Hematology — MCQs

A 32-year-old woman with systemic lupus erythematosus (SLE) and chronic renal failure manifests rapidly progressive weakness. On physical examination, she appears pale and has slightly yellow sclerae and an enlarged spleen. Blood tests reveal severe anemia and mild, mostly unconjugated, hyperbilirubinemia. Coombs test is positive at 37 C but negative at 0-4 C. This patient developed anemia because of?

Q576Easy

Which leukemia is associated with a translocation involving chromosomes 15 and 17?

Q577Medium

Which of the following is NOT a feature of sideroblastic anemia?

Q578Medium

A 5-year-old child presents with a history of fever off and on for the past 2 weeks, petechial spots all over the body, and increasing pallor for the past 1 month. Examination reveals splenomegaly of 2 cm below the costal margin. What is the most likely diagnosis?

Q579Easy

Which of the following is NOT a cause of iron deficiency anemia?

Q580Easy

Increased fetal hemoglobin is seen in which of the following conditions?

Hematology Indian Medical PG Practice Questions and MCQs

Question 571: What is true about alpha-thalassemia trait?

A. Increased HbF
B. Increased HbA
C. Microcytosis (Correct Answer)
D. Severe anemia

Explanation: Explanation: Alpha-thalassemia trait (also known as $\alpha$-thalassemia minor) occurs when there is a deletion of two of the four $\alpha$-globin genes ($--/\alpha\alpha$ or $-\alpha/-\alpha$). **1. Why Microcytosis is correct:** In $\alpha$-thalassemia trait, the reduction in $\alpha\{0}-globin chain synthesis leads to a decrease in the total amount of hemoglobin produced per red cell. This results in **microcytosis** (low MCV) and **hypochromia** (low MCH). Characteristically, the MCV is very low (often <75 fL), while the red cell count (RBC count) remains normal or is slightly elevated, distinguishing it from iron deficiency anemia. **2. Why the other options are incorrect:** * **Increased HbF/HbA2:** Unlike $\beta$-thalassemia trait, where HbA2 and HbF increase to compensate for the lack of $\beta$-chains, $\alpha$-thalassemia involves a deficiency in the $\alpha$-chain, which is a component of **all** adult hemoglobins (HbA, HbA2, and HbF). Therefore, the ratios remain normal, and hemoglobin electrophoresis is typically **normal** in $\alpha$-thalassemia trait [1]. * **Severe Anemia:** $\alpha$-thalassemia trait usually presents with **mild anemia** or is asymptomatic. Severe anemia is characteristic of HbH disease (3-gene deletion) or Hydrops Fetalis (4-gene deletion). **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** $\alpha$-thalassemia trait is a "diagnosis of exclusion" because electrophoresis is normal [1]. Definitive diagnosis requires **Genetic Testing (PCR)**. * **Mentzer Index:** (MCV/RBC count) is typically **<13** in thalassemia, helping differentiate it from iron deficiency (>13). * **Hb Barts:** Composed of $\gamma_4$ tetramers; seen in neonates with $\alpha$-thalassemia. * **HbH:** Composed of $\beta_4$ tetramers; seen in 3-gene deletion (HbH disease), appearing as "golf ball cells" on supra-vital staining.

Question 572: All of the following are causes of eosinophilia except:

A. Allergic Rhinitis
B. Trichinosis
C. Corticosteroid therapy (Correct Answer)
D. Rheumatoid arthritis

Explanation: The correct answer is **Corticosteroid therapy**. Corticosteroids are a classic cause of **eosinopenia** (a decrease in the number of circulating eosinophils). They act by inducing the sequestration of eosinophils in the bone marrow and lymphoid tissues, as well as promoting their apoptosis. **Why the other options are incorrect:** * **Allergic Rhinitis:** Allergic and atopic conditions (Type I hypersensitivity) are the most common causes of mild-to-moderate eosinophilia in developed countries [1], [2]. Eosinophils are recruited to the nasal mucosa in response to IL-5 and other Th2 cytokines. * **Trichinosis:** Helminthic parasitic infections (like *Trichinella spiralis*) are notorious for causing profound eosinophilia, especially during the tissue-invasion phase [2]. * **Rheumatoid Arthritis:** Eosinophilia can occur in systemic autoimmune and connective tissue diseases (CTDs). In RA, it is often a marker of severe disease or systemic vasculitis. **NEET-PG High-Yield Pearls:** 1. **Causes of Eosinopenia (The "S" Rule):** **S**teroids, **S**tress (due to endogenous cortisol), and **S**evere acute bacterial infections (sepsis). 2. **NAACP Mnemonic for Eosinophilia:** **N**eoplasia (Hodgkin’s, CTCL), **A**llergy (Asthma, Rhinitis), **A**ddison’s disease (low cortisol leads to high eosinophils), **C**onnective tissue diseases (Churg-Strauss/EGPA), and **P**arasites [2]. 3. **Drug Reaction:** DRESS syndrome (Drug Reaction with Eosinophilia and Systemic Symptoms) is a frequently tested cause of significant eosinophilia. 4. **Addison’s vs. Cushing’s:** Remember that **hypo**cortisolism (Addison’s) causes eosinophilia, while **hyper**cortisolism (Cushing’s or exogenous steroids) causes eosinopenia.

