American Board of Internal Medicine Certification (ABIM Board Certification) Hematology & Oncology Flashcards

24 sample cards from the Hematology & Oncology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. What are the reversal agents for warfarin, dabigatran, and factor Xa inhibitors?

   Warfarin: vitamin K plus 4-factor prothrombin complex concentrate (or FFP). Dabigatran: idarucizumab. Apixaban/rivaroxaban (factor Xa inhibitors): andexanet alfa (or PCC if unavailable).

2. Why must warfarin be bridged with heparin initially, and what is the mechanism behind warfarin-induced skin necrosis?

   Warfarin inhibits vitamin K-dependent factors II, VII, IX, X and proteins C and S. Protein C (short half-life) falls first, creating a transient hypercoagulable state — hence overlap with heparin and the risk of skin necrosis, especially in protein C deficiency.

3. List the inherited thrombophilias from most to least common and the strongest one.

   Most common: Factor V Leiden (activated protein C resistance), then prothrombin G20210A mutation, then protein C, protein S, and antithrombin III deficiencies. Antithrombin deficiency confers the highest thrombosis risk per case.

4. When should a thrombophilia workup be deferred, and what affects test accuracy?

   Defer during acute thrombosis and while on anticoagulation. Acute thrombosis consumes antithrombin/proteins C and S; heparin lowers antithrombin; warfarin lowers proteins C and S; DOACs interfere with lupus anticoagulant testing. Test after completing therapy when feasible.

5. What diagnostic criteria define antiphospholipid syndrome (APS)?

   Clinical (vascular thrombosis or pregnancy morbidity) plus persistent antiphospholipid antibodies on two occasions ≥12 weeks apart: lupus anticoagulant, anticardiolipin, or anti-beta-2 glycoprotein I. Paradoxically prolongs aPTT in vitro but causes thrombosis in vivo.

6. What is the most common acute leukemia in adults vs children, and the cytogenetic emergency among AML subtypes?

   Adults: acute myeloid leukemia (AML). Children: acute lymphoblastic leukemia (ALL). Acute promyelocytic leukemia (APL, AML M3) with t(15;17) is an emergency due to DIC; treat urgently with ATRA (all-trans retinoic acid) plus arsenic trioxide.

7. What morphologic finding is pathognomonic for AML and how is acute leukemia distinguished from chronic?

   Auer rods (azurophilic cytoplasmic inclusions) indicate AML. Acute leukemia: ≥20% blasts in marrow/blood, rapid course. Chronic leukemia: more mature cells, indolent course.

8. What defines chronic myeloid leukemia (CML) and its targeted therapy?

   BCR-ABL1 fusion from t(9;22) (Philadelphia chromosome) causing constitutive tyrosine kinase activity; marked leukocytosis with left-shifted granulocytes, basophilia, low LAP score. Treat with tyrosine kinase inhibitors (imatinib, dasatinib, nilotinib).

9. What characterizes chronic lymphocytic leukemia (CLL) on smear and flow cytometry?

   Mature small lymphocytosis with smudge cells on smear; flow shows CD5+, CD19+, CD20(dim), CD23+ monoclonal B cells. Complications: autoimmune hemolytic anemia, hypogammaglobulinemia/infections, Richter transformation to DLBCL.

10. What distinguishes Hodgkin lymphoma from non-Hodgkin lymphoma clinically and pathologically?

    Hodgkin: Reed-Sternberg cells (CD15+, CD30+), contiguous nodal spread, bimodal age, often presents in young adults with cervical adenopathy and B symptoms; highly curable. NHL: heterogeneous, noncontiguous/extranodal spread, more common overall.

11. Compare diffuse large B-cell lymphoma (DLBCL) and follicular lymphoma.

    DLBCL: aggressive but potentially curable, treated with R-CHOP. Follicular lymphoma: indolent, t(14;18) overexpressing BCL2, often incurable but slow; can transform to DLBCL. CD20+ B-cell origin in both.

12. What is Burkitt lymphoma's hallmark genetics and clinical urgency?

    t(8;14) translocation overexpressing MYC; 'starry sky' histology with extremely high proliferation (Ki-67 ~100%). Highly aggressive — high tumor lysis syndrome risk; associated with EBV (endemic/jaw) and HIV.

