NURS 231 PATHOPHYSIOLOGY FINAL EXAM | PORTAGE LEARNING (2026/2027)
Portage Learning NURS 231: Pathophysiology Comprehensive Final Examination | Core Domains:
Cellular Injury & Adaptation, Inflammation & Healing, Fluid, Electrolyte & Acid-Base Imbalances,
Genetic Disorders & Neoplasia, Cardiovascular Pathophysiology, Respiratory Pathophysiology, Renal &
Urinary Pathophysiology, Endocrine & Metabolic Pathophysiology, Neurological Pathophysiology, and
Musculoskeletal Pathophysiology | Nursing Program Focus | Comprehensive Pathophysiology Final
Exam Format
Exam Structure
The NURS 231 Pathophysiology Final Exam for the 2026/2027 academic cycle at Portage Learning is a
120-question, multiple-choice question (MCQ) examination.
Introduction
This NURS 231 Pathophysiology Final Exam guide for the 2026/2027 cycle prepares Portage Learning
nursing students for the comprehensive assessment of disease processes across all body systems. The
content emphasizes understanding the mechanisms of cellular and systemic dysfunction, connecting
etiologies to clinical manifestations, and predicting compensatory responses and complications, which
forms the essential scientific foundation for clinical nursing practice.
Answer Format
All correct answers and pathophysiological concepts must be presented in bold and green, followed by
detailed rationales that explain disease mechanisms at the cellular and systemic levels, connect etiologies
to clinical manifestations, and predict compensatory responses and potential complications.
Questions (120 Total)
1. Which cellular adaptation involves an increase in cell size?
A. Hyperplasia
B. Hypertrophy
C. Atrophy
D. Metaplasia
Rationale: Hypertrophy is an increase in the size of individual cells, leading to an enlarged organ
(e.g., cardiac muscle in hypertension). Hyperplasia is an increase in cell number (e.g., endometrial
thickening). Atrophy is cell shrinkage; metaplasia is reversible replacement of one mature cell type with
another (e.g., squamous in bronchial epithelium of smokers).
2. A patient with severe vomiting develops metabolic alkalosis. Which arterial blood gas (ABG) result
supports this diagnosis?
,A. pH 7.30, PaCO₂ 50 mm Hg, HCO₃⁻ 26 mEq/L
B. pH 7.50, PaCO₂ 45 mm Hg, HCO₃⁻ 32 mEq/L
C. pH 7.28, PaCO₂ 30 mm Hg, HCO₃⁻ 18 mEq/L
D. pH 7.40, PaCO₂ 40 mm Hg, HCO₃⁻ 24 mEq/L
Rationale: Metabolic alkalosis is characterized by elevated pH (>7.45) and increased HCO₃⁻ (>26
mEq/L). Vomiting causes loss of gastric acid (HCl), leading to excess bicarbonate. PaCO₂ may be normal
or slightly elevated due to compensatory hypoventilation. Option B matches these values.
3. In acute inflammation, which mediator is primarily responsible for increased vascular permeability?
A. Prostaglandins
B. Histamine
C. Leukotrienes
D. Cytokines
Rationale: Histamine, released by mast cells and basophils, causes immediate vasodilation and
increased capillary permeability, leading to edema and redness. Prostaglandins amplify pain and fever;
leukotrienes sustain inflammation; cytokines (e.g., TNF-α, IL-1) regulate leukocyte recruitment.
4. A patient with chronic kidney disease (CKD) develops hyperkalemia. What ECG change is expected?
A. Prolonged QT interval
B. Peaked T waves
C. U waves
D. ST depression
Rationale: Hyperkalemia initially causes tall, peaked T waves due to accelerated repolarization. As
levels rise, QRS widens, P waves disappear, and ventricular fibrillation may occur. Hypokalemia causes
U waves and flattened T waves. Immediate treatment includes calcium gluconate for cardioprotection.
5. Which genetic disorder is caused by a trisomy of chromosome 21?
A. Turner syndrome
B. Klinefelter syndrome
,C. Down syndrome
D. Cri du chat syndrome
Rationale: Down syndrome (trisomy 21) results from nondisjunction during meiosis, leading to three
copies of chromosome 21. Features include intellectual disability, flat facial profile, and congenital heart
defects. Turner syndrome is 45,X; Klinefelter is 47,XXY; Cri du chat is deletion on chromosome 5p.
6. In atherosclerosis, the primary component of the fatty streak is:
A. Smooth muscle cells
B. Foam cells (lipid-laden macrophages)
C. Platelets
D. Collagen fibers
Rationale: Fatty streaks are the earliest visible lesion in atherosclerosis, composed of macrophages
that have ingested oxidized LDL cholesterol, becoming “foam cells.” Over time, smooth muscle
proliferation, lipid accumulation, and fibrous cap formation lead to advanced plaques that can rupture
and cause thrombosis.
