Hematology — MCQs
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Thrombocytopenia due to increased platelet destruction is seen in which of the following conditions?
Which of the following is a characteristic feature of hypoproliferative anemia?
A 22-year-old woman from a large Italian family is screened for a familial blood disorder. Laboratory studies reveal a hemoglobin of 9.5 g/dL and a peripheral smear showing mild microcytosis, hypochromia, and a few target cells. Hemoglobin electrophoresis demonstrates a mild increase in hemoglobin A2 (7.5%). What is the most likely diagnosis?
The use of desmopressin is best indicated for therapy in which of the following bleeding disorders?
A 65-year-old male patient presents with nonspecific symptoms and moderate splenomegaly. His lab tests show a WBC count of 2000, a normal differential count, Hb 6 g/dL, platelets 80,000/mm³, and 6% blast cells. What is the most likely diagnosis?
The presence of small-sized platelets on the peripheral smear is characteristic of:
Which drug is used for the treatment of Acute Myeloid Leukemia (AML) with FLT-3 mutation?
Increased iron absorption is seen in which of the following conditions?
What is characteristic of anemia of chronic disease?
A 58-year-old woman presents with a 6-month history of backache and recurrent chest infections. She develops sudden weakness of the legs and urinary retention. Investigations reveal a hemoglobin of 7.3 g/dL, serum calcium of 12.6 mg/dL, phosphate of 2.5 mg/dL, alkaline phosphatase of 100 U/L, serum albumin of 3 g/dL, globulin of 7.1 g/dL, and urea of 178 mg/dL. What is the most likely diagnosis?
Hematology Indian Medical PG Practice Questions and MCQs
Question 351: Thrombocytopenia due to increased platelet destruction is seen in which of the following conditions?
- A. Aplastic anemia
- B. Cancer chemotherapy
- C. Acute leukemia
- D. Systemic lupus erythematosus (Correct Answer)
Explanation: ### Explanation Thrombocytopenia can be broadly classified into two mechanisms: **decreased production** (bone marrow failure) and **increased destruction/consumption** (peripheral loss) [1]. **1. Why Systemic Lupus Erythematosus (SLE) is correct:** SLE is an autoimmune multisystem disorder where the body produces autoantibodies against various self-antigens. In SLE, thrombocytopenia occurs due to the production of **anti-platelet antibodies** (similar to Immune Thrombocytopenic Purpura or ITP) [1]. These antibody-coated platelets are prematurely cleared by the splenic macrophages, leading to **increased peripheral destruction**. The bone marrow in these cases typically shows normal or increased megakaryocytes as it attempts to compensate for the loss. Patients with active SLE typically show findings of anaemia, haemolytic anaemia, and thrombocytopenia on laboratory testing [2]. **2. Why the other options are incorrect:** * **Aplastic Anemia:** This is a primary bone marrow failure syndrome characterized by pancytopenia. Thrombocytopenia here is due to **decreased production** because the hematopoietic stem cells are replaced by fat. * **Cancer Chemotherapy:** Most chemotherapeutic agents are myelosuppressive. They inhibit rapidly dividing cells in the bone marrow, leading to **decreased production** of platelets. * **Acute Leukemia:** In leukemia, the bone marrow is "crowded out" by malignant blast cells. This infiltration prevents normal hematopoiesis, resulting in **decreased production** of functional platelets. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism Check:** Always look at the bone marrow. If megakaryocytes are **decreased**, it’s a production house problem (Options A, B, C). If megakaryocytes are **increased/normal**, it’s a peripheral destruction problem (Option D). * **SLE Association:** Up to 25-50% of SLE patients develop thrombocytopenia [2]. If it occurs with autoimmune hemolytic anemia, it is known as **Evans Syndrome**. * **Drug-induced destruction:** Aside from SLE, always remember **Heparin-Induced Thrombocytopenia (HIT)** as a classic cause of increased destruction/consumption [1].
Question 352: Which of the following is a characteristic feature of hypoproliferative anemia?
