Oncology — MCQs

A 41-year-old man presented with a 9-month history of cough, exertional dyspnea, nocturnal diaphoresis, and weight loss of 10 kg. Physical examination revealed painless, massive, discrete, rubbery cervical, supraclavicular, and axillary lymphadenopathy. Chest radiography showed bilateral hilar lymphadenopathy. The serum calcium level was elevated at 16.2 mg/dL, with serum parathyroid hormone within the normal range. What is the urgent treatment to be instituted?

Q88Easy

All of the following are carcinogenic except?

Q89Hard

A 62-year-old man with a history of hypertension and gout, treated with metoprolol and allopurinol, presents with 4 weeks of drowsiness and generalized weakness. He experienced a tonic-clonic seizure. He is a long-term smoker (1 pack/day for 40 years) and has had unintentional weight loss of 20 lb over the past 2 months. His laboratory findings include hemoglobin 10.2 gm/dL, serum sodium 122 mEq/L, serum osmolality 258 mOsm/kg, urine osmolality 300 mOsm/kg, and urine sodium 48 mmol/L. TSH and cortisol levels are normal. What is the most likely diagnosis?

Q90Medium

A 57-year-old man presents with a serum sodium of 125 mEq/L. On examination, he has pitting edema and elevated neck veins. His urine sodium is 10 mEq/L and urine osmolality is 350 mOsm/kg. What is the most likely diagnosis for this patient's hyponatremia?

Oncology Indian Medical PG Practice Questions and MCQs

Question 81: Trousseau's sign is seen in all the following conditions except:

A. Lung carcinoma
B. Gastric carcinoma
C. Pancreatic carcinoma
D. Liposarcoma (Correct Answer)

Explanation: **Explanation:** **Trousseau’s sign of malignancy** (also known as Migratory Thrombophlebitis) refers to spontaneous, recurrent episodes of venous thrombosis at changing (migratory) sites. This phenomenon is a **paraneoplastic syndrome** caused by the release of procoagulants (like tissue factor and mucins) from tumor cells, which activate the coagulation cascade [1]. **Why Liposarcoma is the correct answer:** Trousseau’s sign is classically associated with **mucin-secreting adenocarcinomas**. Liposarcoma is a mesenchymal tumor (sarcoma) arising from fat cells and does not typically secrete the mucins or procoagulants required to trigger migratory thrombophlebitis. Therefore, it is the "except" in this list. **Analysis of other options:** * **Pancreatic Carcinoma:** This is the **most common** association [1]. Trousseau’s sign is frequently the presenting feature of occult pancreatic tail/body cancer. * **Gastric Carcinoma:** As a mucin-producing adenocarcinoma, it is a well-documented cause of hypercoagulability and Trousseau’s sign [1]. * **Lung Carcinoma:** Specifically, **Adenocarcinoma of the lung** is a known cause of paraneoplastic migratory thrombophlebitis. **NEET-PG Clinical Pearls:** 1. **Distinction:** Do not confuse this with *Trousseau’s sign of latent tetany* (carpal spasm induced by BP cuff inflation in hypocalcemia). 2. **Mechanism:** Tumor-derived **mucin** interacts with P-selectin and L-selectin, leading to the formation of platelet-rich microthrombi. 3. **High-Yield Association:** If a patient presents with migratory thrombophlebitis, the first investigation should often be an abdominal CT to rule out **Pancreatic Cancer**. 4. **Treatment:** Heparin is generally more effective than warfarin in managing cancer-associated thrombosis.

Question 82: A 60-year-old patient presents with diarrhea and abdominal pain for 5 days. Ultrasound abdomen is normal, and CT abdomen shows a local mass in the jejunum. 24-hour urine test shows elevated 5-HIAA. What is the most common site for a primary tumor that causes these findings?

