CHAMBERLAIN NR507 MIDTERM EXAM (2026/2027) | CERTIFIED EXAM QUESTIONS
AND ANSWERS
Chamberlain University NR507: Advanced Pathophysiology - Midterm Examination | Core Domains:
Cellular Adaptation, Injury & Death, Fluid, Electrolyte & Acid-Base Imbalances, Inflammation,
Infection & Immunity, Genetic Disorders & Neoplasia, Cardiovascular Pathophysiology, Respiratory
Pathophysiology, and Renal & Urological Pathophysiology | Advanced Nursing Program Focus |
Comprehensive Midterm Exam Format
Exam Structure
The Chamberlain NR507 Midterm Exam for the 2026/2027 academic cycle is a 125-question,
multiple-choice question (MCQ) examination.
Introduction
This Chamberlain NR507 Midterm Exam guide for the 2026/2027 cycle prepares advanced nursing
students for the comprehensive assessment of foundational and intermediate pathophysiological
principles. The content emphasizes understanding disease mechanisms at cellular and systemic levels,
focusing on alterations in homeostasis, immune responses, genetic factors, and the pathophysiology of
key body systems essential for diagnostic reasoning and therapeutic intervention.
Answer Format
All correct answers and pathophysiological concepts must be presented in bold and green, followed by
detailed rationales that explain cellular injury mechanisms (e.g., hypoxia, free radicals), differentiate
types of inflammation and immune responses, analyze genetic and neoplastic disease processes, and
connect systemic pathophysiology (cardiovascular, respiratory, renal) to clinical manifestations and
compensatory mechanisms.
Questions (125 Total)
1. A patient with chronic hypoxia due to COPD develops clubbing of the fingers. This is an example of:
A. Dysplasia
B. Adaptive change (hypertrophy/hyperplasia response to chronic hypoxia)
C. Necrosis
D. Apoptosis
Rationale: Clubbing is a chronic adaptive response to long-term hypoxia, involving soft tissue
proliferation at the nail beds. It is not dysplasia (abnormal cell growth) or cell death
(necrosis/apoptosis). It reflects the body’s attempt to increase capillary density and oxygen delivery.
,2. A patient has a serum sodium of 128 mEq/L, headache, and confusion. What type of fluid imbalance is
present?
A. Hypernatremia
B. Hyponatremia
C. Hypokalemia
D. Hypercalcemia
Rationale: Normal sodium is 135–145 mEq/L. Hyponatremia (<135) causes water to shift into brain
cells, leading to cerebral edema, headache, confusion, and seizures. Common causes include SIADH,
diuretics, or heart failure.
3. A patient with diabetic ketoacidosis (DKA) has Kussmaul respirations. This is a compensatory
mechanism for:
A. Metabolic alkalosis
B. Metabolic acidosis
C. Respiratory acidosis
D. Respiratory alkalosis
Rationale: DKA produces ketoacids, causing metabolic acidosis. The lungs compensate by increasing
respiratory rate and depth (Kussmaul breathing) to blow off CO₂, lowering PaCO₂ and partially
correcting pH.
4. Which type of necrosis is typically seen in tuberculosis?
A. Coagulative
B. Caseous
C. Liquefactive
D. Fat
Rationale: Caseous necrosis ("cheese-like") is characteristic of granulomatous infections like TB. It
combines features of coagulative and liquefactive necrosis, forming soft, friable, white debris within
granulomas.
5. A patient with HIV has a CD4+ count of 180 cells/μL. This places them at high risk for:
,A. Allergic rhinitis
B. Pneumocystis jirovecii pneumonia (PCP)
C. Common cold
D. Seasonal influenza
Rationale: CD4+ counts <200 cells/μL indicate severe immunosuppression and AIDS diagnosis. PCP is
an opportunistic infection that commonly occurs when CD4+ drops below 200. Prophylaxis with
TMP-SMX is standard.
6. Down syndrome is caused by:
A. Deletion on chromosome 5
B. Trisomy 21
C. Monosomy X
D. Trisomy 18
Rationale: Down syndrome results from trisomy 21 (three copies of chromosome 21), usually due to
nondisjunction during meiosis. Features include intellectual disability, flat facial profile, and congenital
heart defects.
