Hematology — MCQs

A 46-year-old male presents to the outpatient department with a history of lower back pain and painful urination. Upon investigation, he is found to have normocytic normochromic anemia and hypercalcemia. Serum protein electrophoresis reveals an M-spike in the gamma region. Which of the following tests is most appropriate to confirm the diagnosis of multiple myeloma?

Hematology Indian Medical PG Practice Questions and MCQs

Question 841: A 65-year-old man presents with anaemia and posterior column dysfunction. What is the likely cause?

A. Vitamin B1 deficiency
B. Vitamin B12 deficiency (Correct Answer)
C. Subacute sclerosing panencephalitis
D. Multiple sclerosis

Explanation: ### Explanation **Correct Answer: B. Vitamin B12 deficiency** The clinical presentation of **anaemia** combined with **posterior column dysfunction** (loss of vibration and proprioception) is a classic hallmark of Vitamin B12 deficiency. This neurological manifestation is known as **Subacute Combined Degeneration (SCD)** of the spinal cord [1]. * **Mechanism:** Vitamin B12 is a cofactor for the enzyme *methylmalonyl-CoA mutase*. Deficiency leads to an accumulation of methylmalonic acid (MMA), which results in the synthesis of abnormal fatty acids. These are incorporated into neuronal lipids, causing **demyelination** of the **dorsal (posterior) columns** and **lateral corticospinal tracts**. * **Hematology:** It typically causes a **megaloblastic macrocytic anaemia** (High MCV, hypersegmented neutrophils) [1]. **Why other options are incorrect:** * **A. Vitamin B1 (Thiamine) deficiency:** Primarily presents as **Wernicke-Korsakoff syndrome** (ataxia, ophthalmoplegia, confusion) or Beriberi. It does not typically cause macrocytic anaemia or isolated posterior column loss. * **C. Subacute Sclerosing Panencephalitis (SSPE):** A progressive neurological disorder caused by a persistent **Measles virus** infection. It presents with cognitive decline and myoclonus, not anaemia or spinal cord syndromes. * **D. Multiple Sclerosis (MS):** While MS causes demyelination, it presents with disseminated neurological deficits (e.g., optic neuritis, internuclear ophthalmoplegia) and is not associated with megaloblastic anaemia. **NEET-PG High-Yield Pearls:** * **Triad of SCD:** Loss of vibration/position sense (Posterior columns), Spastic paresis (Corticospinal tracts), and Upper Motor Neuron signs. * **Peripheral Smear:** Look for **Hypersegmented Neutrophils** (>5 lobes). * **Biochemical marker:** Elevated **Methylmalonic acid (MMA)** and **Homocysteine** levels are diagnostic [1]. (Note: In Folate deficiency, only Homocysteine is elevated). * **Schilling Test:** Historically used to determine the cause of B12 malabsorption (e.g., Pernicious anaemia).

Question 842: Which of the following is a good prognostic factor in ALL?

A. High WBC count
B. Male sex
C. Age < 2 years
D. Hyperdiploidy (Correct Answer)

Explanation: **Explanation:** In Acute Lymphoblastic Leukemia (ALL), prognosis is determined by a combination of clinical features and cytogenetic abnormalities. **Why Hyperdiploidy is Correct:** **Hyperdiploidy** (defined as >50 chromosomes per cell) is one of the most significant **favorable prognostic factors** in ALL [1]. It is associated with a high sensitivity to chemotherapy, particularly methotrexate and corticosteroids, leading to excellent cure rates. Other favorable genetic markers include the **t(12;21) [ETV6-RUNX1]** translocation. **Why the other options are Incorrect:** * **High WBC count:** A high initial leukocyte count (typically >50,000/µL for B-ALL or >100,000/µL for T-ALL) is a **poor prognostic factor** [1], indicating a higher tumor burden and risk of CNS involvement. * **Male sex:** Historically, males have a **worse prognosis** than females, partly due to the risk of late relapses in sanctuary sites like the testes. * **Age < 2 years:** The "sweet spot" for age in ALL prognosis is **1 to 10 years**. Infants (<1 year) and older children/adults have a significantly **poorer prognosis**. Infants often present with the unfavorable t(4;11) MLL gene rearrangement. **High-Yield Clinical Pearls for NEET-PG:** * **Best Prognosis:** Age 1–10 years, Low WBC count, Hyperdiploidy, and t(12;21). * **Worst Prognosis:** Age <1 or >10 years, High WBC count, **Hypodiploidy**, and **t(9;22) [Philadelphia chromosome]** [1]. * **CNS/Testes:** These are considered "sanctuary sites" where leukemic cells can evade systemic chemotherapy. * **Commonest Subtype:** L1 (Small uniform cells) is the most common in children and has the best prognosis compared to L2 and L3 (FAB classification).

