South College NSG 5140 Advanced Pathophysiology Midterm
Exam | Latest Update 2026/2027 | 200 Questions and Verified
Answers | Complete Q&A Guide | A+ Graded
1. A 62yearold male with chronic heart failure presents with worsening dyspnea, jugular venous
distension, and peripheral edema. Which cellular adaptation is most likely occurring in his myocardium
as a compensatory mechanism?
A. Hyperplasia
B. Metaplasia
C. Hypertrophy
D. Dysplasia
Answer: C. Hypertrophy
Explanation: Hypertrophy is an increase in cell size due to increased workload, as seen in heart failure
where myocytes enlarge to compensate for pressure or volume overload. Hyperplasia (increase in cell
number) is not typical in terminally differentiated cardiac muscle. Metaplasia is replacement of one cell
type with another. Dysplasia is disordered cellular growth, often preneoplastic.
2. During ischemia, the switch from aerobic to anaerobic metabolism leads to which immediate
intracellular change?
A. Increased intracellular pH
B. Decreased intracellular sodium
C. Accumulation of lactic acid
D. Increased ATP production
Answer: C. Accumulation of lactic acid
,Explanation: Ischemia causes reduced oxygen supply, forcing cells to shift to anaerobic glycolysis. This
results in lactic acid accumulation, decreased intracellular pH, and reduced ATP production. Sodium
accumulates intracellularly due to Na+/K+ pump failure.
3. In Alzheimer disease, extracellular deposition of which protein is primarily responsible for neuritic
plaque formation?
A. Tau protein
B. Alphasynuclein
C. Betaamyloid
D. Prion protein
Answer: C. Betaamyloid
Explanation: Betaamyloid (Aβ) peptides aggregate into extracellular plaques. Tau protein forms
intracellular neurofibrillary tangles. Alphasynuclein is seen in Parkinson disease. Prion protein causes
spongiform encephalopathies.
4. A 45yearold woman presents with fatigue, pallor, and paresthesias. Laboratory findings show
macrocytic anemia, hypersegmented neutrophils, and low vitamin B12. Which cellular process is most
directly impaired?
A. Heme synthesis
B. Globin chain assembly
C. DNA synthesis
D. Iron transport
Answer: C. DNA synthesis
,Explanation: Vitamin B12 deficiency impairs thymidine synthesis, leading to defective DNA replication
and megaloblastic changes. Heme synthesis is impaired in iron deficiency. Globin defects cause
hemoglobinopathies. Iron transport involves transferrin.
5. A patient develops urticaria, angioedema, and stridor within 10 minutes of penicillin administration.
This reaction is mediated primarily by which immunoglobulin?
A. IgA
B. IgE
C. IgG
D. IgM
Answer: B. IgE
Explanation: Type I hypersensitivity reactions are IgEmediated, causing mast cell degranulation and
release of histamine and other mediators. IgA is mucosal immunity. IgG and IgM are involved in Type II
and III reactions.
6. Which of the following is a hallmark of systemic lupus erythematosus at the cellular level?
A. Deficiency of C1 esterase inhibitor
B. Formation of antinuclear antibodies and immune complexes
C. Selective loss of regulatory T cells
D. Overproduction of IgE
Answer: B. Formation of antinuclear antibodies and immune complexes
Explanation: SLE is a Type III hypersensitivity disorder characterized by autoantibodies (ANA, antidsDNA)
forming immune complexes that deposit in tissues, causing inflammation. C1 esterase inhibitor
, deficiency causes hereditary angioedema. Treg loss is seen in some autoimmune diseases but is not
hallmark. IgE overproduction is atopic.
7. A 68yearold with chronic obstructive pulmonary disease has a PaCO2 of 68 mmHg and pH of 7.31.
Which compensatory mechanism is expected?
A. Increased urinary bicarbonate excretion
B. Increased respiratory rate
C. Increased renal hydrogen ion secretion
D. Decreased renal ammonium excretion
Answer: C. Increased renal hydrogen ion secretion
Explanation: Chronic respiratory acidosis (high PaCO2) is compensated by renal retention of bicarbonate
and increased H+ secretion (as NH4+). Urinary bicarbonate excretion would worsen acidosis. Respiratory
compensation is limited in COPD. Ammonium excretion increases, not decreases.
8. A 30yearold woman with a history of deep vein thrombosis and recurrent miscarriages is found to
have a prolonged aPTT that does not correct with mixing study. Which antibody is most likely present?
A. Anticardiolipin antibody
B. AntiJo1 antibody
C. AntiSSA antibody
D. Antineutrophil cytoplasmic antibody
Answer: A. Anticardiolipin antibody
Explanation: Lupus anticoagulant (a type of antiphospholipid antibody, often anticardiolipin) causes a
paradoxical prolonged aPTT that does not correct with mixing due to phospholipidbinding inhibition.
