Oncology Practice Questions

Q: A 14-year-old girl presents with a rash, abdominal pain, arthralgias, nausea, vomiting, and bloody stools. Physical examination reveals a palpable purpuric rash on her buttocks and lower legs, a tender abdomen, and no active joint inflammation. Urinalysis shows RBCs and RBC casts, and her renal function deteriorates rapidly. A renal biopsy is performed. Considering the clinical presentation and biopsy, what is the most likely diagnosis on renal biopsy for this patient with glomerulonephritis (GN)?

Diffuse proliferative GN. **Explanation:** The clinical presentation of a palpable purpuric rash (buttocks/legs), abdominal pain, arthralgia, and hematuria in a young patient is classic for **Henoch-Schönlein Purpura (HSP)**, also known as IgA Vasculitis. When HSP involves the kidneys, it is termed HSP nephritis. **Why Option A is Correct:** The renal manifestations of HSP are histologically identical to IgA Nephropathy [1]. The severity of the biopsy findings correlates with the clinical presentation. While HSP can show a spectrum of changes, in cases where there is **rapidly deteriorating renal function** and significant hematuria (RBC casts), the most common underlying histological pattern is **Diffuse Proliferative Glomerulonephritis (DPGN)**. This involves global involvement of more than 50% of glomeruli with significant mesangial and endocapillary proliferation. **Why other options are incorrect:** * **B. Crescentic GN:** While this represents the most severe form (Type VI) and can cause rapid deterioration [2], DPGN is the broader pathological category often associated with the initial aggressive proliferative phase in systemic vasculitis. * **C. Focal Proliferative GN:** This is seen in milder clinical cases of HSP where renal function is usually preserved. * **D. Membranoproliferative GN (MPGN):** This is characterized by "tram-track" basement membrane splitting and is typically associated with Hepatitis C or complement dysregulation, not classic HSP. **High-Yield Clinical Pearls for NEET-PG:** * **HSP Tetrad:** Purpura (non-thrombocytopenic), Arthralgia, Abdominal pain, and Renal disease. * **Pathogenesis:** Systemic deposition of **IgA1-containing immune complexes**. * **Biopsy Gold Standard:** Immunofluorescence showing **mesangial IgA deposits** [1]. * **Prognosis:** Generally excellent in children, but the presence of RBC casts and nephritic/nephrotic range proteinuria indicates a higher risk of chronic kidney disease.

Q: Which of the following statements regarding the Philadelphia chromosome is NOT true?

Specific for CML.. The Philadelphia (Ph) chromosome is the hallmark of Chronic Myeloid Leukemia (CML), but it is not exclusive to it. **Explanation of the Correct Answer (C):** The statement "Specific for CML" is **incorrect** because the Philadelphia chromosome is also found in other hematological malignancies. It is present in approximately **25-30% of adults with Acute Lymphoblastic Leukemia (ALL)**, 2-5% of pediatric ALL, and occasionally in Acute Myeloid Leukemia (AML). In ALL, its presence signifies a poor prognosis [1]. **Analysis of Other Options:** * **Option A:** It is present in **>95% of CML patients**. The remaining 5% are "Ph-negative" but usually harbor the cryptic *BCR-ABL1* fusion gene detectable by FISH or PCR. * **Option B & D:** The Ph chromosome is a **reciprocal translocation** between chromosomes 9 and 22, designated as **t(9;22)(q34;q11)** [2]. This results in the fusion of the *ABL1* proto-oncogene (Ch 9) with the *BCR* gene (Ch 22), creating a chimeric protein with constitutive tyrosine kinase activity [2]. **High-Yield Clinical Pearls for NEET-PG:** 1. **Molecular Weight:** The fusion protein in CML is typically **p210**, whereas in Ph+ ALL, it is often **p190**. 2. **Diagnosis:** While karyotyping identifies the Ph chromosome, **FISH** is more sensitive, and **RT-PCR** is the gold standard for monitoring Minimal Residual Disease (MRD) [3]. 3. **Treatment:** The first-line treatment for Ph+ CML is **Imatinib** (a Tyrosine Kinase Inhibitor) [2], [3]. 4. **Blast Crisis:** CML can transform into either AML (70%) or ALL (30%) during a blast crisis.

Q: A 50-year-old woman presents with pain and swelling in her proximal interphalangeal joints, wrists, and knees, accompanied by morning stiffness. She has a history of hysterectomy 10 years ago. Physical examination reveals swelling and synovial thickening of the proximal interphalangeal (PIP) joints. Her laboratory findings include: Hemoglobin 10.3 g/dL, MCV 80 fL, serum iron 28 mg/dL, iron-binding capacity 200 mg/dL, and saturation 14%. What is the most likely explanation for this woman's anemia?

