Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 341: Which of the following is NOT a feature of Antiphospholipid Syndrome (APS)?

A. Haemolytic anemia
B. False positive VDRL
C. Thrombocytopenia
D. Decreased PT with increased APTT (Correct Answer)

Explanation: Antiphospholipid Syndrome (APS) is an autoimmune prothrombotic state characterized by arterial/venous thrombosis and pregnancy complications. [1] **Why Option D is the Correct Answer:** In APS, the presence of **Lupus Anticoagulant (LA)** interferes with phospholipid-dependent coagulation tests *in vitro*. This leads to a **prolonged (increased) APTT** that does not correct with a mixing study. However, the **Prothrombin Time (PT) is typically normal**, not decreased. [1] The hallmark of APS is this "laboratory paradox": an increased APTT (suggesting bleeding risk) despite the patient being in a hypercoagulable state (thrombosis risk). **Analysis of Incorrect Options:** * **A. Haemolytic Anemia:** Autoimmune hemolytic anemia (AIHA) and Evans Syndrome (AIHA + thrombocytopenia) are well-recognized hematologic manifestations associated with APS and SLE. * **B. False positive VDRL:** The reagin antibodies in syphilis cross-react with the cardiolipin antigen used in the VDRL/RPR tests. Since anti-cardiolipin antibodies are a staple of APS, a false positive syphilis screen is a classic diagnostic clue. * **C. Thrombocytopenia:** Mild to moderate thrombocytopenia (100,000–150,000/mm³) occurs in nearly 30% of APS patients due to increased platelet consumption and anti-platelet antibodies. **NEET-PG High-Yield Pearls:** * **Sapporo Criteria:** Diagnosis requires 1 clinical (thrombosis or pregnancy loss) + 1 lab criterion (Anti-cardiolipin, Anti-β2 glycoprotein I, or Lupus Anticoagulant) positive on two occasions 12 weeks apart. * **Mixing Study:** APTT remains prolonged in APS (presence of inhibitor), whereas it corrects in factor deficiencies (e.g., Hemophilia). [1] * **Treatment:** Lifelong anticoagulation with Warfarin (INR 2-3) is preferred; DOACs are generally avoided in triple-positive APS. [2]

Question 342: The BCRABL gene mutation is characteristically associated with which of the following hematologic malignancies?

A. Chronic Myeloid Leukemia (CML) (Correct Answer)
B. Acute Myeloid Leukemia (AML)
C. Chronic Lymphocytic Leukemia (CLL)
D. Acute Lymphoblastic Leukemia (ALL)

Explanation: **Explanation:** The **BCR-ABL1** fusion gene is the hallmark of **Chronic Myeloid Leukemia (CML)** [3]. It results from a reciprocal translocation between chromosomes 9 and 22, known as the **Philadelphia chromosome [t(9;22)(q34;q11)]** [3]. This mutation creates a chimeric protein with constitutive **tyrosine kinase activity**, leading to uncontrolled proliferation of the myeloid lineage [3]. **Analysis of Options:** * **Chronic Myeloid Leukemia (CML):** Correct. The Philadelphia chromosome is present in >95% of CML cases and is essential for diagnosis. * **Acute Myeloid Leukemia (AML):** While t(9;22) can occur in rare de novo AML cases (1%), it is not characteristic. AML is more commonly associated with t(8;21), t(15;17), or inv(16) [4]. * **Chronic Lymphocytic Leukemia (CLL):** CLL is characterized by the deletion of 13q, 11q, or 17p, and trisomy 12. BCR-ABL is not involved. * **Acute Lymphoblastic Leukemia (ALL):** BCR-ABL is found in ~25-30% of adult ALL and ~3-5% of pediatric ALL. While it is a significant prognostic marker (indicating poor prognosis), it is not the *defining* characteristic of the disease as it is for CML [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Treatment:** Imatinib (a Tyrosine Kinase Inhibitor) is the first-line targeted therapy for BCR-ABL positive malignancies [2]. * **Monitoring:** Quantitative PCR for BCR-ABL mRNA transcripts is the gold standard for monitoring "Molecular Response" to therapy [2]. * **Leukocyte Alkaline Phosphatase (LAP) Score:** Characteristically **decreased** in CML, helping differentiate it from a Leukemoid reaction (where LAP is increased). * **Blast Crisis:** CML can transform into AML (70%) or ALL (30%).

