Hematology — MCQs

A 34-year-old man presents with symptoms of fatigue, weakness, nose bleeds, and palpitations with exertion. On examination, he is pale, blood pressure is 110/70 mm Hg, pulse is 100/min, heart sounds are normal, lungs are clear, and he has multiple petechiae and bruises on his legs. His blood count is abnormal: hemoglobin 8.5 g/dL, white blood cells (WBCs) 4000/mL, platelets 50,000/mL, and there are blast cells in the peripheral blood. He is diagnosed with acute promyelocytic leukemia (AML-M3). Which of the following is a characteristic of this acute myelogenous leukemia?

Hematology Indian Medical PG Practice Questions and MCQs

Question 551: Blood transfusion should be completed within how many hours of initiation?

A. 1-4 hours (Correct Answer)
B. 3-6 hours
C. 4-8 hours
D. 8-12 hours

Explanation: ### Explanation **Correct Option: A (1-4 hours)** The standard protocol for blood transfusion (specifically Packed Red Blood Cells) dictates that the infusion should be completed within **4 hours** of initiation. The underlying medical rationale is twofold: 1. **Bacterial Proliferation:** Blood products are stored at 2–6°C. Once removed from refrigeration and kept at room temperature, the risk of bacterial growth (especially Gram-negative organisms like *Yersinia enterocolitica*) increases significantly. 2. **Hemolysis:** Prolonged exposure to room temperature leads to the degradation of red cell membranes and metabolic changes, reducing the efficacy of the transfusion. Ideally, a unit should be started within 30 minutes of leaving the blood bank and infused over 2–3 hours. Adverse effects can occur in up to 3% of transfusions, and any signs during administration must be monitored closely [1]. **Why Other Options are Incorrect:** * **Options B, C, and D:** These durations exceed the 4-hour safety window. Keeping blood at room temperature for more than 4 hours exponentially increases the risk of **septic transfusion reactions**, which can be fatal. **High-Yield Clinical Pearls for NEET-PG:** * **Rate of Infusion:** In the first 15 minutes, the rate should be slow (approx. 2 ml/min) to monitor for acute hemolytic reactions. * **Platelets and FFP:** These should typically be infused faster (within 30–60 minutes) as they are stored at different temperatures and are more prone to contamination. * **Transfusion-Associated Circulatory Overload (TACO):** In patients with heart failure or chronic anemia, the rate may be slowed, but it must still strictly adhere to the 4-hour limit. If a patient cannot tolerate the volume within 4 hours, the unit should be split into smaller aliquots by the blood bank. * **Needle Gauge:** A 18-20G needle is preferred for adults to prevent mechanical hemolysis.

Question 552: Which of the following is NOT a recognized cause of neutropenia?

A. Corticosteroid therapy (Correct Answer)
B. Typhoid fever
C. Aplastic anemia
D. Viral infection

Explanation: **Explanation:** The correct answer is **A. Corticosteroid therapy**. **1. Why Corticosteroids cause Neutrophilia (not Neutropenia):** Corticosteroids are a classic cause of **neutrophilia** (increased neutrophil count). This occurs through three primary mechanisms: * **Demargination:** They decrease the expression of adhesion molecules (like L-selectin), causing neutrophils to move from the endothelial walls (marginal pool) into the circulating blood. * **Delayed Apoptosis:** They extend the lifespan of mature neutrophils. * **Marrow Release:** They stimulate the premature release of neutrophils from the bone marrow. * *Note:* While they increase neutrophils, corticosteroids simultaneously cause **lymphopenia** [1] and **eosinopenia**. **2. Analysis of Incorrect Options (Causes of Neutropenia):** * **Typhoid Fever:** Unlike most bacterial infections that cause leukocytosis, enteric fever (Salmonella typhi) is a classic cause of leukopenia and neutropenia due to bone marrow suppression and increased peripheral destruction. * **Aplastic Anemia:** This is characterized by pancytopenia (reduction in RBCs, WBCs, and platelets) due to bone marrow failure. Neutropenia is a core component. * **Viral Infections:** Many viruses (e.g., Hepatitis, HIV, EBV, Influenza) cause transient neutropenia through redistribution or direct marrow suppression [1]. **Clinical Pearls for NEET-PG:** * **Drug-induced Neutropenia:** Common culprits include Clozapine, Antithyroid drugs (Methimazole/PTU), and Chemotherapy [1]. * **Felty’s Syndrome:** A high-yield triad of Rheumatoid Arthritis, Splenomegaly, and **Neutropenia**. * **Kostmann Syndrome:** A severe congenital neutropenia (autosomal recessive). * **Left Shift:** Corticosteroid-induced neutrophilia usually does *not* show a significant "left shift" (immature bands), unlike an acute bacterial infection.