Question 573: What is the most sensitive marker for iron deficiency anemia?

A. Increased iron binding capacity
B. Decreased serum ferritin level (Correct Answer)
C. Decreased serum iron level
D. Increased serum free transferrin

Explanation: **Explanation:** Iron deficiency anemia (IDA) develops in stages: first, the depletion of storage iron, followed by iron-deficient erythropoiesis, and finally, overt anemia [1]. **Why Serum Ferritin is the Correct Answer:** Serum ferritin reflects the total body iron stores [2]. It is the **first biochemical marker to decline** as iron stores are depleted, even before the hemoglobin level or red cell indices (MCV/MCH) change [1][2]. Therefore, a low serum ferritin level is the **most sensitive and specific** initial lab finding for diagnosing IDA. A value of <15–30 ng/mL is virtually diagnostic of iron deficiency. **Analysis of Incorrect Options:** * **A & D (Increased TIBC/Free Transferrin):** Total Iron Binding Capacity (TIBC) and free transferrin levels increase as the body attempts to capture more iron [2]. While highly suggestive of IDA, these changes occur after the initial drop in ferritin and can be influenced by other conditions like pregnancy or oral contraceptive use. * **C (Decreased Serum Iron):** Serum iron levels fluctuate significantly due to diurnal variation, recent dietary intake, or infection. It is a late marker and is also low in Anemia of Chronic Disease (ACD), making it less specific and sensitive than ferritin. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard:** The most definitive (Gold Standard) test for IDA is **bone marrow aspiration** (Prussian blue staining) to visualize absent hemosiderin, but it is rarely performed clinically [2]. * **The "Acute Phase" Caveat:** Ferritin is an acute-phase reactant. In the presence of inflammation, infection, or malignancy, ferritin may be falsely normal or elevated even if IDA is present. * **Soluble Transferrin Receptor (sTfR):** This marker is useful to differentiate IDA (where sTfR is high) from Anemia of Chronic Disease (where sTfR is normal).

Question 574: What is the most common site for lytic lesions in multiple myeloma?

A. Femur
B. Clavicle
C. Pelvis
D. Vertebral column (Correct Answer)

Explanation: Multiple myeloma is a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells [1]. These cells secrete osteoclast-activating factors (such as RANK-ligand and IL-6), leading to the classic "punched-out" lytic lesions. [1] **Why the Vertebral Column is Correct:** Lytic lesions in multiple myeloma primarily occur in areas of the **active (red) bone marrow**. The **vertebral column** is the most common site for these lesions (found in approximately 65-70% of patients), followed by the ribs, skull, pelvis, and femur [1]. The high concentration of axial bone marrow in the vertebrae makes it the most frequent location for plasma cell infiltration and subsequent bone destruction, often leading to pathological compression fractures. [1] **Analysis of Incorrect Options:** * **Femur (A):** While the proximal femur is a common site for pathological fractures in myeloma, it is less frequently involved than the axial skeleton (spine and ribs). * **Clavicle (B):** The clavicle is rarely the primary or most common site for lytic lesions compared to the central skeleton. * **Pelvis (C):** The pelvis is frequently involved (approx. 40%), but statistically, it ranks lower than the vertebral column. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Myeloma (CRAB):** **C**alcium (elevated), **R**enal failure, **A**nemia, **B**one lesions [1]. * **Skull X-ray:** Classically shows "Raindrop" or "Punched-out" lytic lesions. * **Bone Scan Caution:** Technetium-99m bone scans are often **negative** in myeloma because they detect osteoblastic activity, whereas myeloma is purely **osteolytic** [1]. Skeletal surveys (X-rays) or MRI/CT are preferred. * **Bence-Jones Proteins:** These are free light chains found in urine; they do not show up on a standard dipstick (which detects albumin) [1].

