Hematology — MCQs

A 39-year-old man has experienced chronic fatigue and weight loss for the past 3 months. There are no remarkable findings on physical examination. Laboratory studies show hemoglobin, 10.0 g/dL; hematocrit, 30.3%; MCV, 91 mm3; platelet count, 240,000/mm3; WBC count, 7550/mm3; serum iron 80 mg/dL; total iron-binding capacity, 145 mg/dL; and serum ferritin, 565 ng/mL. Serum erythropoietin levels are low for the level of Hb and hepcidin levels are elevated. Which of the following is the most likely diagnosis?

Q527Medium

A 40-year-old male patient is hospitalized with huge splenomegaly, marked sternal tenderness, and a total leukocyte count of 85,000 per cubic millimeter with a large percentage of myelocytes and metamyelocytes. Which one of the following drugs is best indicated for his disease?

Q528Medium

Which of the following is NOT true about adult autologous stem cell transplant?

Q529Medium

Which of the following indicates a poor prognosis in multiple myeloma?

Q530Medium

Direct Coombs test is positive in hemolytic anemia due to which of the following conditions?

Hematology Indian Medical PG Practice Questions and MCQs

Question 521: Splenomegaly may be a feature of:

A. Megaloblastic anemia
B. Sickle cell anemia (Correct Answer)
C. Thalassemia
D. G6PD deficiency

Explanation: **Explanation:** Splenomegaly is a common clinical finding in various hematological disorders, particularly those involving chronic hemolysis or extramedullary hematopoiesis. **1. Why Sickle Cell Anemia (SCA) is the correct answer:** In the **early stages** of Sickle Cell Anemia (especially in children), the spleen becomes enlarged due to the sequestration of sickled red blood cells and reactive hypertrophy of the reticuloendothelial system [1]. While it is true that recurrent splenic infarcts eventually lead to "autosplenectomy" (a shrunken, fibrotic spleen) by adulthood, **splenomegaly is a classic feature of the pediatric presentation** and the life-threatening "Splenic Sequestration Crisis" [1]. **2. Analysis of Incorrect Options:** * **Megaloblastic Anemia:** This is a maturation defect due to Vitamin B12 or Folate deficiency. While mild splenomegaly can rarely occur, it is not a characteristic or diagnostic feature. * **Thalassemia:** While Thalassemia major is a classic cause of **massive splenomegaly** due to extreme extramedullary hematopoiesis, in the context of standard NEET-PG questioning, if SCA is provided as a specific option regarding the *mechanism* of sequestration or early presentation, it is often highlighted. (Note: In many clinical scenarios, Thalassemia actually causes more persistent splenomegaly than SCA). * **G6PD Deficiency:** This typically presents as episodic, acute intravascular hemolysis triggered by oxidative stress (e.g., fava beans, drugs). Because the hemolysis is acute and transient, the spleen usually does not have time to enlarge. **High-Yield Clinical Pearls for NEET-PG:** * **Autosplenectomy:** Occurs in SCA by age 5–8 years due to repeated micro-infarctions [1]. Look for **Howell-Jolly bodies** on a peripheral smear. * **Massive Splenomegaly:** Defined as the spleen crossing the midline or reaching the left iliac fossa. Common causes: Myelofibrosis, CML, Malaria, Kala-azar, and Thalassemia Major. * **Splenic Sequestration Crisis:** A pediatric emergency in SCA where a sudden trap of blood in the spleen leads to hypovolemic shock and rapid splenic enlargement [1].

Question 522: A 50-year-old male presents with massive splenomegaly. Which of the following is NOT a likely diagnosis?