Question 843: Which of the following investigations is least useful in the diagnosis of multiple myeloma?

A. Erythrocyte Sedimentation Rate (ESR)
B. X-ray
C. Bone scan (Correct Answer)
D. Bone marrow biopsy

Explanation: The diagnosis of Multiple Myeloma (MM) relies on identifying monoclonal plasma cell proliferation and associated end-organ damage (CRAB features) [1]. **Why Bone Scan is the least useful:** In Multiple Myeloma, bone destruction is mediated by **osteoclast** activation and the inhibition of osteoblasts. A **Technetium-99m bone scan** detects areas of increased osteoblastic activity (bone formation). Because myeloma lesions are purely **lytic** (punched-out) with little to no osteoblastic reaction, bone scans often yield false-negative results. Therefore, they are not recommended for screening or diagnosis. **Analysis of other options:** * **X-ray (Skeletal Survey):** Traditionally the first-line imaging. It identifies classic "punched-out" lytic lesions, especially in the skull, spine, and pelvis [1]. * **Bone Marrow Biopsy:** A mandatory diagnostic tool. It confirms the presence of clonal plasma cells (≥10% required for diagnosis) and allows for cytogenetic studies (FISH) [1]. * **ESR:** While non-specific, ESR is almost always markedly elevated (often >100 mm/hr) in MM due to the "Rouleaux formation" caused by high levels of monoclonal paraproteins (M-spike) [1]. **NEET-PG High-Yield Pearls:** * **Imaging Gold Standard:** Whole-body low-dose CT (WBLDCT) or MRI is now preferred over X-ray for higher sensitivity. * **Mnemonic CRAB:** **C**alcium (elevated), **R**enal insufficiency, **A**nemia, **B**one lesions. * **Bence-Jones Proteins:** These are free light chains found in urine; they are *not* detected by standard dipsticks (which detect albumin). * **Diagnostic Hallmark:** Presence of **M-spike** on Serum Protein Electrophoresis (SPEP), usually in the Gamma globulin region.

Question 844: Calculate the iron deficit for a 60 kg person with a hemoglobin of 5 g/dL, assuming 1000 mg is required for iron stores.

A. 1500 mg
B. 2500 mg (Correct Answer)
C. 3500 mg
D. 4000 mg

Explanation: ### Explanation The calculation of iron deficit is a high-yield topic for NEET-PG, typically determined using the **Ganzoni Formula**. This formula accounts for both the iron needed to restore hemoglobin to normal levels and the iron required to replenish body stores. **The Ganzoni Formula:** $\text{Total Iron Deficit (mg)} = \text{Body weight (kg)} \times (\text{Target Hb} - \text{Actual Hb}) \times 2.4 + \text{Iron Stores (mg)}$ **Step-by-Step Calculation:** 1. **Target Hb:** Usually taken as 15 g/dL for adults. 2. **Hb Deficit:** $15 - 5 = 10 \text{ g/dL}$. 3. **Iron for Hb restoration:** $60 \text{ kg} \times 10 \text{ g/dL} \times 2.4 = 1440 \text{ mg}$. 4. **Iron for Stores:** $1000 \text{ mg}$ (as specified in the question). 5. **Total Deficit:** $1440 + 1000 = 2440 \text{ mg}$. Rounding to the nearest clinical value, **2500 mg (Option B)** is the correct answer. --- ### Analysis of Incorrect Options * **Option A (1500 mg):** This value roughly covers only the hemoglobin deficit ($1440 \text{ mg}$) while neglecting the $1000 \text{ mg}$ required for iron stores. * **Option C (3500 mg) & D (4000 mg):** These values significantly overestimate the deficit for a $60 \text{ kg}$ individual. Such high doses could lead to iron toxicity if administered parenterally without calculation. --- ### Clinical Pearls for NEET-PG * **The Constant (2.4):** This factor is derived from the blood volume ($0.07 \text{ L/kg}$) and the iron content of hemoglobin ($0.34\%$). * **Iron Stores:** If not specified in the question, use $500 \text{ mg}$ for individuals $<35 \text{ kg}$ and $1000 \text{ mg}$ for those $>35 \text{ kg}$. * **Indication:** Parenteral iron is indicated when oral iron is poorly tolerated, in cases of malabsorption (e.g., Celiac disease), or when rapid replenishment is needed (e.g., 3rd-trimester pregnancy) [1].