A. Gastrointestinal tract
B. Bronchus (Correct Answer)
C. Kidney
D. Adrenal gland

Explanation: **Explanation:** The patient presents with the classic triad of **Carcinoid Syndrome** (diarrhea, abdominal pain, and elevated urinary 5-HIAA). Carcinoid syndrome occurs when neuroendocrine tumors (NETs) secrete vasoactive substances like serotonin directly into the systemic circulation [1]. **Why Bronchus is the correct answer:** In the context of this specific question, the key is the **absence of liver metastases** (implied by a normal ultrasound). * **Midgut/GI Carcinoids:** Serotonin produced by GI tumors is normally metabolized by the liver (first-pass metabolism) into inactive 5-HIAA [1]. Therefore, GI carcinoids **only** cause systemic carcinoid syndrome once they have metastasized to the liver, bypassing this metabolism [1]. * **Bronchial Carcinoids:** These tumors release serotonin directly into the pulmonary veins and then into the systemic circulation, bypassing the liver entirely. Thus, a primary bronchial carcinoid can cause carcinoid syndrome **without** liver metastasis [1]. Given the normal ultrasound and the presence of symptoms, the primary site is most likely the bronchus. **Analysis of Incorrect Options:** * **A. Gastrointestinal tract:** While the GI tract (specifically the ileum) is the most common site for NETs overall, they rarely cause carcinoid syndrome unless liver metastases are present [1][2]. * **C & D. Kidney and Adrenal gland:** These are not typical sites for serotonin-secreting neuroendocrine tumors and do not present with elevated 5-HIAA. **High-Yield Clinical Pearls for NEET-PG:** * **Most common site for NETs:** Small Intestine (specifically the Ileum) [2]. * **Most common site for NETs causing Carcinoid Syndrome:** Ileum (but requires liver metastasis) [1]. * **Diagnostic Test of Choice:** 24-hour urinary 5-HIAA (metabolite of serotonin). * **Localization:** Chromogranin A (tumor marker) and Octreoscan (Somatostatin receptor scintigraphy). * **Management:** Octreotide (Somatostatin analog) is used to control symptoms.

Question 83: Tumour lysis syndrome is associated with the treatment of which condition?

A. Hairy cell leukemia
B. Burkitt's lymphoma (Correct Answer)
C. Plasmacytoma
D. All of the above

Explanation: **Explanation:** **Tumor Lysis Syndrome (TLS)** is an oncologic emergency caused by the rapid destruction of a large number of tumor cells, leading to the release of intracellular contents into the bloodstream. **Why Burkitt’s Lymphoma is the Correct Answer:** TLS is most commonly associated with **high-grade hematologic malignancies** characterized by a high tumor burden, rapid cell turnover (high proliferation rate), and high sensitivity to chemotherapy [1]. **Burkitt’s lymphoma** is the classic prototype for this; it has a doubling time of approximately 24 hours [1]. When chemotherapy is initiated, the massive release of potassium, phosphate, and nucleic acids (which metabolize into uric acid) overwhelms the body's homeostatic mechanisms. **Why Other Options are Incorrect:** * **Hairy Cell Leukemia:** This is a chronic, indolent B-cell lymphoproliferative disorder. Because the cells divide slowly and the tumor burden is typically lower compared to high-grade lymphomas, the risk of TLS is minimal [1]. * **Plasmacytoma:** This is a localized collection of plasma cells [2]. While it is a plasma cell dyscrasia, it lacks the rapid proliferative kinetics required to trigger systemic TLS upon treatment. [2] **High-Yield Clinical Pearls for NEET-PG:** * **Metabolic Profile of TLS:** Hyperuricemia, Hyperkalemia, Hyperphosphatemia, and **Hypocalcemia** (due to calcium-phosphate precipitation). * **Renal Impact:** Acute Kidney Injury (AKI) occurs due to the precipitation of uric acid crystals or calcium phosphate in the renal tubules. * **Prophylaxis/Treatment:** Aggressive hydration is the mainstay. **Allopurinol** (prevents new uric acid formation) or **Rasburicase** (recombinant urate oxidase that breaks down existing uric acid) are used for management. * **Risk Factors:** High LDH levels and pre-existing renal insufficiency.

Question 84: What is the initial treatment for tumor lysis syndrome?