A. Chronic myeloid leukemia (CML)
B. Polycythemia vera
C. Hairy cell leukemia
D. Aplastic anemia (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Aplastic anemia**. **1. Why Aplastic Anemia is the Correct Answer:** Aplastic anemia is characterized by **pancytopenia** resulting from bone marrow failure (hypocellular marrow). By definition, the absence of hematopoietic cells in the marrow means there is no extramedullary hematopoiesis or infiltration. Therefore, **splenomegaly is characteristically absent** in aplastic anemia. If a patient with pancytopenia presents with an enlarged spleen, clinicians must look for alternative diagnoses like aleukemic leukemia or hypersplenism. **2. Analysis of Incorrect Options:** * **Chronic Myeloid Leukemia (CML):** This is a classic cause of **massive splenomegaly**. The spleen enlarges due to the massive proliferation of mature and maturing granulocytes (extramedullary hematopoiesis) [1]. * **Polycythemia Vera (PV):** Splenomegaly occurs in about 75% of PV patients due to congestion and extramedullary hematopoiesis. It can become massive if the disease progresses to the "spent phase" (myelofibrosis) [1]. * **Hairy Cell Leukemia (HCL):** This is a B-cell lymphoproliferative disorder where the hallmark clinical finding is **massive splenomegaly** (due to red pulp infiltration) and "dry tap" on bone marrow aspiration. **3. NEET-PG High-Yield Pearls:** * **Massive Splenomegaly (Spleen >8cm below costal margin or >1000g):** Remember the mnemonic **"CHCC"** — **C**ML, **H**airy cell leukemia, **C**hronic Malaria (Tropical Splenomegaly Syndrome), and **C**ala-azar (Visceral Leishmaniasis). Other causes include Myelofibrosis and Gaucher’s disease [1]. * **Aplastic Anemia Rule:** If you see "Splenomegaly" in a clinical vignette of a patient with low blood counts, **rule out** Aplastic Anemia immediately. * **Hairy Cell Leukemia:** Associated with TRAP (Tartrate-Resistant Acid Phosphatase) positivity and BRAF V600E mutation.

Question 523: What is the best treatment for Sickle cell anemia?

A. Hydroxyurea (Correct Answer)
B. Sulphonamide
C. Iron Injection
D. Blood transfusion

Explanation: **Explanation:** **Hydroxyurea (Option A)** is the mainstay of disease-modifying therapy in Sickle Cell Anemia (SCA) [1]. Its primary mechanism of action is the **induction of Fetal Hemoglobin (HbF)** synthesis. HbF inhibits the polymerization of deoxygenated Hemoglobin S (HbS), thereby preventing the sickling of red blood cells [1]. Clinically, this translates to a significant reduction in the frequency of painful Vaso-occlusive Crises (VOC), Acute Chest Syndrome, and the need for blood transfusions [1]. **Why other options are incorrect:** * **Sulphonamides (Option B):** These are contraindicated or used with caution in many hemolytic anemias (like G6PD deficiency) as they can trigger oxidative stress. They have no role in treating the underlying pathology of SCA. * **Iron Injection (Option C):** Patients with SCA often develop **hemosiderosis** (iron overload) due to chronic hemolysis and repeated transfusions. Administering iron is generally contraindicated unless a concomitant iron deficiency is proven. * **Blood Transfusion (Option D):** While vital for managing acute complications (e.g., stroke, severe anemia, or splenic sequestration), it is not the "best" long-term treatment due to risks of alloimmunization and iron overload [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Hydroxyurea:** Inhibits the enzyme **Ribonucleotide Reductase**, but its benefit in SCA is specifically via increasing γ-globin chain production [1]. * **Monitoring:** Hydroxyurea can cause bone marrow suppression; monitor CBC for neutropenia or thrombocytopenia. * **Cure:** The only definitive **curative** treatment for SCA is Allogeneic Hematopoietic Stem Cell Transplantation (HSCT) [1]. * **Vaccination:** Patients are functionally asplenic; ensure vaccination against encapsulated organisms (*S. pneumoniae, H. influenzae, N. meningitidis*).

Question 524: What is the blood product of choice for the treatment of hemophilia?

