Hematology — MCQs

A 61-year-old man presents with a several-month history of back pain. Radiographs of the spine reveal multiple 1-2 cm lytic lesions in the vertebral bodies. Physical examination shows no lymphadenopathy or splenomegaly. Serum chemistries reveal sodium 140 mmol/L, potassium 4.4 mmol/L, chloride 101 mmol/L, CO2 26 mmol/L, glucose 78 mg/dL, urea nitrogen 49 mg/dL, creatinine 5 mg/dL, total protein 8.3 g/dL, albumin 3.7 g/dL, alkaline phosphatase 176 U/L, AST 45 U/L, ALT 22 U/L, and total bilirubin 1.2 mg/dL. He recently developed a cough productive of yellowish sputum, and a sputum culture grew Streptococcus pneumoniae. During his hospitalization, a bone marrow biopsy is performed. What is the most likely finding on the bone marrow biopsy?

Q155Medium

A 30-year-old female presents with an RBC count of 4.5 million/µL, MCV of 55 fL, and TLC of 8000/µL. She has no history of blood transfusion. What is the most likely diagnosis?

Q156Easy

All are laboratory findings in iron deficiency anemia EXCEPT:

Q157Easy

A patient presents with macroglossia and decreased hemoglobin. Laboratory investigations reveal low vitamin B12 levels and low folic acid levels. What is the most likely diagnosis?

Q158Easy

Megaloblastic anemia is caused by all EXCEPT:

Q159Medium

What is the most appropriate drug used in the management of iron chelation in beta-thalassemia major?

Q160Easy

Renal involvement in multiple myeloma is characterized by:

Hematology Indian Medical PG Practice Questions and MCQs

Question 151: What is the cause of congestive splenomegaly?

A. Visceral Leishmaniasis
B. Budd Chiari Syndrome (Correct Answer)
C. Gaucher's Disease
D. Hodgkin's Lymphoma

Explanation: **Explanation:** **Congestive splenomegaly** occurs when there is an obstruction to the venous outflow of the spleen, leading to chronic passive congestion and subsequent enlargement. **Why Budd-Chiari Syndrome is Correct:** Budd-Chiari Syndrome (BCS) is characterized by the obstruction of hepatic venous outflow (at the level of the hepatic veins or the inferior vena cava). This leads to increased intrahepatic pressure, which is transmitted backward into the portal venous system (**Portal Hypertension**) [1]. Since the splenic vein drains into the portal vein, this back-pressure causes blood to pool in the splenic sinusoids, resulting in congestive splenomegaly. Other common causes include Cirrhosis and Portal Vein Thrombosis [1]. **Analysis of Incorrect Options:** * **Visceral Leishmaniasis (Kala-azar):** Causes massive splenomegaly due to **reticuloendothelial hyperplasia** (proliferation of macrophages containing Amastigote/LD bodies), not venous congestion. * **Gaucher’s Disease:** This is a lysosomal storage disorder where glucocerebroside accumulates in macrophages (Gaucher cells). The splenomegaly is due to **infiltrative storage**, making it a "storage splenomegaly." * **Hodgkin’s Lymphoma:** Splenomegaly here is due to **neoplastic infiltration** by malignant cells (Reed-Sternberg cells) and reactive lymphoid hyperplasia. **NEET-PG High-Yield Pearls:** * **Massive Splenomegaly (crosses midline/umbilicus):** Chronic Myeloid Leukemia (CML), Myelofibrosis, Visceral Leishmaniasis, and Malaria (Tropical Splenomegaly Syndrome). * **Gaucher’s Disease:** Most common lysosomal storage disorder; look for "crinkled paper" cytoplasm in macrophages. * **Budd-Chiari Triad:** Abdominal pain, ascites, and hepatomegaly. * **Splenic Infarction:** Common in Sickle Cell Anemia and Infective Endocarditis; presents with acute left upper quadrant pain.

Question 152: Christmas disease is treated by?

