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IM13.1-19 | Common Malignancies and Oncology — Practice Quiz

Practice 10 questions · Untimed · Unlimited attempts

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Q1 IM13.4 1 pt

A 55-year-old man from rural Maharashtra presents with a 4-month history of dysphagia to solids progressively worsening to liquids, 8 kg weight loss, and hoarseness. He has chewed gutka for 30 years. On examination there is a hard, non-tender left supraclavicular lymph node. Which eponym describes this clinical sign and what is its significance?

A Virchow's node — signifies disseminated upper abdominal or thoracic malignancy via the thoracic duct
B Sister Mary Joseph's nodule — signifies peritoneal metastasis from gastric cancer
C Trotter's triad — signifies nasopharyngeal carcinoma invasion of the skull base
D Horner's syndrome — signifies apical lung tumour involving the cervical sympathetic chain

Correct. A firm, non-tender left supraclavicular lymph node is Virchow's node (Troisier sign) — the clinical hallmark of disseminated upper abdominal or thoracic malignancy. The thoracic duct drains abdominal and left thoracic lymphatics and empties at the left subclavian-internal jugular junction. A palpable node here indicates retrograde lymphatic permeation by tumour cells, most commonly from gastric, oesophageal, lung, or pancreatic cancer. In this case with tobacco exposure, progressive dysphagia, and hoarseness, oesophageal squamous cell carcinoma with mediastinal/nodal spread is the likely primary.

Virchow's node (Troisier sign) = firm, non-tender left supraclavicular lymph node = hallmark of disseminated upper abdominal or thoracic malignancy. Always palpate the left supraclavicular fossa in any patient with unexplained weight loss, dysphagia, or upper GI symptoms.

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Q2 IM13.2 1 pt

A 38-year-old woman is found on routine blood work to have a WBC of 220 × 10^9/L. The peripheral smear shows a spectrum of myeloid cells at all stages of maturation — myeloblasts 3%, promyelocytes, myelocytes, metamyelocytes, bands, and segmented neutrophils — alongside basophilia and eosinophilia. Platelets are elevated at 680 × 10^9/L. Spleen is palpable 8 cm below the costal margin. What chromosomal abnormality and its molecular product are pathognomonic of this diagnosis?

A t(15;17) producing PML-RARA fusion — diagnostic of acute promyelocytic leukaemia
B t(9;22) producing BCR-ABL1 fusion (Philadelphia chromosome) — diagnostic of chronic myeloid leukaemia
C t(8;14) producing MYC-IGH fusion — diagnostic of Burkitt lymphoma
D del(17p) with TP53 loss — diagnostic of CLL with adverse prognosis

Correct. The clinical picture — markedly elevated WBC with a full myeloid maturation spectrum (myelocytes and metamyelocytes prominent), basophilia, eosinophilia, thrombocytosis, and massive splenomegaly — is classic for chronic myeloid leukaemia (CML). The pathognomonic abnormality is the Philadelphia chromosome: translocation t(9;22), which juxtaposes the BCR gene on chromosome 22 with the ABL1 gene on chromosome 9, producing the BCR-ABL1 fusion oncogene. The resulting p210 BCR-ABL1 protein is a constitutively active tyrosine kinase driving myeloid proliferation. CML has three phases: chronic (as here), accelerated (blasts 10–19%), and blast crisis (blasts ≥20%). First-line treatment is imatinib or a second-generation TKI.

CML = t(9;22) Philadelphia chromosome → BCR-ABL1 fusion → constitutively active tyrosine kinase. Peripheral smear shows myelocyte peak. Basophilia and eosinophilia are characteristic clues. Blast crisis: blasts ≥20% = transformation to acute leukaemia.

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Q3 IM13.4 1 pt

A 62-year-old man presents with fatigue, recurrent infections, and painless bilateral cervical and axillary lymphadenopathy over 8 months. CBC shows WBC 85 × 10^9/L, with 78% mature-appearing small lymphocytes. Peripheral smear shows smudge (smear) cells. He has no systemic symptoms. Which of the following best describes this condition?