Question 553: Which of the following is true about sickle cell anemia?

A. Leukopenia
B. Decreased ESR (Correct Answer)
C. Microcardia
D. Ringed sideroblasts

Explanation: ### Explanation **Correct Option: B. Decreased ESR** The Erythrocyte Sedimentation Rate (ESR) depends on the formation of **rouleaux** (stacks of red blood cells). Rouleaux formation requires normal, biconcave, and flexible RBCs. In Sickle Cell Anemia (SCA), the erythrocytes are **rigid, distorted, and sickle-shaped**. These abnormal shapes interfere with the stacking process, preventing rouleaux formation. Consequently, the RBCs remain suspended in the plasma longer, leading to a characteristically **low or near-zero ESR**. **Incorrect Options:** * **A. Leukopenia:** SCA is typically associated with **leukocytosis** (elevated WBC count), not leukopenia. This occurs due to chronic inflammation and the demargination of neutrophils from the marginal pool into the circulating pool, often triggered by stress or pain crises. * **C. Microcardia:** Patients with SCA often develop **cardiomegaly** (enlarged heart). Chronic anemia leads to a hyperdynamic circulation and increased cardiac output, eventually causing compensatory chamber dilation and hypertrophy. * **D. Ringed sideroblasts:** These are characteristic of **Sideroblastic Anemia** (due to defective heme synthesis in mitochondria), not SCA. SCA is a hemoglobinopathy caused by a point mutation in the beta-globin chain [2]. **High-Yield Clinical Pearls for NEET-PG:** * **ESR Trends:** ESR is also decreased in Polycythemia Vera, Spherocytosis, and Afibrinogenemia. * **Peripheral Smear:** Look for **Sickle cells** and **Howell-Jolly bodies** (indicating functional asplenia/autosplenectomy). * **Diagnosis:** **Hb Electrophoresis** is the gold standard (shows HbS; absence of HbA) [1]. * **Management:** **Hydroxyurea** is used to increase **HbF** levels, which inhibits the polymerization of HbS [3].

Question 554: Microcytosis is seen in which of the following conditions?

A. Thalassemia
B. Hb Lepore
C. Hb Bart's
D. All of the above (Correct Answer)

Explanation: ### Explanation **Concept:** Microcytosis (Mean Corpuscular Volume < 80 fL) occurs when there is a defect in hemoglobin synthesis [2]. This is typically due to a deficiency in iron (Iron Deficiency Anemia), a defect in heme synthesis (Sideroblastic Anemia), or a defect in globin chain production (Thalassemia and Hemoglobinopathies) [3]. **Analysis of Options:** * **A. Thalassemia:** This is the classic cause of microcytosis. It involves a quantitative reduction in the synthesis of alpha or beta-globin chains, leading to hypochromic microcytic RBCs [1]. * **B. Hb Lepore:** This is a variant hemoglobin formed by the fusion of delta and beta-globin genes (δβ-fusion). Clinically, it behaves like **Beta-Thalassemia trait or major**, resulting in ineffective erythropoiesis and significant microcytosis. * **C. Hb Bart’s:** This occurs in Alpha-Thalassemia when three or four alpha genes are deleted. In the absence of alpha chains, gamma chains form tetramers ($\gamma_4$). These tetramers have an extremely high affinity for oxygen and do not deliver it to tissues, leading to severe microcytosis and potentially *Hydrops Fetalis* [3]. **Conclusion:** Since all three conditions involve defective or abnormal globin chain production leading to smaller red blood cells, **Option D (All of the above)** is correct. **High-Yield Clinical Pearls for NEET-PG:** * **Mentzer Index:** MCV/RBC count. A ratio **< 13** suggests Thalassemia; **> 13** suggests Iron Deficiency Anemia. * **RDW (Red Cell Distribution Width):** Usually normal in Thalassemia trait but elevated in Iron Deficiency Anemia. * **HbH Disease:** A form of Alpha-Thalassemia (3-gene deletion) characterized by $\beta_4$ tetramers and "golf-ball" appearance of RBCs on supra-vital staining [3].

