Hematology — MCQs

A 42-year-old female presents with bleeding gums for the past 20 days. Intra-oral examination shows thickened and friable gums. She also has hepatosplenomegaly and generalized non-tender lymphadenopathy. Laboratory findings include: Hemoglobin 11.4 g/dL, Platelet count 90,000/mm³, WBC count 4600/mm³. Bone marrow biopsy shows 100% cellularity with many large blasts that are peroxidase negative and non-specific esterase positive. What is the most likely diagnosis for this patient?

Q810Medium

Chronic hemolysis from which of the following conditions may be associated with iron deficiency?

Hematology Indian Medical PG Practice Questions and MCQs

Question 801: Megaloblastic anemia occurs due to deficiency of which of the following?

A. Iron deficiency
B. Folate deficiency (Correct Answer)
C. Protein deficiency
D. Vitamin C deficiency

Explanation: **Explanation:** Megaloblastic anemia is a subtype of macrocytic anemia characterized by impaired DNA synthesis, leading to a "nuclear-cytoplasmic asynchrony." While the cytoplasm matures normally, the nucleus remains immature, resulting in large, fragile cells [1]. **Why Folate Deficiency is Correct:** Folate (Vitamin B9) and Vitamin B12 are essential cofactors for the synthesis of thymidine triphosphate. When folate is deficient, the conversion of dUMP to dTMP is impaired, halting DNA replication. This leads to the formation of **megaloblasts** in the bone marrow and **macro-ovalocytes** with **hypersegmented neutrophils** (≥5 lobes) in the peripheral blood [1]. **Analysis of Incorrect Options:** * **Iron Deficiency:** Causes **Microcytic Hypochromic** anemia due to impaired hemoglobin synthesis [1]. It is the most common cause of anemia worldwide. * **Protein Deficiency:** Generally leads to normocytic normochromic anemia (Anemia of Chronic Disease/Malnutrition) due to decreased erythropoietin production and global marrow suppression. * **Vitamin C Deficiency:** Causes Scurvy. While Vitamin C aids iron absorption, its deficiency primarily leads to defective collagen synthesis and perifollicular hemorrhages, not megaloblastic changes. **High-Yield Clinical Pearls for NEET-PG:** * **Drug-Induced Megaloblastic Anemia:** Common culprits include Methotrexate, Phenytoin, and Trimethoprim (all interfere with folate metabolism) [2]. * **Neurological Symptoms:** These occur in Vitamin B12 deficiency (Subacute Combined Degeneration) but are **absent** in pure Folate deficiency. * **Biochemical Markers:** Both B12 and Folate deficiency show elevated **Homocysteine**, but only B12 deficiency shows elevated **Methylmalonic Acid (MMA)** [2]. * **Schilling Test:** Historically used to differentiate causes of B12 malabsorption (e.g., Pernicious Anemia).

Question 802: Which of the following statements is true regarding Chronic Myeloid Leukemia (CML)?

A. The size of splenomegaly can indicate prognosis. (Correct Answer)
B. Phagocytic activity of white blood cells is reduced.
C. Sudan black stain is specific for myeloblasts.
D. Myeloblasts, granuloblasts, and lymphoblasts become Philadelphia chromosome positive following remission.

Explanation: In Chronic Myeloid Leukemia (CML), the clinical and laboratory findings are critical for staging and predicting outcomes. ### **Explanation of the Correct Option** **A. The size of splenomegaly can indicate prognosis:** This is correct. Splenomegaly is the most common physical finding in CML. The degree of splenic enlargement is a key component of prognostic scoring systems like the **Sokal Score** and **Hasford Score**. Massive splenomegaly often correlates with a higher tumor burden, an increased risk of transformation to the accelerated or blast phase, and a poorer overall prognosis. ### **Why the Other Options are Incorrect** * **B. Phagocytic activity of white blood cells is reduced:** In the chronic phase of CML, the mature neutrophils produced are functionally normal. Their phagocytic and bactericidal activities are generally **preserved**, which is why patients rarely present with opportunistic infections until they progress to the blast crisis. * **C. Sudan black stain is specific for myeloblasts:** Sudan Black B (SBB) stains phospholipids in the granules of myeloid cells. While it is used to differentiate AML from ALL, it is **not specific** for myeloblasts; it also stains promyelocytes and mature granulocytes. * **D. Philadelphia chromosome (Ph+):** The Ph chromosome ($t[9;22]$) is the hallmark of CML and is present in the **pluripotent stem cell**. While it is found in myeloid, erythroid, and megakaryocytic lineages, "granuloblasts" is not a standard term, and the goal of modern therapy (TKIs) is to achieve a **complete cytogenetic remission**, meaning the Ph chromosome should become **undetectable**, not remain positive [1]. ### **High-Yield Clinical Pearls for NEET-PG** * **Leukocyte Alkaline Phosphatase (LAP) Score:** Characteristically **decreased** in CML (helps differentiate it from a Leukemoid reaction where LAP is high). * **Cytogenetics:** $t(9;22)$ creates the *BCR-ABL1* fusion gene, encoding a constitutively active tyrosine kinase [1]. * **Peripheral Smear:** Shows a "myelocyte bulge" (predominance of myelocytes and metamyelocytes) and **basophilia** (a classic sign of CML). * **Drug of Choice:** Imatinib (Tyrosine Kinase Inhibitor) [1].