Question 575: A 32-year-old woman with systemic lupus erythematosus (SLE) and chronic renal failure manifests rapidly progressive weakness. On physical examination, she appears pale and has slightly yellow sclerae and an enlarged spleen. Blood tests reveal severe anemia and mild, mostly unconjugated, hyperbilirubinemia. Coombs test is positive at 37 C but negative at 0-4 C. This patient developed anemia because of?

A. Bone marrow aplasia
B. IgG directed against red blood cells (Correct Answer)
C. IgM directed against red blood cells
D. Renal failure

Explanation: ### Explanation This patient presents with **Warm Autoimmune Hemolytic Anemia (WAIHA)**, a common hematologic complication of Systemic Lupus Erythematosus (SLE). **1. Why Option B is Correct:** The clinical triad of anemia, jaundice (unconjugated hyperbilirubinemia), and splenomegaly suggests extravascular hemolysis [3]. The definitive clue is the **Coombs test (Direct Antiglobulin Test)**, which is positive at **37°C (body temperature)** [1]. This characterizes "Warm" antibodies, which are almost exclusively **IgG**. These IgG-coated RBCs are partially phagocytosed by splenic macrophages, leading to the formation of spherocytes and subsequent splenic sequestration (splenomegaly) [1]. **2. Why the Other Options are Incorrect:** * **Option C (IgM):** IgM antibodies are associated with **Cold Agglutinin Disease** [2]. These react at low temperatures (**0–4°C**) and typically cause complement-mediated hemolysis. The question specifically states the test was negative at 0–4°C. * **Option A (Bone marrow aplasia):** While SLE can cause pancytopenia, aplasia would not present with jaundice or a positive Coombs test. The hyperbilirubinemia here confirms an active hemolytic process, not a production failure. * **Option D (Renal failure):** Chronic renal failure causes anemia due to **Erythropoietin (EPO) deficiency**. However, this is a normocytic, normochromic anemia and would not cause jaundice, splenomegaly, or a positive Coombs test. **3. High-Yield Clinical Pearls for NEET-PG:** * **WAIHA Associations:** SLE (most common autoimmune cause), CLL, and drugs (e.g., α-methyldopa). * **Cold AIHA Associations:** *Mycoplasma pneumoniae* and Infectious Mononucleosis (EBV). * **Peripheral Smear:** Look for **Spherocytes** in WAIHA (similar to Hereditary Spherocytosis, but Coombs positive) [1]. * **Treatment:** First-line treatment for WAIHA is **Corticosteroids**, whereas Cold AIHA is managed by avoiding cold and treating the underlying cause (steroids are often ineffective for Cold AIHA) [2].

Question 576: Which leukemia is associated with a translocation involving chromosomes 15 and 17?

A. Acute Promyelocytic Leukemia (APML) (Correct Answer)
B. Chronic Myeloid Leukemia (CML)
C. Chronic Lymphocytic Leukemia (CLL)
D. None of the above

Explanation: The correct answer is **Acute Promyelocytic Leukemia (APML)**, which is categorized as AML-M3 in the FAB classification [1]. **1. Why APML is correct:** APML is characteristically defined by the reciprocal translocation **t(15;17)(q22;q12)** [1]. This translocation involves the **PML** (Promyelocytic Leukemia) gene on chromosome 15 and the **RARα** (Retinoic Acid Receptor alpha) gene on chromosome 17. The resulting fusion gene, *PML-RARα*, produces a chimeric protein that arrests myeloid differentiation at the promyelocyte stage. This is a high-yield concept because it dictates treatment: high doses of **All-Trans Retinoic Acid (ATRA)** and Arsenic Trioxide can overcome this block and induce differentiation of the blast cells. **2. Why other options are incorrect:** * **Chronic Myeloid Leukemia (CML):** Associated with the "Philadelphia Chromosome," which is a translocation between chromosomes 9 and 22, **t(9;22)**, creating the *BCR-ABL1* fusion gene [1]. * **Chronic Lymphocytic Leukemia (CLL):** Does not have a single pathognomonic translocation; it is more commonly associated with deletions, such as **del 13q** (most common), del 11q, or trisomy 12. **3. NEET-PG High-Yield Pearls:** * **DIC Risk:** APML is a medical emergency due to the high risk of **Disseminated Intravascular Coagulation (DIC)** triggered by the release of procoagulants from promyelocyte granules. * **Morphology:** Look for **Auer rods**, specifically "Faggot cells" (cells containing bundles of Auer rods). * **Treatment:** ATRA is the mainstay. Watch for **"Differentiation Syndrome"** (fever, dyspnea, pulmonary infiltrates) as a side effect of treatment.