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

Explanation: **Explanation:** The treatment of choice for Hemophilia A (Factor VIII deficiency) among the given options is **Cryoprecipitate**. **1. Why Cryoprecipitate is correct:** Cryoprecipitate is a concentrated subset of plasma proteins obtained by thawing Fresh Frozen Plasma (FFP) at 4°C. It is the "product of choice" among these options because it contains a significantly higher concentration of **Factor VIII**, **von Willebrand Factor (vWF)**, and **Fibrinogen** in a much smaller volume compared to FFP. This allows for effective replacement therapy without the risk of volume overload. **2. Why other options are incorrect:** * **Fresh Frozen Plasma (FFP):** While FFP contains all coagulation factors, the concentration of Factor VIII is low [1]. To achieve therapeutic levels in a hemophilic patient, massive volumes of FFP would be required, leading to **Transfusion-Associated Circulatory Overload (TACO)**. * **Fresh Blood/Plasma:** These contain very dilute amounts of clotting factors and are insufficient for managing acute bleeding episodes in hemophilia. **3. NEET-PG High-Yield Pearls:** * **Gold Standard:** While Cryoprecipitate is the best *blood product* listed, the modern **treatment of choice** is **Recombinant Factor VIII concentrate** [1]. * **Hemophilia B:** Cryoprecipitate does **not** contain Factor IX. Therefore, for Hemophilia B (Christmas Disease), the product of choice is **FFP** (if specific Factor IX concentrates are unavailable). * **Contents of Cryoprecipitate:** Remember the mnemonic **"8, 13, vWF, and Fibrinogen"** (Factors VIII, XIII, von Willebrand Factor, and Fibrinogen). * **Desmopressin (DDAVP):** Used in mild Hemophilia A to release stored Factor VIII from endothelial cells [1]. It is ineffective in Hemophilia B.

Question 525: Regarding anemia of chronic diseases, all are true except?

A. Decreased serum iron
B. Decreased ferritin (Correct Answer)
C. Decreased total iron-binding capacity
D. Increased bone marrow iron

Explanation: **Explanation:** Anemia of Chronic Disease (ACD), also known as Anemia of Inflammation, is driven by the cytokine **Hepcidin** [1]. In chronic inflammatory states (infections, malignancies, autoimmune disorders), IL-6 stimulates the liver to produce Hepcidin. Hepcidin degrades ferroportin, which inhibits iron absorption from the gut and, more importantly, **sequesters iron within macrophages** and hepatocytes [1]. **Why Option B is the correct answer (The "Except"):** In ACD, iron is trapped inside storage cells. **Serum Ferritin**, which reflects total body iron stores and acts as an acute-phase reactant, is **increased or normal**, never decreased. A decreased ferritin is the hallmark of Iron Deficiency Anemia (IDA), not ACD [2]. **Analysis of Incorrect Options:** * **A. Decreased serum iron:** True. Because iron is trapped inside macrophages and not released into the plasma, the circulating (serum) iron level falls [1]. * **C. Decreased TIBC:** True. Total Iron Binding Capacity (TIBC) is a measure of transferrin. In inflammation, the body downregulates transferrin to "starve" pathogens of iron [2]. This helps differentiate ACD (Low TIBC) from IDA (High TIBC). * **D. Increased bone marrow iron:** True. Since iron is sequestered in the reticuloendothelial system, Prussian blue staining of a bone marrow aspirate will show abundant iron in macrophages. **NEET-PG High-Yield Pearls:** 1. **Key Mediator:** Hepcidin (The "Master Regulator" of iron). 2. **Differentiating ACD from IDA:** * **Ferritin:** High/Normal in ACD; Low in IDA [2]. * **TIBC:** Low in ACD; High in IDA [2]. * **Transferrin Saturation:** Low in both. 3. **Soluble Transferrin Receptor (sTfR):** Normal in ACD; Elevated in IDA. This is the most sensitive test to distinguish the two when they coexist.

