Hematology — MCQs
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Which of the following is the mechanism of action of Fondaparinux?
A 28-year-old female presented with malaise and generalized weakness for the past 6 months. Her appetite is reduced, and she experiences intermittent giddiness and palpitations. There was no organomegaly. Laboratory studies showed normochromic to hypochromic anemia with an MCV of 80. What is the diagnosis?
Which of the following is NOT true regarding multiple myeloma?
Which of the following is NOT a characteristic finding in paroxysmal nocturnal hemoglobinuria?
Which drug(s) are used in the treatment of multiple myeloma?
Both APTT and PT are prolonged in which of the following conditions?
Which of the following inherited neutropenias has a self-limited course?
Which of the following is NOT a hypercoagulable state?
A patient with a blood pressure of 90/60 mm Hg presents with pronounced cyanosis. Blood drawn from peripheral veins is observed to be chocolate brown in colour. What is the most likely diagnosis?
A patient presents with ecchymosis and petechiae all over the body, with no hepato-splenomegaly. All of the following are true regarding this condition EXCEPT:
Hematology Indian Medical PG Practice Questions and MCQs
Question 821: Which of the following is the mechanism of action of Fondaparinux?
- A. Factor Xa inhibition and Thrombin inhibition
- B. Factor Xa inhibition (Correct Answer)
- C. Antithrombin inhibitor
- D. Thrombin inhibition
Explanation: **Explanation:** **Fondaparinux** is a synthetic pentasaccharide that acts as a **selective Factor Xa inhibitor**. Its mechanism is mediated through **Antithrombin III (ATIII)**. When Fondaparinux binds to ATIII, it induces a conformational change that increases the neutralization rate of Factor Xa [1]. Unlike Heparin, the pentasaccharide chain of Fondaparinux is too short to bridge ATIII to Thrombin (Factor IIa); therefore, it has **no activity against Thrombin.** [1] **Analysis of Options:** * **Option B (Correct):** Fondaparinux selectively accelerates the neutralization of Factor Xa. * **Option A & D (Incorrect):** These describe the action of Unfractionated Heparin (UFH) and, to a lesser extent, Low Molecular Weight Heparin (LMWH) [1]. Fondaparinux does not inhibit Thrombin (Factor IIa). * **Option C (Incorrect):** Fondaparinux is an **Antithrombin activator/enhancer**, not an inhibitor. It requires endogenous Antithrombin to exert its anticoagulant effect. **High-Yield Clinical Pearls for NEET-PG:** 1. **HIT Safety:** Fondaparinux does not bind to Platelet Factor 4 (PF4). Therefore, it does **not** cause Heparin-Induced Thrombocytopenia (HIT) and is often used as an alternative treatment for it. 2. **Monitoring:** Routine monitoring (like PT or aPTT) is not required. If necessary, anti-Xa levels are measured. 3. **Excretion:** It is strictly renally excreted. It is **contraindicated** if Creatinine Clearance (CrCl) is **<30 mL/min**. 4. **Half-life:** It has a long half-life (~17–21 hours), allowing for once-daily subcutaneous dosing.
Question 822: A 28-year-old female presented with malaise and generalized weakness for the past 6 months. Her appetite is reduced, and she experiences intermittent giddiness and palpitations. There was no organomegaly. Laboratory studies showed normochromic to hypochromic anemia with an MCV of 80. What is the diagnosis?
- A. Thalassemia minor
- B. Iron deficiency anemia (Correct Answer)
- C. Chronic malaria
- D. Folate deficiency
Explanation: **Explanation:** The clinical presentation of a young female with chronic malaise, weakness, palpitations, and reduced appetite is highly suggestive of **Iron Deficiency Anemia (IDA)**, the most common cause of anemia worldwide, especially in women of reproductive age [1], [2]. **Why Iron Deficiency Anemia is correct:** IDA typically presents as a **microcytic hypochromic** anemia. However, in the early stages (Stage 2: Iron-deficient erythropoiesis), the MCV may still be within the **low-normal range (around 80 fL)** before it progressively drops [2]. The absence of organomegaly is a key negative finding that supports IDA over hemolytic or infiltrative disorders [2]. **Analysis of Incorrect Options:** * **Thalassemia minor:** While it presents with microcytosis, the MCV is usually significantly lower (often <70 fL) and disproportionate to the degree of anemia (Mentzer Index <13). Patients are usually asymptomatic. * **Chronic malaria:** This typically presents with **splenomegaly** and intermittent fevers. While it can cause anemia, the lack of organomegaly in this vignette makes it unlikely. * **Folate deficiency:** This causes **megaloblastic anemia**, characterized by a high MCV (>100 fL) and macrocytic blood picture, which contradicts the normo-hypochromic findings here [3]. **NEET-PG High-Yield Pearls:** * **Mentzer Index:** MCV/RBC count. <13 suggests Thalassemia; >13 suggests IDA. * **Best Initial Test for IDA:** Serum Ferritin (decreased). It is the most sensitive and specific lab test. * **Earliest Sign of Response to Iron Therapy:** Reticulocytosis (usually peaks within 7–10 days). * **Pica and Koilonychia:** Specific clinical signs associated with chronic, severe iron deficiency.