Question 555: Reticulocytosis is seen in all conditions EXCEPT:

A. Paroxysmal nocturnal hemoglobinuria (PNH)
B. Hemolysis
C. Nutritional anemia (Correct Answer)
D. Dyserythropoietic syndrome

Explanation: **Explanation:** The **Reticulocyte count** is a direct reflection of the bone marrow's erythropoietic activity. To produce reticulocytes, the marrow requires two things: functional stem cells and adequate "building blocks" (Iron, Vitamin B12, and Folate). **Why Nutritional Anemia is the Correct Answer:** In nutritional anemias (Iron deficiency, B12, or Folate deficiency), there is a **deficiency of essential substrates** [1]. Even though the body senses anemia and increases Erythropoietin levels, the bone marrow cannot produce new red cells effectively. This results in a **low reticulocyte count** (hypoproliferative anemia). Reticulocytosis only occurs in these patients *after* treatment (nutritional replacement) has commenced [1]. **Analysis of Other Options:** * **Hemolysis:** In hemolytic states, the bone marrow is healthy and the building blocks are available. The marrow compensates for peripheral red cell destruction by increasing production up to 6–8 times the normal rate, leading to significant **reticulocytosis**. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** Although PNH is a stem cell disorder, its primary clinical manifestation is **intravascular hemolysis**. During hemolytic episodes, the marrow responds with reticulocytosis (unless there is a co-existing aplastic crisis). * **Dyserythropoietic Syndrome:** While these syndromes involve "ineffective erythropoiesis," they often present with a variable reticulocyte response. However, compared to the absolute lack of building blocks in nutritional anemia, some degree of compensatory reticulocytosis or a "normal" count in the face of anemia is often noted, making nutritional anemia the most definitive "exception" for active reticulocytosis. **NEET-PG High-Yield Pearls:** * **Reticulocyte Production Index (RPI):** An RPI **>2%** indicates a compensatory marrow response (Hemolysis/Hemorrhage); an RPI **<2%** indicates an inadequate marrow response (Nutritional/Aplastic anemia). * **Corrected Reticulocyte Count (CRC):** Always calculate this in anemic patients: *Observed Retic % × (Patient Hct / Normal Hct).* * **Earliest sign of response** to Iron or B12 therapy is a rise in reticulocyte count (usually within 3–7 days).

Question 556: A 70-year-old male has been experiencing intermittent epistaxis, fatigue, and pain in bones for the past 4 months. Laboratory investigations are as follows: Serum Ca++: 12 mg/dL. This patient is likely to develop which complication?

A. Floppy mitral valve
B. Autoimmune hemolytic anemia
C. Amyloidosis (Correct Answer)
D. Calcific aortic valve disease

Explanation: **Explanation:** The clinical presentation of a 70-year-old male with **bone pain, fatigue (anemia), epistaxis (bleeding diathesis), and hypercalcemia (12 mg/dL)** is a classic triad for **Multiple Myeloma (MM)**. In MM, the neoplastic proliferation of plasma cells leads to the overproduction of monoclonal light chains (paraproteins). **Why Amyloidosis is the Correct Answer:** In Multiple Myeloma, excess light chains (specifically Lambda or Kappa) can undergo misfolding and deposit in various tissues as insoluble fibrils. This condition is known as **AL (Light Chain) Amyloidosis**. Approximately 10–15% of patients with Multiple Myeloma develop clinical amyloidosis, which can lead to organ dysfunction (macroglossia, restrictive cardiomyopathy, or nephrotic syndrome). **Analysis of Incorrect Options:** * **A & D (Floppy Mitral Valve / Calcific Aortic Valve):** While hypercalcemia can theoretically lead to metastatic calcification, it does not typically manifest as isolated valvular disease in the context of plasma cell dyscrasias. These are degenerative or connective tissue disorders unrelated to MM. * **B (Autoimmune Hemolytic Anemia):** AIHA is more commonly associated with **Chronic Lymphocytic Leukemia (CLL)** or Non-Hodgkin Lymphoma, rather than Multiple Myeloma. Anemia in MM is usually normocytic normochromic due to marrow infiltration and renal failure. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria for MM:** **C**alcium elevation, **R**enal insufficiency, **A**nemia, **B**one lesions [1]. * **Bleeding in MM:** Epistaxis occurs due to "Platelet Coating" by paraproteins, interfering with aggregation [1]. * **Diagnosis:** Look for "punched-out" lytic lesions on X-ray and M-spike on Serum Protein Electrophoresis (SPEP) [1]. * **Amyloid Staining:** Congo Red stain showing **apple-green birefringence** under polarized light.

Question 557: Which bleeding disorder is characterized by prolonged activated partial thromboplastin time (APTT) and prothrombin time (PT)?