Question 803: A 42-year-old female diagnosed with iron deficiency anemia was treated with oral iron therapy. Her hemoglobin level during review was 8 g%. What is the most likely cause for the failure of treatment?

A. Acquired sideroblastic anemia
B. Inadequate iron dosage
C. Poor compliance to oral iron (Correct Answer)
D. Folate deficiency

Explanation: ### Explanation **1. Why "Poor compliance to oral iron" is correct:** The most common cause of failure of response to oral iron therapy in clinical practice is **poor patient compliance**. Oral iron supplements (like Ferrous Sulfate) are notorious for causing gastrointestinal side effects, including epigastric pain, nausea, constipation, and metallic taste. These adverse effects often lead patients to discontinue the medication prematurely. In a patient with confirmed iron deficiency anemia (IDA) who shows no improvement in hemoglobin (Hb) levels, clinicians must first rule out non-adherence before investigating rare malabsorptive disorders or incorrect diagnoses. **2. Analysis of Incorrect Options:** * **Acquired sideroblastic anemia:** This is a microcytic anemia characterized by impaired heme synthesis and iron overload in mitochondria (ring sideroblasts). It does not respond to iron; however, it is a rare condition and not the primary suspicion when a patient fails initial IDA therapy. * **Inadequate iron dosage:** While a possible cause, modern formulations usually provide sufficient elemental iron. Standard practice ensures the dose is adequate; thus, the patient's failure to take the prescribed dose (compliance) is statistically more likely than the doctor prescribing an insufficient one. * **Folate deficiency:** While megaloblastic anemia can coexist with IDA (dimorphic anemia), folate deficiency alone causes macrocytic anemia [2]. It would not explain a lack of response in a patient specifically diagnosed with and treated for iron deficiency. **3. Clinical Pearls for NEET-PG:** * **First sign of response:** The earliest hematological response to iron therapy is an **increase in reticulocyte count**, which peaks between **5–10 days**. * **Hb Rise:** Hemoglobin typically rises by **2 g/dL every 3 weeks**. * **Duration:** Therapy should continue for **3–6 months** after Hb normalizes to replenish iron stores (Ferritin). * **Other causes of failure:** If compliance is confirmed, consider **persistent blood loss** (e.g., occult GI bleed), malabsorption [1] (Celiac disease, *H. pylori*), or an incorrect diagnosis (e.g., Thalassemia trait).

Question 804: Reticulocytosis is NOT a feature of which of the following conditions?

A. Paroxysmal nocturnal hemoglobinuria
B. Following acute bleeding
C. Hereditary spherocytosis
D. Anemia in chronic renal failure (CRF) (Correct Answer)