7. A patient with emphysema has destruction of alveolar walls. This leads to:
A. Increased elastic recoil
B. Loss of elastic recoil and air trapping
C. Enhanced gas exchange
D. Decreased residual volume
Rationale: Emphysema involves protease-mediated destruction of alveolar walls, reducing surface
area and elastic recoil. This causes airway collapse during expiration, leading to air trapping, increased
residual volume, and impaired gas exchange. Patients develop a “barrel chest” and use pursed-lip
breathing to maintain airway pressure.
8. In diabetic ketoacidosis (DKA), the primary driver of metabolic acidosis is:
A. Lactic acid accumulation
B. Ketone body production (acetoacetic acid and beta-hydroxybutyric acid)
C. Uric acid buildup
, D. Carbonic acid retention
Rationale: Insulin deficiency in DKA causes lipolysis and ketogenesis. Ketone bodies are strong acids
that lower serum pH, causing anion gap metabolic acidosis. Lactic acidosis occurs in shock; uric acid in
tumor lysis; carbonic acid in respiratory failure. ABG shows low pH, low HCO₃⁻, and compensatory
hyperventilation (low PaCO₂).
9. Which neurotransmitter is deficient in Parkinson’s disease?
A. Acetylcholine
B. Dopamine
C. Serotonin
D. GABA
Rationale: Parkinson’s disease involves degeneration of dopaminergic neurons in the substantia
nigra, leading to dopamine deficiency in the basal ganglia. This disrupts motor control, causing
bradykinesia, rigidity, and resting tremor. Acetylcholine becomes relatively excessive, contributing to
symptoms.
10. Osteoporosis is characterized by:
A. Increased bone density
B. Decreased bone mass and microarchitectural deterioration
C. Excessive bone formation
D. Inflammation of joint synovium
Rationale: Osteoporosis results from imbalance between osteoclast (bone resorption) and osteoblast
(bone formation) activity, leading to reduced bone mineral density and increased fracture risk (e.g., hip,
spine). It is distinct from osteoarthritis (joint degeneration) or rheumatoid arthritis (autoimmune
synovitis).
11. During the proliferative phase of wound healing, which process dominates?
A. Vasodilation
B. Fibroblast proliferation and collagen deposition
C. Neutrophil infiltration
D. Clot formation
Portage Learning NURS 231: Pathophysiology Comprehensive Final Examination | Core Domains:
Cellular Injury & Adaptation, Inflammation & Healing, Fluid, Electrolyte & Acid-Base Imbalances,
Genetic Disorders & Neoplasia, Cardiovascular Pathophysiology, Respiratory Pathophysiology, Renal &
Urinary Pathophysiology, Endocrine & Metabolic Pathophysiology, Neurological Pathophysiology, and
Musculoskeletal Pathophysiology | Nursing Program Focus | Comprehensive Pathophysiology Final
Exam Format
Exam Structure
The NURS 231 Pathophysiology Final Exam for the 2026/2027 academic cycle at Portage Learning is a
120-question, multiple-choice question (MCQ) examination.
Introduction
This NURS 231 Pathophysiology Final Exam guide for the 2026/2027 cycle prepares Portage Learning
nursing students for the comprehensive assessment of disease processes across all body systems. The
content emphasizes understanding the mechanisms of cellular and systemic dysfunction, connecting
etiologies to clinical manifestations, and predicting compensatory responses and complications, which
forms the essential scientific foundation for clinical nursing practice.
Answer Format
All correct answers and pathophysiological concepts must be presented in bold and green, followed by
detailed rationales that explain disease mechanisms at the cellular and systemic levels, connect etiologies
to clinical manifestations, and predict compensatory responses and potential complications.
Questions (120 Total)
1. Which cellular adaptation involves an increase in cell size?
A. Hyperplasia
B. Hypertrophy
C. Atrophy
D. Metaplasia
Rationale: Hypertrophy is an increase in the size of individual cells, leading to an enlarged organ
(e.g., cardiac muscle in hypertension). Hyperplasia is an increase in cell number (e.g., endometrial
thickening). Atrophy is cell shrinkage; metaplasia is reversible replacement of one mature cell type with
another (e.g., squamous in bronchial epithelium of smokers).
2. A patient with severe vomiting develops metabolic alkalosis. Which arterial blood gas (ABG) result
supports this diagnosis?