Anemia of chronic disease. The patient presents with clinical features classic for **Rheumatoid Arthritis (RA)**: symmetrical inflammatory polyarthritis involving the PIP joints and wrists with significant morning stiffness [1]. In the context of a chronic inflammatory state like RA, the most common cause of anemia is **Anemia of Chronic Disease (ACD)**. [2] **1. Why Anemia of Chronic Disease is correct:** In chronic inflammation, cytokines (especially IL-6) trigger the liver to produce **Hepcidin** [1]. Hepcidin inhibits **ferroportin**, preventing iron release from macrophages and decreasing intestinal iron absorption. This leads to "iron sequestration" [3]. * **Lab Profile in ACD:** Low serum iron, **low Total Iron Binding Capacity (TIBC)**, and normal-to-high ferritin. * In this case, the TIBC is low (200 mg/dL; normal 250–450), which is the hallmark that distinguishes ACD from Iron Deficiency Anemia (IDA). **2. Why the other options are incorrect:** * **A. Occult blood loss:** This leads to Iron Deficiency Anemia. While IDA also has low serum iron, it is characterized by a **high TIBC** (compensatory increase in transferrin), which is not present here. [3] * **B. Vitamin deficiency:** B12 or Folate deficiency causes megaloblastic anemia with a **high MCV** (>100 fL). This patient has a low-normal MCV (80 fL). * **C. Sideroblastic anemia:** This typically presents with **increased** serum iron and saturation due to the inability to incorporate iron into hemoglobin, often showing "ringed sideroblasts" in the bone marrow. **High-Yield Clinical Pearls for NEET-PG:** * **ACD vs. IDA:** The most reliable differentiator is **Ferritin** (Low in IDA, Normal/High in ACD) and **TIBC** (High in IDA, Low in ACD). * **Hepcidin** is the "master regulator" of iron metabolism and an acute-phase reactant [3]. * In RA, the severity of anemia usually correlates with the degree of joint inflammation and ESR/CRP levels.

Q: What is the most common cause of carcinomatous meningitis?

Carcinoma of the breast. **Explanation:** **Carcinomatous meningitis** (also known as Leptomeningeal Carcinomatosis) occurs when cancer cells infiltrate the subarachnoid space and spread via the cerebrospinal fluid (CSF). **1. Why Breast Carcinoma is the Correct Answer:** Statistically, **Breast Carcinoma** is the most common solid tumor to cause leptomeningeal metastasis, accounting for approximately 30–40% of cases. [1] This is followed closely by lung cancer. The high prevalence is attributed to the biological tendency of breast cancer cells to seed the CNS and the prolonged survival of these patients due to improved systemic therapies, allowing time for late-stage meningeal seeding to manifest. **2. Analysis of Incorrect Options:** * **Carcinoma of the Lung (Option B):** This is the second most common cause. While lung cancer is the most common cause of *parenchymal* brain metastases, it ranks just behind breast cancer for purely leptomeningeal involvement. * **Malignant Melanoma (Option D):** Melanoma has the highest *relative risk* or "propensity" per case to spread to the meninges; however, because melanoma is less common than breast or lung cancer in the general population, it is not the most common cause overall. * **Gastrointestinal Tract (Option C):** GI malignancies (like gastric or colorectal cancer) can cause carcinomatous meningitis, but this is significantly rarer compared to breast, lung, and melanoma. **3. NEET-PG High-Yield Pearls:** * **Clinical Presentation:** Characterized by "multifocal" neurological deficits (e.g., cranial nerve palsies + radiculopathy + headache). * **Gold Standard Diagnosis:** CSF Cytology (shows malignant cells). Note: The first tap may be negative; sensitivity increases with repeated taps (up to 3 taps). [2] * **MRI Finding:** "Sugar coating" or linear enhancement of the leptomeninges and cranial nerves (Zuckerguss appearance). * **Most common primary in children:** Medulloblastoma and Ependymoma.

Q: Which of the following is NOT a paraneoplastic manifestation of bronchogenic carcinoma?