Question 577: Which of the following is NOT a feature of sideroblastic anemia?

A. Microcytosis with hypochromia
B. Increased iron stores in bone marrow
C. Response to pyridoxine therapy
D. Response to folic acid therapy (Correct Answer)

Explanation: **Explanation:** Sideroblastic anemia is a group of disorders characterized by defective heme synthesis despite adequate iron levels. The hallmark is the presence of **ringed sideroblasts** in the bone marrow—erythroblasts with iron-laden mitochondria encircling the nucleus. **Why Option D is the Correct Answer:** Folic acid deficiency causes megaloblastic anemia, not sideroblastic anemia. While some patients with chronic hemolytic or sideroblastic anemias may develop secondary folate deficiency due to high cell turnover, **folic acid therapy is not a primary treatment** for the underlying defect in sideroblastic anemia. **Analysis of Incorrect Options:** * **Option A (Microcytosis with hypochromia):** Since heme synthesis is impaired, hemoglobin production is reduced. This typically results in a microcytic, hypochromic blood picture (though a dimorphic population of cells is often seen). * **Option B (Increased iron stores):** Because iron cannot be incorporated into protoporphyrin to form heme, it accumulates in the mitochondria and systemic stores. This leads to high serum iron, high ferritin, and increased marrow iron. * **Option C (Response to pyridoxine):** The hereditary form (X-linked) is often due to a mutation in the **ALAS2 enzyme**, which requires **Vitamin B6 (Pyridoxine)** as a cofactor. High-dose B6 can overcome this defect in many patients. **NEET-PG High-Yield Pearls:** 1. **Prussian Blue Stain:** The gold standard for identifying ringed sideroblasts in bone marrow. 2. **Acquired Causes:** Lead poisoning (inhibits ALAD and Ferrochelatase), Isoniazid (antagonizes B6), and Alcoholism (most common cause of acquired sideroblastic anemia). 3. **Pappenheimer Bodies:** Siderotic granules seen on peripheral smears in these patients. 4. **MDS connection:** Refractory Anemia with Ringed Sideroblasts (RARS) is a subtype of Myelodysplastic Syndrome.

Question 578: A 5-year-old child presents with a history of fever off and on for the past 2 weeks, petechial spots all over the body, and increasing pallor for the past 1 month. Examination reveals splenomegaly of 2 cm below the costal margin. What is the most likely diagnosis?

A. Acute leukemia (Correct Answer)
B. Idiopathic thrombocytopenic purpura
C. Hypersplenism
D. Aplastic anemia

Explanation: **Explanation:** The clinical triad of **fever** (due to neutropenia/infection), **petechiae** (due to thrombocytopenia), and **pallor** (due to anemia) in a child strongly suggests **bone marrow failure** or infiltration [1]. 1. **Why Acute Leukemia is correct:** In children, Acute Lymphoblastic Leukemia (ALL) is the most common malignancy. The presence of **splenomegaly** is the key differentiating factor here [1]. It indicates an infiltrative process where leukemic cells have spread to the reticuloendothelial system [2]. The combination of pancytopenia (fever, spots, pallor) plus organomegaly is a classic presentation of Acute Leukemia. 2. **Why other options are incorrect:** * **Idiopathic Thrombocytopenic Purpura (ITP):** While it causes petechiae [1], it typically presents as "isolated thrombocytopenia." The child is usually otherwise healthy (no pallor or fever) and splenomegaly is characteristically absent. * **Aplastic Anemia:** This presents with pancytopenia (fever, pallor, bleeding), but **splenomegaly is never a feature** of primary aplastic anemia. Its presence points toward an alternative diagnosis [1]. * **Hypersplenism:** While it can cause cytopenias, it is usually secondary to portal hypertension or chronic malaria. It does not typically present with the acute, febrile, and rapidly progressive symptoms seen in this 5-year-old. **Clinical Pearls for NEET-PG:** * **Most common childhood cancer:** ALL (Peak age: 2–5 years). * **Pancytopenia + Splenomegaly:** Think Leukemia, Lymphoma, or Gaucher’s disease [2]. * **Pancytopenia WITHOUT Splenomegaly:** Think Aplastic Anemia or Vitamin B12 deficiency. * **Diagnostic Gold Standard:** Bone marrow aspiration showing >20% blasts.

