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D236 Objective Assessment Study Guide – WGU Pathophysiology OA V2 (2026) Megan/Shay’s & Casey’s Notes | Pass the OA

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Prepare for the WGU D236 Pathophysiology Objective Assessment with this study guide covering key pathophysiology concepts, mechanisms of disease, common disorders, signs and symptoms, and clinical concepts relevant to OA V2. The guide is designed to organize important course material into a focused review resource for students preparing for the 2026 assessment. The material incorporates Megan/Shay’s and Casey’s notes to provide a structured study aid for reviewing major topics and reinforcing core concepts before the OA. Use it alongside your course materials to identify knowledge gaps and focus your final review.

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WESTERN GOVERNORS UNIVERSITY

COURSE D236: PATHOPHYSIOLOGY
OBJECTIVE ASSESSMENT V2


Comprehensive Professional Practice Examination & Study Guide
(100 Questions)



Prepared for Professional Nursing & Healthcare Candidates
Academic Year 2026

, D236 PATHOPHYSIOLOGY OBJECTIVE ASSESSMENT V2 -
100 QUESTION MASTER EXAM

Question 1: A 45-year-old male presents with sudden-onset crushing
chest pain radiating to the left arm and diaphoresis. Lab results
show elevated troponin I and CK-MB. Which cellular mechanism
causes irreversible myocardial cell injury in acute myocardial
infarction?
A) Reversible depletion of intracellular ATP stores
B) Massive influx of extracellular calcium activating intracellular
lytic enzymes
C) Transient mitochondrial swelling due to osmotic imbalance
D) Compensatory glycogenolysis in ischemic myocardial tissue
Answer: B
Rationale: Ischemia leads to ATP depletion, halting Na+/K+-ATPase
and causing calcium influx, which activates destructive intracellular
lytic enzymes.

Question 2: A patient with chronic poorly controlled hypertension
develops left ventricular hypertrophy. Which cellular adaptation
accounts for this thickening?
A) Metaplasia
B) Hyperplasia
C) Hypertrophy
D) Dysplasia
Answer: C
Rationale: Cardiac myocytes have limited mitotic capacity and
respond to increased hemodynamic afterload by increasing protein
synthesis and cell size (hypertrophy).

,Question 3: A 60-year-old female with a 30 pack-year smoking
history has bronchial biopsy showing replacement of ciliated
columnar epithelium with stratified squamous epithelium. This
represents:
A) Hypertrophy
B) Metaplasia
C) Dysplasia
D) Anaplasia
Answer: B
Rationale: Metaplasia is the reversible replacement of one adult cell
type by another adult cell type in response to chronic irritation.

Question 4: A patient with dehydration and acute kidney injury has
ABG: pH 7.31, PaCO2 38 mmHg, HCO3- 18 mEq/L. Which
imbalance is present?
A) Respiratory acidosis with renal compensation
B) Metabolic alkalosis with respiratory compensation
C) Metabolic acidosis with inadequate respiratory compensation
D) Respiratory alkalosis with metabolic compensation
Answer: C
Rationale: Low pH (< 7.35) and low HCO3- (< 22) indicate primary
metabolic acidosis with normal PaCO2 reflecting
inadequate/uncompensated respiratory response.

Question 5: Which clinical manifestation is most characteristic of
acute hypokalemia (serum potassium < 3.5 mEq/L)?
A) Peaked T waves and widened QRS complexes
B) Muscle weakness, lethargy, and U waves on ECG
C) Paresthesias and hyperactive deep tendon reflexes
D) Severe muscle tetany and Chvostek's sign

, Answer: B
Rationale: Hypokalemia hyperpolarizes resting membrane potentials,
causing generalized skeletal muscle weakness and ECG changes
including flattened T waves and prominent U waves.

Question 6: A 52-year-old male has hemoglobin 9.2 g/dL, MCV 70
fL, and decreased serum ferritin. The underlying pathophysiology
is:
A) Defective DNA synthesis due to vitamin B12 deficiency
B) Premature destruction of erythrocytes in hemolytic anemia
C) Depleted iron stores leading to impaired hemoglobin synthesis
D) Bone marrow suppression secondary to chronic renal failure
Answer: C
Rationale: Microcytic hypochromic anemia with low ferritin is
characteristic of iron deficiency anemia, impairing heme synthesis.

Question 7: A patient with type 1 diabetes presents with nausea,
fruity breath, and Kussmaul respirations. Blood glucose is 425
mg/dL and HCO3- is 12 mEq/L. The primary driver of Kussmaul
respirations is:
A) Direct central nervous system stimulation by hyperglycemia
B) Respiratory compensation for metabolic acidosis via elimination
of carbon dioxide
C) Hypoxemia resulting from secondary pulmonary edema
D) Increased sympathetic tone and catecholamine release
Answer: B
Rationale: Kussmaul respirations represent rapid hyperventilation to
eliminate CO2 (carbonic acid) to compensate for severe ketoacidosis.

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