Hematology & Oncology USMLE Practice Questions

A. Deficient Von Willebrand factor

This option implies von Willebrand disease, which causes mucosal bleeding and ↑ bleeding time, BUT PTT is often prolonged due to factor VIII involvement; here PTT is normal and platelets are severely decreased, pointing instead to immune-mediated platelet destruction.

B. Shiga-like toxin

This option implies EHEC-associated HUS, which causes hemolytic anemia, thrombocytopenia, and acute kidney injury, BUT this patient has normal hemoglobin and creatinine and no evidence of hemolysis, so it doesn’t fit HUS.

C. Bone marrow infiltration

This option implies marrow replacement (eg, leukemia, metastases) causing pancytopenia or multiple cytopenias, BUT this patient has isolated thrombocytopenia with normal WBC and Hb, which argues against primary marrow failure or infiltration.

D. Consumptive coagulopathy

This option implies DIC, which causes prolonged PT and PTT, low platelets, and often schistocytes with organ dysfunction, BUT this patient’s PT/PTT are normal and there is no systemic illness or organ failure, making DIC unlikely.

F. Decrease in ADAMTS13 activity

This option implies TTP, which presents with thrombocytopenia, microangiopathic hemolytic anemia, neurologic symptoms, fever, and renal dysfunction, BUT this patient lacks anemia, neurologic changes, fever, and has normal creatinine, so TTP is not supported.

A. Rh Incompatibility

This option implies Rh hemolytic disease (usually D antigen) causing severe anemia and often hydrops, BUT both mother and infant are Rh+ and fetomaternal hemorrhage screen is negative, making Rh disease unlikely.

C. G6PD deficiency

This option implies an intrinsic RBC enzyme defect causing oxidative hemolysis with bite cells/heinz bodies, BUT the G6PD level is normal and smear shows normocytic cells without oxidative damage features.

D. Physiological jaundice

This option implies benign unconjugated hyperbilirubinemia peaking days 2–3, BUT this infant’s jaundice starts at 8 hours with anemia, positive Coombs, and reticulocytosis—findings of pathologic hemolysis.

E. Sickle cell disease

This option implies HbS causing vaso-occlusive crises and hemolysis, BUT newborns are largely protected by high HbF, screen is negative, and there are no sickled cells described.

A. MHC II

This option implies expression on antigen-presenting cells (B cells, macrophages, dendritic cells), which is very nonspecific. It does not distinguish immature neoplastic B cells from normal B cells and would not by itself confirm B-ALL.

B. CD 3, TCR

This option implies T-cell lineage (T-ALL or peripheral T-cell neoplasms), which commonly involves anterior mediastinal mass and older children/teens. BUT the hematologist specifically suspects immature B cells, not T cells, and the question asks what confirms that suspicion.

D. CD56

This option implies NK cell phenotype (often with CD16), associated with NK-cell neoplasms or some plasma cell disorders, BUT this child’s presentation and the clinician’s suspicion are for immature B-cell leukemia, not NK-cell malignancy.

E. CD16

This option implies NK cells or neutrophils (Fc receptor), suggesting innate immune cells rather than lymphoblasts. It would not confirm a TdT-positive B-lymphoblast leukemia and does not match the suspected immature B-cell neoplasm.

A. IgM monoclonal gammopathy of undetermined significance (MGUS)

This option implies asymptomatic clonal IgM production with no end-organ damage, BUT this patient has symptomatic hyperviscosity (blurry vision, headache, memory decline) and constitutional symptoms, indicating overt malignancy rather than MGUS.

B. Multiple myeloma

This option implies a plasma cell myeloma usually with IgG or IgA spike, lytic bone lesions, hypercalcemia, and renal failure, BUT this patient has an IgM spike, no bone pain, no hypercalcemia, and classic hyperviscosity symptoms, which are more characteristic of Waldenstrom’s macroglobulinemia.

D. Non-Hodgkin’s lymphoma

This option implies nodal or extranodal lymphoid malignancy that can cause B symptoms, BUT the key feature here is a monoclonal IgM spike with hyperviscosity symptoms, specifically pointing to Waldenstrom’s macroglobulinemia (a specific lymphoplasmacytic lymphoma) rather than generic NHL without defined paraprotein pattern.

E. Chronic lymphocytic leukemia

This option implies CD5+ B-cell lymphocytosis with lymphadenopathy, splenomegaly, and often hypogammaglobulinemia, BUT the question highlights a high monoclonal IgM spike and hyperviscosity symptoms, which are not classic for CLL and instead indicate an IgM-secreting lymphoma (Waldenstrom’s).

A. Atrophy of G cells

This option implies loss of gastrin-secreting G cells (usually in the antrum), which would decrease acid but is not the classic lesion in pernicious anemia. Pernicious anemia is due to autoimmune destruction of parietal cells in the fundus/body, not primarily G cells; the key diagnostic feature is anti–intrinsic factor antibodies.

C. Decreased methylmalonic acid levels

This option implies adequate or excess B12, since methylmalonic acid is converted to succinyl-CoA by a B12-dependent enzyme. In B12 deficiency, methylmalonic acid increases, BUT this patient clearly has B12 deficiency (neurologic deficits plus megaloblastic anemia), so levels would be elevated, not decreased.

D. Antithrombotic state

This option implies reduced clotting tendency, such as from anticoagulation or specific coagulopathies. Megaloblastic anemia from B12 deficiency does not produce an antithrombotic state; if anything, severe anemia can increase cardiac workload, BUT there is no indication of bleeding or clotting abnormalities here.

E. B12 malabsorption due to Diphyllobothrium latum

This option implies tapeworm infection from raw freshwater fish leading to B12 deficiency. While that can cause similar neurologic and hematologic findings, there is no travel or dietary history suggesting fish tapeworm infection, BUT the patient does have strong evidence of autoimmune disease (Hashimoto), making autoimmune pernicious anemia more likely.