A. Rasburicase, hydration, potassium binder, and urinary alkalization (Correct Answer)
B. Allopurinol, hydration, potassium binder, and alkalization
C. Both rasburicase and allopurinol, with hydration and a potassium binder
D. Hydration alone is sufficient

Explanation: Tumor Lysis Syndrome (TLS) is an oncologic emergency caused by the rapid breakdown of tumor cells, leading to the release of intracellular contents into the bloodstream [1]. This results in the "TLS metabolic quartet": **Hyperuricemia, Hyperkalemia, Hyperphosphatemia, and Hypocalcemia.** **Why Option A is Correct:** The management of TLS focuses on aggressive hydration and correcting metabolic derangements. * **Hydration:** Increases glomerular filtration and helps flush out uric acid and phosphates. * **Rasburicase:** This is a recombinant urate oxidase enzyme that converts existing uric acid into **allantoin**, which is 5-10 times more soluble. It is the preferred agent for established TLS or high-risk patients because it works rapidly. * **Potassium Binders:** Essential to manage life-threatening hyperkalemia. * **Urinary Alkalization:** Historically used to increase uric acid solubility; however, its role is now debated as it may promote calcium-phosphate precipitation. In many standard protocols and NEET-PG contexts, it remains a recognized component of initial management. **Why Other Options are Wrong:** * **Option B:** **Allopurinol** is a xanthine oxidase inhibitor. It prevents the *formation* of new uric acid but does nothing to reduce existing uric acid levels. It is used for **prophylaxis**, not the treatment of established TLS. * **Option C:** While both drugs target uric acid, Allopurinol is generally redundant once Rasburicase is started, as Rasburicase is significantly more potent and rapid. * **Option D:** Hydration is the cornerstone but is insufficient alone to manage the severe electrolyte imbalances and high uric acid levels seen in clinical TLS. **High-Yield Clinical Pearls for NEET-PG:** * **Cairo-Bishop Definition:** Used to classify Laboratory vs. Clinical TLS. * **Drug of Choice for Prophylaxis:** Allopurinol. * **Drug of Choice for Treatment:** Rasburicase. * **Contraindication:** Rasburicase is contraindicated in **G6PD deficiency** (risk of hemolysis). * **Most common cancers:** High-grade lymphomas (Burkitt’s) and Acute Leukemias (ALL) [1].

Question 85: Kaposi's sarcoma is associated with which of the following conditions?

A. Bronchial asthma
B. HIV (Correct Answer)
C. Hepatitis B
D. Hairy cell leukaemia

Explanation: **Explanation:** **Kaposi’s Sarcoma (KS)** is a vascular neoplasm caused by **Human Herpesvirus 8 (HHV-8)**, also known as Kaposi Sarcoma-associated Herpesvirus (KSHV). While HHV-8 is the primary oncogenic driver, the clinical manifestation of the disease is heavily dependent on the host's immune status. **Why HIV is the correct answer:** The most common and aggressive form of the disease is **AIDS-associated (Epidemic) Kaposi’s Sarcoma** [1]. In patients with HIV, the profound depletion of CD4+ T-cells and the presence of the HIV-Tat protein synergize with HHV-8 to promote spindle cell proliferation and angiogenesis. It is currently the most common neoplasm associated with HIV/AIDS and is considered an **AIDS-defining illness** [1]. **Analysis of Incorrect Options:** * **Bronchial Asthma:** This is a chronic inflammatory airway disease with no known association with HHV-8 or vascular malignancies. * **Hepatitis B:** While HBV is strongly associated with Hepatocellular Carcinoma (HCC), it does not play a role in the pathogenesis of Kaposi’s Sarcoma. * **Hairy Cell Leukaemia:** This is a rare B-cell lymphoproliferative disorder characterized by the BRAF V600E mutation; it is not linked to HHV-8. **Clinical Pearls for NEET-PG:** * **Morphology:** Presents as painless, non-blanching, violaceous (purple) macules, plaques, or nodules [1]. * **Histology:** Characterized by **spindle-shaped cells**, slit-like vascular spaces, and extravasated RBCs. * **Four Clinical Variants:** 1. Classic (Elderly Mediterranean men), 2. Endemic (African), 3. Iatrogenic (Transplant-related), 4. AIDS-associated [1]. * **Treatment:** Highly Active Antiretroviral Therapy (HAART) is the first-line management for AIDS-related KS. For localized lesions, intralesional vinblastine or cryotherapy is used; systemic chemotherapy (Liposomal Doxorubicin) is reserved for visceral involvement.