- A. Normocytic normochromic anemia with reticulocyte index < 2-2.5 (Correct Answer)
- B. Microcytic hypochromic anemia with reticulocyte index < 2-2.5
- C. Microcytic hypochromic anemia with reticulocyte index > 2-2.5
- D. Microcytic anemia with ringed sideroblasts
Explanation: Explanation: Hypoproliferative anemias are characterized by a failure of the bone marrow to produce an appropriate number of erythrocytes in response to a decrease in hemoglobin. This failure is objectively measured by the **Reticulocyte Index (RI)**. 1. **Why Option A is Correct:** In hypoproliferative states (such as early iron deficiency, inflammation, or renal disease), the bone marrow cannot mount an appropriate erythropoietic response [1]. Therefore, the RI remains low (**< 2–2.5**). Morphologically, these anemias are typically **normocytic and normochromic** because the RBCs that *are* produced are of normal size and hemoglobin content, but they are simply produced in insufficient quantities. 2. **Why the other options are incorrect:** * **Option B:** While the RI is low, microcytic hypochromic anemia is more characteristic of **maturation disorders** (like established iron deficiency or thalassemia) rather than pure hypoproliferative states [1]. * **Option C:** An RI **> 2.5** indicates an appropriate marrow response, typically seen in **hemolytic anemias** or acute blood loss, where the marrow is hyperproliferative. * **Option D:** Ringed sideroblasts are the hallmark of **Sideroblastic Anemia**, which is classified as a cytoplasmic maturation defect, not a primary hypoproliferative anemia. **High-Yield Clinical Pearls for NEET-PG:** * **The RI Formula:** $\text{Reticulocyte Count} \times (\text{Observed Hct} / \text{Normal Hct}) \times (1 / \text{Maturation Correction Factor})$. * **Common Causes:** The most common cause of hypoproliferative anemia is **Iron Deficiency** (early stage), followed by **Anemia of Chronic Disease/Inflammation** [1]. * **Key Differentiator:** If the MCV is abnormal (high or low) with a low RI, think of **Maturation Disorders**. If the MCV is normal with a low RI, think **Hypoproliferative Anemia**.
Question 353: A 22-year-old woman from a large Italian family is screened for a familial blood disorder. Laboratory studies reveal a hemoglobin of 9.5 g/dL and a peripheral smear showing mild microcytosis, hypochromia, and a few target cells. Hemoglobin electrophoresis demonstrates a mild increase in hemoglobin A2 (7.5%). What is the most likely diagnosis?
- A. Anemia of chronic disease
- B. G6PD deficiency
- C. Heterozygous beta-thalassemia (Correct Answer)
- D. Homozygous beta-thalassemia
Explanation: ### **Explanation** The correct diagnosis is **Heterozygous beta-thalassemia** (also known as Beta-thalassemia minor). **1. Why the correct answer is right:** The patient presents with mild microcytic hypochromic anemia (Hb 9.5 g/dL) and target cells on the peripheral smear. The diagnostic hallmark in this case is the **Hemoglobin Electrophoresis** result showing an **elevated HbA2 (7.5%)** [3]. * In Beta-thalassemia minor, there is a reduced synthesis of $\beta$-globin chains due to point mutations affecting mRNA production [4]. To compensate, the body increases the production of $\delta$-chains, which combine with $\alpha$-chains to form **HbA2 ($\alpha_2\delta_2$)**. * Normal HbA2 levels are <3.5%. A value between 4% and 9% is classically diagnostic of Beta-thalassemia trait. The patient's Italian ethnicity is also a clinical clue, as the condition is prevalent in Mediterranean populations. **2. Why the incorrect options are wrong:** * **Anemia of chronic disease:** Usually presents as microcytic, hypochromic anemia that is refractory to iron supplementation, often due to inflammation-mediated upregulation of hepcidin [2]. HbA2 levels remain normal. * **G6PD deficiency:** This is an episodic hemolytic anemia triggered by oxidative stress [1]. It presents with normocytic anemia, Heinz bodies, and "bite cells," not chronic microcytosis or elevated HbA2. * **Homozygous beta-thalassemia (Thalassemia Major):** This presents much more severely in early childhood (infancy) with profound anemia (Hb <7 g/dL), hepatosplenomegaly, and skeletal deformities. Electrophoresis would show predominantly HbF with little to no HbA. **3. High-Yield Pearls for NEET-PG:** * **Mentzer Index:** (MCV/RBC count). If **<13**, it suggests Thalassemia; if **>13**, it suggests Iron Deficiency Anemia (IDA). * **Target Cells:** Seen in Thalassemia, Liver disease, Asplenia, and HbC disease (Mnemonic: **HALT**). * **HbA2 levels:** Always check HbA2 to differentiate Thalassemia trait from IDA (HbA2 is normal or low in IDA). * **Iron Studies:** In Thalassemia trait, serum iron and ferritin are typically normal or slightly elevated, unlike IDA.