Question 526: A 39-year-old man has experienced chronic fatigue and weight loss for the past 3 months. There are no remarkable findings on physical examination. Laboratory studies show hemoglobin, 10.0 g/dL; hematocrit, 30.3%; MCV, 91 mm3; platelet count, 240,000/mm3; WBC count, 7550/mm3; serum iron 80 mg/dL; total iron-binding capacity, 145 mg/dL; and serum ferritin, 565 ng/mL. Serum erythropoietin levels are low for the level of Hb and hepcidin levels are elevated. Which of the following is the most likely diagnosis?

A. Anemia of chronic disease (Correct Answer)
B. Aplastic anemia
C. Iron deficiency anemia
D. Megaloblastic anemia

Explanation: ### Explanation **Correct Answer: A. Anemia of chronic disease (ACD)** The clinical and laboratory profile is classic for **Anemia of Chronic Disease (ACD)**, also known as Anemia of Inflammation. The key diagnostic markers in this case are: 1. **Normocytic Anemia:** MCV of 91 fL (normal range 80–100 fL). 2. **Low TIBC:** This is the most specific finding for ACD. In iron deficiency, TIBC increases; in ACD, it decreases as the body attempts to sequester iron. 3. **High Ferritin:** Ferritin acts as an acute-phase reactant. High levels indicate adequate iron stores but poor utilization. 4. **Elevated Hepcidin:** This is the central mediator of ACD. Induced by inflammatory cytokines (mainly IL-6), hepcidin inhibits **ferroportin**, preventing iron release from macrophages and reducing intestinal absorption. It also directly suppresses erythropoietin (EPO) production. --- ### Why the other options are incorrect: * **B. Aplastic anemia:** This typically presents with **pancytopenia** (low WBCs and platelets) and a hypocellular bone marrow. This patient has normal WBC and platelet counts. * **C. Iron deficiency anemia (IDA):** In IDA, you would expect **low ferritin** (<30 ng/mL) and **high TIBC**. The MCV is usually low (microcytic), whereas it is normal here. * **D. Megaloblastic anemia:** This is characterized by **macrocytosis** (MCV >100 fL) and often hypersegmented neutrophils on a peripheral smear, which does not match this patient's normocytic indices. --- ### NEET-PG High-Yield Pearls: * **Hepcidin** is the "master regulator" of iron metabolism. High hepcidin = Iron sequestration (ACD); Low hepcidin = Iron overload (Hemochromatosis). * **TIBC vs. Ferritin:** In NEET-PG questions, if **Ferritin is high** and **TIBC is low**, always think **ACD**. If **Ferritin is low** and **TIBC is high**, think **IDA**. * ACD is the **most common** cause of anemia in hospitalized patients worldwide. * **Treatment:** Focus on the underlying inflammatory condition; recombinant EPO may be used in specific cases (e.g., CKD or malignancy).

Question 527: A 40-year-old male patient is hospitalized with huge splenomegaly, marked sternal tenderness, and a total leukocyte count of 85,000 per cubic millimeter with a large percentage of myelocytes and metamyelocytes. Which one of the following drugs is best indicated for his disease?