Question 823: Which of the following is NOT true regarding multiple myeloma?
- A. Bone pain
- B. Lytic lesions
- C. Increased alkaline phosphatase (Correct Answer)
- D. Tartrate-resistant acid phosphatase positive
Explanation: In Multiple Myeloma (MM), the hallmark of bone involvement is **purely osteoclastic (lytic) activity** without any compensatory osteoblastic activity [1]. **Explanation of the Correct Answer:** * **Option C (Increased Alkaline Phosphatase):** This is the correct answer because it is **NOT** true. Serum Alkaline Phosphatase (ALP) is a marker of osteoblastic (bone-forming) activity. In MM, malignant plasma cells produce "Osteoclast Activating Factors" (like RANKL and IL-6) and simultaneously secrete DKK-1, which **inhibits osteoblasts**. Since there is no new bone formation, ALP levels typically remain **normal**, even in the presence of extensive bone destruction. This distinguishes MM from bone metastases (e.g., prostate cancer) or Paget’s disease [3], where ALP is elevated. **Explanation of Incorrect Options:** * **Option A & B (Bone pain & Lytic lesions):** These are classic features [1]. Over 80% of patients present with bone pain. Lytic "punched-out" lesions are caused by uncontrolled osteoclast activation, commonly seen in the skull, spine, and pelvis. * **Option D (TRAP positive):** Tartrate-Resistant Acid Phosphatase (TRAP) is a histochemical marker for **osteoclasts** [2]. Since MM is characterized by intense osteoclastic resorption, TRAP staining is positive in areas of active bone destruction. (Note: TRAP is also a classic marker for Hairy Cell Leukemia). **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** Calcium (High), Renal insufficiency, Anemia, Bone lesions. * **Imaging:** X-rays (Skeletal Survey) are preferred over Bone Scans [1]. Bone scans (Technetium-99m) are often **false negative** because they require osteoblastic activity to show "hot spots." * **M-Spike:** Found on Serum Protein Electrophoresis (usually IgG > IgA) [1]. * **Bence-Jones Proteins:** Free light chains in urine (detected by sulfosalicylic acid test, not by standard dipstick).
Question 824: Which of the following is NOT a characteristic finding in paroxysmal nocturnal hemoglobinuria?
- A. Haemosiderinuria
- B. Pancytopenia
- C. Increased alkaline phosphatase (Correct Answer)
- D. Cellular marrow
Explanation: Paroxysmal Nocturnal Hemoglobinuria (PNH) is an acquired clonal stem cell disorder caused by a mutation in the PIGA gene, leading to a deficiency of GPI-anchored proteins (CD55 and CD59) on the surface of blood cells. This makes cells highly susceptible to complement-mediated lysis [1]. Why Option C is correct: In PNH, the Leukocyte Alkaline Phosphatase (LAP) score is characteristically decreased, not increased. LAP is a GPI-anchored enzyme found in the membranes of mature neutrophils. Since PNH involves a global deficiency of GPI-anchored proteins, the level of this enzyme is significantly reduced. This is a classic diagnostic marker used to differentiate PNH from other causes of hemolysis or leukocytosis. Why other options are incorrect: * A. Haemosiderinuria: Chronic intravascular hemolysis leads to the release of free hemoglobin. This is filtered by the kidneys, and iron is deposited in the renal tubular cells as hemosiderin. When these cells slough off into the urine, it results in hemosiderinuria, a hallmark of chronic intravascular hemolysis [1]. * B. Pancytopenia: Because PNH is a stem cell disorder, it often coexists with or evolves from bone marrow failure syndromes like Aplastic Anemia. Deficiency in all three cell lines (RBCs, WBCs, and platelets) is common. * D. Cellular marrow: While PNH can be associated with a hypocellular marrow (Aplastic Anemia), the marrow is frequently cellular as a compensatory response to the ongoing peripheral destruction of red blood cells (erythroid hyperplasia). NEET-PG High-Yield Pearls: * Gold Standard Diagnosis: Flow cytometry (showing absence of CD55/CD59). * Classic Triad: Hemolytic anemia, pancytopenia, and venous thrombosis (often in unusual sites like the Budd-Chiari syndrome). * Treatment: Eculizumab (a monoclonal antibody against C5 complement). * Ham’s Test & Sucrose Lysis Test: Historical tests (now largely replaced by flow cytometry).