A Chronic lymphocytic leukaemia — a B-cell neoplasm of mature small lymphocytes; smudge cells are the hallmark; Rai staging guides management
B Acute lymphoblastic leukaemia — blastic transformation with CNS tropism requiring immediate induction therapy
C Follicular lymphoma — nodal B-cell lymphoma with BCL-2 overexpression; smudge cells are not typical
D Hairy cell leukaemia — characterised by BRAF V600E, pancytopenia, and monocytopenia; no smudge cells

Correct. The presentation of an elderly man with slowly progressive lymphocytosis (mature small lymphocytes), painless lymphadenopathy, smudge (basket) cells on smear, and absence of systemic symptoms is classic for chronic lymphocytic leukaemia (CLL). CLL is the most common adult leukaemia in Western countries and is increasingly diagnosed in India. Smudge cells represent fragile tumour lymphocytes disrupted during smear preparation. Rai staging (0–IV, based on lymphocytosis, lymphadenopathy, hepatosplenomegaly, anaemia, and thrombocytopenia) determines prognosis and timing of treatment. Many patients with early-stage CLL are managed with watch-and-wait.

CLL = mature small B-cell lymphocytosis + smudge cells on smear + painless lymphadenopathy in older adults. Distinguish from ALL (blasts, aggressive, younger patients). Rai staging (0–IV) guides management. CD5+/CD23+ B-cell immunophenotype confirms diagnosis.

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Q4 IM13.4 1 pt

A 16-year-old boy presents with 3 months of painless right cervical lymph node enlargement, low-grade fever, night sweats, and 6 kg weight loss. Excision biopsy shows large binucleate cells with prominent eosinophilic 'owl-eye' nucleoli surrounded by a mixed inflammatory background of eosinophils, plasma cells, and lymphocytes. What is the diagnosis, and which staging system is used?

A Non-Hodgkin lymphoma — staged by Ann Arbor but usually presents as advanced-stage disease
B Hodgkin lymphoma (nodular sclerosis subtype) — staged by Ann Arbor (I–IV); characteristic Reed-Sternberg cells
C Burkitt lymphoma — staged by Murphy/St Jude; starry-sky pattern on biopsy
D Infectious mononucleosis — EBV-driven polyclonal B-cell activation; atypical lymphocytes not RS cells

Correct. The combination of painless cervical lymphadenopathy in a young patient, B symptoms (fever, night sweats, weight loss >10% in 6 months), and the pathognomonic Reed-Sternberg (RS) cells — large binucleate or bilobed cells with prominent eosinophilic 'owl-eye' nucleoli in a mixed inflammatory background — confirms Hodgkin lymphoma. The nodular sclerosis subtype (RS cells within lacunae in a collagen-banded background) is the most common subtype and typically involves mediastinal or cervical nodes in young adults. Staging uses the Ann Arbor system (I–IV, with A/B suffix for absence/presence of B symptoms and E/S modifiers for extranodal/splenic involvement).

Hodgkin lymphoma = Reed-Sternberg cells (owl-eye nucleoli) in mixed inflammatory background. B symptoms: unexplained fever >38°C, drenching night sweats, weight loss >10% in 6 months. Staged by Ann Arbor (I–IV, A/B). Curable in most stages with ABVD chemotherapy ± radiation.

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Q5 IM13.4 1 pt

A 70-year-old man with known large B-cell lymphoma on salvage chemotherapy presents to the casualty with confusion, oliguria, and muscle cramps 48 hours after his second cycle of chemotherapy. Investigations show: serum uric acid 14 mg/dL, potassium 6.8 mEq/L, phosphate 8.2 mg/dL, calcium 6.9 mg/dL, creatinine 4.1 mg/dL. What is the diagnosis, and what is the FIRST-LINE pharmacological prevention for this complication?

A Hypercalcaemia of malignancy; first-line treatment is IV bisphosphonate (zoledronic acid)
B Tumour lysis syndrome; first-line prevention is allopurinol plus aggressive IV hydration; rasburicase for high-risk patients
C Disseminated intravascular coagulation; first-line treatment is fresh frozen plasma and platelet transfusion
D Febrile neutropenia; first-line treatment is broad-spectrum IV antibiotics within 1 hour

Correct. The tetrad of hyperuricaemia, hyperkalaemia, hyperphosphataemia, and hypocalcaemia (due to calcium-phosphate precipitation) with acute kidney injury occurring after chemotherapy for a high-burden lymphoma is tumour lysis syndrome (TLS). TLS results from massive release of intracellular contents — uric acid (from purine catabolism), potassium, and phosphate — when tumour cells are rapidly destroyed. Prevention: aggressive IV hydration (to maintain urine output ≥100 mL/hr) + allopurinol (inhibits xanthine oxidase, reducing uric acid synthesis) started 24–48 hours before chemotherapy. Rasburicase (recombinant uricase) is reserved for high-risk patients (high tumour burden, elevated baseline uric acid) — it enzymatically degrades uric acid more rapidly than allopurinol.