Question 354: The use of desmopressin is best indicated for therapy in which of the following bleeding disorders?
- A. Severe hemophilia A
- B. Severe hemophilia B
- C. Von Willebrand disease (VWD) (Correct Answer)
- D. Glanzmann thrombasthenia
Explanation: **Explanation:** **Desmopressin (DDAVP)** is a synthetic analogue of vasopressin that stimulates the release of **von Willebrand factor (vWF)** and **Factor VIII** from endothelial storage sites (Weibel-Palade bodies) [2]. 1. **Why Option C is Correct:** In **Von Willebrand Disease (VWD)**, particularly Type 1 (the most common form), there is a quantitative deficiency of vWF [2]. DDAVP effectively increases endogenous plasma levels of vWF and Factor VIII, making it the treatment of choice for minor bleeding episodes or surgical prophylaxis in these patients [2]. 2. **Why Other Options are Incorrect:** * **Severe Hemophilia A (Option A):** DDAVP can be used in *mild* Hemophilia A. However, in *severe* cases (Factor VIII <1%), there are no endogenous stores to release; therefore, exogenous Factor VIII replacement is mandatory. [1] * **Severe Hemophilia B (Option B):** Hemophilia B is a deficiency of Factor IX. DDAVP has no effect on Factor IX levels; these patients require Factor IX concentrates. * **Glanzmann Thrombasthenia (Option D):** This is a qualitative platelet disorder (deficiency of GpIIb/IIIa) [3]. DDAVP does not correct this receptor defect; treatment usually involves platelet transfusions or recombinant Factor VIIa. **NEET-PG High-Yield Pearls:** * **Route:** DDAVP can be administered IV, SC, or via a highly concentrated nasal spray (Stimate). * **Side Effects:** The most critical side effect is **hyponatremia** (due to the antidiuretic effect), which can lead to seizures. Patients should be advised on fluid restriction. * **Tachyphylaxis:** Repeated doses lead to a diminishing response as endothelial stores become exhausted. * **Contraindication:** Avoid DDAVP in **VWD Type 2B**, as it can cause paradoxical thrombocytopenia due to the release of abnormal vWF that induces platelet aggregation.
Question 355: A 65-year-old male patient presents with nonspecific symptoms and moderate splenomegaly. His lab tests show a WBC count of 2000, a normal differential count, Hb 6 g/dL, platelets 80,000/mm³, and 6% blast cells. What is the most likely diagnosis?
- A. Acute myeloid leukemia (Correct Answer)
- B. Aplastic anemia
- C. Idiopathic thrombocytopenic purpura
- D. Hemolytic anemia
Explanation: The clinical presentation of pancytopenia (low WBC, Hb, and platelets) combined with **splenomegaly** and the presence of **circulating blasts** is a classic indicator of an acute hematological malignancy [1]. **1. Why Acute Myeloid Leukemia (AML) is correct:** In AML, the bone marrow is replaced by malignant blast cells, leading to bone marrow failure (pancytopenia). While the total WBC count is low in this case (aleukemic/subleukemic leukemia), the presence of **6% blasts** in the peripheral blood is the definitive clue. In a patient over 60, AML is a primary consideration when marrow failure is accompanied by splenomegaly and blasts. The diagnosis is suspected from an abnormal blood count and confirmed by bone marrow [1]. **2. Why the other options are incorrect:** * **Aplastic Anemia:** While it presents with pancytopenia, it is characterized by an empty bone marrow. Crucially, **splenomegaly is characteristically absent**, and there are no circulating blasts. * **Idiopathic Thrombocytopenic Purpura (ITP):** This typically presents with isolated thrombocytopenia. Hemoglobin and WBC counts remain normal, and there is no splenomegaly or blasts. * **Hemolytic Anemia:** This would show a decrease in Hb and potentially splenomegaly, but it would be associated with an *increase* in reticulocytes and jaundice, not pancytopenia or circulating blasts. **High-Yield NEET-PG Pearls:** * **Aleukemic Leukemia:** A condition where the total WBC count is normal or low, but the bone marrow is packed with blasts. * **Splenomegaly Rule:** If a patient has pancytopenia **with** splenomegaly, think of AML, Myelofibrosis [2], or Gaucher’s disease. If **without** splenomegaly, think of Aplastic Anemia. * **Diagnosis:** The WHO criteria for AML require ≥20% blasts in the bone marrow or peripheral blood [1]. The presence of any blasts in a pancytopenic elderly patient should immediately trigger a bone marrow biopsy.
