Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 111: During an evaluation of hypoproliferative anemia, a patient was found to have mild normocytic anemia, serum iron was low (< 50), increased TIBC, with elevated serum ferritin and adequate bone marrow iron stores. What is the most likely diagnosis in this scenario?

A. Thalassemia
B. Iron deficiency anemia
C. Anemia of chronic inflammation (Correct Answer)
D. Renal disease

Explanation: The clinical scenario describes **Anemia of Chronic Inflammation (ACI)**, also known as Anemia of Chronic Disease. The hallmark of ACI is the **sequestration of iron** within the reticuloendothelial system (macrophages), mediated by **Hepcidin** [1], [3]. 1. **Why ACI is correct:** In response to inflammation (IL-6), the liver produces Hepcidin, which degrades ferroportin [2]. This prevents iron release from macrophages and absorption from the gut. Consequently, **Serum Iron is low**, but **Serum Ferritin is high** (reflecting trapped iron stores) [3]. Bone marrow examination shows **adequate iron stores** but poor incorporation into RBC precursors [3]. 2. **Why other options are wrong:** * **Iron Deficiency Anemia (IDA):** While IDA also has low serum iron and high TIBC, it is characterized by **low Serum Ferritin** and **absent bone marrow iron stores**. * **Thalassemia:** This is a microcytic anemia with **normal or high serum iron** and ferritin levels due to ineffective erythropoiesis and hemolysis. * **Renal Disease:** Anemia in chronic kidney disease is primarily due to **Erythropoietin (EPO) deficiency**. While it is normocytic, it does not typically present with the classic "iron trapping" profile unless comorbid inflammation is present. **High-Yield Pearls for NEET-PG:** * **Hepcidin** is the "Master Regulator" of iron metabolism; it is an acute-phase reactant [2]. * **TIBC vs. Ferritin:** In IDA, TIBC is high and Ferritin is low. In ACI, TIBC is low/normal and Ferritin is high [3]. * **Soluble Transferrin Receptor (sTfR):** This is the best test to differentiate IDA from ACI. sTfR is **elevated in IDA** but **normal in ACI**. * ACI is typically **normocytic normochromic**, but can become microcytic in long-standing cases [1].

Question 112: All of the following conditions typically cause reticulocytosis EXCEPT:

A. Aplastic anemia (Correct Answer)
B. Thalassemia
C. Sickle cell anemia
D. Chronic blood loss

Explanation: ### Explanation The **reticulocyte count** is a direct reflection of the bone marrow's ability to produce new red blood cells (erythropoiesis) in response to anemia. **1. Why Aplastic Anemia is the Correct Answer:** Aplastic anemia is characterized by **bone marrow failure** (pancytopenia with hypocellular marrow). In this condition, the "factory" itself is damaged, meaning the marrow cannot produce new cells despite the presence of anemia. Therefore, the hallmark of aplastic anemia is **reticulocytopenia** (a low reticulocyte count). **2. Analysis of Incorrect Options:** * **Sickle Cell Anemia:** This is a hemolytic anemia. When RBCs are destroyed prematurely, the healthy bone marrow compensates by increasing production, leading to a high reticulocyte count (**reticulocytosis**). * **Thalassemia:** While thalassemia involves ineffective erythropoiesis, it is often associated with a compensatory (though inadequate) increase in reticulocytes compared to the baseline, especially after treatment or in milder forms. * **Chronic Blood Loss:** Persistent blood loss leads to iron deficiency over time. However, as long as iron stores are sufficient or during the early stages of compensation, the marrow increases RBC production to replace lost cells, resulting in reticulocytosis. **3. NEET-PG High-Yield Pearls:** * **Reticulocyte Production Index (RPI):** In anemia, always look for the RPI. An **RPI > 2-3%** indicates an appropriate marrow response (Hemolysis/Hemorrhage), while an **RPI < 2%** indicates an inadequate response (Nutritional deficiencies or Marrow failure). * **Corrected Reticulocyte Count (CRC):** Formula = Observed Reticulocyte % × (Patient's Hct / Normal Hct). * **Mnemonic for Low Retic Count:** "Marrow is **SAD**" (**S**ideroblastic anemia, **A**plastic anemia/Anemia of chronic disease, **D**eficiency of B12/Folate/Iron).