Question 343: Which of the following sets of findings is seen in Disseminated Intravascular Coagulation (DIC)?

A. Increased fibrinogen, increased antithrombin III, increased thrombin-antithrombin III complexes
B. Increased FDP, decreased PT, increased antithrombin III
C. Increased FDP, prolonged PT, increased thrombin-antithrombin complexes
D. Increased FDP, prolonged PT, reduced platelets (Correct Answer)

Explanation: Disseminated Intravascular Coagulation (DIC) is a thrombo-hemorrhagic disorder characterized by systemic activation of the coagulation cascade, leading to widespread fibrin deposition and the subsequent "consumption" of clotting factors and platelets [1]. **Why Option D is Correct:** The pathophysiology of DIC involves two main phases: 1. **Consumption Phase:** Rapid formation of microthrombi consumes **platelets** and clotting factors [1], leading to thrombocytopenia and **prolonged Prothrombin Time (PT)** and Activated Partial Thromboplastin Time (aPTT) [1]. 2. **Fibrinolysis Phase:** To counteract clotting, the body activates plasmin, which breaks down fibrin. This results in elevated **Fibrin Degradation Products (FDPs)** and D-dimers [1]. **Analysis of Incorrect Options:** * **Option A:** In DIC, **fibrinogen** and **antithrombin III** are **decreased** because they are consumed during the massive clotting process. * **Option B:** While FDP is increased, the **PT is prolonged** (not decreased) due to factor depletion [1], and **antithrombin III is decreased** as it is used up trying to neutralize thrombin. * **Option C:** While these findings can occur, Option D represents the classic "diagnostic triad" (Thrombocytopenia, Prolonged PT, High FDP) most commonly tested in exams. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause:** Sepsis (Gram-negative organisms) [1]. * **Peripheral Smear:** Presence of **Schistocytes** (fragmented RBCs) due to microangiopathic hemolytic anemia (MAHA). * **Best Screening Test:** Platelet count (usually low) [1]. * **Most Sensitive/Specific Test:** D-dimer (elevated) [1]. * **Acute Promyelocytic Leukemia (M3):** A classic association where DIC is triggered by the release of procoagulants from leukemic cells.

Question 344: Which of the following is not associated with a high reticulocyte count?

A. Acute bleed
B. Hemolytic anemia
C. Megaloblastic anemia (Correct Answer)
D. Response to treatment in nutrition deficiency anemia

Explanation: The **Reticulocyte Count** is a direct reflection of the bone marrow's erythropoietic activity. A high count (reticulocytosis) indicates that the marrow is healthy and responding to a decrease in red blood cells (RBCs) or a stimulus like erythropoietin. **Why Megaloblastic Anemia is the Correct Answer:** Megaloblastic anemia (caused by Vitamin B12 or Folate deficiency) is characterized by **ineffective erythropoiesis** [1]. Although the bone marrow is hypercellular, the RBC precursors die within the marrow due to defective DNA synthesis. Consequently, the marrow cannot release mature cells or reticulocytes into the peripheral blood, leading to a **low reticulocyte count** (reticulocytopenia) [1]. **Analysis of Incorrect Options:** * **Acute Bleed:** Following a sudden loss of blood, the body increases erythropoietin production, stimulating a healthy marrow to release young RBCs (reticulocytes) within 3–5 days to compensate. * **Hemolytic Anemia:** In conditions like G6PD deficiency or Hereditary Spherocytosis, RBCs are destroyed prematurely. The marrow remains functional and compensates by significantly increasing reticulocyte production. * **Response to Treatment:** When a nutritional deficiency (Iron, B12, or Folate) is treated, the "block" in RBC production is removed, leading to a "reticulocyte flare" (usually peaking at 5–10 days), signaling a positive response to therapy. **NEET-PG High-Yield Pearls:** * **Corrected Reticulocyte Count (CRC):** In anemia, always use CRC [% Retic × (Patient Hct / Normal Hct)] to assess marrow response accurately. * **Reticulocyte Production Index (RPI):** An RPI > 2% indicates an adequate marrow response (Hemolysis/Hemorrhage); an RPI < 2% indicates an inadequate response (Hypoproliferative/Megaloblastic anemias). * **Supravital Stains:** Reticulocytes are visualized using **New Methylene Blue** or **Brilliant Cresyl Blue**, which stain the residual ribosomal RNA.

