1
NR 507 Advanced Pathophysiology Midterm Exam –
Chamberlain – 2025/2026 Latest Update with Verified
Questions and 100% Correct Answers
SECTION 1: CELLULAR INJURY, ADAPTATION & NEOPLASIA
1. The irreversible marker of cell death on electron microscopy is:
A. Cellular swelling
B. Nuclear pyknosis
C. Mitochondrial amorphous (flocculent) densities
D. Membrane blebbing
Correct Answer-: C. Mitochondrial amorphous (flocculent) densities
Rationale: Flocculent densities in the mitochondrial matrix are an irreversible marker of cell death,
indicating severe membrane damage. This is the "point of no return" where cell death is inevitable even
if the stressor is removed .
2. What is the earliest reversible morphologic sign of cell injury?
A. Nuclear fragmentation
B. Cellular swelling (hydropic change)
C. Karyolysis
D. Fatty change
Correct Answer-: B. Cellular swelling (hydropic change)
Rationale: Cellular swelling is the earliest reversible sign of cell injury, caused by ATP depletion leading
to failure of the Na⁺/K⁺ pump and subsequent water influx. This is followed by fatty change in some
organs .
3. The process where a normal cell becomes a cancer cell is called:
A. Metaplasia
B. Dysplasia
C. Cell transformation
D. Anaplasia
Correct Answer-: C. Cell transformation
Rationale: Cell transformation is the process by which a normal cell acquires the characteristics of a
,2
cancer cell. It involves genetic mutations that lead to uncontrolled growth, loss of differentiation, and
the ability to invade and metastasize .
4. Cachexia in cancer patients is primarily mediated by which cytokine?
A. Interleukin-2 (IL-2)
B. Interferon-gamma (IFN-γ)
C. Tumor Necrosis Factor-alpha (TNF-α)
D. Interleukin-10 (IL-10)
Correct Answer-: C. Tumor Necrosis Factor-alpha (TNF-α)
Rationale: TNF-α, formerly called cachectin, is a key mediator of cancer cachexia. It promotes fat and
muscle wasting, anorexia, and systemic inflammation seen in advanced malignancies .
5. The "two-hit hypothesis" applies to which type of genes?
A. Proto-oncogenes
B. Tumor suppressor genes
C. Oncogenes
D. DNA repair genes
Correct Answer-: B. Tumor suppressor genes
Rationale: The two-hit hypothesis states that both alleles of a tumor suppressor gene must be
inactivated (mutated or deleted) for cancer to develop. Examples include the retinoblastoma (Rb) and
p53 genes .
SECTION 2: FLUID, ELECTROLYTE & ACID-BASE BALANCE
6. What is the primary cause of hypokalemia during treatment of diabetic ketoacidosis (DKA)?
A. Vomiting from acidosis
B. Insulin driving potassium into cells
C. Renal loss of potassium
D. Increased aldosterone secretion
Correct Answer-: B. Insulin driving potassium into cells
Rationale: During DKA treatment, insulin administration activates the Na⁺/K⁺-ATPase pump, driving
potassium from the extracellular space into cells. This can cause life-threatening hypokalemia even if
initial potassium levels are normal or elevated .
7. Winter's formula for calculating expected PaCO₂ in metabolic acidosis is:
,3
A. PaCO₂ = (0.5 × HCO₃⁻) + 10
B. PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2
C. PaCO₂ = (HCO₃⁻) + 15
D. PaCO₂ = (2 × HCO₃⁻) – 10
Correct Answer-: B. PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2
Rationale: Winter's formula predicts the appropriate respiratory compensation for primary metabolic
acidosis. If the measured PaCO₂ is higher than calculated, there is a concurrent respiratory acidosis; if
lower, a concurrent respiratory alkalosis .
8. What is the most common cause of hypercalcemia in ambulatory patients?
A. Malignancy
B. Hyperparathyroidism
C. Vitamin D toxicity
D. Sarcoidosis
Correct Answer-: B. Hyperparathyroidism
Rationale: Primary hyperparathyroidism is the leading cause of hypercalcemia in ambulatory
(outpatient) settings. Malignancy is the most common cause in hospitalized patients .