Question 86: Which type of lung carcinoma responds best to chemotherapy?

A. Squamous cell type
B. Oat cell type (Correct Answer)
C. Adenocarcinoma
D. All respond equally

Explanation: **Explanation:** The correct answer is **Oat cell type**, also known as **Small Cell Lung Carcinoma (SCLC)**. **1. Why Oat cell type is correct:** Small cell lung carcinoma is characterized by a very high growth fraction and a rapid doubling time. In oncology, the "Law of Bergonie and Tribondeau" dictates that cells with high mitotic activity are more sensitive to cytotoxic agents. Because SCLC is highly aggressive and almost always disseminated at the time of diagnosis, it is treated primarily as a systemic disease [1]. It shows a dramatic initial response to chemotherapy (typically Etoposide + Cisplatin/Carboplatin), with objective response rates often exceeding 60-80%. **2. Why other options are incorrect:** * **Squamous cell type & Adenocarcinoma:** These are subtypes of Non-Small Cell Lung Carcinoma (NSCLC). Unlike SCLC, NSCLC is characterized by slower growth and is relatively chemoresistant. While chemotherapy is used in advanced stages, the response is much less dramatic than in SCLC. Surgery is the primary treatment for early-stage NSCLC. * **All respond equally:** This is incorrect because lung cancers are biologically heterogeneous. The distinction between SCLC (chemosensitive) and NSCLC (chemoresistant) is a fundamental principle in thoracic oncology. **Clinical Pearls for NEET-PG:** * **Strongest Association:** SCLC and Squamous cell carcinoma have the strongest association with **smoking** [1]. * **Location:** SCLC and Squamous cell carcinoma are typically **central/hilar**, while Adenocarcinoma is usually **peripheral** [1]. * **Paraneoplastic Syndromes:** SCLC is most commonly associated with **SIADH** and **ACTH production** (Cushing’s), as well as Lambert-Eaton Myasthenic Syndrome [1]. * **Prognosis:** Despite being the most chemo-responsive, SCLC has a poor long-term prognosis due to early metastasis and frequent recurrence.

Question 87: A 41-year-old man presented with a 9-month history of cough, exertional dyspnea, nocturnal diaphoresis, and weight loss of 10 kg. Physical examination revealed painless, massive, discrete, rubbery cervical, supraclavicular, and axillary lymphadenopathy. Chest radiography showed bilateral hilar lymphadenopathy. The serum calcium level was elevated at 16.2 mg/dL, with serum parathyroid hormone within the normal range. What is the urgent treatment to be instituted?

A. Intravenous administration of normal saline and a bisphosphonate (Correct Answer)
B. Oxygen 6 L/min by mask
C. Antibiotics and anti-inflammatory drugs
D. Antitussive and chest physiotherapy

Explanation: The patient presents with classic constitutional symptoms (weight loss, night sweats), generalized rubbery lymphadenopathy, and hilar adenopathy, highly suggestive of a hematologic malignancy (likely **Lymphoma**) [1] or Sarcoidosis. However, the acute clinical priority is dictated by his laboratory findings: a life-threatening **Serum Calcium level of 16.2 mg/dL** (Severe Hypercalcemia). [3] **1. Why Option A is Correct:** Severe hypercalcemia (defined as >14 mg/dL) is a medical emergency. The immediate management goals are volume expansion and inhibition of bone resorption: * **Normal Saline (IV):** Restores intravascular volume and promotes urinary calcium excretion. [3] * **Bisphosphonates (e.g., Zoledronic acid):** The gold standard for Hypercalcemia of Malignancy; they inhibit osteoclast activity to provide sustained reduction in calcium levels. [2] * *Note:* In lymphoma, hypercalcemia is often mediated by increased 1,25-dihydroxyvitamin D (Calcitriol) production by malignant cells. **2. Why Incorrect Options are Wrong:** * **Option B:** While the patient has dyspnea, oxygen is supportive and does not address the metabolic emergency (hypercalcemia) which can cause cardiac arrhythmias and coma. * **Option C:** Antibiotics are indicated for infections. While TB is a differential for hilar adenopathy, the acute hypercalcemia takes precedence. [1] * **Option D:** These are symptomatic treatments for cough and do not address the underlying pathology or the life-threatening calcium level. **Clinical Pearls for NEET-PG:** * **Hypercalcemia of Malignancy:** Most common cause of hypercalcemia in hospitalized patients (Primary Hyperparathyroidism is the most common in outpatients). * **Mechanism in Lymphoma:** Extra-renal conversion of 25-OH Vit D to 1,25-(OH)₂ Vit D by 1-alpha-hydroxylase in tumor cells. * **Treatment Sequence:** 1st: Rehydration (NS); 2nd: Bisphosphonates; 3rd: Loop diuretics (only *after* rehydration is complete); 4th: Calcitonin (for rapid, short-term reduction). [2]

