WGU D115 Advanced
Pathophysiology OA Exam
2025/2026 – Complete Exam
Questions and answers
1. A patient presents with cellular atrophy in the skeletal muscles after
prolonged immobilization. Which cellular process primarily explains this
finding?
A) Increased protein synthesis and cell proliferation
B) Decreased protein synthesis and increased proteolysis via the ubiquitin-
proteasome pathway
C) Increased mitochondrial biogenesis
D) Accumulation of intracellular lipids
,,,,answer,,,,: B
Rationale: Atrophy is characterized by a reduction in cell size due to decreased
protein synthesis and increased protein degradation, often mediated by the
ubiquitin-proteasome system. This occurs when cells are underused or have
reduced metabolic demands.
2. Which of the following best describes the mechanism of cellular injury in
ischemia-reperfusion injury?
A) Decreased production of reactive oxygen species upon reperfusion
B) Restoration of blood flow leads to increased oxidative stress, calcium overload,
and inflammation
C) Permanent vasodilation preventing further injury
D) Immediate restoration of ATP levels with no tissue damage
,,,,,answer,,,,: B
Rationale: Reperfusion of ischemic tissues paradoxically worsens injury through
production of reactive oxygen species (ROS), calcium influx, opening of
mitochondrial permeability transition pores, and recruitment of inflammatory cells.
3. A mutation in the TP53 tumor suppressor gene can lead to cancer because
p53 normally:
A) Stimulates cell division and angiogenesis
B) Repairs double-strand breaks without error
C) Halts the cell cycle at the G1/S checkpoint to allow DNA repair or triggers
apoptosis
D) Activates oncogenes
,,,,answer,,,,: C
Rationale: p53 is a guardian of the genome; it arrests the cell cycle for DNA repair
or induces apoptosis if damage is irreparable. Loss of p53 function allows cells
with damaged DNA to proliferate.
4. Which of the following is an example of a Type II hypersensitivity reaction?
A) Anaphylaxis to bee venom
B) Serum sickness from antitoxins
C) Autoimmune hemolytic anemia
D) Contact dermatitis from poison ivy
,,,,answer,,,,: C
Rationale: Type II hypersensitivity involves IgG or IgM antibodies directed against
cell surface or extracellular matrix antigens, leading to cell lysis or phagocytosis.
Autoimmune hemolytic anemia (antibodies against red blood cells) is a classic
example. Type I is IgE-mediated; Type III is immune complex deposition; Type IV is
T-cell mediated.
5. In systemic lupus erythematosus (SLE), which of the following is a
characteristic immunologic finding?
A) Decreased complement levels (C3, C4) and anti-dsDNA antibodies
,B) Increased complement levels and rheumatoid factor
C) Anti-centromere antibodies and normal complement
D) Anti-mitochondrial antibodies and elevated IgM
,,,,answer,,,,: A
Rationale: Active SLE often presents with low complement levels due to
consumption by immune complexes and the presence of anti-double-stranded
DNA (anti-dsDNA) antibodies, which are specific for SLE.
6. A patient with chronic hypertension develops left ventricular hypertrophy.
This cellular adaptation is best described as:
A) Hyperplasia
B) Metaplasia
C) Hypertrophy
D) Atrophy
,,,,answer,,,,: C
Rationale: Hypertrophy is an increase in cell size (not number) due to increased
workload. In hypertension, the left ventricle works against increased afterload,
leading to myocyte hypertrophy.
7. Which cytokine is the primary mediator of fever by acting on the
hypothalamus?
A) Interleukin-10 (IL-10)
B) Tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1)
C) Interferon-gamma (IFN-γ)
D) Transforming growth factor-beta (TGF-β)
,,,,answer,,,,: B
Rationale: IL-1 and TNF-α are endogenous pyrogens that stimulate the production
of prostaglandin E2 in the hypothalamus, raising the thermal set point and causing
fever.
8. A patient with chronic renal failure has a normocytic, normochromic anemia.
The primary pathophysiologic mechanism is:
, A) Iron deficiency due to chronic blood loss
B) Decreased production of erythropoietin by the kidneys
C) Hemolysis due to uremic toxins
D) Vitamin B12 deficiency
,,,,answer,,,,: B
Rationale: The kidneys produce erythropoietin in response to hypoxia. In renal
failure, erythropoietin production decreases, leading to anemia of chronic disease
with normocytic, normochromic indices.
9. Which of the following characterizes the pathophysiology of acute
respiratory distress syndrome (ARDS)?
A) Bronchoconstriction and mucus plugging
B) Diffuse alveolar damage with increased capillary permeability and
noncardiogenic pulmonary edema
C) Chronic inflammation and fibrosis of the bronchial walls
D) Granulomatous inflammation with caseating necrosis
,,,,answer,,,,: B
Rationale: ARDS is a form of acute lung injury caused by direct or indirect insults,
leading to diffuse alveolar damage, increased permeability of the alveolar-capillary
barrier, and protein-rich pulmonary edema, often refractory to oxygen therapy.
10. In the pathogenesis of atherosclerosis, which of the following is an early
event?
A) Endothelial dysfunction and accumulation of oxidized LDL in the arterial intima
B) Calcification of the vessel wall
C) Rupture of the fibrous cap
D) Thrombosis without underlying plaque
,,,,answer,,,,: A
Rationale: Atherosclerosis begins with endothelial injury/dysfunction, which
increases permeability to LDL. Oxidized LDL is taken up by macrophages, forming
foam cells and fatty streaks.