Exam | Latest Update 2026/2027 | 200 Questions and Verified
Answers | Complete Q&A Guide | A+ Graded
1. A 62yearold male with chronic heart failure presents with worsening dyspnea, jugular venous
distension, and peripheral edema. Which cellular adaptation is most likely occurring in his myocardium
as a compensatory mechanism?
A. Hyperplasia
B. Metaplasia
C. Hypertrophy
D. Dysplasia
Answer: C. Hypertrophy
Explanation: Hypertrophy is an increase in cell size due to increased workload, as seen in heart failure
where myocytes enlarge to compensate for pressure or volume overload. Hyperplasia (increase in cell
number) is not typical in terminally differentiated cardiac muscle. Metaplasia is replacement of one cell
type with another. Dysplasia is disordered cellular growth, often preneoplastic.
2. During ischemia, the switch from aerobic to anaerobic metabolism leads to which immediate
intracellular change?
A. Increased intracellular pH
B. Decreased intracellular sodium
C. Accumulation of lactic acid
D. Increased ATP production
Answer: C. Accumulation of lactic acid
,Explanation: Ischemia causes reduced oxygen supply, forcing cells to shift to anaerobic glycolysis. This
results in lactic acid accumulation, decreased intracellular pH, and reduced ATP production. Sodium
accumulates intracellularly due to Na+/K+ pump failure.
3. In Alzheimer disease, extracellular deposition of which protein is primarily responsible for neuritic
plaque formation?
A. Tau protein
B. Alphasynuclein
C. Betaamyloid
D. Prion protein
Answer: C. Betaamyloid
Explanation: Betaamyloid (Aβ) peptides aggregate into extracellular plaques. Tau protein forms
intracellular neurofibrillary tangles. Alphasynuclein is seen in Parkinson disease. Prion protein causes
spongiform encephalopathies.
4. A 45yearold woman presents with fatigue, pallor, and paresthesias. Laboratory findings show
macrocytic anemia, hypersegmented neutrophils, and low vitamin B12. Which cellular process is most
directly impaired?
A. Heme synthesis
B. Globin chain assembly
C. DNA synthesis
D. Iron transport
Answer: C. DNA synthesis
,Explanation: Vitamin B12 deficiency impairs thymidine synthesis, leading to defective DNA replication
and megaloblastic changes. Heme synthesis is impaired in iron deficiency. Globin defects cause
hemoglobinopathies. Iron transport involves transferrin.
5. A patient develops urticaria, angioedema, and stridor within 10 minutes of penicillin administration.
This reaction is mediated primarily by which immunoglobulin?
A. IgA
B. IgE
C. IgG
D. IgM
Answer: B. IgE
Explanation: Type I hypersensitivity reactions are IgEmediated, causing mast cell degranulation and
release of histamine and other mediators. IgA is mucosal immunity. IgG and IgM are involved in Type II
and III reactions.
6. Which of the following is a hallmark of systemic lupus erythematosus at the cellular level?
A. Deficiency of C1 esterase inhibitor
B. Formation of antinuclear antibodies and immune complexes
C. Selective loss of regulatory T cells
D. Overproduction of IgE
Answer: B. Formation of antinuclear antibodies and immune complexes
Explanation: SLE is a Type III hypersensitivity disorder characterized by autoantibodies (ANA, antidsDNA)
forming immune complexes that deposit in tissues, causing inflammation. C1 esterase inhibitor
, deficiency causes hereditary angioedema. Treg loss is seen in some autoimmune diseases but is not
hallmark. IgE overproduction is atopic.
7. A 68yearold with chronic obstructive pulmonary disease has a PaCO2 of 68 mmHg and pH of 7.31.
Which compensatory mechanism is expected?
A. Increased urinary bicarbonate excretion
B. Increased respiratory rate
C. Increased renal hydrogen ion secretion
D. Decreased renal ammonium excretion
Answer: C. Increased renal hydrogen ion secretion
Explanation: Chronic respiratory acidosis (high PaCO2) is compensated by renal retention of bicarbonate
and increased H+ secretion (as NH4+). Urinary bicarbonate excretion would worsen acidosis. Respiratory
compensation is limited in COPD. Ammonium excretion increases, not decreases.
8. A 30yearold woman with a history of deep vein thrombosis and recurrent miscarriages is found to
have a prolonged aPTT that does not correct with mixing study. Which antibody is most likely present?
A. Anticardiolipin antibody
B. AntiJo1 antibody
C. AntiSSA antibody
D. Antineutrophil cytoplasmic antibody
Answer: A. Anticardiolipin antibody
Explanation: Lupus anticoagulant (a type of antiphospholipid antibody, often anticardiolipin) causes a
paradoxical prolonged aPTT that does not correct with mixing due to phospholipidbinding inhibition.