Question 825: Which drug(s) are used in the treatment of multiple myeloma?
- A. Bortezomib (Correct Answer)
- B. Methotrexate
- C. Hydroxyurea
- D. Ketoconazole
Explanation: **Explanation:** **Multiple Myeloma (MM)** is a plasma cell dyscrasia characterized by the malignant proliferation of plasma cells in the bone marrow. **Why Bortezomib is correct:** Bortezomib is a **Proteasome Inhibitor**. Malignant plasma cells produce massive amounts of monoclonal proteins (M-proteins). Proteasomes are responsible for degrading misfolded proteins; by inhibiting them, Bortezomib causes an accumulation of toxic proteins within the cell, leading to endoplasmic reticulum stress and apoptosis. It is a cornerstone of induction therapy in MM (often used in the VRd regimen: Velcade/Bortezomib, Lenalidomide, and Dexamethasone). **Why other options are incorrect:** * **Methotrexate:** An antimetabolite (folate antagonist) used primarily in leukemias (ALL), lymphomas, and autoimmune conditions like Rheumatoid Arthritis. It is not a standard treatment for MM. * **Hydroxyurea:** An inhibitor of ribonucleotide reductase used for cytoreduction in myeloproliferative neoplasms (CML, Polycythemia Vera) and to increase HbF in Sickle Cell Anemia. * **Ketoconazole:** An antifungal agent. While it can inhibit steroidogenesis (used in Cushing’s syndrome), it has no role in treating plasma cell malignancies. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** Remember the classic presentation of MM: **C**alcium elevation, **R**enal insufficiency, **A**nemia, and **B**one lesions (lytic). * **Drug Side Effects:** A common side effect of Bortezomib is **peripheral neuropathy**. Prophylaxis for **Herpes Zoster** (Acyclovir) is mandatory during treatment. * **Other MM Drugs:** Immunomodulatory drugs (IMiDs) like **Lenalidomide** and Monoclonal Antibodies like **Daratumumab** (anti-CD38) are also frequently tested.
Question 826: Both APTT and PT are prolonged in which of the following conditions?
- A. Factor II deficiency (Correct Answer)
- B. Factor XIII deficiency
- C. Heparin administration
- D. Thrombocytopenia
Explanation: To understand why **Factor II (Prothrombin) deficiency** prolongs both PT and APTT, one must visualize the coagulation cascade as three distinct pathways: 1. **Extrinsic Pathway:** Measured by **PT** (Prothrombin Time). Involves Factor VII [1]. 2. **Intrinsic Pathway:** Measured by **APTT** (Activated Partial Thromboplastin Time). Involves Factors XII, XI, IX, and VIII [1]. 3. **Common Pathway:** Measured by **both PT and APTT**. Involves Factors **X, V, II (Prothrombin), and I (Fibrinogen)** [1]. Since Factor II is a key component of the **Common Pathway**, its deficiency disrupts the final stages of clot formation regardless of whether the cascade was initiated via the intrinsic or extrinsic route [1]. Therefore, both PT and APTT will be prolonged. **Analysis of Incorrect Options:** * **Factor XIII deficiency:** Factor XIII stabilizes the fibrin clot *after* it has formed. Since PT and APTT measure the time taken to reach the initial fibrin formation, they remain **normal**. Diagnosis requires a Urea Solubility Test. * **Heparin administration:** Unfractionated Heparin primarily inhibits Factor IIa and Xa via Antithrombin III. While very high doses can affect PT, its primary clinical effect is a **prolonged APTT** [1]. * **Thrombocytopenia:** This is a quantitative platelet disorder. PT and APTT measure secondary hemostasis (clotting factors) and are **unaffected** by platelet count [2]. **NEET-PG High-Yield Pearls:** * **Isolated prolonged PT:** Think Factor VII deficiency (or early Vitamin K deficiency/Warfarin use). * **Isolated prolonged APTT:** Think Hemophilia A (VIII), B (IX), or C (XI), and Von Willebrand Disease. * **Prolonged PT + APTT:** Think Common Pathway deficiency (X, V, II, I), severe Vitamin K deficiency, Liver disease, or DIC [1], [2]. * **Mixing Studies:** If PT/APTT corrects with normal plasma, it indicates a **factor deficiency**; if it doesn't correct, an **inhibitor** (like Lupus Anticoagulant) is present [1].
