OBJECTIVE ASSESSMENT COMPREHENSIVE EXAMINATION | 200 VERIFIED QUESTIONS & RATIONALES | NEWEST EXAM 2026/2027
WGU D236
PATHOPHYSIOLOGY
WESTERN GOVERNORS UNIVERSITY
200 QUESTIONS PATHO RATIONALES 2026/2027 NEWEST
, EXAM COVERAGE AREAS
Domain 1: Cellular Injury, Immunity & Inflammation
• Cellular injury necrosis apoptosis
• Inflammation acute chronic
• Immunity innate adaptive hypersensitivity
• Genetics
Domain 2: Fluid Electrolyte Acid-Base & Hematology
• Fluid electrolyte Na K Ca
• Acid-base ABG metabolic respiratory
• Hematology anemia coagulation
• Blood
Domain 3: Cardiovascular, Pulmonary & Renal
• Cardiovascular HTN HF MI
• Pulmonary COPD asthma pneumonia
• Renal AKI CKD
• Shock
Domain 4: Endocrine, GI, Neuro & Musculoskeletal
• Endocrine diabetes thyroid
• GI liver pancreatitis
• Neuro stroke seizures
• MSK fractures
Latest OA High Yield 2026/2027
• D236 OA focus cellular immunity fluid acid-base hematology CV pulmonary renal endocrine neuro
• Patho mechanisms
• 200 verified rationales
WGU D236 Pathophysiology 2026/2027 OA 200 Questions Page 2
, QUESTION 1: Necrosis vs apoptosis?
A) Necrosis pathological cell death swelling membrane rupture inflammation, apoptosis programmed
shrinkage fragmentation no inflammation
B) Same
C) Only necrosis
D) Only apoptosis
CORRECT ANSWER: A) Necrosis pathological cell death swelling membrane rupture
inflammation, apoptosis programmed shrinkage fragmentation no inflammation
RATIONALE: Cell injury: necrosis pathological uncontrolled swelling membrane rupture release enzymes
inflammation, apoptosis programmed controlled shrinkage chromatin condensation fragmentation apoptotic
bodies no inflammation normal development. Types coagulative liquefactive caseous fat.
QUESTION 2: Type I hypersensitivity mechanism?
A) IgE mediated mast cell degranulation histamine immediate anaphylaxis
B) IgG
C) T cell
D) Immune complex
CORRECT ANSWER: A) IgE mediated mast cell degranulation histamine immediate
anaphylaxis
RATIONALE: Hypersensitivity: Type I IgE mast cell histamine immediate anaphylaxis allergic rhinitis
asthma. Type II cytotoxic IgG IgM lysis hemolytic transfusion. Type III immune complex deposition serum
sickness. Type IV delayed T cell contact dermatitis TB test.
QUESTION 3: Metabolic acidosis ABG interpretation?
A) pH less than 7.35 HCO3 less than 22, causes DKA lactic renal failure
B) pH high
C) Only respiratory
D) No acidosis
CORRECT ANSWER: A) pH less than 7.35 HCO3 less than 22, causes DKA lactic renal
failure
RATIONALE: Acid-base: pH 7.35-7.45 HCO3 22-26 PaCO2 35-45. Metabolic acidosis pH down HCO3
down causes DKA lactic acidosis renal failure. Metabolic alkalosis pH up HCO3 up vomiting. Respiratory
acidosis pH down PaCO2 up hypoventilation, alkalosis pH up PaCO2 down hyperventilation. Compensation.
QUESTION 4: Heart failure left vs right pathophysiology?
A) Left HF dyspnea crackles pulmonary edema fatigue, right HF peripheral edema JVD hepatomegaly
B) Same
C) Only left
D) Only right
CORRECT ANSWER: A) Left HF dyspnea crackles pulmonary edema fatigue, right HF
peripheral edema JVD hepatomegaly
RATIONALE: HF: left HF unable pump forward pulmonary congestion dyspnea orthopnea crackles
pulmonary edema fatigue low EF. Right HF systemic congestion peripheral edema JVD ascites
hepatomegaly. Compensatory RAAS SNS hypertrophy. NYHA classes. Causes HTN MI CAD.
WGU D236 Pathophysiology 2026/2027 OA 200 Questions Page 3
, QUESTION 5: COPD vs asthma pathophysiology?