13. What are the CRAB criteria and diagnostic findings of multiple myeloma?

    CRAB: hyperCalcemia, Renal insufficiency, Anemia, Bone lytic lesions. Diagnosis: ≥10% clonal plasma cells in marrow plus end-organ damage; monoclonal (M) spike on SPEP, rouleaux on smear, free light chains in urine (Bence Jones).

14. How does MGUS differ from smoldering myeloma and multiple myeloma?

    MGUS: M-protein <3 g/dL, <10% marrow plasma cells, no CRAB (~1%/yr progression). Smoldering myeloma: M-protein ≥3 g/dL and/or 10-60% plasma cells, no CRAB. Multiple myeloma: ≥10% plasma cells with CRAB or myeloma-defining biomarkers.

15. What is Waldenström macroglobulinemia and its characteristic complication?

    Lymphoplasmacytic lymphoma producing monoclonal IgM (MYD88 mutation). The large IgM causes hyperviscosity syndrome (blurred vision, headache, mucosal bleeding, confusion); treat hyperviscosity with plasmapheresis.

16. Name the three classic BCR-ABL-negative myeloproliferative neoplasms and their driver mutation.

    Polycythemia vera, essential thrombocythemia, and primary myelofibrosis — most commonly driven by the JAK2 V617F mutation (also CALR or MPL in ET/MF).

17. What distinguishes polycythemia vera from secondary polycythemia?

    PV: JAK2 mutation, low serum EPO, elevated RBC mass, often with pruritus (after warm shower), splenomegaly, thrombosis. Secondary polycythemia: high EPO from hypoxia/tumor. Treat PV with phlebotomy and aspirin (add hydroxyurea if high risk).

18. What defines myelodysplastic syndrome (MDS) and its major risks?

    Clonal stem cell disorder with ineffective hematopoiesis: peripheral cytopenias with a hypercellular dysplastic marrow and <20% blasts. Risks: progression to AML and transfusion-dependent cytopenias. Risk-stratify with IPSS-R; 5q- syndrome responds to lenalidomide.

19. What is the most common cancer in women, the screening test, and the key receptor subtypes guiding therapy?

    Breast cancer; screen with mammography. Subtypes: ER/PR-positive (endocrine therapy — tamoxifen, aromatase inhibitors), HER2-positive (trastuzumab), and triple-negative (chemotherapy). BRCA mutations greatly increase risk.

20. What are the USPSTF lung cancer and colorectal cancer screening recommendations?

    Lung: annual low-dose CT for adults 50-80 with a ≥20 pack-year history who currently smoke or quit within 15 years. Colorectal: begin at age 45 (e.g., colonoscopy every 10 years, or FIT/stool tests) through age 75.

21. What is the USPSTF cervical and prostate cancer screening guidance?

    Cervical: ages 21-29 cytology every 3 years; ages 30-65 cytology every 3 years, HPV testing every 5 years, or co-testing every 5 years. Prostate: shared decision-making for PSA in men 55-69; not routinely recommended at age ≥70.

22. List the major oncologic emergencies and the immediate management of spinal cord compression and tumor lysis syndrome.

    Emergencies: febrile neutropenia, tumor lysis syndrome, hypercalcemia, SVC syndrome, spinal cord compression, hyperviscosity, leukostasis. Cord compression: immediate dexamethasone + emergent MRI + radiation/surgery. TLS (high K, high phosphate, high uric acid, low calcium): aggressive IV fluids, rasburicase/allopurinol, treat hyperkalemia.

23. How is malignancy-associated hypercalcemia managed and what are its mechanisms?

    Mechanisms: PTHrP secretion (most common, e.g., squamous cell), osteolytic metastases, and 1,25-OH vitamin D (lymphoma). Treat with aggressive IV normal saline first, then bisphosphonates (zoledronic acid) or denosumab; calcitonin for rapid temporary lowering.

24. Match these paraneoplastic syndromes to their cancers: SIADH, ectopic ACTH/Cushing, Lambert-Eaton, hypercalcemia (PTHrP).

    SIADH and ectopic ACTH (Cushing) — small cell lung cancer. Lambert-Eaton myasthenic syndrome (anti-voltage-gated calcium channel antibodies) — small cell lung cancer. Hypercalcemia from PTHrP — squamous cell carcinoma (lung, head/neck). Immunotherapy with checkpoint inhibitors causes autoimmune 'itis' toxicities (colitis, pneumonitis, hepatitis, thyroiditis, hypophysitis) treated with corticosteroids.

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