Question 88: All of the following are carcinogenic except?

A. H. pylori
B. Hepatitis B virus
C. Epstein-Barr virus
D. All the above (Correct Answer)

Explanation: **Explanation:** The correct answer is **D (All the above)** because all three listed organisms are classified as **Group 1 Carcinogens** by the International Agency for Research on Cancer (IARC). These biological agents are known to induce oncogenesis through chronic inflammation, integration of viral DNA, or the expression of oncoproteins [1]. 1. **H. pylori (Option A):** This gram-negative bacterium is the most common cause of **Gastric Adenocarcinoma** and **MALT Lymphoma** [3]. It induces carcinogenesis through chronic mucosal inflammation and the action of virulence factors like **CagA** (Cytotoxin-associated gene A), which interferes with host cell signaling [2]. 2. **Hepatitis B Virus (Option B):** HBV is a DNA virus that integrates into the host genome. It causes **Hepatocellular Carcinoma (HCC)** via chronic necro-inflammation and the **HBx protein**, which inactivates the p53 tumor suppressor gene and promotes cell proliferation [1]. 3. **Epstein-Barr Virus (Option C):** EBV is associated with several malignancies, most notably **Burkitt Lymphoma** (starry-sky appearance), **Nasopharyngeal Carcinoma**, and Hodgkin Lymphoma. It transforms B-cells using proteins like **LMP-1** (Latent Membrane Protein 1), which mimics CD40 signaling [1]. **Clinical Pearls for NEET-PG:** * **H. pylori** is the only bacterium classified as a Type 1 carcinogen [3]. * **HBV vs. HCV:** While both cause HCC, HBV is a DNA virus that can cause cancer without preceding cirrhosis, whereas HCV (RNA virus) almost always requires cirrhosis to develop HCC. * **EBV Association:** Classically associated with the **t(8;14)** translocation in Burkitt Lymphoma involving the *c-myc* gene. * **Other high-yield carcinogens:** Human Papillomavirus (HPV 16, 18) for Cervical Cancer and *Schistosoma haematobium* for Squamous Cell Carcinoma of the bladder.

Question 89: A 62-year-old man with a history of hypertension and gout, treated with metoprolol and allopurinol, presents with 4 weeks of drowsiness and generalized weakness. He experienced a tonic-clonic seizure. He is a long-term smoker (1 pack/day for 40 years) and has had unintentional weight loss of 20 lb over the past 2 months. His laboratory findings include hemoglobin 10.2 gm/dL, serum sodium 122 mEq/L, serum osmolality 258 mOsm/kg, urine osmolality 300 mOsm/kg, and urine sodium 48 mmol/L. TSH and cortisol levels are normal. What is the most likely diagnosis?

A. Trousseau syndrome
B. Sezary syndrome
C. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) (Correct Answer)
D. Tumor lysis syndrome