7. A patient with heart failure has jugular venous distension (JVD) and peripheral edema. This is
primarily due to:
A. Decreased preload
B. Increased hydrostatic pressure from fluid overload
C. Hypoalbuminemia
D. Lymphatic obstruction
Rationale: In heart failure, poor cardiac output leads to fluid retention and increased venous pressure.
This raises hydrostatic pressure in capillaries, forcing fluid into interstitial spaces—causing JVD and
pitting edema.
8. A patient with COPD has an ABG: pH 7.36, PaCO₂ 58 mm Hg, HCO₃⁻ 32 mEq/L. This indicates:
A. Acute respiratory acidosis
B. Chronic respiratory acidosis with renal compensation
, C. Metabolic alkalosis
D. Normal ABG
Rationale: Elevated PaCO₂ with normal pH and elevated HCO₃⁻ indicates chronic respiratory acidosis.
The kidneys compensate by retaining bicarbonate over days. This is typical in stable COPD patients.
9. Acute tubular necrosis (ATN) is most commonly caused by:
A. Glomerulonephritis
B. Ischemia or nephrotoxins
C. Urinary tract infection
D. Autoimmune disease
Rationale: ATN—the most common cause of intrinsic acute kidney injury—results from prolonged
renal hypoperfusion (e.g., shock) or exposure to nephrotoxins (e.g., aminoglycosides, contrast dye). It
causes oliguria and “muddy brown casts” in urine sediment.
10. A patient with systemic lupus erythematosus (SLE) develops a malar rash and joint pain. This is due
to:
A. Bacterial infection
B. Type III hypersensitivity (immune complex deposition)
C. Type I allergy
D. Viral reactivation
Rationale: SLE is a classic Type III hypersensitivity disorder where autoantibodies form immune
complexes that deposit in tissues (skin, joints, kidneys), triggering inflammation and damage via
complement activation.
11. The primary mediator of fever during acute inflammation is:
A. Histamine
B. Interleukin-1 (IL-1) and prostaglandin E2 (PGE2)
C. Bradykinin
D. Complement C3a
AND ANSWERS
Chamberlain University NR507: Advanced Pathophysiology - Midterm Examination | Core Domains:
Cellular Adaptation, Injury & Death, Fluid, Electrolyte & Acid-Base Imbalances, Inflammation,
Infection & Immunity, Genetic Disorders & Neoplasia, Cardiovascular Pathophysiology, Respiratory
Pathophysiology, and Renal & Urological Pathophysiology | Advanced Nursing Program Focus |
Comprehensive Midterm Exam Format
Exam Structure
The Chamberlain NR507 Midterm Exam for the 2026/2027 academic cycle is a 125-question,
multiple-choice question (MCQ) examination.
Introduction
This Chamberlain NR507 Midterm Exam guide for the 2026/2027 cycle prepares advanced nursing
students for the comprehensive assessment of foundational and intermediate pathophysiological
principles. The content emphasizes understanding disease mechanisms at cellular and systemic levels,
focusing on alterations in homeostasis, immune responses, genetic factors, and the pathophysiology of
key body systems essential for diagnostic reasoning and therapeutic intervention.
Answer Format
All correct answers and pathophysiological concepts must be presented in bold and green, followed by
detailed rationales that explain cellular injury mechanisms (e.g., hypoxia, free radicals), differentiate
types of inflammation and immune responses, analyze genetic and neoplastic disease processes, and
connect systemic pathophysiology (cardiovascular, respiratory, renal) to clinical manifestations and
compensatory mechanisms.
Questions (125 Total)
1. A patient with chronic hypoxia due to COPD develops clubbing of the fingers. This is an example of:
A. Dysplasia
B. Adaptive change (hypertrophy/hyperplasia response to chronic hypoxia)
C. Necrosis
D. Apoptosis
Rationale: Clubbing is a chronic adaptive response to long-term hypoxia, involving soft tissue
proliferation at the nail beds. It is not dysplasia (abnormal cell growth) or cell death
(necrosis/apoptosis). It reflects the body’s attempt to increase capillary density and oxygen delivery.