TLS = hyperuricaemia + hyperkalaemia + hyperphosphataemia + hypocalcaemia + AKI after cytotoxic therapy. Most common in Burkitt lymphoma, ALL, and high-grade NHL. Prevention: IV hydration + allopurinol pre-chemo; rasburicase for high-risk. Monitor electrolytes, uric acid, and creatinine every 6–8 hours.

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Q6 IM13.4 1 pt

A 58-year-old woman with metastatic breast cancer presents with severe back pain, progressive bilateral lower limb weakness over 3 days, and difficulty voiding. MRI spine shows a T6 vertebral body metastasis compressing the spinal cord. What is the IMMEDIATE management priority?

A Urgent CT-guided biopsy of the vertebral lesion for tissue diagnosis before any treatment
B High-dose dexamethasone immediately, followed by urgent radiation oncology and spinal surgery review within 24 hours
C IV bisphosphonate infusion to reduce skeletal-related events and analgesics for pain control
D Start systemic chemotherapy within 24 hours to shrink the metastatic lesion

Correct. Malignant spinal cord compression (MSCC) is an oncological emergency. The degree of neurological recovery is directly proportional to the neurological function at the time treatment is initiated — patients still ambulatory at presentation have the best outcomes. Immediate management: high-dose dexamethasone (typically 16 mg IV loading, then 8 mg twice daily) to reduce perilesional oedema, followed by urgent multidisciplinary review for emergency radiotherapy (treatment of choice for most) or surgical decompression (for spinal instability, progressive neurology despite RT, or radioresistant tumour). Bladder dysfunction indicates cord compromise at sacral level; catheterisation may be needed.

MSCC = back pain + progressive limb weakness + sphincter disturbance in a cancer patient = emergency. Immediate dexamethasone; urgent MRI if not done; radiotherapy within 24 hours. Ambulatory status at treatment determines outcome. Never delay treatment awaiting biopsy in known malignancy.

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Q7 IM13.4 1 pt

A 45-year-old woman with advanced ovarian cancer is admitted with somnolence, severe constipation, polyuria, and polydipsia. Serum calcium is 3.8 mmol/L (corrected). She is not on thiazide diuretics or calcium supplements. Which of the following correctly pairs the mechanism of hypercalcaemia and its first-line treatment?

A PTH-related peptide (PTHrP) secreted by tumour cells mimics PTH → osteoclast activation; first-line treatment is IV 0.9% saline hydration followed by zoledronic acid
B Calcitonin deficiency from thyroid metastasis; first-line treatment is calcitonin infusion
C Hypervitaminosis D from 1-alpha-hydroxylase overexpression; first-line treatment is oral prednisolone
D Direct bone dissolution by primary ovarian cancer cells; first-line treatment is emergency surgery

Correct. Hypercalcaemia of malignancy is the most common life-threatening metabolic complication of cancer. The most frequent mechanism in solid tumours (squamous cell cancers, renal, breast, ovarian) is ectopic secretion of PTH-related peptide (PTHrP), which binds PTH receptors on osteoclasts and renal tubular cells, activating osteoclastic bone resorption and reducing renal calcium excretion. First-line treatment: aggressive IV 0.9% saline hydration (3–4 L/day) to restore intravascular volume and promote renal calcium excretion, followed by IV zoledronic acid (bisphosphonate) which inhibits osteoclast function and is the most potent and durable agent for hypercalcaemia of malignancy. Furosemide after hydration may be added if volume overloaded.

Hypercalcaemia of malignancy: most common mechanism = PTHrP (solid tumours); osteolytic metastases (breast, myeloma); 1,25-OH vitamin D excess (lymphoma). Symptoms: moans, groans, bones, psychic overtones. Treatment: IV saline hydration → IV bisphosphonate (zoledronic acid). Calcitonin for rapid acute effect (tachyphylaxis limits long-term use).

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Q8 IM13.4 1 pt

A 65-year-old man with AML receiving induction chemotherapy (7+3 regimen: cytarabine + anthracycline) develops fever of 39.2°C on day 12. He appears unwell. Blood counts show WBC 0.4 × 10^9/L with ANC 0.2 × 10^9/L. Blood cultures are drawn. What is the correct next step?