Explanation: ### Explanation **Correct Option: C. Syndrome of inappropriate antidiuretic hormone secretion (SIADH)** The patient presents with symptomatic **euvolemic hyponatremia**, characterized by low serum sodium (122 mEq/L) and low serum osmolality (<275 mOsm/kg), alongside inappropriately concentrated urine (urine osmolality >100 mOsm/kg) and elevated urine sodium (>40 mmol/L) [1]. Normal TSH and cortisol levels rule out hypothyroidism and adrenal insufficiency as causes. In the context of a heavy smoker with significant weight loss, the most likely underlying etiology is **Small Cell Lung Cancer (SCLC)**, which is a classic paraneoplastic cause of SIADH due to ectopic ADH production [2]. The neurological symptoms (drowsiness, seizures) are a direct consequence of cerebral edema from acute/severe hyponatremia. **Analysis of Incorrect Options:** * **A. Trousseau syndrome:** Refers to migratory superficial thrombophlebitis associated with visceral malignancy (usually pancreatic). It presents with tender, cord-like venous inflammation, not hyponatremia. * **B. Sezary syndrome:** A leukemic form of Cutaneous T-cell Lymphoma characterized by erythroderma, lymphadenopathy, and atypical T-cells (Sezary cells). It does not typically cause SIADH. * **D. Tumor lysis syndrome:** Characterized by hyperuricemia, hyperkalemia, hyperphosphatemia, and **hypocalcemia** following chemotherapy. While this patient has gout (hyperuricemia), his primary presentation is hyponatremia, and he has not yet started treatment. **NEET-PG High-Yield Pearls:** * **SIADH Criteria:** Serum Osm <275; Urine Osm >100; Urine Na >40; Euvolemia; Normal thyroid/adrenal/renal function [1]. * **SCLC Paraneoplastic Syndromes:** SIADH (most common), ACTH production (Cushing syndrome), and Lambert-Eaton Myasthenic Syndrome [2]. * **Management:** Fluid restriction is first-line for mild SIADH. For severe symptoms (seizures, coma), use **3% hypertonic saline**. * **Caution:** Correct sodium slowly (<8–10 mEq/L in 24h) to avoid **Osmotic Demyelination Syndrome (Central Pontine Myelinolysis)**.

Question 90: A 57-year-old man presents with a serum sodium of 125 mEq/L. On examination, he has pitting edema and elevated neck veins. His urine sodium is 10 mEq/L and urine osmolality is 350 mOsm/kg. What is the most likely diagnosis for this patient's hyponatremia?

A. Congestive heart failure (CHF) (Correct Answer)
B. Extrarenal sodium and fluid losses
C. Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
D. Polydipsia

Explanation: ### Explanation The patient presents with **hypovolemic hyponatremia** (Sodium 125 mEq/L) and clinical signs of **volume overload** (pitting edema, elevated neck veins). This combination is the hallmark of hypervolemic hyponatremia [1]. **1. Why Congestive Heart Failure (CHF) is Correct:** In CHF, there is a decrease in "effective arterial blood volume" (EABV) despite an increase in total body water. This triggers the **Renin-Angiotensin-Aldosterone System (RAAS)** and the release of **Antidiuretic Hormone (ADH)** [2]. * **Low Urine Sodium (< 20 mEq/L):** Aldosterone causes the kidneys to avidly reabsorb sodium to compensate for perceived low perfusion [1]. * **High Urine Osmolality (> 100 mOsm/kg):** ADH causes water reabsorption, concentrating the urine [2]. * **Edema/Elevated JVP:** Reflects the increased total body sodium and water [3]. **2. Why Incorrect Options are Wrong:** * **Extrarenal losses (e.g., vomiting/diarrhea):** These cause *hypovolemic* hyponatremia [1]. While urine sodium would be low (<20), the patient would show signs of dehydration (dry mucus membranes, flat neck veins), not edema. * **SIADH:** This causes *euvolemic* hyponatremia [1]. Patients do not have edema or elevated JVP. Furthermore, urine sodium in SIADH is typically **high (> 40 mEq/L)** because there is no stimulus for aldosterone-mediated sodium retention. * **Polydipsia:** This also causes euvolemic hyponatremia, but the urine would be **maximally dilute** (Urine Osmolality < 100 mOsm/kg) as the body tries to excrete the excess water [2]. **Clinical Pearls for NEET-PG:** * **Hypervolemic Hyponatremia + Low Urine Sodium (<20):** Think CHF, Cirrhosis, or Nephrotic Syndrome [1]. * **Hypervolemic Hyponatremia + High Urine Sodium (>20):** Think Acute or Chronic Renal Failure (kidneys cannot retain sodium) [1]. * **Key Differentiator:** The presence of edema/JVP separates hypervolemic causes from SIADH [3].

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