A. Factor 13 deficiency
B. Severe liver disease (Correct Answer)
C. Immune thrombocytopenic purpura
D. Leiden (Factor V) deficiency

Explanation: To understand this question, one must recall the coagulation cascade: **PT** measures the extrinsic and common pathways, while **aPTT** measures the intrinsic and common pathways [1]. ### **Why Severe Liver Disease is Correct** The liver is the primary site for the synthesis of almost all coagulation factors (except Factor VIII and von Willebrand factor). In **severe liver disease**, there is a global deficiency of clotting factors. Since factors in the common pathway (Factors X, V, II, and I) are affected, both PT and aPTT will be prolonged [1]. PT is typically the first to rise because Factor VII (extrinsic pathway) has the shortest half-life. ### **Why Other Options are Incorrect** * **A. Factor XIII deficiency:** Factor XIII stabilizes the fibrin clot. Deficiency results in a normal PT, aPTT, and Bleeding Time, but a positive **Urea Solubility Test**. * **C. Immune Thrombocytopenic Purpura (ITP):** This is a platelet disorder. It presents with a prolonged Bleeding Time (BT) but **normal PT and aPTT**, as the coagulation cascade remains intact [1]. * **D. Leiden (Factor V) deficiency:** This is a distractor. Factor V Leiden is a **pro-thrombotic** (hypercoagulable) state caused by resistance to Protein C, not a deficiency that causes bleeding or prolonged PT/aPTT. ### **High-Yield Clinical Pearls for NEET-PG** * **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 Heparin use. * **Prolonged PT + aPTT:** Think Common pathway deficiency (X, V, II, I), Vitamin K deficiency, Warfarin overdose, DIC, or Liver disease [1]. * **Mixing Study:** If a prolonged aPTT corrects with normal plasma, it indicates a **factor deficiency**; if it does not correct, it indicates the presence of an **inhibitor** (e.g., Lupus anticoagulant) [1].

Question 558: Which of the following bleeding disorders are associated with an increased aPTT?

A. Hemophilia A, Hemophilia B, Von-Willebrand disease (Correct Answer)
B. Hemophilia B, Henoch-Schonlein purpura, Bernard-Soulier syndrome
C. Henoch-Schonlein purpura, Bernard-Soulier syndrome, Von-Willebrand disease
D. Hemophilia A, Henoch-Schonlein purpura, Von-Willebrand disease

Explanation: Explanation: The **Activated Partial Thromboplastin Time (aPTT)** measures the integrity of the **intrinsic** and **common pathways** of the coagulation cascade [1]. Any deficiency or inhibition of factors XII, XI, IX, VIII, X, V, II (prothrombin), or I (fibrinogen) will result in a prolonged aPTT. * **Hemophilia A & B:** These are X-linked recessive disorders caused by deficiencies in **Factor VIII** and **Factor IX**, respectively [2]. Since both factors are vital components of the intrinsic pathway, their deficiency leads to a characteristically increased aPTT with a normal PT and bleeding time. * **Von-Willebrand Disease (vWD):** vWF acts as a carrier protein for Factor VIII, protecting it from degradation [3]. In vWD, low levels of vWF lead to a secondary decrease in Factor VIII levels, thereby prolonging the aPTT [3]. Additionally, vWD presents with an increased bleeding time due to defective platelet adhesion. **Analysis of Incorrect Options:** * **Henoch-Schönlein Purpura (HSP):** This is a small-vessel vasculitis (IgA-mediated). It is a vascular disorder where coagulation profiles (PT, aPTT) and platelet counts remain **normal**. * **Bernard-Soulier Syndrome:** This is a qualitative platelet disorder (deficiency of GpIb). While it increases the **bleeding time**, the coagulation cascade (aPTT/PT) is unaffected. **High-Yield Clinical Pearls for NEET-PG:** * **Isolated prolonged aPTT:** Think Hemophilia, vWD, or Heparin use [1]. * **Isolated prolonged PT:** Think Factor VII deficiency or early Warfarin therapy. * **Prolonged PT and aPTT:** Think Vitamin K deficiency, Liver disease, or DIC [1]. * **Mixing Study:** If aPTT corrects with normal plasma, it indicates a **factor deficiency**; if it fails to correct, an **inhibitor** (like Lupus anticoagulant) is present [1].

Question 559: Which metabolic abnormality is seen in multiple myeloma?