Question 356: The presence of small-sized platelets on the peripheral smear is characteristic of:
- A. Idiopathic thrombocytopenic purpura.
- B. Bernard Soulier syndrome
- C. Disseminated intravascular coagulation
- D. Wiskott Aldrich syndrome (Correct Answer)
Explanation: ### Explanation **Correct Answer: D. Wiskott-Aldrich Syndrome (WAS)** **Medical Concept:** Wiskott-Aldrich Syndrome is an X-linked recessive disorder caused by a mutation in the **WAS protein (WASP)**, which is essential for actin cytoskeleton remodeling in hematopoietic cells. The hallmark of WAS is the triad of **thrombocytopenia, eczema, and recurrent infections** (due to combined B and T-cell deficiency). Crucially, WAS is the classic condition associated with **microthrombocytes (small-sized platelets)** [1]. This occurs because the defective cytoskeleton leads to abnormal pro-platelet formation and fragmentation in the bone marrow. **Analysis of Incorrect Options:** * **A. Idiopathic Thrombocytopenic Purpura (ITP):** Characterized by peripheral destruction of platelets [1]. The bone marrow compensates by releasing immature "stress platelets," which are typically **large (megathrombocytes)**. * **B. Bernard-Soulier Syndrome (BSS):** A defect in the GpIb-IX-V receptor [2]. It is famously associated with **Giant Platelets** (often as large as red blood cells) and a failure of platelets to agglutinate with Ristocetin. * **C. Disseminated Intravascular Coagulation (DIC):** This is a consumptive coagulopathy [1]. While it causes thrombocytopenia, the platelets present on the smear are usually of **normal size**, though schistocytes (fragmented RBCs) are a prominent feature. **High-Yield Clinical Pearls for NEET-PG:** * **Small Platelets:** Think **Wiskott-Aldrich Syndrome** and **TAR syndrome** (Thrombocytopenia with Absent Radii). * **Large/Giant Platelets:** Think **Bernard-Soulier Syndrome**, **May-Hegglin anomaly** (look for Dohle-like bodies), and **ITP**. * **WAS Triad Mnemonic:** **W**-**A**-**S** (**W**iskott, **A**ctin mutation, **S**mall platelets). * **Laboratory Finding:** Low Mean Platelet Volume (MPV) is a diagnostic clue for WAS.
Question 357: Which drug is used for the treatment of Acute Myeloid Leukemia (AML) with FLT-3 mutation?