Question 345: A 69-year-old woman presents with fatigue. Her hemoglobin is 9.0 g/dL (14 g/dL one year prior) with no other symptoms. A blood film is provided. What is the most appropriate next diagnostic step?

A. Serum B12 level
B. Hemoglobin electrophoresis
C. Colonoscopy (Correct Answer)
D. Bone marrow aspiration

Explanation: ***Colonoscopy*** - In a **post-menopausal** 69-year-old woman with **microcytic hypochromic anemia**, the most likely cause is **iron deficiency** from **occult GI bleeding**. - **Colonoscopy** is essential to rule out **colorectal malignancy** and identify sources of chronic blood loss in this age group. *Serum B12 level* - **B12 deficiency** typically causes **macrocytic anemia** with **megaloblastic** changes on blood film, not microcytic hypochromic RBCs. - The blood film shows **microcytic** RBCs, making B12 deficiency unlikely as the primary cause. *Hemoglobin electrophoresis* - Used to diagnose **hemoglobinopathies** like **thalassemia** or **sickle cell disease**, which are congenital conditions. - This 69-year-old woman had **normal hemoglobin** (14 g/dL) one year prior, making acquired **iron deficiency** more likely than congenital hemoglobinopathy. *Bone marrow aspiration* - Reserved for cases where the diagnosis remains unclear after initial investigations or when **hematologic malignancy** is suspected. - **Iron deficiency anemia** can usually be diagnosed and managed without bone marrow examination, especially when **GI source** is likely.

Question 346: To which of the following diseases is pyruvate kinase deficiency most similar clinically?

A. Alpha thalassemia
B. Beta thalassemia
C. Glucose-6-phosphate dehydrogenase deficiency (Correct Answer)
D. Hereditary spherocytosis

Explanation: ### Explanation **Correct Answer: C. Glucose-6-phosphate dehydrogenase (G6PD) deficiency** **Reasoning:** Pyruvate Kinase (PK) deficiency and G6PD deficiency are both **enzymopathies** that lead to **normocytic hemolytic anemia** [1]. * **PK Deficiency:** Affects the glycolytic pathway (Embden-Meyerhof pathway), leading to decreased ATP production [1]. This causes rigid RBCs that are destroyed in the spleen. * **G6PD Deficiency:** Affects the Hexose Monophosphate (HMP) shunt, leading to decreased NADPH and glutathione, making RBCs susceptible to oxidative stress [1], [2]. Clinically, both present as episodic or chronic hemolysis, jaundice, and gallstones. While PK deficiency is typically autosomal recessive and G6PD is X-linked, they are grouped together as the most common red cell enzyme defects causing non-spherocytic hemolytic anemia [1]. **Analysis of Incorrect Options:** * **A & B (Thalassemias):** These are **hemoglobinopathies** characterized by quantitative defects in globin chain synthesis [3]. They typically present as **microcytic hypochromic** anemia with characteristic target cells and skeletal changes, which are not features of PK deficiency. * **D (Hereditary Spherocytosis):** This is a **membranopathy** (defect in proteins like Ankyrin or Spectrin) [4]. While it also causes extravascular hemolysis, it is distinguished by the presence of spherocytes and a positive osmotic fragility test, whereas PK deficiency presents with "echinocytes" (burr cells). **NEET-PG High-Yield Pearls:** * **PK Deficiency:** Most common enzyme deficiency of the **glycolytic pathway**. It causes a **right shift** in the oxygen dissociation curve due to increased 2,3-BPG levels (allowing better oxygen delivery to tissues). * **G6PD Deficiency:** Most common red cell enzyme deficiency overall [2]. Look for **Heinz bodies** and **Bite cells** on peripheral smear. * **Diagnostic Test:** PK deficiency is diagnosed via a quantitative enzyme assay; it is a **non-spherocytic** hemolytic anemia (Coombs test negative).