Question 579: Which of the following is NOT a cause of iron deficiency anemia?

A. Chronic renal failure (CRF) (Correct Answer)
B. Young female
C. Celiac sprue
D. Hookworm infestation

Explanation: The correct answer is **A. Chronic renal failure (CRF)**. In Chronic Renal Failure, the primary cause of anemia is a **deficiency of Erythropoietin (EPO)**, which is produced by the peritubular interstitial cells of the kidney. This results in a **normocytic normochromic anemia**, not iron deficiency anemia (IDA). While patients on dialysis may develop IDA due to blood loss or frequent sampling, the hallmark of CRF-related anemia is "Anemia of Chronic Disease" (ACD), characterized by poor iron utilization rather than a lack of iron stores [2]. **Analysis of Incorrect Options:** * **Young female:** This is a classic cause of IDA due to physiological blood loss during **menstruation** [1, 2] and increased iron demands during pregnancy [3]. * **Celiac sprue:** This condition causes malabsorption [2]. Since iron is primarily absorbed in the **duodenum and upper jejunum**, the villous atrophy seen in Celiac disease directly impairs iron absorption. * **Hookworm infestation:** (*Ancylostoma duodenale* and *Necator americanus*) is a leading cause of IDA in developing countries [2]. The worms attach to the intestinal mucosa and suck blood, leading to chronic occult GI blood loss [1]. **NEET-PG High-Yield Pearls:** * **Most common cause of IDA worldwide:** Nutritional deficiency/Hookworm [1, 2]. * **Most common cause of IDA in adult males/post-menopausal females:** Occult GI bleed (must rule out malignancy) [1]. * **Absorption Site:** Iron is absorbed in the **Duodenum** (Ferrous form, $Fe^{2+}$) [4]. * **CRF Anemia Treatment:** Recombinant Human Erythropoietin (target Hb: 10–11 g/dL). Always ensure adequate iron stores before starting EPO.

Question 580: Increased fetal hemoglobin is seen in which of the following conditions?

A. Juvenile chronic myeloid leukemia (Correct Answer)
B. Congenital red cell aplasia
C. Hereditary spherocytosis
D. Acute myeloid leukemia

Explanation: **Explanation:** The correct answer is **Juvenile chronic myeloid leukemia (JMML)**. **Why JMML is correct:** Juvenile Myelomonocytic Leukemia (formerly known as Juvenile CML) is a rare clonal hematopoietic stem cell disorder of childhood. A hallmark feature of JMML is the **reversion to fetal erythropoiesis**, leading to a significantly **elevated Fetal Hemoglobin (HbF)** level, often disproportionate to the child's age. This occurs because the malignant clone retains or reverts to a fetal pattern of gene expression. Other key features include a lack of the Philadelphia chromosome (t:9,22), monocytosis, and hypersensitivity to Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF). **Analysis of Incorrect Options:** * **B. Congenital red cell aplasia (Diamond-Blackfan Anemia):** While HbF can be elevated in DBA as a sign of "stress erythropoiesis," JMML is a more classic and frequently tested association for markedly high HbF in pediatric hematologic malignancies. However, in the context of this specific question, JMML is the primary diagnostic marker. * **C. Hereditary spherocytosis:** This is a membrane defect (ankyrin/spectrin deficiency) leading to extravascular hemolysis. It does not involve a switch in hemoglobin chains; therefore, HbF levels remain normal. * **D. Acute myeloid leukemia:** While some cases of erythroleukemia (AML-M6) might show minor elevations, it is not a characteristic or diagnostic feature of AML in general. **High-Yield Clinical Pearls for NEET-PG:** * **HbF in JMML:** It is one of the diagnostic criteria. Levels >10% (often much higher) are common. * **Philadelphia Chromosome:** JMML is **Ph-negative**. If a child has Ph+ leukemia, it is "Pediatric CML," not JMML. * **Other conditions with high HbF:** Beta-thalassemia major, Sickle cell anemia [1], Hereditary Persistence of Fetal Hemoglobin (HPFH), and Aplastic anemia (during recovery). * **JMML Associations:** Strongly associated with **Neurofibromatosis type 1 (NF1)** and Noonan syndrome (PTPN11 mutations).

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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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