Question 113: A 35-year-old man was admitted with a history of painless cervical and axillary lymphadenopathy. He had a history of loss of weight, fever, and night sweats and was found to have cutaneous allergy. There was no hepatosplenomegaly. What is the most likely diagnosis?

A. Diffuse large B-cell lymphoma
B. Hodgkin's lymphoma (Correct Answer)
C. Burkitt lymphoma
D. Follicular lymphoma

Explanation: The clinical presentation of painless cervical and axillary lymphadenopathy associated with "B symptoms" (fever, night sweats, and weight loss) in a young adult is classic for Hodgkin’s Lymphoma (HL) [1]. A key diagnostic clue in this question is "cutaneous anergy" (implied by cutaneous allergy/lack of delayed-type hypersensitivity). In HL, there is a progressive defect in T-cell mediated immunity, even in early stages, leading to a failure to respond to skin antigens (like Tuberculin). Unlike Non-Hodgkin Lymphomas (NHL), HL typically spreads in a predictable, contiguous fashion and often involves the mediastinal or cervical nodes without early hepatosplenomegaly [1]. **Why other options are incorrect:** * **Diffuse Large B-cell Lymphoma (DLBCL):** While it can present with B symptoms, it is usually more aggressive, often involves extranodal sites, and does not characteristically present with cutaneous anergy as a primary feature [2]. * **Burkitt Lymphoma:** This is a very high-grade B-cell lymphoma [2]. It typically presents as a rapidly growing jaw mass (Endemic/African) or abdominal mass (Sporadic), rather than chronic painless peripheral lymphadenopathy. * **Follicular Lymphoma:** This is an indolent (slow-growing) lymphoma usually seen in older adults (median age >60) [2]. B symptoms and cutaneous anergy are uncommon in the early stages. **High-Yield Pearls for NEET-PG:** * **Bimodal Age Distribution:** HL has peaks in the 20s and 50s. * **Reed-Sternberg (RS) Cells:** The hallmark "Owl’s eye" appearance (CD15+ and CD30+) [1]. * **Alcohol-induced pain:** Pain in the lymph nodes after drinking alcohol is a rare but highly specific sign of HL. * **Pel-Ebstein Fever:** Characterized by alternating bouts of high fever and afebrile periods.

Question 114: Cold haemagglutinin is associated with which antibody type?

A. Anti IgM (Correct Answer)
B. Anti IgG
C. Anti IgA
D. Donath-Landsteiner antibody

Explanation: ### Explanation **Cold Agglutinin Disease (CAD)** is a type of autoimmune hemolytic anemia (AIHA) characterized by autoantibodies that react with red blood cells (RBCs) at low temperatures (optimally at 0–4°C) [1]. **1. Why Anti-IgM is Correct:** The autoantibodies in Cold AIHA are almost exclusively of the **IgM class** [1]. Due to its pentameric structure, IgM is highly efficient at binding to RBC antigens (usually the **I-antigen**) in the cooler peripheral circulation (fingers, toes, nose) [1]. This binding triggers the classical complement pathway, leading to C3b opsonization and subsequent extravascular hemolysis in the liver. **2. Analysis of Incorrect Options:** * **Anti-IgG:** This is the hallmark of **Warm AIHA**, where IgG antibodies bind to RBCs at body temperature (37°C), leading to splenic sequestration [1]. * **Anti-IgA:** While IgA can rarely cause AIHA, it is not the primary antibody associated with cold agglutinins. * **Donath-Landsteiner Antibody:** This refers specifically to a **biphasic IgG** antibody found in **Paroxysmal Cold Hemoglobinuria (PCH)**. Unlike CAD, it binds in the cold but causes brisk intravascular hemolysis upon rewarming. **3. High-Yield Clinical Pearls for NEET-PG:** * **Associations:** Acute CAD is often seen post-infection (**Mycoplasma pneumoniae** or **EBV/Infectious Mononucleosis**). Chronic CAD is associated with B-cell lymphoproliferative disorders [1]. * **Peripheral Smear:** Characterized by **RBC agglutination** (clumping), which can cause a falsely elevated MCV on automated counters [1]. * **Direct Coombs Test (DAT):** Positive for **C3 only** (IgM dissociates at warm temperatures, leaving only complement behind). * **Clinical Sign:** Patients may present with **acrocyanosis** (bluish discoloration of extremities) upon cold exposure [1].