Explanation: **Explanation:** The **Reticulocyte Count** is a direct indicator of the bone marrow's erythropoietic activity. To produce reticulocytes, the marrow requires two things: a functional stimulus (Erythropoietin) and a healthy "factory" (bone marrow). **Why Option D is Correct:** In **Chronic Renal Failure (CRF)**, the primary cause of anemia is the **deficiency of Erythropoietin (EPO)**, which is produced by the peritubular interstitial cells of the kidney [1]. Without EPO, the bone marrow is not stimulated to produce new red cells despite the anemia. Therefore, CRF is characterized by a **hypoproliferative anemia** with a low reticulocyte count (reticulocytopenia) [1]. **Why the other options are incorrect:** * **A. Paroxysmal Nocturnal Hemoglobinuria (PNH):** This is an acquired hemolytic anemia. In response to the destruction of RBCs, a healthy bone marrow compensates by increasing RBC production, leading to reticulocytosis. * **B. Acute Bleeding:** Following a sudden loss of blood, the body increases EPO production to replace the lost volume, resulting in a physiological rise in reticulocytes within 3–5 days. * **C. Hereditary Spherocytosis:** This is a congenital hemolytic anemia due to membrane defects. The marrow remains hyperactive to compensate for the shortened lifespan of the spherocytes, resulting in a high reticulocyte count. **High-Yield Clinical Pearls for NEET-PG:** * **Corrected Reticulocyte Count (CRC):** In anemia, always use CRC to assess marrow response. $CRC = \text{Observed Retic \%} \times (\text{Patient Hct} / \text{Normal Hct})$. * **Reticulocyte Production Index (RPI):** An RPI > 2% indicates an adequate marrow response (hemolysis/hemorrhage); RPI < 2% indicates an inadequate response (nutritional deficiency/marrow failure). * **Other causes of Reticulocytopenia:** Iron/B12/Folate deficiency, Aplastic anemia, and Bone marrow suppression (e.g., chemotherapy).

Question 805: What is the typical Vitamin B level in chronic myeloid leukemia?

A. Elevated (Correct Answer)
B. Decreased
C. Normal
D. Markedly decreased

Explanation: **Explanation:** In Chronic Myeloid Leukemia (CML), serum Vitamin B12 levels are characteristically **elevated**, often reaching several times the normal limit. This occurs due to the massive expansion of the granulocytic series (neutrophils and their precursors). These cells synthesize and secrete **Transcobalamin I (TCI)**, an R-binder protein responsible for transporting Vitamin B12 in the plasma. As the total white blood cell count rises, the concentration of TCI increases proportionally, leading to an increased total B12 binding capacity and elevated serum B12 levels. **Analysis of Options:** * **Option A (Correct):** Elevated levels are a classic biochemical marker of CML due to increased Transcobalamin I production by leukemic cells. * **Option B & D (Incorrect):** Decreased levels are seen in megaloblastic anemias (pernicious anemia, dietary deficiency). In CML, despite high serum levels, there is often "functional" deficiency because the B12 is tightly bound to TCI and less available for tissue uptake. * **Option C (Incorrect):** Normal levels are rare in untreated CML with high tumor burden. **High-Yield Clinical Pearls for NEET-PG:** * **Transcobalamin I (TCI):** Derived from specific granules of granulocytes; elevated in CML. * **Transcobalamin II (TCII):** The primary protein responsible for delivering B12 to tissues (liver, bone marrow). * **LAP Score:** In CML, the Leukocyte Alkaline Phosphatase (LAP) score is characteristically **low**, helping differentiate it from a Leukemoid Reaction (where LAP is high). * **Uric Acid:** Also frequently elevated in CML due to high cell turnover [1].

Question 806: Which of the following is NOT a true feature of Multiple Myeloma?

A. Proteinuria
B. Visual disturbance
C. Bleeding
D. Dystrophic calcification (Correct Answer)

Explanation: In Multiple Myeloma (MM), hypercalcemia occurs due to increased osteoclast activity (mediated by RANKL and IL-6), leading to bone resorption. This results in **Metastatic Calcification**—calcium deposition in previously normal tissues (like kidneys or lungs) due to high serum calcium levels. In contrast, **Dystrophic Calcification** occurs in dead or degenerated tissues despite normal serum calcium levels, which is not the mechanism in MM. **Analysis of Incorrect Options:** * **A. Proteinuria:** This is a classic feature. It is primarily **Bence-Jones proteinuria** (monoclonal light chains), which are not detected on standard dipsticks [1]. Additionally, amyloidosis or light chain deposition can lead to albuminuria. * **B. Visual Disturbance:** This occurs due to **Hyperviscosity Syndrome**, typically seen when M-protein levels are very high [1]. It leads to retinal hemorrhages and "sausage-link" appearance of retinal veins. * **C. Bleeding:** Patients often present with mucosal bleeding or purpura. This is caused by **thrombocytopenia** (bone marrow infiltration) and the interference of M-proteins with clotting factors and platelet aggregation. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** **C**alcium (elevated), **R**enal insufficiency, **A**nemia, **B**one lesions (lytic "punched-out" lesions) [2]. * **Diagnosis:** Bone marrow plasmacytosis >10% is the gold standard [2]. * **Blood Smear:** **Rouleaux formation** (due to decreased zeta potential between RBCs). * **Urine:** Bence-Jones proteins precipitate at 40-60°C and redissolve at 100°C. * **M-Spike:** Found on Serum Protein Electrophoresis (SPEP), usually IgG (most common) or IgA [1].