- A. Crizotinib
- B. Gilteritinib (Correct Answer)
- C. Acalabrutinib
- D. Ibrutinib
Explanation: **Explanation:** **Acute Myeloid Leukemia (AML)** management has evolved with the identification of specific molecular markers. The **FLT3 (Fms-like tyrosine kinase 3)** mutation is one of the most common genetic alterations in AML (seen in ~30% of cases) and is associated with a poor prognosis and high relapse rates. * **Why Gilteritinib is correct:** **Gilteritinib** is a highly potent, selective **second-generation FLT3 inhibitor**. It targets both FLT3-ITD (Internal Tandem Duplication) and FLT3-TKD (Tyrosine Kinase Domain) mutations. It is specifically FDA-approved for the treatment of adult patients with **relapsed or refractory AML** with a FLT3 mutation. Other FLT3 inhibitors used in AML include Midostaurin (used in induction) and Quizartinib. **Analysis of Incorrect Options:** * **A. Crizotinib:** An ALK (Anaplastic Lymphoma Kinase) and ROS1 inhibitor primarily used in **Non-Small Cell Lung Cancer (NSCLC)** and ALK-positive Anaplastic Large Cell Lymphoma. * **C. Acalabrutinib:** A second-generation **Bruton Tyrosine Kinase (BTK) inhibitor** used in Chronic Lymphocytic Leukemia (CLL) and Mantle Cell Lymphoma. * **D. Ibrutinib:** The first-generation **BTK inhibitor** used for CLL, Small Lymphocytic Lymphoma (SLL), and Waldenström Macroglobulinemia. **High-Yield Clinical Pearls for NEET-PG:** * **FLT3-ITD** mutation is a marker of **poor prognosis** in AML [1]. * **Midostaurin** is the first-generation FLT3 inhibitor added to standard "7+3" chemotherapy for newly diagnosed FLT3+ AML. * **All-trans retinoic acid (ATRA)** and **Arsenic Trioxide** remain the drugs of choice for the M3 subtype (APML) characterized by t(15,17) [1]. * **Venetoclax** (BCL-2 inhibitor) is another high-yield drug now used in AML for elderly patients unfit for intensive chemotherapy.
Question 358: Increased iron absorption is seen in which of the following conditions?
- A. Iron deficiency anemia (Correct Answer)
- B. Hypoxia
- C. Inflammation
- D. Antacids
Explanation: The regulation of iron absorption is primarily controlled by **Hepcidin**, a peptide hormone synthesized by the liver. Hepcidin acts as a negative regulator by binding to and degrading **ferroportin**, the only known cellular iron exporter found on enterocytes and macrophages [1]. **1. Why Iron Deficiency Anemia (IDA) is correct:** In IDA, the body’s iron stores are depleted. This signals the liver to **decrease Hepcidin production** [1]. Low levels of hepcidin allow ferroportin to remain active on the basolateral membrane of enterocytes, significantly increasing the absorption of dietary iron into the bloodstream to compensate for the deficiency. **2. Analysis of Incorrect Options:** * **Hypoxia:** While chronic hypoxia (via HIF-2α) can stimulate erythropoiesis and eventually lower hepcidin, the most direct and potent stimulus for increased absorption in clinical scenarios is iron deficiency itself [1]. (Note: In some contexts, hypoxia increases absorption, but IDA is the classic physiological "gold standard" answer). * **Inflammation:** Inflammation (via IL-6) **increases Hepcidin** levels [1]. This leads to the degradation of ferroportin, "locking" iron inside cells and decreasing intestinal absorption. This is the pathophysiology behind *Anemia of Chronic Disease*. * **Antacids:** Iron requires an acidic environment (gastric HCl) to be reduced from the ferric ($Fe^{3+}$) to the ferrous ($Fe^{2+}$) state, which is the form absorbed by the DMT-1 transporter. Antacids neutralize gastric acid, thereby **decreasing** iron absorption. **High-Yield Clinical Pearls for NEET-PG:** * **Hepcidin** is an "Acute Phase Reactant." * **Vitamin C** (Ascorbic acid) increases iron absorption by maintaining iron in the ferrous state. * **Hereditary Hemochromatosis** is characterized by a deficiency in Hepcidin, leading to uncontrolled iron overload [1]. * **Site of absorption:** Iron is primarily absorbed in the **Duodenum** and upper Jejunum.
Question 359: What is characteristic of anemia of chronic disease?