Acanthosis nigricans. **Explanation:** Paraneoplastic syndromes are clinical syndromes involving non-metastatic systemic effects that accompany malignant disease [3]. While many cancers share similar paraneoplastic manifestations, certain signs are classically associated with specific primary tumors. **Why Acanthosis Nigricans is the correct answer:** Acanthosis nigricans (specifically the malignant type) is most strongly associated with **intra-abdominal adenocarcinomas**, with **gastric carcinoma** being the most common (approx. 55-60% of cases). While it can rarely occur with other cancers, it is not a classic paraneoplastic manifestation of bronchogenic carcinoma. **Analysis of other options:** * **Dermatomyositis (A):** This inflammatory myopathy has a strong association with several malignancies, particularly **Small Cell Lung Cancer (SCLC)** and non-small cell lung cancer, as well as ovarian and breast cancers [1]. * **Cerebellar degeneration (C):** Paraneoplastic cerebellar degeneration is a well-documented neurological manifestation of **Small Cell Lung Cancer**, often mediated by anti-Hu or anti-VGCC antibodies [3]. * **Hyperkeratosis of palms and soles (D):** Also known as **Tylosis**, this is a recognized paraneoplastic feature of **Squamous Cell Carcinoma of the Lung** (and esophagus). **NEET-PG High-Yield Pearls:** * **Small Cell Lung Cancer (SCLC):** Most common cause of SIADH, Ectopic ACTH (Cushing’s), and Lambert-Eaton Myasthenic Syndrome [1], [3]. * **Squamous Cell Carcinoma:** Most common cause of Hypercalcemia (due to PTHrP) [1]. * **Hypertrophic Osteoarthropathy (HOA):** Classically associated with Adenocarcinoma of the lung [2]. * **Leser-Trélat sign:** Sudden onset of multiple seborrheic keratoses; like malignant acanthosis nigricans, it points toward **Gastric Adenocarcinoma**.

Q: Which of the following drugs has been found to increase survival in locally advanced pancreatic cancer?

Gemcitabine. **Explanation:** **Gemcitabine** (Option C) is the correct answer. It is a pyrimidine antimetabolite that inhibits DNA synthesis. For decades, Gemcitabine has been the cornerstone of chemotherapy for locally advanced and metastatic pancreatic adenocarcinoma. Clinical trials demonstrated that Gemcitabine provides a significant "clinical benefit response" (improvement in pain, performance status, and weight) and a modest but statistically significant survival advantage compared to older agents like 5-Fluorouracil. **Analysis of Incorrect Options:** * **Doxorubicin (A):** An anthracycline primarily used in breast cancer, lymphomas, and sarcomas. It has minimal efficacy in pancreatic cancer and is not a standard treatment. * **Streptozocin (B):** This is an alkylating agent specifically toxic to pancreatic islet cells. While it is used in the management of **Pancreatic Neuroendocrine Tumors (PNETs)** like insulinomas, it is ineffective against the more common pancreatic adenocarcinoma. * **Paclitaxel (D):** While standard Paclitaxel is not used alone, its albumin-bound formulation (**Nab-paclitaxel**) is used *in combination* with Gemcitabine. However, as a monotherapy, it does not hold the same historical or clinical weight as Gemcitabine for survival. **High-Yield Clinical Pearls for NEET-PG:** * **First-line regimens:** For patients with good performance status, **FOLFIRINOX** (5-FU, Leucovorin, Irinotecan, and Oxaliplatin) or **Gemcitabine + Nab-paclitaxel** are the current preferred regimens, offering better survival than Gemcitabine alone. * **Radiosensitizer:** Gemcitabine also acts as a potent radiosensitizer in locally advanced cases. * **Tumor Marker:** **CA 19-9** is the most specific marker used to monitor treatment response and recurrence in pancreatic cancer.

Q: A 56-year-old man is evaluated for a recent onset painful skin lesion involving his abdominal wall. The lesion started 3 days ago as a small erythematous macule which has gradually increased in size to a large purpuric lesion with bulla formation. He is afebrile and does not recall any trauma. His medical history is significant for atrial fibrillation; he was recently switched from rivaroxaban to warfarin due to the high cost of rivaroxaban. What is the most probable cause of the condition?

Warfarin. ### Explanation The clinical presentation describes **Warfarin-induced Skin Necrosis (WISN)**, a rare but serious complication of oral anticoagulant therapy. **1. Why Warfarin is Correct:** Warfarin inhibits Vitamin K epoxide reductase, leading to a decrease in Vitamin K-dependent clotting factors (II, VII, IX, X) and anticoagulant proteins (Protein C and Protein S). Protein C has a significantly shorter half-life (~6 hours) compared to procoagulant factors like Factor II (~60 hours) and Factor X (~40 hours). During the initial phase of warfarin therapy, Protein C levels drop rapidly, creating a transient **prothrombotic state**. This leads to microvascular thrombosis, skin ischemia, and subsequent necrosis. It typically occurs 3–10 days after starting therapy, often in areas with high subcutaneous fat (breasts, thighs, abdomen). **2. Why Incorrect Options are Wrong:** * **Rivaroxaban (A):** As a direct Factor Xa inhibitor, it does not affect Protein C/S levels and is not associated with skin necrosis. In fact, switching *from* rivaroxaban *to* warfarin triggered this event. * **Low-molecular-weight heparin (B):** LMWH is actually used to *prevent* WISN by providing "bridging" anticoagulation until a stable INR is reached. * **Low dose aspirin (D):** Aspirin is an antiplatelet agent. While it can cause bruising, it does not cause the characteristic purpuric bullae and necrosis seen in this patient. **3. High-Yield Pearls for NEET-PG:** * **Risk Factor:** Underlying **Protein C deficiency** is the most common predisposing factor. * **Prevention:** Always "bridge" with Heparin/LMWH when starting Warfarin in high-risk patients. * **Management:** Immediate cessation of Warfarin, administration of Vitamin K, and giving **Protein C concentrate** or Fresh Frozen Plasma (FFP). * **Differential:** Do not confuse with *Calciphylaxis* (seen in ESRD) or *Heparin-induced Thrombocytopenia (HIT)*.