9. Which of the following causes a normal anion gap (hyperchloremic) metabolic acidosis?
A. Diabetic ketoacidosis
B. Lactic acidosis
C. Massive diarrhea
D. Methanol poisoning
Correct Answer-: C. Massive diarrhea
Rationale: Diarrhea causes loss of bicarbonate-rich intestinal fluid, leading to a normal anion gap
metabolic acidosis. Other causes include renal tubular acidosis and certain medications. MUDPILES
conditions cause elevated anion gap acidosis .
SECTION 3: IMMUNITY & HYPERSENSITIVITY REACTIONS
10. Which hypersensitivity reaction is mediated solely by T cells (no antibody involvement)?
A. Type I
B. Type II
C. Type III
D. Type IV
Correct Answer-: D. Type IV
Rationale: Type IV hypersensitivity is a delayed, cell-mediated reaction involving T lymphocytes (Th1,
, 4
Th17, and CTLs) and macrophages. It does not involve antibodies. Examples include contact dermatitis
(poison ivy), tuberculin skin test, and graft rejection .
11. Allergic contact dermatitis (e.g., poison ivy) is an example of which hypersensitivity reaction?
A. Type I
B. Type II
C. Type III
D. Type IV
Correct Answer-: D. Type IV
Rationale: Poison ivy causes a delayed-type hypersensitivity (Type IV) reaction mediated by T cells. The
rash appears 24-72 hours after contact and is localized to the area of exposure, unlike Type I reactions
which are immediate .
12. Hives (urticaria) are an example of which hypersensitivity reaction?
A. Type I
B. Type II
C. Type III
D. Type IV
Correct Answer-: A. Type I
Rationale: Urticaria (hives) is an immediate hypersensitivity reaction (Type I) mediated by IgE and mast
cell degranulation. Histamine release causes vasodilation, increased vascular permeability, and itching .
13. Which laboratory finding would be expected with urticaria?
A. Neutrophilia
B. Lymphocytosis
C. Eosinophilia
D. Monocytosis
Correct Answer-: C. Eosinophilia
Rationale: Eosinophilia is often seen in allergic conditions, including urticaria, due to the release of
eosinophil chemotactic factors from mast cells during Type I hypersensitivity reactions .
14. Anaphylaxis is what type of hypersensitivity reaction, and what is the primary treatment?
A. Type II, antihistamines
B. Type III, corticosteroids
C. Type I, epinephrine
D. Type IV, topical steroids
NR 507 Advanced Pathophysiology Midterm Exam –
Chamberlain – 2025/2026 Latest Update with Verified
Questions and 100% Correct Answers
SECTION 1: CELLULAR INJURY, ADAPTATION & NEOPLASIA
1. The irreversible marker of cell death on electron microscopy is:
A. Cellular swelling
B. Nuclear pyknosis
C. Mitochondrial amorphous (flocculent) densities
D. Membrane blebbing
Correct Answer-: C. Mitochondrial amorphous (flocculent) densities
Rationale: Flocculent densities in the mitochondrial matrix are an irreversible marker of cell death,
indicating severe membrane damage. This is the "point of no return" where cell death is inevitable even
if the stressor is removed .
2. What is the earliest reversible morphologic sign of cell injury?
A. Nuclear fragmentation
B. Cellular swelling (hydropic change)
C. Karyolysis
D. Fatty change
Correct Answer-: B. Cellular swelling (hydropic change)
Rationale: Cellular swelling is the earliest reversible sign of cell injury, caused by ATP depletion leading
to failure of the Na⁺/K⁺ pump and subsequent water influx. This is followed by fatty change in some
organs .
3. The process where a normal cell becomes a cancer cell is called:
A. Metaplasia
B. Dysplasia
C. Cell transformation
D. Anaplasia
Correct Answer-: C. Cell transformation
Rationale: Cell transformation is the process by which a normal cell acquires the characteristics of a
,2
cancer cell. It involves genetic mutations that lead to uncontrolled growth, loss of differentiation, and
the ability to invade and metastasize .
4. Cachexia in cancer patients is primarily mediated by which cytokine?
A. Interleukin-2 (IL-2)
B. Interferon-gamma (IFN-γ)
C. Tumor Necrosis Factor-alpha (TNF-α)
D. Interleukin-10 (IL-10)
Correct Answer-: C. Tumor Necrosis Factor-alpha (TNF-α)
Rationale: TNF-α, formerly called cachectin, is a key mediator of cancer cachexia. It promotes fat and
muscle wasting, anorexia, and systemic inflammation seen in advanced malignancies .
