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

Hematology & Oncology syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Hematology & Oncology in American Board of Internal Medicine Certification (ABIM Board Certification), not a summary of it.

1. 1

   Anemias & Red Cell Disorders

   4 topics

   • Microcytic anemias
     • Iron deficiency and thalassemia
   • Macrocytic and megaloblastic anemias
   • Hemolytic anemias
   • Anemia of chronic disease and bone marrow failure
2. 2

   Hemostasis & Thrombosis

   4 topics

   • Bleeding disorders and platelet dysfunction
   • Thrombocytopenia
     • ITP, TTP, HIT, DIC
   • Venous thromboembolism and anticoagulation management
   • Hypercoagulable states and thrombophilia workup
3. 3

   Hematologic Malignancies

   4 topics

   • Acute and chronic leukemias
   • Lymphomas (Hodgkin and non-Hodgkin)
   • Plasma cell disorders
     • Multiple myeloma and MGUS
   • Myeloproliferative neoplasms and myelodysplastic syndromes
4. 4

   Solid Tumor Oncology

   5 topics

   • Breast, lung, colorectal, and prostate cancer
   • Cancer screening guidelines
   • Oncologic emergencies
     • Tumor lysis, spinal cord compression, hypercalcemia, febrile neutropenia
   • Paraneoplastic syndromes and cancer of unknown primary
   • Principles of systemic therapy and immunotherapy toxicity

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

25 of 51 cards from the Hematology & Oncology deck — real questions with worked answers.

1. What is the classic CBC pattern and most common cause of microcytic anemia worldwide?

   Low MCV (<80 fL) with low hemoglobin; iron deficiency anemia is the most common cause. Labs show low ferritin, low serum iron, high TIBC/transferrin, and low transferrin saturation.

2. How do you distinguish iron deficiency anemia from anemia of chronic disease (inflammation) on iron studies?

   Iron deficiency: low ferritin, high TIBC, low transferrin saturation. Anemia of chronic disease: normal-to-high ferritin (acute phase reactant), low TIBC, and low/normal iron due to hepcidin-mediated iron sequestration.

3. What is the Mentzer index and how does it help differentiate thalassemia trait from iron deficiency?

   Mentzer index = MCV / RBC count. <13 suggests thalassemia trait (normal/high RBC count); >13 suggests iron deficiency anemia (low RBC count).

4. What hemoglobin electrophoresis finding confirms beta-thalassemia minor?

   Elevated HbA2 (>3.5%), often with mildly elevated HbF. The patient has microcytosis with a normal or elevated RBC count and target cells on smear.

5. What are the two major causes of macrocytic megaloblastic anemia and the unifying biochemical defect?

   Vitamin B12 (cobalamin) deficiency and folate deficiency. Both impair DNA synthesis, causing nuclear-cytoplasmic asynchrony with hypersegmented neutrophils and oval macrocytes.

6. Which labs distinguish B12 deficiency from folate deficiency, and which neurologic finding is unique to B12 deficiency?

   Both raise homocysteine; only B12 deficiency raises methylmalonic acid (MMA). B12 deficiency causes subacute combined degeneration (dorsal columns/corticospinal tracts) — neurologic disease that folate replacement does not correct.

7. What is pernicious anemia and which antibodies/tests support the diagnosis?

   Autoimmune destruction of gastric parietal cells causing intrinsic factor deficiency and B12 malabsorption. Anti-intrinsic factor antibodies (specific) and anti-parietal cell antibodies are positive; associated with atrophic gastritis and increased gastric cancer risk.

8. List common causes of non-megaloblastic macrocytosis.

   Alcohol use, liver disease, hypothyroidism, myelodysplastic syndrome, reticulocytosis (e.g., hemolysis/bleeding), and drugs (hydroxyurea, methotrexate, zidovudine). Smear lacks hypersegmented neutrophils.

9. What lab pattern indicates hemolysis?

   Elevated indirect (unconjugated) bilirubin, elevated LDH, low haptoglobin, and reticulocytosis. Intravascular hemolysis adds hemoglobinuria and hemosiderinuria.

10. How do you differentiate intravascular from extravascular hemolysis?

    Intravascular: very low haptoglobin, markedly high LDH, hemoglobinemia/hemoglobinuria, schistocytes (e.g., TTP, mechanical valve, PNH). Extravascular: splenic RBC destruction, spherocytes, less hemoglobinuria (e.g., warm AIHA, hereditary spherocytosis).

11. What does a positive direct antiglobulin (Coombs) test indicate and how do warm vs cold AIHA differ?

    DAT detects antibody/complement on RBCs, confirming autoimmune hemolytic anemia. Warm AIHA: IgG-mediated, optimal at 37°C, spherocytes, treat with steroids (associated with CLL, SLE, drugs). Cold agglutinin disease: IgM/complement, agglutination in cold, associated with Mycoplasma and EBV; treat by avoiding cold/rituximab.