A) COPD irreversible airflow obstruction emphysema alveolar destruction chronic bronchitis
productive, asthma reversible bronchospasm inflammation
B) Same
C) Only COPD
D) Only asthma
CORRECT ANSWER: A) COPD irreversible airflow obstruction emphysema alveolar
destruction chronic bronchitis productive, asthma reversible bronchospasm
inflammation
RATIONALE: Pulmonary: COPD irreversible airflow obstruction smoking causes emphysema alveolar wall
destruction loss recoil chronic bronchitis productive cough 3 months 2 years. Asthma reversible
bronchospasm inflammation hyperresponsiveness triggers allergy. Spirometry FEV1/FVC less than 70%
COPD.
QUESTION 6: DKA pathophysiology?
A) Absolute insulin deficiency hyperglycemia ketosis acidosis pH down HCO3 down ketones positive
B) No ketosis
C) Only hyperglycemia
D) Only type 2
CORRECT ANSWER: A) Absolute insulin deficiency hyperglycemia ketosis acidosis pH
down HCO3 down ketones positive
RATIONALE: Diabetes: Type 1 absolute insulin deficiency autoimmune DKA hyperglycemia ketosis acidosis
dehydration Kussmaul. Type 2 insulin resistance HHS hyperglycemia no ketosis. Patho polyuria polydipsia
polyphagia. Complications retinopathy nephropathy neuropathy.
QUESTION 7: Necrosis vs apoptosis?
A) Necrosis pathological cell death swelling membrane rupture inflammation, apoptosis programmed
shrinkage fragmentation no inflammation
B) Same
C) Only necrosis
D) Only apoptosis
CORRECT ANSWER: A) Necrosis pathological cell death swelling membrane rupture
inflammation, apoptosis programmed shrinkage fragmentation no inflammation
RATIONALE: Cell injury: necrosis pathological uncontrolled swelling membrane rupture release enzymes
inflammation, apoptosis programmed controlled shrinkage chromatin condensation fragmentation apoptotic
bodies no inflammation normal development. Types coagulative liquefactive caseous fat.
QUESTION 8: Type I hypersensitivity mechanism?
A) IgE mediated mast cell degranulation histamine immediate anaphylaxis
B) IgG
C) T cell
D) Immune complex
WGU D236 Pathophysiology 2026/2027 OA 200 Questions Page 4
WGU D236
PATHOPHYSIOLOGY
WESTERN GOVERNORS UNIVERSITY
200 QUESTIONS PATHO RATIONALES 2026/2027 NEWEST
, EXAM COVERAGE AREAS
Domain 1: Cellular Injury, Immunity & Inflammation
• Cellular injury necrosis apoptosis
• Inflammation acute chronic
• Immunity innate adaptive hypersensitivity
• Genetics
Domain 2: Fluid Electrolyte Acid-Base & Hematology
• Fluid electrolyte Na K Ca
• Acid-base ABG metabolic respiratory
• Hematology anemia coagulation
• Blood
Domain 3: Cardiovascular, Pulmonary & Renal
• Cardiovascular HTN HF MI
• Pulmonary COPD asthma pneumonia
• Renal AKI CKD
• Shock
Domain 4: Endocrine, GI, Neuro & Musculoskeletal
• Endocrine diabetes thyroid
• GI liver pancreatitis
• Neuro stroke seizures
• MSK fractures
Latest OA High Yield 2026/2027
• D236 OA focus cellular immunity fluid acid-base hematology CV pulmonary renal endocrine neuro
• Patho mechanisms
• 200 verified rationales
WGU D236 Pathophysiology 2026/2027 OA 200 Questions Page 2
, QUESTION 1: Necrosis vs apoptosis?
A) Necrosis pathological cell death swelling membrane rupture inflammation, apoptosis programmed
shrinkage fragmentation no inflammation
B) Same
C) Only necrosis
D) Only apoptosis
CORRECT ANSWER: A) Necrosis pathological cell death swelling membrane rupture
inflammation, apoptosis programmed shrinkage fragmentation no inflammation
RATIONALE: Cell injury: necrosis pathological uncontrolled swelling membrane rupture release enzymes
inflammation, apoptosis programmed controlled shrinkage chromatin condensation fragmentation apoptotic
bodies no inflammation normal development. Types coagulative liquefactive caseous fat.
QUESTION 2: Type I hypersensitivity mechanism?