A. Fresh frozen plasma (Correct Answer)
B. Fresh frozen blood
C. Cryoprecipitate
D. Steroids

Explanation: Explanation: **Christmas disease**, also known as **Hemophilia B**, is an X-linked recessive bleeding disorder caused by a deficiency of **Clotting Factor IX** [1]. 1. **Why Fresh Frozen Plasma (FFP) is correct:** FFP contains all coagulation factors, including Factor IX. In the absence of specific recombinant Factor IX concentrates (which is the gold standard but often not listed in basic MCQ options), FFP is the primary source used to replenish Factor IX levels and achieve hemostasis [1]. 2. **Why other options are incorrect:** * **Fresh frozen blood:** This is not a standard component therapy. Whole blood is rarely used because it can lead to volume overload and contains lower concentrations of specific factors compared to plasma. * **Cryoprecipitate:** This is a **high-yield trap**. Cryoprecipitate is rich in Factor VIII, Fibrinogen, von Willebrand Factor, and Factor XIII. It **does not contain Factor IX**. Therefore, it is used for Hemophilia A and von Willebrand disease, but is ineffective for Christmas disease. * **Steroids:** These have no role in replacing clotting factors; they are used in immune-mediated hematological conditions like ITP. **Clinical Pearls for NEET-PG:** * **Hemophilia A:** Factor VIII deficiency (Treated with Cryoprecipitate or Factor VIII concentrate). * **Hemophilia B:** Factor IX deficiency (Treated with FFP or Factor IX concentrate) [1]. * **Inheritance:** Both are X-linked recessive (mostly affects males) [1]. * **Lab Findings:** Prolonged **aPTT**, but normal PT and Bleeding Time (BT). * **Most common site of bleeding:** Hemarthrosis (bleeding into joints, most commonly the knee) [1].

Question 153: Splenectomy is expected to cause what change in the number of platelets?

A. Increase in the number of platelets (Correct Answer)
B. Decrease in the number of platelets
C. No change in the number of platelets
D. Complete absence of platelets

Explanation: **Explanation:** **1. Why Option A is Correct:** The spleen normally acts as a major reservoir for platelets, sequestering approximately **one-third (30-33%)** of the total body platelet mass at any given time [1]. These platelets are in a state of dynamic equilibrium with the systemic circulation. When the spleen is removed (splenectomy), this sequestration site is lost [2]. Consequently, the platelets that would have been stored in the spleen are released into the peripheral blood, leading to **thrombocytosis** (an increase in platelet count). This rise is often immediate and can be significant, sometimes exceeding 1,000,000/µL in the postoperative period. **2. Why Other Options are Incorrect:** * **Option B & D:** Platelet production occurs in the bone marrow via megakaryocytes, not the spleen. Therefore, removing the spleen does not stop production or cause a decrease; rather, it removes the primary site of platelet destruction and storage. * **Option C:** Because the spleen holds a significant portion of the circulating mass, its removal invariably alters the peripheral blood count. **3. NEET-PG High-Yield Pearls:** * **Post-Splenectomy Blood Picture:** Look for **Howell-Jolly bodies** (nuclear remnants), **Pappenheimer bodies** (iron granules), **Heinz bodies** (denatured hemoglobin), and **Target cells** on the peripheral smear. * **Clinical Risk:** Extreme thrombocytosis post-splenectomy may rarely require hydroxyurea or aspirin if thrombotic events are a concern, though it is usually transient. * **Infections:** Patients are at lifelong risk of **OPSI (Overwhelming Post-Splenectomy Infection)** caused by encapsulated organisms (*S. pneumoniae, H. influenzae, N. meningitidis*). Vaccination is mandatory. * **Splenomegaly:** In cases of massive splenomegaly (e.g., Myelofibrosis), sequestration can increase to 90% [1], leading to peripheral thrombocytopenia.

Question 154: A 61-year-old man presents with a several-month history of back pain. Radiographs of the spine reveal multiple 1-2 cm lytic lesions in the vertebral bodies. Physical examination shows no lymphadenopathy or splenomegaly. Serum chemistries reveal sodium 140 mmol/L, potassium 4.4 mmol/L, chloride 101 mmol/L, CO2 26 mmol/L, glucose 78 mg/dL, urea nitrogen 49 mg/dL, creatinine 5 mg/dL, total protein 8.3 g/dL, albumin 3.7 g/dL, alkaline phosphatase 176 U/L, AST 45 U/L, ALT 22 U/L, and total bilirubin 1.2 mg/dL. He recently developed a cough productive of yellowish sputum, and a sputum culture grew Streptococcus pneumoniae. During his hospitalization, a bone marrow biopsy is performed. What is the most likely finding on the bone marrow biopsy?