12. What triggers hemolysis in G6PD deficiency and what is seen on smear?

    Oxidative stress — infections, fava beans, drugs (dapsone, primaquine, sulfa, nitrofurantoin). Smear shows bite cells and Heinz bodies. X-linked; enzyme level may be falsely normal during acute crisis (test weeks later).

13. What is the pentad of thrombotic thrombocytopenic purpura (TTP) and the underlying defect?

    Fever, microangiopathic hemolytic anemia, thrombocytopenia, renal dysfunction, neurologic changes (full pentad uncommon). Caused by ADAMTS13 deficiency causing large vWF multimers. Treat urgently with plasma exchange (NOT platelet transfusion).

14. What characterizes anemia of chronic disease pathophysiologically?

    Inflammation-driven hepcidin elevation blocks iron release from macrophages and absorption (ferroportin downregulation), plus blunted EPO response. Typically normocytic (can be microcytic), with low iron, low TIBC, and high/normal ferritin.

15. What is aplastic anemia and its diagnostic hallmark?

    Pancytopenia with a hypocellular bone marrow (fatty marrow) without infiltration or fibrosis, due to immune-mediated stem cell failure. Treat with immunosuppression (ATG + cyclosporine) or allogeneic transplant; eltrombopag can be added.

16. What is paroxysmal nocturnal hemoglobinuria (PNH) and how is it diagnosed?

    Acquired PIGA mutation causing loss of GPI-anchored complement regulators (CD55, CD59), leading to complement-mediated intravascular hemolysis, thrombosis, and cytopenias. Diagnosed by flow cytometry showing CD55/CD59-deficient cells; treat with eculizumab/ravulizumab.

17. What is the difference between PT/INR and aPTT in evaluating bleeding disorders?

    PT/INR assesses the extrinsic and common pathways (factors VII, X, V, II, fibrinogen) and is sensitive to warfarin. aPTT assesses intrinsic and common pathways (factors XII, XI, IX, VIII plus common) and is sensitive to heparin.

18. What is von Willebrand disease and its typical lab and treatment profile?

    Most common inherited bleeding disorder; deficient/defective vWF causes mucocutaneous bleeding. Labs: prolonged bleeding time/PFA, normal platelet count, possibly prolonged aPTT (low factor VIII), low vWF antigen/activity (ristocetin cofactor). Treat with desmopressin (DDAVP) for type 1 or vWF concentrate.

19. Compare hemophilia A and B.

    Both X-linked recessive with deep tissue/joint bleeding (hemarthroses) and prolonged aPTT with normal PT. Hemophilia A = factor VIII deficiency (more common); Hemophilia B (Christmas disease) = factor IX deficiency. Treat with factor concentrate replacement.

20. What is disseminated intravascular coagulation (DIC) and its lab findings?

    Systemic activation of coagulation consuming clotting factors and platelets with secondary fibrinolysis. Labs: low platelets, prolonged PT and aPTT, low fibrinogen, elevated D-dimer, and schistocytes. Treat the underlying cause; support with FFP, cryoprecipitate, platelets.

21. What is the mechanism and platelet defect of uremic bleeding?

    Uremic toxins impair platelet function (qualitative defect) despite often-normal counts, causing mucocutaneous bleeding and prolonged bleeding time. Treat with desmopressin, dialysis, and correction of anemia; cryoprecipitate if severe.

22. How does ITP (immune thrombocytopenia) present and how is it diagnosed?

    Isolated thrombocytopenia from autoantibody-mediated platelet destruction; diagnosis of exclusion (normal smear otherwise, no other cytopenias). First-line treatment: corticosteroids, IVIG; second-line: TPO agonists, rituximab, splenectomy.

23. What defines heparin-induced thrombocytopenia (HIT) and how is it managed?

    IgG antibodies to platelet factor 4-heparin complexes causing platelet activation; platelet drop >50% typically 5-10 days after heparin, with paradoxical thrombosis. Use the 4T score; confirm with PF4 ELISA and serotonin release assay. Stop ALL heparin and start a non-heparin anticoagulant (argatroban, fondaparinux); do NOT give platelets or start warfarin acutely.

24. What is the difference between thrombocytopenia from decreased production vs increased destruction on bone marrow?

    Decreased production (e.g., aplasia, chemotherapy, MDS): reduced megakaryocytes. Increased destruction/consumption (e.g., ITP, DIC, TTP): normal or increased megakaryocytes.

25. What are Wells criteria used for, and what is the next step in a low-probability DVT/PE workup?

    Wells criteria stratify pretest probability of DVT or PE. For low probability, a negative D-dimer rules out VTE; for high probability, proceed directly to imaging (compression ultrasound for DVT, CT pulmonary angiography for PE).

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