Pathophysiology OA Exam
2025/2026 – Complete Exam
Questions and answers
1. A patient presents with cellular atrophy in the skeletal muscles after
prolonged immobilization. Which cellular process primarily explains this
finding?
A) Increased protein synthesis and cell proliferation
B) Decreased protein synthesis and increased proteolysis via the ubiquitin-
proteasome pathway
C) Increased mitochondrial biogenesis
D) Accumulation of intracellular lipids
,,,,answer,,,,: B
Rationale: Atrophy is characterized by a reduction in cell size due to decreased
protein synthesis and increased protein degradation, often mediated by the
ubiquitin-proteasome system. This occurs when cells are underused or have
reduced metabolic demands.
2. Which of the following best describes the mechanism of cellular injury in
ischemia-reperfusion injury?
A) Decreased production of reactive oxygen species upon reperfusion
B) Restoration of blood flow leads to increased oxidative stress, calcium overload,
and inflammation
C) Permanent vasodilation preventing further injury
D) Immediate restoration of ATP levels with no tissue damage
,,,,,answer,,,,: B
Rationale: Reperfusion of ischemic tissues paradoxically worsens injury through
production of reactive oxygen species (ROS), calcium influx, opening of
mitochondrial permeability transition pores, and recruitment of inflammatory cells.
3. A mutation in the TP53 tumor suppressor gene can lead to cancer because
p53 normally:
A) Stimulates cell division and angiogenesis
B) Repairs double-strand breaks without error
C) Halts the cell cycle at the G1/S checkpoint to allow DNA repair or triggers
apoptosis
D) Activates oncogenes
,,,,answer,,,,: C
Rationale: p53 is a guardian of the genome; it arrests the cell cycle for DNA repair
or induces apoptosis if damage is irreparable. Loss of p53 function allows cells
with damaged DNA to proliferate.
4. Which of the following is an example of a Type II hypersensitivity reaction?
A) Anaphylaxis to bee venom
B) Serum sickness from antitoxins
C) Autoimmune hemolytic anemia
D) Contact dermatitis from poison ivy
,,,,answer,,,,: C
Rationale: Type II hypersensitivity involves IgG or IgM antibodies directed against
cell surface or extracellular matrix antigens, leading to cell lysis or phagocytosis.
Autoimmune hemolytic anemia (antibodies against red blood cells) is a classic
example. Type I is IgE-mediated; Type III is immune complex deposition; Type IV is
T-cell mediated.
5. In systemic lupus erythematosus (SLE), which of the following is a
characteristic immunologic finding?
A) Decreased complement levels (C3, C4) and anti-dsDNA antibodies
,B) Increased complement levels and rheumatoid factor
C) Anti-centromere antibodies and normal complement
D) Anti-mitochondrial antibodies and elevated IgM
,,,,answer,,,,: A
Rationale: Active SLE often presents with low complement levels due to
consumption by immune complexes and the presence of anti-double-stranded
DNA (anti-dsDNA) antibodies, which are specific for SLE.
6. A patient with chronic hypertension develops left ventricular hypertrophy.
This cellular adaptation is best described as:
A) Hyperplasia
B) Metaplasia
C) Hypertrophy
D) Atrophy
,,,,answer,,,,: C
Rationale: Hypertrophy is an increase in cell size (not number) due to increased
workload. In hypertension, the left ventricle works against increased afterload,
leading to myocyte hypertrophy.
7. Which cytokine is the primary mediator of fever by acting on the
hypothalamus?
A) Interleukin-10 (IL-10)
B) Tumor necrosis factor-alpha (TNF-α) and interleukin-1 (IL-1)
C) Interferon-gamma (IFN-γ)
D) Transforming growth factor-beta (TGF-β)
,,,,answer,,,,: B
Rationale: IL-1 and TNF-α are endogenous pyrogens that stimulate the production
of prostaglandin E2 in the hypothalamus, raising the thermal set point and causing
fever.
8. A patient with chronic renal failure has a normocytic, normochromic anemia.
The primary pathophysiologic mechanism is:
, A) Iron deficiency due to chronic blood loss
B) Decreased production of erythropoietin by the kidneys
C) Hemolysis due to uremic toxins
D) Vitamin B12 deficiency
,,,,answer,,,,: B
Rationale: The kidneys produce erythropoietin in response to hypoxia. In renal
failure, erythropoietin production decreases, leading to anemia of chronic disease
with normocytic, normochromic indices.
9. Which of the following characterizes the pathophysiology of acute
respiratory distress syndrome (ARDS)?
A) Bronchoconstriction and mucus plugging
B) Diffuse alveolar damage with increased capillary permeability and
noncardiogenic pulmonary edema
C) Chronic inflammation and fibrosis of the bronchial walls
D) Granulomatous inflammation with caseating necrosis
,,,,answer,,,,: B
Rationale: ARDS is a form of acute lung injury caused by direct or indirect insults,
leading to diffuse alveolar damage, increased permeability of the alveolar-capillary
barrier, and protein-rich pulmonary edema, often refractory to oxygen therapy.
10. In the pathogenesis of atherosclerosis, which of the following is an early
event?
A) Endothelial dysfunction and accumulation of oxidized LDL in the arterial intima
B) Calcification of the vessel wall
C) Rupture of the fibrous cap
D) Thrombosis without underlying plaque
,,,,answer,,,,: A
Rationale: Atherosclerosis begins with endothelial injury/dysfunction, which
increases permeability to LDL. Oxidized LDL is taken up by macrophages, forming
foam cells and fatty streaks.