Question 347: What is the most common inherited bleeding disorder?

A. Von Willebrand disease (Correct Answer)
B. Bernard-Soulier syndrome
C. Glanzmann thrombasthenia
D. Idiopathic thrombocytopenic purpura (ITP)

Explanation: **Explanation:** **Von Willebrand Disease (vWD)** is the most common inherited bleeding disorder worldwide, affecting approximately 1% of the general population. It is caused by a quantitative or qualitative deficiency of **Von Willebrand Factor (vWF)**, a large multimeric glycoprotein essential for two primary functions [1]: 1. **Platelet Adhesion:** It acts as a bridge between platelet glycoprotein Ib (GpIb) receptors and the subendothelial collagen [2]. 2. **Factor VIII Carrier:** It stabilizes and protects Factor VIII from rapid degradation in the plasma [1]. **Analysis of Incorrect Options:** * **Bernard-Soulier Syndrome (BSS):** A rare autosomal recessive disorder characterized by a deficiency of the **GpIb-IX-V receptor** [2]. It presents with giant platelets and thrombocytopenia. * **Glanzmann Thrombasthenia (GT):** A rare autosomal recessive disorder caused by a deficiency of **GpIIb/IIIa**, leading to defective platelet aggregation [2]. * **Idiopathic Thrombocytopenic Purpura (ITP):** While a common cause of low platelets, it is an **acquired autoimmune** condition, not an inherited one. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most common type (Type 1) is **Autosomal Dominant**. * **Clinical Presentation:** Mucocutaneous bleeding (epistaxis, menorrhagia, easy bruising) [1]. * **Lab Findings:** Prolonged Bleeding Time (BT) and often a prolonged **aPTT** (due to low Factor VIII levels) [1]. Platelet count is usually normal (except in Type 2B). * **Screening Test:** Ristocetin Cofactor Assay (measures vWF-mediated platelet agglutination) [1]. * **Treatment of Choice:** **Desmopressin (DDAVP)**, which releases stored vWF from Weibel-Palade bodies in endothelial cells [1].

Question 348: The Rumpel Leede test measures what?

A. Bleeding time
B. Platelet count
C. Capillary fragility (Correct Answer)
D. ESR

Explanation: The **Rumpel-Leede test**, also known as the **Capillary Fragility Test** or the Tourniquet Test, is a clinical diagnostic tool used to assess the structural integrity of capillary walls and platelet function. **Why Option C is correct:** The test involves applying a blood pressure cuff to the upper arm and inflating it to a point midway between the systolic and diastolic blood pressure for 5 minutes. If the capillaries are fragile or if there is significant thrombocytopenia, the increased intraluminal pressure causes them to rupture, resulting in the formation of **petechiae** [1]. A positive test (usually >10–20 petechiae in a 1-inch square area) indicates **capillary fragility**. It is classically positive in conditions like **Dengue Hemorrhagic Fever**, Vitamin C deficiency (Scurvy), and various thrombocytopenic states. **Why other options are incorrect:** * **Bleeding Time (A):** Measures the time taken for a standardized skin wound to stop bleeding; it assesses platelet adhesion and aggregation, not capillary wall strength. * **Platelet Count (B):** This is a quantitative laboratory measurement (CBC) and cannot be determined by a physical tourniquet test, though low counts often lead to a positive Rumpel-Leede result [2]. * **ESR (D):** Erythrocyte Sedimentation Rate is a non-specific marker of inflammation and is unrelated to capillary integrity. **High-Yield Clinical Pearls for NEET-PG:** * **Dengue:** The Tourniquet Test is a key WHO criterion for the clinical diagnosis of Dengue. * **Scurvy:** Defective collagen synthesis leads to weak vessel walls and a positive Rumpel-Leede test. * **Hess Test:** Another name for the Rumpel-Leede test. * **Limitation:** It is not specific; it can be positive in both qualitative platelet defects (e.g., Glanzmann's) and quantitative defects (thrombocytopenia).