Question 115: All of the following statements characterize chronic lymphocytic leukemia (CLL), EXCEPT:

A. It is a malignancy of elderly persons.
B. Patients may be asymptomatic at diagnosis.
C. Patients may exhibit hepatosplenomegaly.
D. Hypergammaglobulinemia is usually present. (Correct Answer)

Explanation: **Explanation:** Chronic Lymphocytic Leukemia (CLL) is a monoclonal proliferation of mature-appearing but functionally incompetent B-lymphocytes. **Why Option D is the Correct Answer (The Exception):** In CLL, the neoplastic B-cells do not differentiate into plasma cells effectively. Instead of hypergammaglobulinemia, patients typically develop **Hypogammaglobulinemia** (low antibody levels) as the disease progresses [1]. This occurs due to the suppression of normal B-cell function, leading to an increased risk of recurrent bacterial infections (e.g., *S. pneumoniae*) [1]. **Analysis of Incorrect Options:** * **Option A:** CLL is primarily a disease of the **elderly**, with a median age at diagnosis of approximately 70-72 years. It is rare in individuals under 40. * **Option B:** Approximately 50-70% of patients are **asymptomatic** at the time of diagnosis [1]. The condition is often discovered incidentally during routine blood work showing isolated lymphocytosis. * **Option C:** Physical examination often reveals painless generalized lymphadenopathy and **hepatosplenomegaly** due to the infiltration of lymphoid organs by leukemic cells [1]. **NEET-PG High-Yield Pearls:** * **Peripheral Smear:** Characterized by mature small lymphocytes and **Smudge cells** (basket cells), which are fragile lymphocytes ruptured during slide preparation. * **Immunophenotype:** CLL cells characteristically express **CD5** (a T-cell marker), **CD19, CD20, and CD23**. * **Complications:** Watch for **Richter Transformation**, where CLL evolves into a high-grade Large B-cell Lymphoma, and **Autoimmune Hemolytic Anemia (AIHA)** [1]. * **Staging:** The **Rai** and **Binet** staging systems are used to determine prognosis and treatment initiation [1].

Question 116: What is the most common chemotherapeutic agent used in patients with typical B cell CLL?

A. Fludarabine (Correct Answer)
B. Rituximab
C. Cyclophosphamide
D. Prednisolone

Explanation: **Explanation:** **Chronic Lymphocytic Leukemia (CLL)** is a monoclonal proliferation of mature B-cells. For many years, the purine analog **Fludarabine** has been established as the most effective single-agent chemotherapeutic drug for achieving high response rates in typical B-cell CLL. [1] 1. **Why Fludarabine is correct:** Fludarabine inhibits DNA synthesis and is highly toxic to both dividing and resting lymphocytes. In the classic "FCR" regimen (Fludarabine, Cyclophosphamide, Rituximab), which was the gold standard for fit patients, Fludarabine serves as the primary chemotherapeutic backbone due to its superior efficacy in inducing remission compared to older alkylating agents like Chlorambucil. [1], [2] 2. **Why other options are incorrect:** * **Rituximab:** While frequently used, it is a **monoclonal antibody** (targeting CD20), not a "chemotherapeutic agent." It is usually used in combination with chemotherapy to improve survival. [1] * **Cyclophosphamide:** An alkylating agent often used in the FCR regimen, but it is rarely used as a standalone first-line therapy for CLL compared to Fludarabine. * **Prednisolone:** Glucocorticoids are used to manage autoimmune complications of CLL (like AIHA or ITP) or in palliative settings, but they are not the primary treatment for the leukemia itself. **High-Yield Clinical Pearls for NEET-PG:** * **Most common leukemia in adults:** CLL (Western world). * **Characteristic finding:** Smudge cells (Basket cells) on peripheral smear. * **Immunophenotype:** CD5+, CD19+, CD20+, and CD23+. * **Richter’s Transformation:** Sudden transformation of CLL into Diffuse Large B-cell Lymphoma (DLBCL), signaled by rapidly enlarging lymph nodes and systemic symptoms. * **Modern Shift:** While Fludarabine remains a classic exam answer, clinical practice is shifting toward **Ibrutinib** (BTK inhibitor) and **Venetoclax** (BCL-2 inhibitor) as first-line targeted therapies.

Question 117: All of the following are major criteria for diagnosing Myeloma except?

