Hematology & Oncology for USMLE Step 1 FAQs
| 1. What are the different types of leukemia and how do they differ on USMLE Step 1? |  |
Ans. Leukemia classifies as acute or chronic, and myeloid or lymphoid, creating four main categories: acute myeloid leukaemia (AML), acute lymphoblastic leukaemia (ALL), chronic myeloid leukaemia (CML), and chronic lymphocytic leukaemia (CLL). Each presents distinct blast morphology, chromosomal abnormalities, and prognosis. AML typically affects older adults; ALL commonly strikes children. CML features Philadelphia chromosome translocation; CLL involves abnormal B-lymphocytes with longer disease progression than acute variants.
| 2. How do you differentiate between Hodgkin lymphoma and non-Hodgkin lymphoma for Step 1 exams? |  |
Ans. Hodgkin lymphoma contains pathognomonic Reed-Sternberg cells and shows orderly nodal progression, typically affecting young adults and those over 55. Non-Hodgkin lymphoma lacks Reed-Sternberg cells, demonstrates random dissemination, and subdivides into B-cell and T-cell variants. Hodgkin's presents with B-symptoms and mediastinal involvement; NHL shows extranodal disease more frequently. Prognosis and chemotherapy regimens differ significantly between these lymphoid malignancies.
| 3. What is the mechanism of action of common chemotherapy drugs tested on USMLE Step 1? |  |
Ans. Chemotherapy agents work through distinct mechanisms: alkylating agents cross-link DNA; antimetabolites inhibit nucleotide synthesis; topoisomerase inhibitors prevent DNA unwinding; microtubule inhibitors disrupt mitosis. Anthracyclines intercalate DNA and generate free radicals. Targeted therapies like imatinib inhibit specific tyrosine kinases in leukaemia cells. Understanding drug class, cell-cycle specificity, and toxicity profiles-including cardiotoxicity and bone marrow suppression-is essential for Step 1 success.
| 4. How do you interpret CBC findings in anaemia and identify the specific type? |  |
Ans. Complete blood count analysis begins with haemoglobin and mean corpuscular volume (MCV) to classify anaemia as microcytic, normocytic, or macrocytic. Microcytic suggests iron deficiency or thalassaemia; macrocytic indicates B12/folate deficiency or alcohol use. Reticulocyte count reveals bone marrow response capacity. Peripheral blood smear examination identifies cell morphology abnormalities. Evaluating these parameters systematically determines underlying aetiology and guides appropriate therapeutic intervention for Step 1 questions.
| 5. What are the key genetic mutations and chromosomal abnormalities in hematologic malignancies? |  |
Ans. Critical cytogenetic abnormalities include t(9;22) Philadelphia chromosome in CML, t(15;17) in acute promyelocytic leukaemia (APL), and t(8;14) in Burkitt lymphoma. FAB classification and WHO criteria emphasise mutation testing: FLT3, NPM1, and TP53 mutations in AML; BCR-ABL fusion in CML. FISH and karyotyping identify these abnormalities. Prognostic significance and targeted therapy options depend directly on specific genetic profiles tested extensively on Step 1 examinations.
| 6. How do tumour markers and flow cytometry help diagnose hematologic cancers? |  |
Ans. Flow cytometry identifies abnormal cell populations through CD antigen expression patterns, distinguishing lymphoid subtypes and leukaemia classifications. Tumour markers like lactate dehydrogenase (LDH) and uric acid indicate disease burden and prognosis. PSA, AFP, and beta-hCG serve specific malignancies. Immunophenotyping via flow cytometry establishes immunologic markers for diagnosis confirmation. These diagnostic tools provide rapid, accurate characterisation of haematologic malignancies essential for Step 1 clinical case scenarios.
| 7. What is the role of stem cell transplantation and immunotherapy in treating haematologic malignancies? |  |
Ans. Haematopoietic stem cell transplantation (HSCT) offers curative potential in leukaemia and lymphoma through myeloablation and graft-versus-leukaemia effect. Allogeneic transplants involve donor stem cells; autologous uses patient's own cells. Chimeric antigen receptor T-cell (CAR-T) therapy represents modern immunotherapy, reprogramming T-lymphocytes to target malignant cells. Both approaches carry infection and rejection risks. Understanding indications, timing, and complications distinguishes high-performing Step 1 candidates in haematologic-oncology sections.
| 8. How do you manage tumour lysis syndrome and hyperuricaemia in haematologic malignancies? |  |
Ans. Tumour lysis syndrome develops when massive cell death releases intracellular contents, causing hyperkalaemia, hyperphosphataemia, and hyperuricaemia. Prevention involves aggressive hydration, allopurinol, and rasburicase. Rasburicase converts uric acid to allantoin, preventing nephropathy more effectively than allopurinol. Monitoring electrolytes, calcium, and renal function proves critical. Understanding pathophysiology, risk stratification in high-burden diseases, and prophylactic versus therapeutic intervention separates comprehensive Step 1 knowledge from superficial understanding.
| 9. What are the major side effects and toxicities of chemotherapy agents relevant to USMLE Step 1? |  |
Ans. Chemotherapy toxicities vary by drug class: anthracyclines cause cardiomyopathy and congestive heart failure; bleomycin induces pulmonary fibrosis; cisplatin causes nephrotoxicity and ototoxicity; methotrexate damages hepatic and renal function. Alkylating agents increase secondary malignancy risk. Bone marrow suppression, mucositis, and alopecia occur across agents. Antiemetics, growth factors, and monitoring protocols mitigate toxicity. Step 1 requires recognising drug-toxicity correlations and management strategies for clinical scenarios.
| 10. How do you approach diagnosis and staging of solid tumours in oncology for board exams? |  |
Ans. Solid tumour evaluation combines imaging (CT, MRI, PET scan), biopsy confirmation, and tumour markers. TNM staging classifies cancer extent: T indicates tumour size, N describes nodal involvement, M denotes metastases. Grading reflects differentiation and aggressiveness. Histopathology remains gold standard for diagnosis. Staging guides prognosis and treatment selection. Step 1 emphasises recognising common malignancies, their presentations, typical metastatic sites, and stage-appropriate interventions for comprehensive oncology understanding.