A. Scattered small granulomas
B. Nodules of small mature lymphocytes
C. Occasional Reed-Sternberg cells
D. Numerous plasma cells (Correct Answer)

Explanation: ### Explanation The clinical presentation is classic for **Multiple Myeloma (MM)**, a neoplastic proliferation of plasma cells [1]. The diagnosis is supported by the **CRAB** criteria: * **C (Calcium):** Often elevated (though not provided here). * **R (Renal Insufficiency):** Creatinine is significantly elevated (5 mg/dL), likely due to myeloma kidney (cast nephropathy). * **A (Anemia):** Common in MM (implied by the chronic presentation). * **B (Bone lesions):** Radiographs show characteristic **punched-out lytic lesions** in the vertebrae [1]. The patient also has a **reversed Albumin/Globulin ratio** (Total protein 8.3 - Albumin 3.7 = Globulin 4.6 g/dL), indicating hypergammaglobulinemia. The susceptibility to *Streptococcus pneumoniae* occurs because neoplastic plasma cells produce monoclonal M-proteins, leading to a deficiency in functional, polyclonal immunoglobulins (hypogammaglobulinemia). In MM, the bone marrow typically shows **>10% clonal plasma cells** [1]. #### Why Other Options are Incorrect: * **A. Scattered small granulomas:** Seen in infections (TB, fungal), sarcoidosis, or certain drug reactions, but not associated with lytic bone lesions and renal failure [2]. * **B. Nodules of small mature lymphocytes:** Characteristic of **Chronic Lymphocytic Leukemia (CLL)** or Small Lymphocytic Lymphoma (SLL), which typically present with lymphadenopathy and splenomegaly [3]. * **C. Occasional Reed-Sternberg cells:** The hallmark of **Hodgkin Lymphoma**, which usually presents with painless lymphadenopathy and "B symptoms" rather than lytic bone lesions. #### NEET-PG High-Yield Pearls: * **Most common cause of death in MM:** Infection (due to hypogammaglobulinemia) followed by Renal Failure. * **Radiology:** Lytic lesions are "cold" on bone scans because there is no osteoblastic activity; X-rays or CT/MRI are preferred. * **Renal Failure:** Primarily caused by Bence-Jones proteinuria (light chain casts) obstructing distal tubules. * **Alkaline Phosphatase:** Usually **normal** in MM despite extensive bone destruction, as there is minimal osteoblastic activity (a key differentiator from bone metastases).

Question 155: A 30-year-old female presents with an RBC count of 4.5 million/µL, MCV of 55 fL, and TLC of 8000/µL. She has no history of blood transfusion. What is the most likely diagnosis?

A. Iron deficiency anemia
B. Thalassemia major
C. Thalassemia minor (Correct Answer)
D. Megaloblastic anemia

Explanation: ### Explanation The key to solving this clinical scenario lies in the **Mentzer Index**, which is a high-yield tool for differentiating microcytic anemias. **1. Why Thalassemia Minor is Correct:** The Mentzer Index is calculated as **MCV / RBC count**. * In this patient: $55 / 4.5 = 12.2$. * A Mentzer Index **< 13** strongly suggests **Thalassemia trait/minor**. * In Thalassemia, the bone marrow is hyperactive but produces defective hemoglobin, leading to a high or near-normal RBC count despite a very low MCV (disproportionate microcytosis). A patient with an MCV as low as 55 fL who is otherwise stable and has a normal RBC count is classic for Thalassemia minor. **2. Why the other options are incorrect:** * **Iron Deficiency Anemia (IDA):** The Mentzer Index is typically **> 13**. In IDA, the RBC count decreases because the "building blocks" (iron) are missing [1]. An MCV of 55 fL in IDA would usually be accompanied by a much lower RBC count. * **Thalassemia Major:** This presents in early childhood with severe anemia, hepatosplenomegaly, and skeletal deformities. Patients are transfusion-dependent; this patient is 30 years old with no transfusion history. * **Megaloblastic Anemia:** This is a **macrocytic** anemia characterized by an MCV > 100 fL [1]. The patient’s MCV of 55 fL (microcytic) immediately rules this out. **Clinical Pearls for NEET-PG:** * **Mentzer Index:** $< 13$ = Thalassemia; $> 13$ = Iron Deficiency. * **Red Cell Distribution Width (RDW):** Usually normal in Thalassemia minor but elevated in IDA. * **Confirmatory Test:** Hb Electrophoresis is the gold standard for Thalassemia (showing elevated HbA2 > 3.5%). * **Target Cells:** Commonly seen on the peripheral smear of Thalassemia patients.