A Wait 48–72 hours for blood culture results before starting antibiotics to avoid unnecessary antibiotic exposure
B Start broad-spectrum IV antibiotics (e.g., piperacillin-tazobactam or carbapenem) within 1 hour of fever recognition without waiting for culture results
C Add antifungal therapy (voriconazole) immediately because fever in AML is always fungal after day 7
D Administer G-CSF (filgrastim) urgently to raise the neutrophil count before starting antibiotics

Correct. Febrile neutropenia (fever ≥38.3°C once or ≥38.0°C sustained for 1 hour + ANC <0.5 × 10^9/L, or <1.0 × 10^9/L falling to <0.5) is a medical emergency. Delay in antibiotic initiation of even 1–2 hours significantly increases mortality. Management: draw blood cultures (peripheral and from central line if present) and other appropriate cultures, then immediately start empirical broad-spectrum IV antibiotics covering gram-negative organisms (including Pseudomonas) within 1 hour — piperacillin-tazobactam or carbapenem are standard. Antifungal coverage is added only if fever persists >96 hours despite antibiotics, not empirically from the outset. G-CSF does not substitute for or precede antibiotics.

Febrile neutropenia = ANC <0.5 × 10^9/L + fever ≥38.3°C = oncological emergency. Give broad-spectrum IV antibiotics within 1 hour — NEVER wait for culture results. Add antifungal only after 96 hours of antibiotic failure. MASCC score stratifies low vs high risk for out-patient management.

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Q9 IM13.4 1 pt

A 70-year-old man with known lung cancer develops progressive facial and neck swelling over 3 weeks. His face appears plethoric and oedematous; there are dilated collateral veins over the anterior chest wall. He is dyspnoeic in the supine position. What is the diagnosis, and what is the immediate positioning and diagnostic step?

A Superior vena cava (SVC) syndrome; sit patient upright immediately; CT chest with contrast to assess level and cause of obstruction
B Cardiac tamponade from pericardial metastasis; immediate echocardiography and pericardiocentesis
C Cerebral venous sinus thrombosis; immediate CT brain then anticoagulation
D Bilateral axillary lymph node obstruction; bilateral axillary lymph node biopsy and CT thorax

Correct. The clinical triad of facial/neck oedema, plethora, and dilated anterior chest wall collateral veins (filling from below upward in the supine position) with orthopnoea in a patient with lung cancer is classic for superior vena cava (SVC) syndrome. This is caused by compression or invasion of the SVC, most commonly by right-sided lung cancer (especially small cell lung cancer or squamous cell carcinoma), mediastinal lymphoma, or central venous catheter thrombosis. Immediate management: sit the patient upright (reduces venous pressure in the head/neck), supplemental oxygen if needed, and CT chest with contrast to delineate the level of obstruction, degree of collateral flow, and primary tumour extent. Dexamethasone may provide temporary symptomatic relief. Definitive treatment depends on histology (chemotherapy for SCLC/lymphoma; SVC stenting for rapid relief; radiotherapy for radiosensitive tumours).

SVC syndrome = facial/neck oedema + plethora + dilated chest wall collateral veins in a cancer patient (especially lung/lymphoma). Sit upright immediately. CT chest with contrast to confirm. Dexamethasone for symptom relief; SVC stenting or chemo/radiotherapy per histology.

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Q10 IM13.17 1 pt

A 52-year-old man with advanced lung adenocarcinoma is on regular oral morphine 30 mg every 4 hours for background pain. He develops new-onset nausea and constipation since the dose was increased last week. What is the most appropriate immediate management of his opioid-induced constipation?

A Discontinue morphine and switch to a non-opioid analgesic to avoid further constipation
B Start a stimulant laxative (e.g., bisacodyl or senna) and a stool softener; this should be prescribed prophylactically with every opioid
C Prescribe a bulk-forming laxative (ispaghula husk) as first-line for opioid-induced constipation
D Reduce the morphine dose by 50% to balance analgesia with constipation

Correct. Constipation affects virtually all patients on regular opioids and, unlike nausea and sedation, does not improve with continued use (no tolerance develops). A stimulant laxative (senna, bisacodyl) ± a stool softener (docusate) should be prescribed prophylactically whenever an opioid is started — not added reactively after constipation develops. Bulk-forming agents are contraindicated in opioid-induced constipation because they require adequate fluid intake and gut motility (which opioids reduce) — they cause impaction. Reducing the morphine dose or stopping opioids is inappropriate if the patient's pain is not controlled by lower doses.

Opioid-induced constipation: never develops tolerance; always prescribe a stimulant laxative (senna/bisacodyl) prophylactically. Bulk-forming laxatives are CONTRAINDICATED with opioids. Nausea and sedation usually improve after 1–2 weeks (tolerance develops); constipation does not. WHO analgesic ladder: paracetamol → weak opioids (codeine/tramadol) → strong opioids (morphine/oxycodone).

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