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NURS 611 Advanced Pathophysiology Week 3: Cancer and Hematology 2026 |Maryville

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NURS 611 Advanced Pathophysiology Week 3: Cancer and Hematology 2026 |Maryville

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NURS 611 Advanced Pathophysiology Week 3: Cancer and
Hematology 2026 |Maryville


1. Which of the following describes the ‘Warburg effect’ observed in many
cancer cells?

A. The preference for oxidative phosphorylation over glycolysis in aerobic conditions

B. The total shut down of mitochondrial function to avoid apoptosis

C. The use of aerobic glycolysis to support rapid proliferation even in the presence of oxygen

D. The process of using fatty acid oxidation as the primary energy source

Answer: C
Rationale: The Warburg effect refers to the shift in cancer cells toward aerobic glycolysis,
converting glucose to lactate even when oxygen is available, which provides metabolic
intermediates for rapid growth.

2. A patient is diagnosed with Chronic Myeloid Leukemia (CML). Which genetic
abnormality is most characteristic of this condition?

A. A translocation between chromosomes 9 and 22

B. A translocation between chromosomes 8 and 14

C. A deletion of the short arm of chromosome 5

D. An amplification of the N-myc oncogene

Answer: A
Rationale: The Philadelphia chromosome (t(9;22)) creates the BCR-ABL1 fusion gene,
which is the hallmark of CML and leads to constitutive tyrosine kinase activity.

,3. In the process of metastasis, what is the significance of the Epithelial-
Mesenchymal Transition (EMT)?

A. It causes the tumor cells to become more differentiated and less aggressive

B. It allows cancer cells to regain polarity and adhere more tightly to the basement membrane

C. It triggers the activation of the immune system to clear the metastatic cells

D. It enables cells to lose adhesion, increase motility, and enter the bloodstream

Answer: D
Rationale: EMT is a process where epithelial cells lose their cell-to-cell adhesion and gain
mesenchymal properties, which are essential for migration, invasion, and metastasis.

4. Which type of anemia is characterized by a lack of intrinsic factor, preventing
the absorption of Vitamin B12?

A. Iron deficiency anemia

B. Sideroblastic anemia

C. Aplastic anemia

D. Pernicious anemia

Answer: D
Rationale: Pernicious anemia is a macrocytic-normochromic anemia caused by an
autoimmune-mediated deficiency of intrinsic factor, which is required for B12 absorption
in the ileum.

5. What is the primary pathophysiology underlying Disseminated Intravascular
Coagulation (DIC)?

A. A genetic deficiency of Factor VIII leading to spontaneous bleeds

B. Widespread activation of the coagulation cascade resulting in microvascular thrombi and consumption of
clotting factors

C. A decrease in erythropoietin production leading to systemic hypoxia

D. Increased platelet production leading to arterial occlusion

Answer: B

, Rationale: DIC involves systemic activation of coagulation, leading to microthrombi that
organ damage, followed by consumption of platelets and factors, which results in
hemorrhage.

6. Tumor Suppressor Genes, such as TP53, require how many alleles to be
inactivated to contribute to cancer development?

A. Only one allele (dominant effect)

B. No alleles, they are activated by external toxins only

C. Three alleles (polyploidy effect)

D. Both alleles (recessive effect)

Answer: D
Rationale: Tumor suppressor genes typically follow the ‘two-hit hypothesis,’ meaning both
alleles must be inactivated to lose the regulatory function that prevents cancer.

7. Which clinical manifestation is highly specific for Hodgkin Lymphoma?

A. Presence of Bence-Jones proteins in the urine

B. Pancytopenia with a high percentage of blast cells

C. The presence of Reed-Sternberg cells on lymph node biopsy

D. A butterfly rash on the face

Answer: C
Rationale: Reed-Sternberg cells are large, multinucleated B-cells that are the diagnostic
hallmark of Hodgkin Lymphoma.

8. What is the primary role of Telomerase in cancer cell immortality?

A. It maintains the length of telomeres, preventing senescence and apoptosis

B. It repairs double-stranded DNA breaks caused by radiation

C. It inhibits the cell cycle at the G1 phase

D. It promotes the secretion of vascular endothelial growth factor (VEGF)

Answer: A

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