A. Tissue biopsy suggestive of myeloma
B. Bone marrow plasma cells > 30%
C. IgG level > 35 g/L
D. Lytic bone lesions in X-ray (Correct Answer)

Explanation: The diagnosis of Multiple Myeloma has traditionally been based on the **Salmon-Durie Criteria**, which categorizes findings into Major and Minor criteria. [1] ### **Explanation of the Correct Answer** **Option D (Lytic bone lesions)** is the correct answer because it is classified as a **Minor Criterion**, not a major one. While lytic lesions are a hallmark of myeloma (part of the CRAB features), they do not independently prove the high plasma cell burden required for a major criterion. ### **Analysis of Incorrect Options (Major Criteria)** * **Option A (Tissue biopsy):** A biopsy showing a **plasmacytoma** (localized collection of plasma cells) is a Major Criterion as it provides definitive histological evidence of the disease. * **Option B (Bone marrow plasma cells > 30%):** A high percentage of clonal plasma cells in the marrow is a Major Criterion. (Note: 10–30% is considered a minor criterion). [1] * **Option C (IgG level > 35 g/L):** High levels of monoclonal (M) protein (IgG > 35 g/L, IgA > 20 g/L, or Bence-Jones proteinuria > 1g/24h) signify a massive expansion of a single plasma cell clone, meeting Major Criteria. [1] ### **NEET-PG High-Yield Pearls** * **Updated IMWG Criteria:** Modern diagnosis now relies on the **SLiM-CRAB** criteria. A diagnosis is made if there is ≥10% clonal plasma cells PLUS one or more "Myeloma Defining Events": [1] * **S:** Sixty percent (≥60%) plasma cells in marrow. * **Li:** Light chain ratio (involved:uninvolved) ≥ 100. * **M:** MRI showing >1 focal lesion. * **CRAB:** Calcium elevation, Renal insufficiency, Anemia, and Bone lesions. [1] * **Most Common Presentation:** Bone pain (backache). * **Investigation of Choice for Bone:** Whole-body low-dose CT (more sensitive than X-ray). * **Peripheral Smear:** Characterized by **Rouleaux formation** due to high ESR. [1]

Question 118: Which of the following is NOT a good prognostic factor for acute lymphoblastic leukemia (ALL)?

A. Hyperdiploidy
B. Female sex
C. Pre B cell ALL (Correct Answer)
D. t (12 : 21) translocation

Explanation: ### Explanation In Acute Lymphoblastic Leukemia (ALL), prognosis is determined by age, white blood cell (WBC) count at presentation, cytogenetics, and immunophenotype [1]. **Why "Pre-B cell ALL" is the correct answer:** While the term "Pre-B cell" is often used broadly, in the context of prognostic stratification, **Early Pre-B cell (Common ALL)**—which expresses the CD10 (CALLA) antigen—carries a **favorable** prognosis [1]. However, the specific **Pre-B cell phenotype** (characterized by cytoplasmic immunoglobulin heavy chains) is associated with the **t(1;19)** translocation, which historically carries a **poor to intermediate prognosis**. Compared to the "Common ALL" subtype or the hyperdiploid state, it is considered a less favorable prognostic marker. **Analysis of Incorrect Options:** * **A. Hyperdiploidy (>50 chromosomes):** This is one of the strongest **favorable** prognostic factors in pediatric ALL [1]. It typically responds very well to chemotherapy. * **B. Female sex:** Statistically, girls have a **better prognosis** than boys. Boys have a higher risk of late relapses, partly due to sanctuary sites like the testes. * **D. t(12;21) translocation:** Also known as the *TEL-AML1* (ETV6-RUNX1) fusion, this is the most common genetic rearrangement in childhood ALL and is associated with an **excellent prognosis**. **NEET-PG High-Yield Pearls:** * **Best Prognosis:** Age 1–9 years, low initial WBC count (<50,000/µL), Hyperdiploidy, and t(12;21). * **Worst Prognosis:** Age <1 or >10 years, high WBC count, **t(9;22)** (Philadelphia chromosome/BCR-ABL1), and **t(4;11)** (MLL rearrangement). * **Immunophenotype:** Mature B-cell ALL (Burkitt-type) and T-cell ALL generally carry a worse prognosis than the standard B-cell precursor (Common) ALL.

Question 119: Megaloblastic anemia in blind loop syndrome is due to which of the following?