Question 827: Which of the following inherited neutropenias has a self-limited course?
- A. Shwachman-Diamond syndrome
- B. Dyskeratosis congenita
- C. Chédiak-Higashi syndrome
- D. Autoimmune neutropenia of infancy (Correct Answer)
Explanation: **Explanation:** The correct answer is **Autoimmune Neutropenia of Infancy (AIN)**. **Why it is correct:** AIN is the most common cause of isolated neutropenia in children aged 6 months to 2 years. It is caused by the production of **anti-neutrophil antibodies** (typically against HNA-1a or HNA-1b antigens) which lead to the peripheral destruction of neutrophils. Unlike the other options, AIN is a **self-limited condition**. Spontaneous resolution occurs in approximately 95% of cases within 12 to 24 months as the antibody production ceases. Most children remain asymptomatic or experience only mild skin or respiratory infections. **Why the other options are incorrect:** * **Shwachman-Diamond Syndrome:** An autosomal recessive ribosomopathy characterized by exocrine pancreatic insufficiency and bone marrow failure. It is a chronic, progressive condition with a high risk of transformation to MDS/AML. * **Dyskeratosis Congenita:** A telomere biology disorder presenting with the triad of abnormal skin pigmentation, nail dystrophy, and oral leukoplakia. It leads to progressive, permanent bone marrow failure. * **Chédiak-Higashi Syndrome:** An autosomal recessive disorder of lysosomal trafficking (LYST gene). It presents with partial albinism, recurrent infections, and giant cytoplasmic granules. It is not self-limited and often requires hematopoietic stem cell transplant. **High-Yield Clinical Pearls for NEET-PG:** * **AIN:** Often presents with a "benign" clinical course despite very low absolute neutrophil counts (ANC <500). * **Kostmann Syndrome:** Severe Congenital Neutropenia (SCN); unlike AIN, it is life-threatening and requires G-CSF or transplant. * **Cyclic Neutropenia:** Characterized by a 21-day cycle of neutropenia; associated with *ELANE* gene mutations.
Question 828: Which of the following is NOT a hypercoagulable state?
- A. Protein C resistance
- B. Factor V Leiden deficiency (Correct Answer)
- C. Antiphospholipid antibody
- D. Polycythemia
Explanation: The correct answer is **Factor V Leiden deficiency**. This is a classic "trick" question in hematology that tests your understanding of the pathophysiology of inherited thrombophilia. ### 1. Why Factor V Leiden deficiency is the correct answer: The condition associated with hypercoagulability is **Factor V Leiden mutation**, not deficiency. In this autosomal dominant condition, a point mutation makes Factor V resistant to inactivation by Activated Protein C (APC) [1]. Therefore, Factor V remains active longer, promoting excessive clotting. A *deficiency* of Factor V (also known as Owren’s disease) would actually lead to a **bleeding diathesis**, not a hypercoagulable state [2]. ### 2. Analysis of Incorrect Options: * **Protein C resistance:** This is the functional hallmark of Factor V Leiden. Since Protein C is a natural anticoagulant, any resistance to its action leads to a prothrombotic state [1]. * **Antiphospholipid antibody (APLA):** This is an acquired autoimmune hypercoagulable state. Antibodies (like Lupus Anticoagulant) interfere with phospholipid-binding proteins, leading to arterial and venous thrombosis and recurrent pregnancy loss. * **Polycythemia:** This is a myeloproliferative disorder characterized by an increased red cell mass. The resulting hyperviscosity of the blood significantly increases the risk of both arterial and venous thrombosis. ### 3. High-Yield Clinical Pearls for NEET-PG: * **Factor V Leiden** is the **most common** inherited cause of hypercoagulability in Caucasians. * **Prothrombin G20210A mutation** is the second most common inherited cause. * **Antithrombin III deficiency** is the most "thrombogenic" (highest risk of clot) among inherited causes, though it is less common than Factor V Leiden [1]. * **Warfarin-induced skin necrosis** is a classic complication seen in patients with **Protein C or S deficiency** when starting warfarin without heparin bridging.
Question 829: A patient with a blood pressure of 90/60 mm Hg presents with pronounced cyanosis. Blood drawn from peripheral veins is observed to be chocolate brown in colour. What is the most likely diagnosis?