Question 807: What is the earliest time point at which an increase in reticulocyte count is typically observed following the initiation of iron therapy?

A. 48 - 72 hours (Correct Answer)
B. 24 hours
C. 96 hours
D. 6 hours

Explanation: ### Explanation **Correct Answer: A. 48 - 72 hours** The initiation of iron therapy in a patient with Iron Deficiency Anemia (IDA) triggers a predictable sequence of hematological responses. The **reticulocyte count** is the first objective laboratory marker of a positive response to therapy. 1. **Why 48 - 72 hours is correct:** Once iron is administered, it is transported to the bone marrow and incorporated into developing erythroblasts. It takes approximately **2 to 3 days (48–72 hours)** for these newly stimulated cells to mature into reticulocytes and be released into the peripheral circulation. The reticulocyte count continues to rise, reaching its **peak between 7 to 10 days**. 2. **Why other options are incorrect:** * **6 hours and 24 hours (B & D):** These timeframes are too short for the biological process of erythropoiesis [1]. Even with adequate iron, the bone marrow requires more than a day to synthesize hemoglobin and transition cells from the normoblast stage to the reticulocyte stage. * **96 hours (C):** While the reticulocyte count is certainly elevated by 96 hours, it is not the *earliest* point of detection. Standard medical teaching identifies the 48–72 hour window as the initial onset of the rise. --- ### NEET-PG High-Yield Pearls: Sequence of Response to Iron Therapy * **First sign of improvement:** Subjective feeling of well-being (within 24 hours) due to the restoration of iron-containing enzymes (e.g., cytochromes). * **Earliest Lab Marker:** Increased reticulocyte count (48–72 hours). * **Peak Reticulocytosis:** 7–10 days. * **Hemoglobin Rise:** Starts after 1 week; typically increases by **1 g/dL every 7–10 days**. * **Normalization of Hemoglobin:** Usually occurs within 2 months. * **Last marker to normalize:** **Serum Ferritin** (indicates replenishment of iron stores). Therapy should continue for 3–6 months after Hb normalizes to ensure stores are full [2].

Question 808: All of the following are poor prognostic factors for Hodgkin's disease, except?

A. Younger age (Correct Answer)
B. Systemic manifestations
C. Lymphocyte depletion
D. Mediastinal disease

Explanation: In Hodgkin’s Lymphoma (HL), prognosis is determined by the clinical stage, histological subtype, and specific clinical markers. **Explanation of the Correct Answer:** **Option A (Younger age)** is the correct answer because it is actually a **favorable** prognostic factor. In HL, **older age (>45–50 years)** is consistently associated with a poorer prognosis due to a higher frequency of comorbidities, decreased tolerance to intensive chemotherapy, and a higher prevalence of unfavorable histological subtypes (like Mixed Cellularity). Younger patients typically have better performance status and a higher cure rate. **Explanation of Incorrect Options (Poor Prognostic Factors):** * **Option B (Systemic manifestations):** Also known as **"B symptoms"** (fever, night sweats, weight loss), these indicate a higher tumor burden and more aggressive disease, correlating with a worse prognosis. * **Option C (Lymphocyte depletion):** This is the rarest histological subtype of HL and carries the **worst prognosis**. Conversely, Lymphocyte Predominant HL has the best prognosis. * **Option D (Mediastinal disease):** Specifically "Bulky disease" (mediastinal mass >1/3 of the maximum intrathoracic diameter) is a major poor prognostic factor in early-stage HL, as it increases the risk of local recurrence. **High-Yield Clinical Pearls for NEET-PG:** * **Hasenclever Index (International Prognostic Score):** Used for advanced HL. Poor prognostic factors include: Age ≥45, Male sex, Stage IV disease, Albumin <4 g/dL, Hemoglobin <10.5 g/dL, WBC ≥15,000/µL, and Lymphocytes <600/µL (or <8%). * **Ann Arbor Staging:** The most important factor for determining treatment. * **Reed-Sternberg Cells:** The hallmark "Owl’s eye" appearance; CD15+ and CD30+ (except in Nodular Lymphocyte Predominant HL, which is CD20+).

Question 809: A 42-year-old female presents with bleeding gums for the past 20 days. Intra-oral examination shows thickened and friable gums. She also has hepatosplenomegaly and generalized non-tender lymphadenopathy. Laboratory findings include: Hemoglobin 11.4 g/dL, Platelet count 90,000/mm³, WBC count 4600/mm³. Bone marrow biopsy shows 100% cellularity with many large blasts that are peroxidase negative and non-specific esterase positive. What is the most likely diagnosis for this patient?