Question 845: A young boy presents with joint swelling after a fall. Lab investigations show normal PT and raised aPTT. What is the most likely diagnosis?

A. Von Willebrand Disease
B. Hemophilia (Correct Answer)
C. Platelet function disorder
D. Iron Deficiency Anaemia (IDA)

Explanation: ***Hemophilia***- The presentation of joint swelling after trauma (suggesting **hemarthrosis**) in a young boy is highly characteristic of hemophilia, which is an X-linked recessive disorder [1].- Hemophilia A (Factor VIII deficiency) or B (Factor IX deficiency) affects the **intrinsic coagulation pathway**, leading to an isolated prolongation of the **aPTT** while the PT remains normal. *Von Willebrand Disease*- VWD primarily causes defects in **platelet adhesion** and mild to moderate mucocutaneous bleeding (e.g., epistaxis, menorrhagia), not typically severe spontaneous hemarthrosis [1].- While severe VWD can lower Factor VIII and mildly prolong aPTT, it generally presents differently and often affects both males and females (autosomal pattern) [2].*Iron Deficiency Anaemia (IDA)*- IDA is a nutritional deficiency resulting in **microcytic, hypochromic anemia** and is not a primary bleeding disorder.- It does not involve defects in the coagulation cascade; therefore, PT and aPTT levels would be within the **normal reference range**.*Platelet function disorder*- These disorders (e.g., Glanzmann's or Bernard-Soulier) affect **primary hemostasis** (platelet plug formation), leading mainly to mucocutaneous bleeding [2].- In platelet disorders, the **PT and aPTT** are typically normal, as the coagulation cascade (secondary hemostasis) is intact.

Question 846: A patient presents with fatigue, anemia, and hepatomegaly. Hemoglobin electrophoresis reveals the presence of HbS. What will be the appropriate treatment?

A. Blood transfusion
B. Iron supplementation
C. Vitamin B12 supplementation
D. Hydroxyurea (Correct Answer)

Explanation: Correct: Hydroxyurea - This is the primary disease-modifying therapy for Sickle Cell Disease (SCD), significantly reducing the frequency of vaso-occlusive crises and acute chest syndrome [1]. - It works by increasing the production of fetal hemoglobin (HbF), which interferes with HbS polymerization and subsequent sickling of red blood cells [1]. - Hydroxyurea is the first-line chronic management for symptomatic SCD patients [1]. *Incorrect: Blood transfusion* - Transfusions are reserved for acute, life-threatening complications of SCD, such as aplastic crisis, severe exacerbation of anemia, or prevention of stroke in high-risk patients [1]. - Chronic routine transfusions carry risks of iron overload (hemosiderosis) and alloimmunization, making them generally unsuitable for standard chronic management. *Incorrect: Iron supplementation* - Sickle cell anemia is a hemolytic anemia typically resulting in elevated iron stores due to chronic hemolysis, and if transfusions are given, iron overload (hemosiderosis) is a major concern. - Iron supplementation is contraindicated unless a specific, documented iron deficiency is present, as it can worsen iron deposition in vital organs. *Incorrect: Vitamin B12 supplementation* - Vitamin B12 is primarily used to treat megaloblastic anemia resulting from B12 deficiency (e.g., pernicious anemia). - SCD anemia is caused by chronic extravascular hemolysis, and while folic acid is often required due to high cell turnover, B12 is not the targeted treatment for HbS pathology.

Question 847: A patient has cheilosis with koilonychia and anemia. Diagnosis is?

