
B. Hypertrophy [CORRECT]
C. Hyperplasia
D. Metaplasia
Correct Answer: B
Rationale:
Hypertrophy is an increase in cell SIZE without an increase in cell number, classically seen in cardiac and skeletal muscle
(terminally differentiated cells that cannot undergo mitosis). The increased afterload in hypertension forces ventricular
myocytes to add sarcomeres in parallel, producing concentric hypertrophy. Atrophy is a decrease in cell size, hyperplasia
is an increase in cell number (not possible in cardiac myocytes), and metaplasia is reversible replacement of one
differentiated cell type by another. Verification: this mechanism is emphasized in BIOD 331 Module 2 and NURS 231
cellular adaptation competencies.
Q2: A 55-year-old chronic smoker undergoes bronchoscopy. Biopsy of the bronchial epithelium shows
replacement of the normal ciliated pseudostratified columnar epithelium with stratified squamous
epithelium. Which pathophysiological mechanism BEST explains this finding, and what is its clinical
significance?
A. Dysplasia; reversible upon smoking cessation with no malignant potential
B. Metaplasia; reversible adaptive substitution but a precursor lesion for squamous carcinoma
[CORRECT]
C. Hyperplasia; benign proliferative response with no premalignant implications
D. Anaplasia; irreversible malignant transformation indicating invasive carcinoma
Correct Answer: B
Rationale:
Smoking induces reversible substitution of ciliated columnar epithelium with stratified squamous epithelium, a classic
example of metaplasia—an adaptive substitution of one differentiated cell type for another better able to withstand chronic
irritation. While initially reversible with smoking cessation, persistent injury may progress to dysplasia and squamous cell
carcinoma. Dysplasia (A) implies disordered growth within the same cell type; anaplasia (D) indicates frank malignancy.
Verification: aligned with Portage Learning BIOD 331 cellular adaptation module.
Page 3
, BIOD 331 | NURS 231 Pathophysiology Final Exam | 2026/2027 Update 100% Correct - Verified Q&A
Q3: A researcher is studying a tissue exposed to sustained hypoxia. Cells demonstrate mitochondrial
swelling, blebbing of the plasma membrane, and clumping of nuclear chromatin. Intracellular calcium
rises, ATP depletion is profound, and ROS generation accelerates. Which sequence BEST describes the
irreversible point of cell injury?
A. Depletion of glycogen stores and onset of anaerobic glycolysis
B. Severe ATP depletion leading to Na+/K+ pump failure and massive mitochondrial calcium overload
with membrane permeability transition [CORRECT]
C. Activation of caspase-3 followed by orderly chromatin laddering
D. Rupture of lysosomes with autophagy and adaptive upregulation of HIF-1α
Correct Answer: B
Rationale:
Irreversible injury is defined by severe ATP depletion causing failure of the Na+/K+-ATPase, massive calcium influx, and
opening of the mitochondrial permeability transition pore (mPTP). Calcium activates phospholipases, proteases, and
endonucleases that destroy membranes and chromatin. Option A describes early reversible injury; option C describes
apoptosis (programmed, orderly); option D describes a mixed autophagic response that is generally adaptive. The mPTP
opening and mitochondrial calcium overload mark the point of no return. Verification: consistent with NURS 231 cell
injury pathophysiology objectives.
Q4: A 6-hour-old neonate develops severe seizures. Laboratory testing reveals hyperammonemia,
metabolic acidosis, and elevated orotic acid. The defect is traced to a mitochondrial enzyme. Which
organelle is PRIMARILY implicated, and what is the underlying mechanism?
A. Rough endoplasmic reticulum; defective post-translational protein folding
B. Mitochondrion; defective oxidative phosphorylation and urea cycle enzyme mislocalization
[CORRECT]
C. Golgi apparatus; defective glycosylation of carrier proteins
D. Peroxisome; defective β-oxidation of very-long-chain fatty acids
Correct Answer: B
Rationale:
The combination of hyperammonemia, metabolic acidosis, and elevated orotic acid suggests a mitochondrial urea cycle
disorder (e.g., ornithine transcarbamylase deficiency, which is mitochondrial). Mitochondria generate ATP via oxidative
phosphorylation and house several metabolic enzymes, including OTC and carbamoyl-phosphate synthetase I. Defective
mitochondrial function disrupts the urea cycle and energy production. The rough ER (A) is for protein synthesis/secretion;
Golgi (C) for glycosylation/sorting; peroxisomes (D) for VLCFA β-oxidation. Verification: aligns with BIOD 331
organelle function content.
Page 4