- A. Total iron-binding capacity (TIBC)
- B. Serum iron
- C. Bone marrow iron stores
- D. Serum ferritin (Correct Answer)
Explanation: **Explanation:** Anemia of Chronic Disease (ACD), also known as anemia of inflammation, is primarily driven by **Hepcidin**, an acute-phase reactant produced by the liver in response to inflammatory cytokines (mainly IL-6) [1]. Hepcidin degrades ferroportin, leading to the sequestration of iron within macrophages and hepatocytes [2]. **Why Serum Ferritin is the Correct Answer:** In ACD, iron is trapped inside storage cells. Since **Serum Ferritin** reflects total body iron stores and acts as an acute-phase reactant, its levels are characteristically **normal or increased** [3]. This is the most crucial laboratory finding to differentiate ACD from Iron Deficiency Anemia (IDA), where ferritin is always low. **Analysis of Incorrect Options:** * **A. Total Iron-Binding Capacity (TIBC):** In ACD, TIBC is **decreased**. The body attempts to sequester iron away from potential pathogens by reducing the synthesis of transferrin. In contrast, TIBC is increased in IDA. * **B. Serum Iron:** This is **decreased** in ACD [2]. Despite adequate total body stores, the iron is "locked away" and unavailable in the serum for erythropoiesis. * **C. Bone Marrow Iron Stores:** These are **increased or normal** (visible as abundant hemosiderin in macrophages) [3]. The defect is not a lack of iron, but the inability to mobilize it to erythroid precursors. **NEET-PG High-Yield Pearls:** * **The Hallmark:** Low Serum Iron + Low TIBC + **High/Normal Ferritin** [3]. * **Cytokine Mediator:** IL-6 is the primary trigger for Hepcidin synthesis [1]. * **Morphology:** Usually normocytic normochromic, but can become microcytic in long-standing cases [1]. * **Treatment:** Treat the underlying inflammatory condition; recombinant erythropoietin may be used in specific cases (e.g., CKD or malignancy).
Question 360: A 58-year-old woman presents with a 6-month history of backache and recurrent chest infections. She develops sudden weakness of the legs and urinary retention. Investigations reveal a hemoglobin of 7.3 g/dL, serum calcium of 12.6 mg/dL, phosphate of 2.5 mg/dL, alkaline phosphatase of 100 U/L, serum albumin of 3 g/dL, globulin of 7.1 g/dL, and urea of 178 mg/dL. What is the most likely diagnosis?
- A. Lung cancer
- B. Disseminated tuberculosis
- C. Multiple myeloma (Correct Answer)
- D. Osteoporosis
Explanation: ### **Explanation** The clinical presentation and laboratory findings are classic for **Multiple Myeloma (MM)**, a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells. [1] **Why Multiple Myeloma is Correct:** The patient presents with the **CRAB** criteria, the hallmark of MM: * **C (Calcium elevation):** Serum calcium is 12.6 mg/dL (Normal: 8.5–10.5). * **R (Renal insufficiency):** Urea is significantly elevated (178 mg/dL), likely due to light-chain cast nephropathy ("Myeloma kidney"). * **A (Anemia):** Hemoglobin is 7.3 g/dL (Normocytic normochromic anemia is common). * **B (Bone lesions):** Backache and sudden leg weakness/urinary retention suggest a **pathological vertebral fracture** leading to **spinal cord compression**. [1] * **Hyperglobulinemia:** The "Albumin-Globulin gap" (Albumin 3.0, Globulin 7.1) indicates a massive production of monoclonal immunoglobulins (M-protein). * **Normal Alkaline Phosphatase (ALP):** In MM, bone lesions are purely osteolytic (mediated by osteoclasts) without osteoblastic activity, hence ALP remains normal—a key differentiator from bone metastases. **Why Other Options are Incorrect:** * **Lung Cancer:** While it can cause hypercalcemia and bone metastasis, it usually presents with elevated ALP and would not typically explain such profound hyperglobulinemia. * **Disseminated Tuberculosis:** Can cause back pain (Pott’s spine) and anemia, but it does not cause significant hypercalcemia or the massive protein gap seen here. * **Osteoporosis:** Causes fractures and backache in elderly women, but laboratory parameters (Calcium, Urea, Globulin) remain normal. **NEET-PG High-Yield Pearls:** * **Most common initial symptom:** Bone pain (usually back). * **Gold Standard Investigation:** Bone marrow biopsy (>10% clonal plasma cells). [1] * **Radiology:** "Punched-out" lytic lesions on a skeletal survey. [1] Note: Bone scans (Technetium-99m) are often negative as they detect osteoblastic activity. * **Peripheral Smear:** **Rouleaux formation** due to high globulin levels.
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
Practice Questions
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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