A. Cyclophosphamide
B. Chlorambucil
C. Melphalan
D. Hydroxyurea (Correct Answer)

Explanation: ### Explanation **Diagnosis:** The clinical presentation of **huge splenomegaly**, **sternal tenderness** (due to marrow expansion), and a high leukocyte count with a "left shift" (presence of myelocytes and metamyelocytes) is classic for **Chronic Myeloid Leukemia (CML)** in the chronic phase [1]. **Why Hydroxyurea is the Correct Answer:** In the management of CML, **Hydroxyurea** is the preferred agent for **rapid cytoreduction** (lowering the white blood cell count) [1]. It is an antimetabolite that inhibits the enzyme **ribonucleotide reductase**, thereby interfering with DNA synthesis. While Tyrosine Kinase Inhibitors (like Imatinib) are the definitive long-term treatment for CML [1], Hydroxyurea is the drug of choice for immediate control of hyperleukocytosis and symptomatic splenomegaly. **Why Other Options are Incorrect:** * **A. Cyclophosphamide:** An alkylating agent primarily used in lymphomas, leukemias (like CLL), and as an immunosuppressant. It is not a first-line agent for CML. * **B. Chlorambucil:** An alkylating agent used primarily in Chronic Lymphocytic Leukemia (CLL) and some lymphomas. It has no role in the management of CML. * **C. Melphalan:** An alkylating agent used predominantly in the treatment of Multiple Myeloma. **Clinical Pearls for NEET-PG:** * **CML Hallmark:** Presence of the **Philadelphia Chromosome t(9;22)** creating the *BCR-ABL1* fusion gene [1]. * **Sternal Tenderness:** A sign of rapid bone marrow expansion; highly characteristic of CML. * **LAP Score:** Low Leukocyte Alkaline Phosphatase (LAP) score helps differentiate CML from a Leukemoid reaction (where the score is high). * **Definitive Treatment:** Imatinib (TKI) is the gold standard for long-term management, but Hydroxyurea is used for initial "debulking" of the tumor load [1].

Question 528: Which of the following is NOT true about adult autologous stem cell transplant?

A. Used in the treatment of leukemia
B. Stem cells are collected directly from the peripheral blood (Correct Answer)
C. G-CSF is given to expand the number of stem cells
D. It allows high dose of chemotherapy

Explanation: **Explanation:** In autologous stem cell transplantation (ASCT), the "incorrect" statement (and thus the correct answer) is that stem cells are collected **directly** from the peripheral blood. Under normal physiological conditions, the concentration of hematopoietic stem cells (HSCs) in the peripheral blood is extremely low. To collect a sufficient yield for transplant, patients must first undergo **"mobilization."** This involves administering growth factors (like G-CSF) [1] or chemotherapy to force the stem cells to migrate from the bone marrow niche into the peripheral circulation, from where they are then collected via apheresis. **Analysis of Options:** * **Option A (Used in leukemia):** This is true. ASCT is a standard consolidation therapy for certain leukemias (like Acute Myeloid Leukemia) and is the gold standard for Multiple Myeloma and Relapsed Hodgkin’s Lymphoma. [1] * **Option C (G-CSF is given):** This is true. Granulocyte Colony-Stimulating Factor (G-CSF) is the primary agent used to expand and mobilize CD34+ stem cells into the blood. [1] * **Option D (Allows high dose chemotherapy):** This is true. The primary goal of ASCT is not to treat the disease with the cells themselves, but to "rescue" the bone marrow after the patient receives myeloablative (very high-dose) chemotherapy intended to kill resistant cancer cells. **Clinical Pearls for NEET-PG:** * **CD34+:** The surface marker used to identify and quantify hematopoietic stem cells during collection. * **Plerixafor:** A CXCR4 antagonist often used as a "rescue" mobilizing agent if G-CSF fails to yield enough cells. * **Graft-vs-Host Disease (GVHD):** This occurs in **allogeneic** transplants but is virtually **absent** in autologous transplants because the patient is receiving their own cells.

Question 529: Which of the following indicates a poor prognosis in multiple myeloma?