A. Esophageal cancer
B. Achalasia cardia
C. Plummer-Vinson syndrome (Correct Answer)
D. Tylosis palmaris

Explanation: ***Plummer-Vinson syndrome***- This syndrome is defined by the classic triad of **dysphagia** (due to esophageal webs), **iron deficiency anemia**, and mucosal changes, which include **cheilosis** (angular stomatitis) and **koilonychia** (spoon nails) [1].- It is most common in middle-aged women and results from chronic, severe **iron deficiency**, which causes the epithelial atrophy leading to the observed symptoms [1].*Esophageal cancer*- While **Plummer-Vinson syndrome** is a pre-malignant condition that increases the risk of **esophageal squamous cell carcinoma**, the current presentation describes the syndrome's classic signs, not confirmed malignancy.- Malignancy typically causes progressive **dysphagia** and severe **weight loss**, and the specific triad of **cheilosis** and **koilonychia** is not the primary diagnostic feature.*Achalasia cardia*- This is a **primary esophageal motility disorder** characterized by the poor relaxation of the **lower esophageal sphincter (LES)** and aperistalsis of the esophageal body.- The main symptoms are **dysphagia** (to both solids and liquids) and **regurgitation**, but it is not associated with the systemic features of **iron deficiency anemia**, **cheilosis**, or **koilonychia**.*Tylosis palmaris*- **Tylosis palmaris** is a form of **palmoplantar keratoderma**, an inherited disorder causing marked hyperkeratosis (thickening) of the palms and soles.- Although it is strongly associated with an increased risk for **esophageal squamous cell carcinoma** (Howel-Evans syndrome), it does not cause the specific features of **iron deficiency anemia**, **cheilosis**, and **koilonychia**.

Question 848: A 62-year-old male presents with left leg swelling and pain for 5 days and has a positive D-dimer test. Duplex ultrasonography confirms an extensive DVT involving the left popliteal and femoral veins. Which of the following is the most appropriate initial management strategy?

A. LMWH followed by oral anticoagulant (Correct Answer)
B. Unfractionated heparin followed by warfarin
C. Catheter-directed thrombolysis
D. IVC filter placement

Explanation: LMWH followed by oral anticoagulant - Low Molecular Weight Heparin (LMWH) is the preferred initial treatment for stable patients with extensive DVT due to its predictable response [1], [2], subcutaneous administration, and lower risk of heparin-induced thrombocytopenia (HIT) compared to UFH. - Following the initial parenteral therapy (LMWH or UFH), long-term treatment with an oral anticoagulant (such as a DOAC or warfarin) is necessary for at least 3 to 6 months to prevent thrombus extension and recurrent Pulmonary Embolism (PE) [1]. Unfractionated heparin followed by warfarin - Unfractionated Heparin (UFH) often requires hospitalization for IV administration and intense monitoring of aPTT levels [2], making LMWH the outpatient standard for stable patients. - UFH is typically reserved for patients with severe renal impairment (Creatinine Clearance < 30 mL/min) or those who are hemodynamically unstable and may require urgent reversal. Catheter-directed thrombolysis - This invasive therapy is reserved for patients with DVT accompanied by limb ischemia (phlegmasia cerulea dolens) [1] or for selected young patients with extensive proximal DVT and a low risk of bleeding. - It is associated with a significantly higher risk of major bleeding and is not the standard initial strategy for an uncomplicated extensive DVT [1]. IVC filter placement - An IVC filter is indicated only for patients with acute DVT who have an absolute contraindication to anticoagulation (e.g., active hemorrhage) or who experience recurrent PE despite adequate anticoagulation [1]. - Filter placement does not treat the existing deep vein clot and increases the long-term risk of recurrent DVT.

Question 849: A young woman presents with recurrent headaches, easy bruising, and episodes of visual blurring. Her platelet count is elevated, while her red blood cell (RBC) and white blood cell (WBC) counts are normal. What is the most likely diagnosis?