A. Acute lymphoblastic leukemia
B. Acute megakaryocytic leukemia
C. Acute promyelocytic leukemia
D. Acute monocytic leukemia (Correct Answer)

Explanation: ### Explanation The correct diagnosis is **Acute Monocytic Leukemia (AML-M5)**. **1. Why Acute Monocytic Leukemia is correct:** The clinical hallmark of monocytic leukemia is **extramedullary involvement**, specifically **gingival hypertrophy** (thickened, friable gums) [1], hepatosplenomegaly, and lymphadenopathy [2]. Monoblasts have a high propensity to infiltrate tissues. * **Laboratory Findings:** The bone marrow shows large blasts that are **Myeloperoxidase (MPO) negative** (common in M5) but strongly **Non-Specific Esterase (NSE) positive**. NSE is the characteristic marker for the monocytic lineage. **2. Why other options are incorrect:** * **A. Acute Lymphoblastic Leukemia (ALL):** While common in children and presenting with lymphadenopathy [2], ALL blasts are typically **PAS positive** and would not show NSE positivity or specific gingival infiltration. * **B. Acute Megakaryocytic Leukemia (AML-M7):** This is often associated with myelofibrosis (dry tap) and Down Syndrome. Blasts are identified by platelet markers (CD41/CD61), not NSE. * **C. Acute Promyelocytic Leukemia (AML-M3):** Characterized by Auer rods, DIC, and strong **MPO positivity**. It does not typically present with gingival hypertrophy or NSE positivity. **3. NEET-PG High-Yield Pearls:** * **Gingival Hyperplasia:** Classic for AML-M4 (Myelomonocytic) and **AML-M5 (Monocytic)** [1]. * **NSE Stain:** Highly specific for monocytes. If the stain is inhibited by sodium fluoride, it confirms the monocytic origin. * **MPO Stain:** The most sensitive marker for the myeloid lineage (positive in M1, M2, M3, M4). * **M5 Subtypes:** M5a (mostly monoblasts) and M5b (monoblasts + promonocytes + monocytes).

Question 810: Chronic hemolysis from which of the following conditions may be associated with iron deficiency?

A. Paroxysmal cold Hemoglobinuria (Correct Answer)
B. Thalassemia
C. Hereditary spherocytosis
D. G 6PD deficiency

Explanation: The core concept behind this question is the distinction between **intravascular** and **extravascular** hemolysis. ### **Explanation** **Paroxysmal Cold Hemoglobinuria (PCH)** is a form of **intravascular hemolysis** caused by the Donath-Landsteiner antibody. When hemolysis occurs within the blood vessels, free hemoglobin is released into the plasma. This hemoglobin is filtered by the kidneys, leading to **hemoglobinuria** and **hemosiderinuria** [1]. The chronic loss of iron through the urine (as hemoglobin or sloughed tubular cells containing hemosiderin) eventually depletes the body's iron stores, leading to iron deficiency. ### **Why the other options are incorrect:** * **Thalassemia:** This is a disorder of globin chain synthesis. It is characterized by ineffective erythropoiesis and extravascular hemolysis [2]. Because the iron remains within the body (recycled by macrophages) and patients often require transfusions, they are at risk of **iron overload**, not deficiency. * **Hereditary Spherocytosis (HS):** This involves **extravascular hemolysis** where RBCs are destroyed by splenic macrophages [1]. The iron is recycled and stored as ferritin/hemosiderin within the reticuloendothelial system. * **G6PD Deficiency:** While it can cause acute episodes of intravascular hemolysis, it is typically episodic rather than chronic [3]. Between episodes, iron is conserved. ### **NEET-PG Clinical Pearls:** * **Rule of Thumb:** Chronic **intravascular** hemolysis (e.g., PNH, PCH, Microangiopathic Hemolytic Anemia, or prosthetic heart valves) leads to iron deficiency [1]. Chronic **extravascular** hemolysis (e.g., HS, AIHA) does not. * **PCH Hallmark:** It is mediated by an **IgG biphasic antibody** (binds in the cold, fixes complement in the warm). * **PNH vs. PCH:** Paroxysmal Nocturnal Hemoglobinuria (PNH) is the most classic cause of iron deficiency due to hemolysis mentioned in exams, but PCH follows the same physiological mechanism.

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Hematology — MCQs

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