,2. A patient has a serum sodium of 128 mEq/L, headache, and confusion. What type of fluid imbalance is
present?
A. Hypernatremia
B. Hyponatremia
C. Hypokalemia
D. Hypercalcemia
Rationale: Normal sodium is 135–145 mEq/L. Hyponatremia (<135) causes water to shift into brain
cells, leading to cerebral edema, headache, confusion, and seizures. Common causes include SIADH,
diuretics, or heart failure.
3. A patient with diabetic ketoacidosis (DKA) has Kussmaul respirations. This is a compensatory
mechanism for:
A. Metabolic alkalosis
B. Metabolic acidosis
C. Respiratory acidosis
D. Respiratory alkalosis
Rationale: DKA produces ketoacids, causing metabolic acidosis. The lungs compensate by increasing
respiratory rate and depth (Kussmaul breathing) to blow off CO₂, lowering PaCO₂ and partially
correcting pH.
4. Which type of necrosis is typically seen in tuberculosis?
A. Coagulative
B. Caseous
C. Liquefactive
D. Fat
Rationale: Caseous necrosis ("cheese-like") is characteristic of granulomatous infections like TB. It
combines features of coagulative and liquefactive necrosis, forming soft, friable, white debris within
granulomas.
5. A patient with HIV has a CD4+ count of 180 cells/μL. This places them at high risk for:
,A. Allergic rhinitis
B. Pneumocystis jirovecii pneumonia (PCP)
C. Common cold
D. Seasonal influenza
Rationale: CD4+ counts <200 cells/μL indicate severe immunosuppression and AIDS diagnosis. PCP is
an opportunistic infection that commonly occurs when CD4+ drops below 200. Prophylaxis with
TMP-SMX is standard.
6. Down syndrome is caused by:
A. Deletion on chromosome 5
B. Trisomy 21
C. Monosomy X
D. Trisomy 18
Rationale: Down syndrome results from trisomy 21 (three copies of chromosome 21), usually due to
nondisjunction during meiosis. Features include intellectual disability, flat facial profile, and congenital
heart defects.
7. A patient with heart failure has jugular venous distension (JVD) and peripheral edema. This is
primarily due to:
A. Decreased preload
B. Increased hydrostatic pressure from fluid overload
C. Hypoalbuminemia
D. Lymphatic obstruction
Rationale: In heart failure, poor cardiac output leads to fluid retention and increased venous pressure.
This raises hydrostatic pressure in capillaries, forcing fluid into interstitial spaces—causing JVD and
pitting edema.
8. A patient with COPD has an ABG: pH 7.36, PaCO₂ 58 mm Hg, HCO₃⁻ 32 mEq/L. This indicates:
A. Acute respiratory acidosis
B. Chronic respiratory acidosis with renal compensation
, C. Metabolic alkalosis
D. Normal ABG
Rationale: Elevated PaCO₂ with normal pH and elevated HCO₃⁻ indicates chronic respiratory acidosis.
The kidneys compensate by retaining bicarbonate over days. This is typical in stable COPD patients.
9. Acute tubular necrosis (ATN) is most commonly caused by:
A. Glomerulonephritis
B. Ischemia or nephrotoxins
C. Urinary tract infection
D. Autoimmune disease
Rationale: ATN—the most common cause of intrinsic acute kidney injury—results from prolonged
renal hypoperfusion (e.g., shock) or exposure to nephrotoxins (e.g., aminoglycosides, contrast dye). It
causes oliguria and “muddy brown casts” in urine sediment.
10. A patient with systemic lupus erythematosus (SLE) develops a malar rash and joint pain. This is due
to:
A. Bacterial infection
B. Type III hypersensitivity (immune complex deposition)
C. Type I allergy
D. Viral reactivation
Rationale: SLE is a classic Type III hypersensitivity disorder where autoantibodies form immune
complexes that deposit in tissues (skin, joints, kidneys), triggering inflammation and damage via
complement activation.
11. The primary mediator of fever during acute inflammation is:
A. Histamine
B. Interleukin-1 (IL-1) and prostaglandin E2 (PGE2)
C. Bradykinin
D. Complement C3a