A. Vitamin B12 malabsorption
B. Bacterial overgrowth (Correct Answer)
C. Frequent diarrhea
D. Decreased iron intake

Explanation: **Explanation:** **Blind Loop Syndrome** (also known as Stagnant Loop Syndrome) occurs when there is stasis of intestinal contents due to structural abnormalities (e.g., diverticula, strictures, or surgical blind pouches) [1]. This stasis leads to **Small Intestinal Bacterial Overgrowth (SIBO)**. **Why Bacterial Overgrowth is the correct answer:** The primary mechanism for megaloblastic anemia in this syndrome is the proliferation of aerobic and anaerobic bacteria (such as *E. coli* and *Bacteroides*) within the stagnant segment. these bacteria **competitively utilize dietary Vitamin B12**, depriving the host of the vitamin even if intrinsic factor levels and ileal mucosal function are normal. This leads to a secondary Vitamin B12 deficiency and subsequent megaloblastic anemia [2]. **Analysis of Incorrect Options:** * **Option A (Vitamin B12 malabsorption):** While B12 deficiency occurs, "malabsorption" usually implies a defect in the ileal receptors or lack of Intrinsic Factor (as in Pernicious Anemia). In Blind Loop Syndrome, the primary pathology is the consumption of the vitamin by bacteria before it can be absorbed. * **Option C (Frequent diarrhea):** While diarrhea and steatorrhea are common symptoms of SIBO (due to bacterial deconjugation of bile salts), they are consequences of the syndrome, not the direct cause of the megaloblastic changes. * **Option D (Decreased iron intake):** Iron deficiency causes microcytic hypochromic anemia, not megaloblastic anemia. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** The gold standard is a jejunal aspirate culture (>10⁵ CFU/mL), but the **14C-D-Xylose breath test** or Hydrogen breath test are commonly used non-invasive alternatives. * **Treatment:** Management involves surgical correction of the stasis and a course of **broad-spectrum antibiotics** (e.g., Rifaximin, Tetracycline, or Metronidazole) to eliminate the overgrowth. * **Contrast:** Unlike Vitamin B12, **Folate levels** are often **elevated** in SIBO because the overgrowing bacteria synthesize folate.

Question 120: Intravenous immunoglobulin therapy is effective in some patients with which of the following conditions?

A. Pure red cell aplasia (Correct Answer)
B. Myelodysplasia
C. Paroxysmal nocturnal hemoglobinuria (PNH)
D. Glucose-6-phosphate dehydrogenase (G6PD) deficiency

Explanation: **Explanation:** **Pure Red Cell Aplasia (PRCA)** is a clinical syndrome characterized by a severe reduction in erythroid precursors in the bone marrow, leading to isolated anemia. The underlying pathophysiology is often immune-mediated (T-cell or antibody-driven). Intravenous Immunoglobulin (IVIG) is specifically effective in cases of PRCA caused by **persistent Parvovirus B19 infection**, particularly in immunocompromised patients (e.g., HIV, transplant recipients). IVIG provides neutralizing antibodies against the virus, allowing erythropoiesis to resume. It is also sometimes used in refractory autoimmune PRCA. **Analysis of Incorrect Options:** * **Myelodysplasia (MDS):** This is a clonal stem cell disorder characterized by ineffective hematopoiesis and cytopenias. Treatment involves growth factors (EPO), hypomethylating agents (Azacitidine), or bone marrow transplant, but not IVIG. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** This is a stem cell defect involving a mutation in the *PIGA* gene, leading to a deficiency of GPI-anchored proteins (CD55/CD59) and complement-mediated hemolysis. The treatment of choice is Eculizumab (C5 inhibitor). * **G6PD Deficiency:** This is an X-linked enzymatic defect causing episodic oxidative hemolysis. Management focuses on avoiding triggers (e.g., fava beans, certain drugs) and supportive care; IVIG has no role here. **High-Yield Clinical Pearls for NEET-PG:** * **PRCA Associations:** Thymoma (most common association), Parvovirus B19, SLE, and drugs (e.g., Phenytoin, EPO-alpha). * **Diagnostic Hallmark:** Bone marrow shows a selective absence of erythroid precursors with normal myeloid and megakaryocytic lines. * **First-line treatment for autoimmune PRCA:** Cyclosporine or Corticosteroids. * **Parvovirus B19** specifically targets the **P-antigen** on proerythroblasts.

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Thalassemias

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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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Hematology — MCQs

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