A. Essential Thrombocythemia (Correct Answer)
B. Polycythemia Vera
C. Chronic Myeloid Leukemia (CML)
D. Acute Myeloid Leukemia (AML)

Explanation: ***Essential Thrombocythemia*** - This **myeloproliferative neoplasm (MPN)** is characterized by isolated, persistent elevation of the **platelet count** (thrombocytosis) with relatively normal RBC and WBC counts, fitting the clinical picture. - Symptoms like headaches, visual blurring, and bruising are common because the functionally abnormal platelets can cause both **microvascular thrombosis** and bleeding tendencies. *Polycythemia Vera* - PV is primarily defined by **erythrocytosis** (elevated RBC count or hematocrit), which is inconsistent with this patient's normal red blood cell count. - Although PV often causes thrombocytosis, the core diagnostic feature involves a panmyelosis dominated by excessive **RBC mass** leading to hyperviscosity symptoms. *Chronic Myeloid Leukemia (CML)* - CML is hallmarked by significant **leukocytosis** (elevated WBC count, especially neutrophils and their precursors) due to the **BCR-ABL fusion gene**. - The patient's normal WBC count makes CML an unlikely diagnosis. *Acute Myeloid Leukemia (AML)* - AML typically presents with signs of **bone marrow failure**, such as anemia, neutropenia, and thrombocytopenia (low platelets), indicating acute lack of mature blood cells. - The lab findings in AML usually show cytopenia or the presence of immature **myeloblasts**, not isolated thrombocytosis.

Question 850: A 46-year-old male presents to the outpatient department with a history of lower back pain and painful urination. Upon investigation, he is found to have normocytic normochromic anemia and hypercalcemia. Serum protein electrophoresis reveals an M-spike in the gamma region. Which of the following tests is most appropriate to confirm the diagnosis of multiple myeloma?

A. Liver function test
B. Urine albumin-to-creatinine ratio (UACR) test
C. Bone marrow examination (Correct Answer)
D. Bence Jones protein in urine

Explanation: ***Bone marrow examination*** - The **definitive confirmatory test** for multiple myeloma is bone marrow examination showing **≥10% clonal plasma cells** (or presence of plasmacytoma on biopsy) [1]. - According to **International Myeloma Working Group (IMWG) criteria**, diagnosis requires: (1) clonal bone marrow plasma cells ≥10% OR biopsy-proven plasmacytoma AND (2) evidence of end-organ damage (CRAB criteria: hypercalcemia, renal insufficiency, anemia, bone lesions) [1]. - This patient has M-spike (monoclonal protein), hypercalcemia, anemia, and bone pain—bone marrow biopsy **confirms the diagnosis** by demonstrating clonal plasma cell proliferation [2]. *Liver function test* - These tests primarily evaluate **hepatic function** (e.g., ALT, AST, bilirubin) and are not diagnostic for multiple myeloma. - While some secondary abnormalities may occur (e.g., elevated **LDH** or **ALP** if bone involvement is extensive), LFTs lack the required specificity for confirming the diagnosis. *Urine albumin-to-creatinine ratio (UACR) test* - UACR is primarily used to screen for **microalbuminuria** in conditions such as **diabetic nephropathy** or hypertensive kidney disease. - The proteinuria seen in multiple myeloma is due to excretion of **kappa or lambda light chains** (Bence Jones protein), not albumin, making UACR inappropriate for MM diagnosis. *Bence Jones protein in urine* - Detection of **monoclonal free light chains** (Bence Jones protein) in urine is a **supportive finding** present in 50-60% of MM cases [1]. - While clinically significant and part of the diagnostic workup, it is **not confirmatory by itself**—bone marrow examination remains the gold standard. - Modern detection uses **urine immunofixation electrophoresis** or serum free light chain assays.

Practice by Chapter

Anemia Evaluation and Management

Practice Questions

Hemoglobinopathies

Practice Questions

Thalassemias

Practice Questions

Platelet Disorders

Practice Questions

Coagulation Disorders

Practice Questions

Thrombotic Disorders

Practice Questions

Leukemias

Practice Questions

Lymphomas

Practice Questions

Multiple Myeloma and Plasma Cell Disorders

Practice Questions

Myeloproliferative Neoplasms

Practice Questions

Transfusion Medicine

Practice Questions

Hematopoietic Stem Cell Transplantation

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Hematology — MCQs

Hematology — MCQs

On this page

Practice by Chapter

Want unlimited practice?