5. The "two-hit hypothesis" applies to which type of genes?
A. Proto-oncogenes
B. Tumor suppressor genes
C. Oncogenes
D. DNA repair genes
Correct Answer-: B. Tumor suppressor genes
Rationale: The two-hit hypothesis states that both alleles of a tumor suppressor gene must be
inactivated (mutated or deleted) for cancer to develop. Examples include the retinoblastoma (Rb) and
p53 genes .
SECTION 2: FLUID, ELECTROLYTE & ACID-BASE BALANCE
6. What is the primary cause of hypokalemia during treatment of diabetic ketoacidosis (DKA)?
A. Vomiting from acidosis
B. Insulin driving potassium into cells
C. Renal loss of potassium
D. Increased aldosterone secretion
Correct Answer-: B. Insulin driving potassium into cells
Rationale: During DKA treatment, insulin administration activates the Na⁺/K⁺-ATPase pump, driving
potassium from the extracellular space into cells. This can cause life-threatening hypokalemia even if
initial potassium levels are normal or elevated .
7. Winter's formula for calculating expected PaCO₂ in metabolic acidosis is:
,3
A. PaCO₂ = (0.5 × HCO₃⁻) + 10
B. PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2
C. PaCO₂ = (HCO₃⁻) + 15
D. PaCO₂ = (2 × HCO₃⁻) – 10
Correct Answer-: B. PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2
Rationale: Winter's formula predicts the appropriate respiratory compensation for primary metabolic
acidosis. If the measured PaCO₂ is higher than calculated, there is a concurrent respiratory acidosis; if
lower, a concurrent respiratory alkalosis .
8. What is the most common cause of hypercalcemia in ambulatory patients?
A. Malignancy
B. Hyperparathyroidism
C. Vitamin D toxicity
D. Sarcoidosis
Correct Answer-: B. Hyperparathyroidism
Rationale: Primary hyperparathyroidism is the leading cause of hypercalcemia in ambulatory
(outpatient) settings. Malignancy is the most common cause in hospitalized patients .
9. Which of the following causes a normal anion gap (hyperchloremic) metabolic acidosis?
A. Diabetic ketoacidosis
B. Lactic acidosis
C. Massive diarrhea
D. Methanol poisoning
Correct Answer-: C. Massive diarrhea
Rationale: Diarrhea causes loss of bicarbonate-rich intestinal fluid, leading to a normal anion gap
metabolic acidosis. Other causes include renal tubular acidosis and certain medications. MUDPILES
conditions cause elevated anion gap acidosis .
SECTION 3: IMMUNITY & HYPERSENSITIVITY REACTIONS
10. Which hypersensitivity reaction is mediated solely by T cells (no antibody involvement)?
A. Type I
B. Type II
C. Type III
D. Type IV
Correct Answer-: D. Type IV
Rationale: Type IV hypersensitivity is a delayed, cell-mediated reaction involving T lymphocytes (Th1,
, 4
Th17, and CTLs) and macrophages. It does not involve antibodies. Examples include contact dermatitis
(poison ivy), tuberculin skin test, and graft rejection .
11. Allergic contact dermatitis (e.g., poison ivy) is an example of which hypersensitivity reaction?
A. Type I
B. Type II
C. Type III
D. Type IV
Correct Answer-: D. Type IV
Rationale: Poison ivy causes a delayed-type hypersensitivity (Type IV) reaction mediated by T cells. The
rash appears 24-72 hours after contact and is localized to the area of exposure, unlike Type I reactions
which are immediate .
12. Hives (urticaria) are an example of which hypersensitivity reaction?
A. Type I
B. Type II
C. Type III
D. Type IV
Correct Answer-: A. Type I
Rationale: Urticaria (hives) is an immediate hypersensitivity reaction (Type I) mediated by IgE and mast
cell degranulation. Histamine release causes vasodilation, increased vascular permeability, and itching .
13. Which laboratory finding would be expected with urticaria?
A. Neutrophilia
B. Lymphocytosis
C. Eosinophilia
D. Monocytosis
Correct Answer-: C. Eosinophilia
Rationale: Eosinophilia is often seen in allergic conditions, including urticaria, due to the release of
eosinophil chemotactic factors from mast cells during Type I hypersensitivity reactions .
14. Anaphylaxis is what type of hypersensitivity reaction, and what is the primary treatment?
A. Type II, antihistamines
B. Type III, corticosteroids
C. Type I, epinephrine
D. Type IV, topical steroids
