Wilkes University | Q & A | 2026/2027 Edition
(PDF)
1. Which pathophysiologic mechanism is primarily responsible for the microcytic, hypochromic anemia
seen in iron deficiency?
A) Impaired DNA synthesis due to vitamin B12 deficiency
B) Decreased iron availability for hemoglobin synthesis
C) Autoimmune destruction of gastric parietal cells
D) Premature destruction of red blood cells in the spleen
Correct Answer: Decreased iron availability for hemoglobin synthesis
Rationale: Iron deficiency anemia results from decreased iron availability for heme and hemoglobin
synthesis, leading to the production of microcytic (small) and hypochromic (pale) red blood cells.
Common causes include chronic blood loss, inadequate dietary intake, and malabsorption. Laboratory
findings show low ferritin, low serum iron, and elevated total iron-binding capacity (TIBC).
2. Which laboratory finding is characteristic of pernicious anemia?
A) Elevated ferritin and low TIBC
B) Macrocytic red blood cells with low serum B12
C) Microcytic red blood cells with elevated serum iron
D) Normal MCV with low serum folate
Correct Answer: Macrocytic red blood cells with low serum B12
Rationale: Pernicious anemia is a macrocytic anemia caused by vitamin B12 deficiency due to lack of
intrinsic factor, often from autoimmune destruction of gastric parietal cells. Laboratory findings include
elevated mean corpuscular volume (MCV), low serum B12, and anti-intrinsic factor antibodies.
Neurologic symptoms such as paresthesia and ataxia may also be present.
,3. A patient with anemia of chronic disease would most likely have which laboratory profile?
A) Low serum iron, low TIBC, elevated ferritin
B) Low serum iron, elevated TIBC, low ferritin
C) Elevated serum iron, low TIBC, low ferritin
D) Low serum iron, low TIBC, low ferritin
Correct Answer: Low serum iron, low TIBC, elevated ferritin
Rationale: Anemia of chronic disease is characterized by low serum iron, low TIBC, and normal or
elevated ferritin due to inflammation-induced hepcidin production. Hepcidin blocks iron absorption and
release from macrophages, trapping iron in stores. This anemia is normocytic and normochromic in early
stages, becoming microcytic with chronicity.
4. What is the primary pathophysiologic mechanism of hemolytic anemia?
A) Decreased production of red blood cells in the bone marrow
B) Premature destruction of red blood cells
C) Impaired hemoglobin synthesis
D) Vitamin B12 deficiency
Correct Answer: Premature destruction of red blood cells
Rationale: Hemolytic anemia results from premature destruction of red blood cells, either from intrinsic
causes (membrane defects, enzyme deficiencies, hemoglobinopathies) or extrinsic causes (immune-
mediated, mechanical, or infectious). Laboratory findings include decreased haptoglobin, elevated LDH,
elevated indirect bilirubin, and reticulocytosis.
5. A patient with sickle cell disease experiences a vaso-occlusive crisis. What is the primary trigger for
hemoglobin S polymerization?
A) Increased oxygen tension
B) Decreased oxygen tension
C) Elevated pH
, D) Increased temperature
Correct Answer: Decreased oxygen tension
Rationale: In sickle cell disease, hemoglobin S polymerizes under conditions of decreased oxygen
tension, causing red blood cells to deform into a sickle shape. These sickled cells obstruct
microcirculation, leading to vaso-occlusion, ischemia, and pain. Dehydration, infection, and cold
temperature can also trigger crises.
6. Which coagulation disorder is characterized by widespread activation of the clotting cascade leading
to microvascular thrombosis and consumption of clotting factors?
A) Hemophilia A
B) von Willebrand disease
C) Disseminated intravascular coagulation (DIC)
D) Idiopathic thrombocytopenic purpura
Correct Answer: Disseminated intravascular coagulation (DIC)
Rationale: DIC is characterized by widespread activation of the coagulation cascade, leading to
microvascular thrombosis and consumption of clotting factors and platelets. This results in a paradoxical
bleeding diathesis. Common triggers include sepsis, trauma, malignancy, and obstetric complications.
7. In hyperthyroidism caused by Graves' disease, what is the mechanism of thyroid hormone excess?
A) Destruction of thyroid follicles by autoantibodies
B) Thyroid-stimulating immunoglobulins that activate the TSH receptor
C) Iodine deficiency leading to TSH hypersecretion
D) Autoimmune destruction of pituitary thyrotropes
Correct Answer: Thyroid-stimulating immunoglobulins that activate the TSH receptor