Question 1

A 14-year-old girl presents with a rash, abdominal pain, arthralgias, nausea, vomiting, and bloody stools. Physical examination reveals a palpable purpuric rash on her buttocks and lower legs, a tender abdomen, and no active joint inflammation. Urinalysis shows RBCs and RBC casts, and her renal function deteriorates rapidly. A renal biopsy is performed. Considering the clinical presentation and biopsy, what is the most likely diagnosis on renal biopsy for this patient with glomerulonephritis (GN)?

Accepted Answer

Diffuse proliferative GN

Answer

Crescentic GN

Answer

Focal proliferative GN

Answer

Membranoproliferative GN

Question 2

Which parameter best predicts the return of renal function in a patient with tumor lysis syndrome?

Accepted Answer

Serum uric acid

Answer

Serum creatinine

Answer

Serum phosphate

Answer

Serum potassium

Question 3

Which of the following statements regarding the Philadelphia chromosome is NOT true?

Accepted Answer

Specific for CML.

Answer

Present in 95% of chronic myeloid leukemia (CML) patients.

Answer

It is the result of a reciprocal translocation.

Answer

Designated as t(9;22)(q34;q11).

Question 4

A 50-year-old woman presents with pain and swelling in her proximal interphalangeal joints, wrists, and knees, accompanied by morning stiffness. She has a history of hysterectomy 10 years ago. Physical examination reveals swelling and synovial thickening of the proximal interphalangeal (PIP) joints. Her laboratory findings include: Hemoglobin 10.3 g/dL, MCV 80 fL, serum iron 28 mg/dL, iron-binding capacity 200 mg/dL, and saturation 14%. What is the most likely explanation for this woman's anemia?

Accepted Answer

Anemia of chronic disease

Answer

Occult blood loss

Answer

Vitamin deficiency

Answer

Sideroblastic anemia

Question 5

A 69-year-old man with a 60 pack-year smoking history presents with dizziness and visual disturbances. Physical examination reveals a purplish discoloration of his face, arms, and neck; retinal vein engorgement; and visible distention of his neck veins. His complete blood count reveals a normocytic anemia. The pathophysiology of this patient’s clinical presentation most likely involves which of the following?

Accepted Answer

Obstruction of the superior vena cava by a primary tumor arising in the lungs

Answer

Right heart failure secondary to left heart failure

Answer

Metastatic disease to the cervical lymph nodes with compression of the jugular veins

Answer

Polycythemia rubra vera

Question 6

Which of the following is NOT recommended for the management of Tumour lysis syndrome?

Accepted Answer

Urinary alkalinisation using soda bicarbonate

Answer

Allopurinol

Answer

Febuxostat

Answer

Rasburicase

Question 7

What is the most common cause of carcinomatous meningitis?

Accepted Answer

Carcinoma of the breast

Answer

Carcinoma of the lung

Answer

Carcinoma of the gastrointestinal tract

Answer

Malignant melanoma

Question 8

Which of the following is NOT a paraneoplastic manifestation of bronchogenic carcinoma?

Accepted Answer

Acanthosis nigricans

Answer

Dermatomyositis

Answer

Cerebellar degeneration

Answer

Hyperkeratosis of palm and soles

Question 9

Which of the following drugs has been found to increase survival in locally advanced pancreatic cancer?

Accepted Answer

Gemcitabine

Answer

Doxorubicin

Answer

Streptozocin

Answer

Paclitaxel

Question 10

A 56-year-old man is evaluated for a recent onset painful skin lesion involving his abdominal wall. The lesion started 3 days ago as a small erythematous macule which has gradually increased in size to a large purpuric lesion with bulla formation. He is afebrile and does not recall any trauma. His medical history is significant for atrial fibrillation; he was recently switched from rivaroxaban to warfarin due to the high cost of rivaroxaban. What is the most probable cause of the condition?

Accepted Answer

Warfarin

Answer

Rivaroxaban

Answer

Low-molecular-weight heparin

Answer

Low dose aspirin (81 mg/d)

Oncology — MCQs

Oncology — MCQs

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