NEET SS Medical Oncology (DM) Flashcards

24 sample cards from the Medical Oncology (DM) deck

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

1. Name the most common renal cell carcinoma subtype and its associated genetic alteration.

   Clear cell renal cell carcinoma; associated with VHL (von Hippel-Lindau) gene inactivation on chromosome 3p, leading to HIF accumulation and angiogenesis.

2. What is the most common primary malignant brain tumor in adults, and its key prognostic molecular markers?

   Glioblastoma (GBM, WHO grade 4 astrocytoma). Better prognosis with IDH mutation and MGMT promoter methylation (predicts temozolomide response).

3. Differentiate AML from ALL by typical age, common cytochemistry, and a defining cytogenetic example.

   AML: adults, myeloperoxidase-positive, Auer rods; t(15;17) in APL (M3). ALL: children, TdT-positive, PAS-positive; t(9;22) Philadelphia chromosome confers poor prognosis (treated with TKI).

4. What is the treatment and pathognomonic emergency of acute promyelocytic leukemia (APL, AML-M3)?

   Treated with ATRA (all-trans retinoic acid) plus arsenic trioxide. Pathognomonic emergency: DIC (disseminated intravascular coagulation) from release of procoagulants; ATRA can also cause differentiation syndrome.

5. What defines chronic myeloid leukemia and the three clinical phases?

   Defined by BCR-ABL1 fusion (Philadelphia chromosome, t(9;22)) producing constitutive tyrosine kinase. Phases: chronic phase, accelerated phase, and blast crisis (>20% blasts). First-line therapy: TKIs (imatinib, dasatinib, nilotinib).

6. What is the most common adult leukemia in the West, its immunophenotype, and a poor-prognosis marker?

   Chronic lymphocytic leukemia (CLL); CD5+, CD19+, CD23+ B cells with smudge cells on smear; del(17p)/TP53 mutation indicates poor prognosis and resistance to chemoimmunotherapy.

7. How are Hodgkin and non-Hodgkin lymphoma distinguished pathologically and by spread?

   Hodgkin lymphoma has Reed-Sternberg cells (CD15+, CD30+), spreads contiguously between nodal groups, and has bimodal age distribution. NHL lacks Reed-Sternberg cells, spreads non-contiguously/extranodally, and is more common.

8. What is the most common non-Hodgkin lymphoma in adults and its first-line treatment?

   Diffuse large B-cell lymphoma (DLBCL); treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone).

9. Name the translocations characteristic of Burkitt lymphoma, follicular lymphoma, and mantle cell lymphoma.

   Burkitt: t(8;14) c-MYC. Follicular: t(14;18) BCL2. Mantle cell: t(11;14) cyclin D1 (BCL1).

10. What is the CRAB criteria for symptomatic multiple myeloma?

    hyperCalcemia, Renal insufficiency, Anemia, Bone lesions (lytic). These end-organ damage features distinguish active myeloma requiring treatment from MGUS/smoldering myeloma.

11. What laboratory and imaging findings support a diagnosis of multiple myeloma?

    Monoclonal (M) protein spike on serum/urine electrophoresis (Bence Jones proteins), >10% clonal plasma cells in marrow, rouleaux formation, lytic 'punched-out' bone lesions, and elevated free light chains.

12. Define MGUS and its relationship to multiple myeloma.

    Monoclonal Gammopathy of Undetermined Significance: M protein <3 g/dL, <10% marrow plasma cells, no CRAB features. It is a premalignant condition that progresses to multiple myeloma at ~1% per year.

13. What is tumor lysis syndrome, its classic metabolic abnormalities, and prophylaxis?

    Massive tumor cell death (often after chemo of bulky/high-turnover tumors) causing hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia, leading to acute kidney injury/arrhythmia. Prophylaxis: aggressive hydration, allopurinol or rasburicase.

14. What is the management of malignant hypercalcemia?

    Aggressive IV isotonic saline hydration, IV bisphosphonates (zoledronic acid) or denosumab; calcitonin for rapid short-term lowering; treat the underlying malignancy. PTHrP-mediated humoral hypercalcemia is the most common mechanism.

15. What are the features and emergency management of malignant spinal cord compression?

    Back pain (worse at night/recumbent), motor weakness, sensory level, and bladder/bowel dysfunction. Emergency: high-dose dexamethasone immediately, urgent MRI of whole spine, then radiotherapy or surgical decompression.

16. What is superior vena cava (SVC) syndrome, its most common malignant cause, and management?

    Obstruction of SVC causing facial/upper limb edema, distended neck veins, and dyspnea. Most common malignant cause is lung cancer (especially SCLC) and lymphoma. Management: airway support, corticosteroids, radiotherapy/chemotherapy, and endovascular stenting.

17. What is febrile neutropenia, its definition, and initial management?

    Temperature >=38.3C once (or >=38.0C sustained 1 hour) with absolute neutrophil count <500 (or <1000 falling). Emergency: blood cultures then immediate empiric broad-spectrum IV antibiotics (anti-pseudomonal beta-lactam e.g. piperacillin-tazobactam or cefepime) within 1 hour.

18. What is the role and main agents of G-CSF (granulocyte colony-stimulating factor) in oncology?

    G-CSF (filgrastim, pegfilgrastim) stimulates neutrophil production to prevent/treat chemotherapy-induced neutropenia and for stem cell mobilization. Used as primary prophylaxis when febrile neutropenia risk is >20%.

19. Classify chemotherapy emetogenicity management: name the antiemetic triple therapy for highly emetogenic regimens.

    A 5-HT3 antagonist (ondansetron/palonosetron) + NK1 antagonist (aprepitant) + dexamethasone; olanzapine may be added as a fourth agent for highly emetogenic chemotherapy like cisplatin.

20. What is SIADH as a paraneoplastic syndrome, its classic associated tumor, and treatment?

    Syndrome of Inappropriate ADH secretion causing euvolemic hyponatremia with concentrated urine; classically caused by small cell lung cancer. Treatment: fluid restriction, and vaptans or hypertonic saline for severe symptomatic hyponatremia.

21. What paraneoplastic syndrome causes Cushing's, and which tumor most commonly produces ectopic ACTH?

    Ectopic ACTH syndrome causes hypokalemic metabolic alkalosis, hyperglycemia, and Cushingoid features; small cell lung cancer (and bronchial carcinoid) is the classic source.

22. What is Lambert-Eaton myasthenic syndrome, its mechanism, and association?

    A paraneoplastic neuromuscular disorder from autoantibodies against presynaptic voltage-gated calcium channels causing proximal weakness that improves with repeated effort; associated with small cell lung cancer.

23. Match these paraneoplastic syndromes to tumors: hypercalcemia (PTHrP), polycythemia (erythropoietin), and acanthosis nigricans.

    PTHrP hypercalcemia: squamous cell carcinoma of lung, renal cell, head/neck. Erythropoietin polycythemia: renal cell carcinoma, hepatocellular carcinoma, cerebellar hemangioblastoma. Acanthosis nigricans: gastric adenocarcinoma.

24. What is the difference between neoadjuvant, adjuvant, and palliative chemotherapy?

    Neoadjuvant: given before primary (surgical) therapy to shrink the tumor and improve resectability. Adjuvant: given after definitive local therapy to eradicate micrometastases and reduce recurrence. Palliative: given to relieve symptoms and prolong life in incurable disease, prioritizing quality of life.

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