- A. Methemoglobinemia (Correct Answer)
- B. Hypovolemic shock
- C. Cardiogenic shock
- D. Hemorrhagic shock
Explanation: The clinical presentation of **pronounced cyanosis** unresponsive to oxygen, combined with **chocolate-brown colored blood**, is a classic hallmark of **Methemoglobinemia**. **1. Why Methemoglobinemia is correct:** Methemoglobinemia occurs when the iron in hemoglobin is oxidized from the **ferrous (Fe²⁺)** state to the **ferric (Fe³⁺)** state. Ferric iron cannot bind oxygen. Furthermore, the presence of ferric iron causes a "left shift" in the oxygen-dissociation curve, meaning the remaining ferrous heme groups bind oxygen too tightly, preventing its release to tissues [2]. The characteristic chocolate-brown color of the blood is due to the dark pigment of methemoglobin, which does not change color even when exposed to 100% oxygen [1]. **2. Why the other options are incorrect:** * **Hypovolemic, Cardiogenic, and Hemorrhagic Shock:** While these conditions can cause hypotension (90/60 mm Hg) and peripheral cyanosis due to poor tissue perfusion (stagnant hypoxia), they **do not** change the color of the blood to chocolate brown. In these types of shock, the blood remains dark red (deoxygenated) but turns bright red upon exposure to oxygen or during arterial sampling. **3. Clinical Pearls for NEET-PG:** * **The "Saturation Gap":** A key diagnostic clue is a significant difference (>5%) between the oxygen saturation measured by pulse oximetry (which is falsely low, often hovering around 85%) and the arterial oxygen saturation (SaO₂) calculated on an ABG. * **Common Triggers:** Exposure to oxidizing agents like **Nitrites, Benzocaine, Dapsone, or Primaquine** [1], [2]. * **Antidote:** The treatment of choice is **Methylene Blue** (acts as an electron donor to reduce Fe³⁺ back to Fe²⁺). * **Note:** Methylene blue is ineffective in patients with **G6PD deficiency**; in such cases, Vitamin C or exchange transfusion is used.
Question 830: A patient presents with ecchymosis and petechiae all over the body, with no hepato-splenomegaly. All of the following are true regarding this condition EXCEPT:
- A. Increased megakaryocytes in bone marrow
- B. Bleeding into the joints (Correct Answer)
- C. Decreased platelets in the blood
- D. The disease resolves spontaneously in 80% of patients within 2-6 weeks
Explanation: The clinical presentation of petechiae and ecchymosis without hepatosplenomegaly strongly suggests **Immune Thrombocytopenic Purpura (ITP)**. In ITP, there is isolated thrombocytopenia due to autoantibody-mediated destruction of platelets [1]. ### **Explanation of Options** * **Option B (Correct Answer):** Bleeding into the joints (**Hemarthrosis**) is a hallmark of **coagulation factor deficiencies** (e.g., Hemophilia), not platelet disorders [1]. Platelet disorders (like ITP) typically present with superficial "mucocutaneous" bleeding, such as petechiae, purpura, epistaxis, and gum bleeding [1]. * **Option A:** In ITP, the bone marrow responds to peripheral platelet destruction by increasing production. Therefore, an **increased number of megakaryocytes** (platelet precursors) is a classic compensatory finding. * **Option C:** The primary pathology is the immune-mediated destruction of platelets in the spleen, leading to **decreased platelets** (thrombocytopenia) in the peripheral blood [1]. * **Option D:** This describes **Acute ITP**, which is most common in children following a viral infection. It is typically self-limiting, with approximately **80% of cases resolving spontaneously** within weeks to months. ### **NEET-PG High-Yield Pearls** * **ITP Diagnosis:** It is a diagnosis of exclusion. The presence of splenomegaly should prompt a search for other causes (e.g., Leukemia, Cirrhosis) [2]. * **First-line Treatment:** Corticosteroids (Prednisolone) or IVIG. * **Platelet Transfusion:** Generally contraindicated in ITP unless there is life-threatening hemorrhage, as the autoantibodies will destroy the transfused platelets rapidly. * **Chronic ITP:** Defined as thrombocytopenia persisting for >12 months; more common in adults [1].
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
Practice Questions
Thalassemias
Practice Questions
Platelet Disorders
Practice Questions
Coagulation Disorders
Practice Questions
Thrombotic Disorders
Practice Questions
Leukemias
Practice Questions
Lymphomas
Practice Questions
Multiple Myeloma and Plasma Cell Disorders
Practice Questions
Myeloproliferative Neoplasms
Practice Questions
Transfusion Medicine
Practice Questions
Hematopoietic Stem Cell Transplantation
Practice Questions
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