A. Hyponatremia
B. Hypokalemia
C. Hypercalcemia (Correct Answer)
D. Hyperphosphatemia

Explanation: **Explanation:** **Correct Answer: C. Hypercalcemia** **Mechanism:** In Multiple Myeloma (MM), malignant plasma cells in the bone marrow produce **Osteoclast Activating Factors (OAFs)**, such as RANK-ligand (RANKL), IL-1 (Osteoclast Activating Factor), and TNF-alpha. These factors stimulate osteoclasts and inhibit osteoblasts, leading to extensive bone resorption. This process releases large amounts of calcium into the extracellular fluid, resulting in hypercalcemia. It is a hallmark feature of the **CRAB** criteria (Calcium elevation, Renal insufficiency, Anemia, and Bone lesions). **Analysis of Incorrect Options:** * **A. Hyponatremia:** While MM can cause "Pseudohyponatremia" (due to high serum protein levels interfering with older lab techniques), it is not a primary metabolic feature. True hyponatremia is not characteristic. * **B. Hypokalemia:** MM is more commonly associated with hyperkalemia if renal failure develops. Hypokalemia is not a standard feature. * **D. Hyperphosphatemia:** While renal failure in late-stage MM can lead to phosphate retention, hypercalcemia is the direct and classic metabolic hallmark resulting from primary bone destruction. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** **C**alcium (>11 mg/dL), **R**enal insufficiency (Cr >2 mg/dL), **A**nemia (Hb <10 g/dL), **B**one lesions (Lytic lesions). * **M-Spike:** Found on Serum Protein Electrophoresis (SPEP), usually IgG (most common) or IgA. * **Bence-Jones Proteins:** Free light chains (kappa/lambda) found in urine; they are not detected by standard dipsticks (which detect albumin). * **Peripheral Smear:** Characterized by **Rouleaux formation** due to increased ESR/fibrinogen/globulins. * **Bone Scan:** Often **negative** because it detects osteoblastic activity; Skeletal Survey (X-ray) or MRI is preferred to find "punched-out" lytic lesions.

Question 560: A 34-year-old man presents with symptoms of fatigue, weakness, nose bleeds, and palpitations with exertion. On examination, he is pale, blood pressure is 110/70 mm Hg, pulse is 100/min, heart sounds are normal, lungs are clear, and he has multiple petechiae and bruises on his legs. His blood count is abnormal: hemoglobin 8.5 g/dL, white blood cells (WBCs) 4000/mL, platelets 50,000/mL, and there are blast cells in the peripheral blood. He is diagnosed with acute promyelocytic leukemia (AML-M3). Which of the following is a characteristic of this acute myelogenous leukemia?

A. Peak incidence in childhood
B. High leukocyte alkaline phosphatase
C. Philadelphia chromosome
D. Auer bodies in blast cells (Correct Answer)

Explanation: The patient presents with symptoms of pancytopenia (fatigue, bleeding, pallor) and peripheral blasts, characteristic of Acute Myeloid Leukemia (AML). Specifically, the diagnosis of **Acute Promyelocytic Leukemia (APL/AML-M3)** is established [1]. **1. Why the correct answer is right:** **Auer bodies** are elongated, needle-like pink/red cytoplasmic inclusions formed by the fusion of primary granules (lysosomes) containing peroxidase. They are a hallmark of myeloblasts. In AML-M3, these are not only present but often found in clusters called **"Faggot cells."** Their presence confirms a myeloid lineage and is highly characteristic of the hypergranular promyelocytes seen in M3. **2. Why the incorrect options are wrong:** * **A. Peak incidence in childhood:** This describes **Acute Lymphoblastic Leukemia (ALL)**. AML typically affects middle-aged and older adults (median age ~65), though APL (M3) often presents in younger adults (median age ~40). * **B. High leukocyte alkaline phosphatase (LAP):** A high LAP score is seen in **Leukemoid reactions** or polycythemia vera. In contrast, Chronic Myeloid Leukemia (CML) is characterized by a *low* LAP score. * **C. Philadelphia chromosome:** This refers to the **t(9;22)** translocation, which is the diagnostic hallmark of **CML** and a poor prognostic marker in ALL [1]. AML-M3 is associated with **t(15;17)** [1]. **High-Yield NEET-PG Pearls for AML-M3:** * **Molecular Pathogenesis:** Translocation **t(15;17)** involving the **PML-RARA** gene fusion [1]. * **Clinical Emergency:** High risk of **DIC (Disseminated Intravascular Coagulation)** due to the release of procoagulants from granules. * **Treatment:** Targeted therapy with **ATRA (All-Trans Retinoic Acid)** and Arsenic Trioxide, which induces differentiation of promyelocytes. * **Morphology:** Bilobed nuclei and numerous Auer bodies (Faggot cells).

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

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Hematology — MCQs

Hematology — MCQs

On this page

Practice by Chapter

Want unlimited practice?