Question 349: What is the typical number of platelets in a single bag of Single Donor Platelets (SDP)?

A. 1 x 10^11
B. 2 x 10^11
C. 1 x 10^12 (Correct Answer)
D. 2 x 10^12

Explanation: Explanation: Platelet transfusions are primarily available in two forms: **Random Donor Platelets (RDP)** and **Single Donor Platelets (SDP)**. Understanding the quantitative difference between them is a high-yield topic for NEET-PG. **1. Why Option C is Correct:** A single unit of **SDP**, obtained via apheresis from a single donor, typically contains approximately **3 x 10¹¹ to 1 x 10¹² platelets**. In the context of standard medical examinations and blood bank protocols, **1 x 10¹²** is recognized as the upper-tier yield for a high-quality SDP bag. One unit of SDP is therapeutically equivalent to 6–8 units of RDP and is expected to raise the recipient's platelet count by **30,000–60,000/µL**. **2. Why Other Options are Incorrect:** * **Option A & B (1–2 x 10¹¹):** These values are too low for a standard SDP. A single unit of **RDP** contains roughly **5.5 x 10¹⁰** platelets. Therefore, a pool of 4–6 RDPs would reach the 2 x 10¹¹ range, but a full SDP bag significantly exceeds this. * **Option D (2 x 10¹²):** This value is physiologically and technically improbable for a single apheresis session and exceeds standard bag concentrations. **Clinical Pearls for NEET-PG:** * **Dose Response:** 1 unit of RDP increases platelet count by **5,000–10,000/µL**, whereas 1 unit of SDP increases it by **30,000–60,000/µL**. * **Shelf Life:** Platelets are stored at **20–24°C** (room temperature) with continuous agitation for a maximum of **5 days**. * **Advantage of SDP:** Reduced risk of HLA alloimmunization and transfusion-transmitted infections (TTIs) because the recipient is exposed to only one donor. * **Trigger for Prophylactic Transfusion:** Usually **<10,000/µL** in stable patients.

Question 350: Which of the following is a feature of disseminated intravascular coagulation (DIC)?

A. Normal prothrombin time
B. Reduced plasma fibrinogen (Correct Answer)
C. Normal platelet count
D. Normal clotting time

Explanation: **Explanation:** Disseminated Intravascular Coagulation (DIC) is a complex consumptive coagulopathy characterized by systemic activation of the coagulation cascade [1]. This leads to the widespread formation of fibrin microthrombi, which paradoxically results in the **exhaustion of clotting factors and platelets**, leading to severe hemorrhage. **Why Option B is Correct:** In DIC, there is massive conversion of fibrinogen to fibrin due to excess thrombin [1]. Simultaneously, secondary fibrinolysis is activated, leading to the breakdown of fibrinogen. This dual process results in **hypofibrinogenemia (reduced plasma fibrinogen)**, which is a hallmark laboratory finding of the condition [1]. **Why Other Options are Incorrect:** * **A & D (Normal PT and Clotting Time):** Because DIC consumes clotting factors (Factors V, VIII, and X), the **Prothrombin Time (PT)**, **Activated Partial Thromboplastin Time (aPTT)**, and **Clotting Time (CT)** are all characteristically **prolonged**, not normal [1][2]. * **C (Normal Platelet Count):** Platelets are rapidly consumed during the formation of microthrombi [3]. Therefore, **thrombocytopenia** (reduced platelet count) is a consistent feature of DIC [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Best Screening Test:** Platelet count and PT (both will be abnormal) [1][2]. * **Most Specific Test:** Elevated **D-dimer** or Fibrin Degradation Products (FDPs) [1]. * **Peripheral Smear:** Presence of **Schistocytes** (fragmented RBCs) due to microangiopathic hemolytic anemia (MAHA). * **Common Triggers:** Sepsis (most common), Obstetric complications (Abruptio placentae), and Malignancy (APML - M3) [1].

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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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