A) IgE mediated mast cell degranulation histamine immediate anaphylaxis
B) IgG
C) T cell
D) Immune complex
CORRECT ANSWER: A) IgE mediated mast cell degranulation histamine immediate
anaphylaxis
RATIONALE: Hypersensitivity: Type I IgE mast cell histamine immediate anaphylaxis allergic rhinitis
asthma. Type II cytotoxic IgG IgM lysis hemolytic transfusion. Type III immune complex deposition serum
sickness. Type IV delayed T cell contact dermatitis TB test.
QUESTION 3: Metabolic acidosis ABG interpretation?
A) pH less than 7.35 HCO3 less than 22, causes DKA lactic renal failure
B) pH high
C) Only respiratory
D) No acidosis
CORRECT ANSWER: A) pH less than 7.35 HCO3 less than 22, causes DKA lactic renal
failure
RATIONALE: Acid-base: pH 7.35-7.45 HCO3 22-26 PaCO2 35-45. Metabolic acidosis pH down HCO3
down causes DKA lactic acidosis renal failure. Metabolic alkalosis pH up HCO3 up vomiting. Respiratory
acidosis pH down PaCO2 up hypoventilation, alkalosis pH up PaCO2 down hyperventilation. Compensation.
QUESTION 4: Heart failure left vs right pathophysiology?
A) Left HF dyspnea crackles pulmonary edema fatigue, right HF peripheral edema JVD hepatomegaly
B) Same
C) Only left
D) Only right
CORRECT ANSWER: A) Left HF dyspnea crackles pulmonary edema fatigue, right HF
peripheral edema JVD hepatomegaly
RATIONALE: HF: left HF unable pump forward pulmonary congestion dyspnea orthopnea crackles
pulmonary edema fatigue low EF. Right HF systemic congestion peripheral edema JVD ascites
hepatomegaly. Compensatory RAAS SNS hypertrophy. NYHA classes. Causes HTN MI CAD.
WGU D236 Pathophysiology 2026/2027 OA 200 Questions Page 3
, QUESTION 5: COPD vs asthma pathophysiology?
A) COPD irreversible airflow obstruction emphysema alveolar destruction chronic bronchitis
productive, asthma reversible bronchospasm inflammation
B) Same
C) Only COPD
D) Only asthma
CORRECT ANSWER: A) COPD irreversible airflow obstruction emphysema alveolar
destruction chronic bronchitis productive, asthma reversible bronchospasm
inflammation
RATIONALE: Pulmonary: COPD irreversible airflow obstruction smoking causes emphysema alveolar wall
destruction loss recoil chronic bronchitis productive cough 3 months 2 years. Asthma reversible
bronchospasm inflammation hyperresponsiveness triggers allergy. Spirometry FEV1/FVC less than 70%
COPD.
QUESTION 6: DKA pathophysiology?
A) Absolute insulin deficiency hyperglycemia ketosis acidosis pH down HCO3 down ketones positive
B) No ketosis
C) Only hyperglycemia
D) Only type 2
CORRECT ANSWER: A) Absolute insulin deficiency hyperglycemia ketosis acidosis pH
down HCO3 down ketones positive
RATIONALE: Diabetes: Type 1 absolute insulin deficiency autoimmune DKA hyperglycemia ketosis acidosis
dehydration Kussmaul. Type 2 insulin resistance HHS hyperglycemia no ketosis. Patho polyuria polydipsia
polyphagia. Complications retinopathy nephropathy neuropathy.
QUESTION 7: Necrosis vs apoptosis?
A) Necrosis pathological cell death swelling membrane rupture inflammation, apoptosis programmed
shrinkage fragmentation no inflammation
B) Same
C) Only necrosis
D) Only apoptosis
CORRECT ANSWER: A) Necrosis pathological cell death swelling membrane rupture
inflammation, apoptosis programmed shrinkage fragmentation no inflammation
RATIONALE: Cell injury: necrosis pathological uncontrolled swelling membrane rupture release enzymes
inflammation, apoptosis programmed controlled shrinkage chromatin condensation fragmentation apoptotic
bodies no inflammation normal development. Types coagulative liquefactive caseous fat.
QUESTION 8: Type I hypersensitivity mechanism?
A) IgE mediated mast cell degranulation histamine immediate anaphylaxis
B) IgG
C) T cell
D) Immune complex
WGU D236 Pathophysiology 2026/2027 OA 200 Questions Page 4