,A. pH 7.30, PaCO₂ 50 mm Hg, HCO₃⁻ 26 mEq/L
B. pH 7.50, PaCO₂ 45 mm Hg, HCO₃⁻ 32 mEq/L
C. pH 7.28, PaCO₂ 30 mm Hg, HCO₃⁻ 18 mEq/L
D. pH 7.40, PaCO₂ 40 mm Hg, HCO₃⁻ 24 mEq/L
Rationale: Metabolic alkalosis is characterized by elevated pH (>7.45) and increased HCO₃⁻ (>26
mEq/L). Vomiting causes loss of gastric acid (HCl), leading to excess bicarbonate. PaCO₂ may be normal
or slightly elevated due to compensatory hypoventilation. Option B matches these values.
3. In acute inflammation, which mediator is primarily responsible for increased vascular permeability?
A. Prostaglandins
B. Histamine
C. Leukotrienes
D. Cytokines
Rationale: Histamine, released by mast cells and basophils, causes immediate vasodilation and
increased capillary permeability, leading to edema and redness. Prostaglandins amplify pain and fever;
leukotrienes sustain inflammation; cytokines (e.g., TNF-α, IL-1) regulate leukocyte recruitment.
4. A patient with chronic kidney disease (CKD) develops hyperkalemia. What ECG change is expected?
A. Prolonged QT interval
B. Peaked T waves
C. U waves
D. ST depression
Rationale: Hyperkalemia initially causes tall, peaked T waves due to accelerated repolarization. As
levels rise, QRS widens, P waves disappear, and ventricular fibrillation may occur. Hypokalemia causes
U waves and flattened T waves. Immediate treatment includes calcium gluconate for cardioprotection.
5. Which genetic disorder is caused by a trisomy of chromosome 21?
A. Turner syndrome
B. Klinefelter syndrome
,C. Down syndrome
D. Cri du chat syndrome
Rationale: Down syndrome (trisomy 21) results from nondisjunction during meiosis, leading to three
copies of chromosome 21. Features include intellectual disability, flat facial profile, and congenital heart
defects. Turner syndrome is 45,X; Klinefelter is 47,XXY; Cri du chat is deletion on chromosome 5p.
6. In atherosclerosis, the primary component of the fatty streak is:
A. Smooth muscle cells
B. Foam cells (lipid-laden macrophages)
C. Platelets
D. Collagen fibers
Rationale: Fatty streaks are the earliest visible lesion in atherosclerosis, composed of macrophages
that have ingested oxidized LDL cholesterol, becoming “foam cells.” Over time, smooth muscle
proliferation, lipid accumulation, and fibrous cap formation lead to advanced plaques that can rupture
and cause thrombosis.
7. A patient with emphysema has destruction of alveolar walls. This leads to:
A. Increased elastic recoil
B. Loss of elastic recoil and air trapping
C. Enhanced gas exchange
D. Decreased residual volume
Rationale: Emphysema involves protease-mediated destruction of alveolar walls, reducing surface
area and elastic recoil. This causes airway collapse during expiration, leading to air trapping, increased
residual volume, and impaired gas exchange. Patients develop a “barrel chest” and use pursed-lip
breathing to maintain airway pressure.
8. In diabetic ketoacidosis (DKA), the primary driver of metabolic acidosis is:
A. Lactic acid accumulation
B. Ketone body production (acetoacetic acid and beta-hydroxybutyric acid)
C. Uric acid buildup
, D. Carbonic acid retention
Rationale: Insulin deficiency in DKA causes lipolysis and ketogenesis. Ketone bodies are strong acids
that lower serum pH, causing anion gap metabolic acidosis. Lactic acidosis occurs in shock; uric acid in
tumor lysis; carbonic acid in respiratory failure. ABG shows low pH, low HCO₃⁻, and compensatory
hyperventilation (low PaCO₂).
9. Which neurotransmitter is deficient in Parkinson’s disease?
A. Acetylcholine
B. Dopamine
C. Serotonin
D. GABA
Rationale: Parkinson’s disease involves degeneration of dopaminergic neurons in the substantia
nigra, leading to dopamine deficiency in the basal ganglia. This disrupts motor control, causing
bradykinesia, rigidity, and resting tremor. Acetylcholine becomes relatively excessive, contributing to
symptoms.
10. Osteoporosis is characterized by:
A. Increased bone density
B. Decreased bone mass and microarchitectural deterioration
C. Excessive bone formation
D. Inflammation of joint synovium
Rationale: Osteoporosis results from imbalance between osteoclast (bone resorption) and osteoblast
(bone formation) activity, leading to reduced bone mineral density and increased fracture risk (e.g., hip,
spine). It is distinct from osteoarthritis (joint degeneration) or rheumatoid arthritis (autoimmune
synovitis).
11. During the proliferative phase of wound healing, which process dominates?
A. Vasodilation
B. Fibroblast proliferation and collagen deposition
C. Neutrophil infiltration
D. Clot formation