A. WBC > 20,000
B. Azotemia (Correct Answer)
C. Hypocalcemia
D. Low or normal M component production

Explanation: **Explanation:** In Multiple Myeloma (MM), prognosis is determined by tumor burden, host factors, and end-organ damage. **Azotemia (elevated blood urea nitrogen/creatinine)** is a major poor prognostic indicator because it reflects significant renal impairment [1]. Renal failure in MM is often multifactorial (cast nephropathy, hypercalcemia, amyloidosis) and is the second most common cause of death after infection. **Why the other options are incorrect:** * **WBC > 20,000:** While leukocytosis can occur in infections, it is not a standard prognostic marker for MM. In fact, leukopenia (due to marrow infiltration) is more common. * **Hypocalcemia:** **Hypercalcemia** (not hypo) is a hallmark of MM (part of the CRAB criteria) and indicates high bone resorption and poor prognosis. * **Low or normal M component:** A high M-protein spike (>3 g/dL) correlates with a higher tumor burden. However, a very low M-protein in the presence of extensive marrow involvement (Non-secretory myeloma) can sometimes be aggressive, but "low or normal" is generally not a standard poor prognostic marker compared to azotemia. **Clinical Pearls for NEET-PG:** 1. **International Staging System (ISS):** The most important prognostic markers are **Serum Beta-2 Microglobulin** (high = poor) and **Serum Albumin** (low = poor). 2. **Cytogenetics:** Deletion 17p (p53 locus) and t(4;14) are high-risk markers. 3. **CRAB Criteria:** Calcium (elevated), Renal insufficiency, Anemia, Bone lesions [1]. 4. **Renal Failure:** The most common cause is **Bence-Jones proteinuria** leading to "Myeloma Kidney" (Cast Nephropathy) [1].

Question 530: Direct Coombs test is positive in hemolytic anemia due to which of the following conditions?

A. Paroxysmal cold hemoglobinuria (Correct Answer)
B. Paroxysmal nocturnal hemoglobinuria
C. Idiopathic thrombocytopenic purpura
D. Hemolytic uremic syndrome

Explanation: **Explanation:** The **Direct Coombs Test (Direct Antiglobulin Test - DAT)** is used to detect antibodies (IgG) or complement (C3) bound directly to the surface of red blood cells (RBCs). It is the hallmark of **Immune-Mediated Hemolytic Anemias.** [1] **Why Paroxysmal Cold Hemoglobinuria (PCH) is correct:** PCH is an autoimmune hemolytic anemia caused by the **Donath-Landsteiner antibody**, which is an IgG antibody directed against the P-antigen on RBCs. This antibody binds to RBCs at cold temperatures and fixes complement; when the blood warms, the complement cascade is activated, leading to intravascular hemolysis. Because complement (C3) remains bound to the RBCs, the **Direct Coombs test is positive for C3.** [1] **Analysis of Incorrect Options:** * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** This is a **non-immune** hemolytic anemia caused by an acquired genetic mutation (PIGA gene) leading to a deficiency of GPI-anchored proteins (CD55/CD59). Since the defect is intrinsic to the cell membrane and not antibody-mediated, the Coombs test is **negative**. * **Idiopathic Thrombocytopenic Purpura (ITP):** This is an immune-mediated destruction of **platelets**, not RBCs. While it is an autoimmune condition, it does not cause a positive Coombs test unless it occurs concurrently with AIHA (known as Evans Syndrome). * **Hemolytic Uremic Syndrome (HUS):** This is a **Microangiopathic Hemolytic Anemia (MAHA)** caused by mechanical shearing of RBCs (schistocytes) as they pass through fibrin clots in small vessels [3]. It is a non-immune process; therefore, the Coombs test is **negative**. **NEET-PG High-Yield Pearls:** * **Warm AIHA:** IgG mediated, extravascular hemolysis, positive for IgG [1]. * **Cold Agglutinin Disease:** IgM mediated, but since IgM dissociates, the Coombs test is **positive for C3 only** [2]. * **PCH:** Often follows viral infections in children; characterized by the Donath-Landsteiner test. * **Negative Coombs Hemolysis:** Think of PNH, G6PD deficiency [4], HUS/TTP, or Hereditary Spherocytosis.

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Anemia Evaluation and Management

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Hemoglobinopathies

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Thalassemias

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Platelet Disorders

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Coagulation Disorders

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Thrombotic Disorders

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Leukemias

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Lymphomas

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Multiple Myeloma and Plasma Cell Disorders

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Myeloproliferative Neoplasms

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Transfusion Medicine

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Hematopoietic Stem Cell Transplantation

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Hematology — MCQs

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