Question 156: All are laboratory findings in iron deficiency anemia EXCEPT:

A. Decreased serum iron
B. Increased total iron binding capacity
C. Decreased serum ferritin
D. Increased mean corpuscular volume (Correct Answer)

Explanation: Explanation: Iron Deficiency Anemia (IDA) is characterized by a defect in hemoglobin synthesis due to inadequate iron stores [1]. 1. Why Option D is correct: Mean Corpuscular Volume (MCV) measures the average size of red blood cells. In IDA, the lack of iron leads to fewer hemoglobin molecules being produced. To maintain concentration, the cells undergo additional divisions, resulting in microcytic (small) cells [2]. Therefore, MCV is decreased (<80 fL), not increased. Increased MCV is seen in megaloblastic anemias (Vitamin B12 or Folate deficiency). 2. Why other options are incorrect: * Decreased Serum Iron (A): This is a direct reflection of low circulating iron available for erythropoiesis. * Increased TIBC (B): Total Iron Binding Capacity represents the availability of binding sites on transferrin. In deficiency states, the liver increases transferrin production to maximize iron transport, leading to an elevated TIBC. * Decreased Serum Ferritin (C): Ferritin is the primary storage form of iron. A low serum ferritin is the most specific initial laboratory finding indicating depleted iron stores [1][2]. NEET-PG High-Yield Pearls: * Earliest Sign of IDA: Increased Red Cell Distribution Width (RDW). * Best Screening Test: Serum Ferritin (levels <15-30 ng/mL are diagnostic). * Gold Standard Investigation: Bone marrow aspiration (Perls’ Prussian Blue stain) showing absent hemosiderin [2]. * Mentzer Index: MCV/RBC count. If <13, it suggests Thalassemia trait; if >13, it suggests IDA.

Question 157: A patient presents with macroglossia and decreased hemoglobin. Laboratory investigations reveal low vitamin B12 levels and low folic acid levels. What is the most likely diagnosis?

A. Hemolytic anemia
B. Sideroblastic anemia
C. Megaloblastic anemia (Correct Answer)
D. Anemia of chronic disease

Explanation: ### Explanation **1. Why Megaloblastic Anemia is Correct:** Megaloblastic anemia is characterized by impaired DNA synthesis, most commonly due to a deficiency in **Vitamin B12 (Cobalamin)** and/or **Folic acid**. These vitamins are essential cofactors for nucleic acid synthesis; their deficiency leads to "nuclear-cytoplasmic asynchrony," where the nucleus matures slower than the cytoplasm [1]. * **Clinical Correlation:** **Macroglossia** (beefy red, smooth tongue) is a classic physical finding in megaloblastic anemia due to the atrophy of lingual papillae. * **Laboratory Correlation:** The combination of low hemoglobin (anemia) and low levels of B12/Folate confirms the diagnosis [1]. **2. Why Other Options are Incorrect:** * **Hemolytic Anemia:** Characterized by increased red cell destruction. While it can cause jaundice and splenomegaly, it does not typically present with macroglossia or low B12/Folate levels. * **Sideroblastic Anemia:** This is a microcytic anemia (usually) caused by defective heme synthesis. It is characterized by "ringed sideroblasts" in the bone marrow and iron overload, not B12/Folate deficiency. * **Anemia of Chronic Disease (ACD):** Usually normocytic or mildly microcytic. It is driven by high **Hepcidin** levels due to inflammation, leading to iron sequestration, not vitamin deficiencies [1]. **3. NEET-PG High-Yield Pearls:** * **Peripheral Smear:** Look for **Hypersegmented Neutrophils** (earliest sign) and **Oval Macrocytes**. * **MCV:** Typically >100 fL. * **Neurological Symptoms:** Only seen in Vitamin B12 deficiency (Subacute Combined Degeneration of the spinal cord), NOT in Folate deficiency [1]. * **Biochemical Markers:** Both B12 and Folate deficiency show elevated **Homocysteine**; however, only B12 deficiency shows elevated **Methylmalonic Acid (MMA)**. * **Commonest Cause:** In India, nutritional deficiency is the most common cause of megaloblastic anemia.

Question 158: Megaloblastic anemia is caused by all EXCEPT:

A. Aspirin (Correct Answer)
B. Primidone
C. Methotrexate
D. Nitrous oxide (N2O)

Explanation: **Explanation:** Megaloblastic anemia is characterized by impaired DNA synthesis, leading to large, nucleated red blood cell precursors in the bone marrow [1]. This is most commonly due to deficiencies or interference in the metabolism of Vitamin B12 (Cobalamin) or Folate (Vitamin B9) [2]. **Why Aspirin is the correct answer:** **Aspirin (Acetylsalicylic acid)** is a salicylate that acts as a COX inhibitor. It primarily causes gastrointestinal blood loss or iron deficiency anemia over long-term use, but it does **not** interfere with DNA synthesis, folate metabolism, or B12 absorption. Therefore, it does not cause megaloblastic anemia. **Why the other options are incorrect:** * **Methotrexate:** A potent dihydrofolate reductase (DHFR) inhibitor [2]. It prevents the conversion of dihydrofolate to tetrahydrofolate, directly halting DNA synthesis and causing megaloblastic changes. * **Primidone:** An anticonvulsant (similar to Phenytoin and Phenobarbital) that interferes with folate absorption and metabolism in the gut, leading to folate deficiency. * **Nitrous oxide (N2O):** Known as "laughing gas," it oxidizes the cobalt atom of Vitamin B12, rendering the enzyme methionine synthase inactive [2]. This leads to an acute megaloblastic state and potential subacute combined degeneration of the spinal cord (SCD). **NEET-PG High-Yield Pearls:** * **Drugs causing Megaloblastic Anemia:** Methotrexate, Trimethoprim, Pyrimethamine (DHFR inhibitors); Phenytoin, Primidone (Folate malabsorption); Zidovudine (AZT); and Hydroxyurea. * **N2O Warning:** Repeated exposure to Nitrous Oxide can cause megaloblastic changes within hours. * **MCV:** Megaloblastic anemia is a macrocytic anemia (MCV >100 fL) characterized by **hypersegmented neutrophils** (>5 lobes) on peripheral smear.

Question 159: What is the most appropriate drug used in the management of iron chelation in beta-thalassemia major?

A. Oral desferrioxamine
B. Oral deferiprone (Correct Answer)
C. Intramuscular EDTA
D. Oral succimer

Explanation: **Explanation:** In patients with **Beta-thalassemia major**, chronic blood transfusions lead to secondary iron overload (hemosiderosis). Since the human body lacks an active mechanism to excrete excess iron, chelation therapy is mandatory to prevent organ damage, particularly to the heart and liver. **Why Oral Deferiprone is correct:** **Deferiprone** is an orally active iron chelator. It is particularly noted for its ability to cross cell membranes effectively and remove iron from intracellular sites. In clinical practice, it is highly effective at removing **cardiac iron**, making it a preferred choice for preventing or treating iron-induced cardiomyopathy, the leading cause of death in these patients. **Analysis of Incorrect Options:** * **A. Oral Desferrioxamine:** Desferrioxamine is a potent chelator, but it is **not absorbed orally**. It must be administered via slow subcutaneous or intravenous infusion (usually 8–12 hours daily), which leads to poor patient compliance. * **C. Intramuscular EDTA:** Calcium disodium EDTA is primarily used for **lead poisoning**, not for chronic iron overload in thalassemia. * **D. Oral Succimer:** Succimer (DMSA) is an oral chelating agent used for **lead, mercury, and arsenic poisoning** in children. It has no role in iron chelation. **NEET-PG High-Yield Pearls:** 1. **Deferasirox:** Another common oral chelator; it is often the first-line choice for systemic iron overload due to its once-daily dosing. 2. **Side Effects:** * **Deferiprone:** Agranulocytosis (requires weekly CBC monitoring) and arthralgia. * **Desferrioxamine:** Ototoxicity and retinal damage. 3. **Indication for Chelation:** Usually started when Serum Ferritin >1000 ng/ml or after 10–20 transfusions.

Question 160: Renal involvement in multiple myeloma is characterized by:

A. Nitrogen retention (Correct Answer)
B. Hypertension
C. Edema
D. Hematuria

Explanation: **Explanation:** Renal failure is a hallmark of Multiple Myeloma (MM), occurring in approximately 25–50% of patients. The primary mechanism is **Myeloma Cast Nephropathy** (Myeloma Kidney), where excessive monoclonal light chains (Bence-Jones proteins) precipitate with Tamm-Horsfall protein in the distal tubules, causing obstruction and direct tubular toxicity [1]. **1. Why Nitrogen Retention is Correct:** Nitrogen retention (Azotemia) refers to the accumulation of nitrogenous waste products like urea and creatinine in the blood. In MM, the combination of cast nephropathy, hypercalcemia-induced pre-renal azotemia, and amyloidosis leads to a progressive decline in the Glomerular Filtration Rate (GFR). This results in elevated BUN and Serum Creatinine, making nitrogen retention a classic feature of myeloma-related renal involvement [3]. **2. Why Other Options are Incorrect:** * **Hypertension:** Unlike most chronic kidney diseases, hypertension is **characteristically absent** or rare in Multiple Myeloma, even in the presence of significant renal failure. * **Edema:** While nephrotic syndrome can occur if AL-amyloidosis develops, the primary renal pathology (cast nephropathy) is a tubular process rather than a glomerular one, meaning massive proteinuria/edema is not the standard presentation [2]. * **Hematuria:** Myeloma kidney is a

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Leukemias

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Lymphomas

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Multiple Myeloma and Plasma Cell Disorders

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Hematology — MCQs

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