1. e. In viral lymphadenitis as in the case of infectious mononucleosis, there is follicular and paracortical hyperplasia with proliferation of immunoblasts, tangiblebody macrophages, Reed-Sternberg-like cells, atypical lymphocytes, and monocytoid B cells. Necrosis and viral inclusions can also be seen. Langerhans cells and dendritic cells are not usually prominent. Their presence suggests dermatopathic lymphadenopathy.

2. d. Dermatopathic lymphadenopathy is a proliferation of histiocytes in patchy aggregates in the cortical or the peripheral areas of the lymph node. The paracortical areas are also expanded by Langerhans cells and interdigitating dendritic cells. 70% of patients with dermatopathic lymphadenopathy have cutaneous T-cell lymphoma or Sézary syndrome.

3. e. The size, shape, distribution, and density of the follicles, overexpression of bcl-2, and expression of CD10 in the compressed interfollicular zone in follicular lymphoma help differentiate it from reactive follicular hyperplasia. In reactive hyperplasia, there is proliferation of dendritic cells, histiocytes, tingible-body macrophages, and plasma cells.

4. e. This fusion transcript results in translocation t(5;17)(q22;q11-12), which is a feature of acute promyelocytic leukemia. Leukemic myeloid cells contain characteristic bundles of Auer rods in the cytoplasm, called “faggot cells.” This type of leukemia has good prognosis if treated with transretinoic acid therapy.

5. d. Section shows diffuse proliferation of blasts that stain with markers of immature cells such as terminal deoxytransferase (Tdt). Of the list, Tdt is the only nuclear stain and is positive in lymphoblastic leukemia/lymphoma. All the other choices have antibodies that stain the cytoplasm.

6. c. Hyaline-vascular Castleman disease is more common than the plasma cell type, which is seen mainly in multicentric Castleman disease. This disease is sometimes associated with the clonal rearrangements of the T-cell receptor gene, and results in a clinical picture similar to that of angioimmunoblastic lymphadenopathy. It is also associated with herpes virus 8, Kaposi sarcoma, large cell lymphoma, and POEMS (polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin changes) syndrome.

7. c. This translocation is one of the most common chromosomal aberrations in acute myeloid leukemia and occurs predominantly in younger patients. Leukemic cells have myeloid differentiation and show cytoplasmic Auer rods. This type of leukemia has good prognosis and good response to chemotherapy.

8. d. Vascular neoplasms, angiomyoid proliferative lesions, angiomatous hamartomas, and HHV-8 positive Kaposi sarcoma have all been reported to occur in patients with Castleman disease. Ewing sarcoma is not associated with Castleman syndrome.

9. d. Rosai-Dorfman disease is mainly seen in young African American children and adolescents. It presents as neck lymphadenopathy and also involves the extranodal areas in one fourth of cases. It is a benign histiocytosis characterized histologically by engulfment of lymphocytes. Phagocytic cells are reactive with S-100 but not with CD1a or Epstein-Barr viral markers.

10. a. Lymphoblastic lymphoma is the most common lymphoma type in children and is usually of the T-cell type. It presents with mediastinal mass with or without lymphadenopathy. It is a high-grade lymphoma that is typically positive for Tdt and not CD30.

11. c. The prognosis of Hodgkin lymphoma is best in nodular sclerosis type, followed by mixed cellularity. The overall 5-year survival rate for Hodgkin lymphoma is 75%, and is worst in lymphocyte-depleted type.

12. c. Clinical stage is the most important prognostic parameter. Stage IV has the worst prognosis. African Americans men, mediastinal tumor, splenic nodules, lymphocyte depletion, and age more than 50 years are other parameters associated with poor prognosis. Favorable prognostic features in Hodgkin lymphoma include female gender, white race, nodular lymphocyte-predominant, and nodular sclerosis histologic types.

13. e. Unlike other types of Hodgkin, nodular lymphocyte-predominant Hodgkin lymphoma cells are negative for CD30 and CD15 and stain with CD20, CD79a, and BSAP.

14. c. Refractory anemia with ringed sideroblasts (RARS) characteristically affects older individuals and shows evidence of iron overload in the bone marrow, spleen, and liver. It is an idiopathic disease that can only be diagnosed after excluding all other possible etiologies of erythroid abnormalities. It evolves to acute leukemia in 1% to 2% of cases.

15. b. In chronic myelogenous leukemia, the breakpoint in the BCR gene is in the major breakpoint cluster region (BCR exons 12-16) and a p210 protein is formed. The fusion gene leads to increased tyrosine kinase receptor activity. Inhibition of tyrosine kinase by Gleevec is a mode of treatment of chronic myelogenous leukemia.

16. c. Blast phase of chronic myelogenous leukemia resembles acute leukemia where the number of blasts exceeds 20%. The blast lineage is mostly myeloid but can be lymphoblastic in 20% of cases. There is gain of additional chromosomal abnormalities. Splenomegaly, thrombocytosis, and thrombocytopenia are seen in both accelerated and blast phases. The white cell count does not decrease.

17. e. Monosomy 5q- syndrome characteristically occurs in women and causes myelodysplastic syndrome with blasts <5%. The disease leads to refractory anemia and increase in megakaryocytes with hypolobated nuclei. Isolated monosomy 5 syndrome is associated with good survival.

18. d. Progressive transformation of germinal centers describes an alteration of lymphoid architecture in which lymphoid follicles become enlarged and infiltrated by small lymphocytes. It occurs in association with nodular lymphocyte-predominant Hodgkin disease and other reactive lymphadenopathies.