Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 651: Polycythemia is not caused by which of the following?

A. Renal carcinoma
B. Liver carcinoma
C. Cerebellar hemangioma
D. Lung carcinoma (Correct Answer)

Explanation: **Explanation:** The question tests the concept of **Secondary Polycythemia** caused by inappropriate **Erythropoietin (EPO)** production. **Why Lung Carcinoma is the correct answer:** While lung carcinoma (specifically Small Cell Lung Cancer) is notorious for paraneoplastic syndromes like SIADH or ectopic ACTH production [1], [3], it is **not** typically associated with ectopic EPO production. Therefore, it does not cause polycythemia. In fact, chronic malignancy often leads to the "anemia of chronic disease." **Analysis of Incorrect Options (Causes of Polycythemia):** Certain tumors are classic "EPO-producers," leading to an absolute increase in red cell mass: * **Renal Cell Carcinoma (RCC):** The most common tumor associated with ectopic EPO production [1]. * **Hepatocellular Carcinoma (Liver):** A well-recognized cause of paraneoplastic polycythemia [1]. * **Cerebellar Hemangioblastoma:** A classic association, often seen in Von Hippel-Ludlau (VHL) syndrome [1]. **Clinical Pearls for NEET-PG:** To remember the common tumors causing ectopic EPO production, use the mnemonic **"Potentially Really High Hematocrit"** [1]: 1. **P**heochromocytoma 2. **R**enal Cell Carcinoma 3. **H**epatocellular Carcinoma 4. **H**emangioblastoma (Cerebellar) 5. **U**terine Fibroids (Leiomyoma) **Distinction:** * **Primary Polycythemia (Polycythemia Vera):** Low EPO levels due to JAK2 mutation [2]. * **Secondary Polycythemia:** High EPO levels due to hypoxia or ectopic tumor production [2].

Question 652: Hemophilia manifests clinically as a rise in which of the following parameters?

A. APTT (Correct Answer)
B. PT
C. CT
D. FDP

Explanation: Hemophilia (A and B) is a X-linked recessive bleeding disorder caused by a deficiency in **Factor VIII** (Hemophilia A) or **Factor IX** (Hemophilia B). Both of these factors are integral components of the **Intrinsic Pathway** of the coagulation cascade. **1. Why APTT is the correct answer:** The **Activated Partial Thromboplastin Time (APTT)** is the screening test used to evaluate the integrity of the intrinsic and common pathways [1]. Since Hemophilia involves a deficiency in intrinsic pathway factors (VIII or IX), the APTT will be characteristically **prolonged (increased)**. **2. Why the other options are incorrect:** * **PT (Prothrombin Time):** This tests the **Extrinsic Pathway** (Factor VII) and the common pathway [1]. Since Factor VII levels are normal in Hemophilia, the PT remains normal. * **CT (Clotting Time):** While CT can be prolonged in severe hemophilia, it is a non-specific, insensitive, and outdated bedside test. APTT is the definitive laboratory parameter for diagnosis. * **FDP (Fibrin Degradation Products):** These are elevated in conditions involving excessive fibrinolysis or clot breakdown, such as **DIC (Disseminated Intravascular Coagulation)**, not in primary factor deficiencies like Hemophilia [1]. **Clinical Pearls for NEET-PG:** * **Mixing Study:** If APTT is prolonged, a mixing study is performed [1]. If the APTT **corrects** after adding normal plasma, it indicates a factor deficiency (Hemophilia). If it does **not correct**, it indicates the presence of an inhibitor (e.g., Lupus anticoagulant). * **Bleeding Profile in Hemophilia:** Prolonged APTT; Normal PT, Normal Bleeding Time (BT), and Normal Platelet Count. * **Clinical Presentation:** Characterized by deep tissue bleeding, **hemarthrosis** (bleeding into joints), and delayed surgical bleeding.

Question 653: Low iron and low TIBC is seen in which condition?

A. Anaemia of chronic disease (Correct Answer)
B. Sideroblastic anaemia
C. Iron deficiency anaemia
D. Aplastic anemia

Explanation: ### Explanation **Correct Answer: A. Anaemia of chronic disease (ACD)** The hallmark of **Anaemia of Chronic Disease** is the body's inability to utilize iron despite adequate stores [1]. This is primarily mediated by **Hepcidin**, an acute-phase reactant [2]. * **Mechanism:** Inflammatory cytokines (like IL-6) increase Hepcidin levels [1]. Hepcidin degrades ferroportin (the iron exporter), leading to iron sequestration in macrophages and decreased intestinal absorption [2]. * **Lab Findings:** Because iron is "locked away," **Serum Iron is low**. Simultaneously, the body downregulates the synthesis of Transferrin (the protein measured by TIBC) as part of the acute-phase response. Therefore, **TIBC is low**. Ferritin (stored iron) is typically normal or high [4]. --- ### Why the other options are incorrect: * **B. Sideroblastic Anaemia:** Characterized by a defect in heme synthesis. Iron is not utilized, leading to **High Serum Iron** and high Ferritin. TIBC is usually normal or low. * **C. Iron Deficiency Anaemia (IDA):** This is the most important differential. In IDA, the body is starved of iron, so **Serum Iron is low**, but the liver compensates by producing more Transferrin to "scout" for iron, resulting in **High TIBC** [3]. * **D. Aplastic Anaemia:** This is a bone marrow failure syndrome. Since the marrow cannot produce RBCs, iron is not consumed, leading to **High Serum Iron** and high Ferritin levels. --- ### NEET-PG High-Yield Pearls: * **TIBC (Total Iron Binding Capacity)** is an indirect measure of **Transferrin**. * **Serum Ferritin** is the most sensitive and specific lab test to differentiate IDA (Low Ferritin) from ACD (Normal/High Ferritin) [4]. * **Transferrin Saturation (TSAT):** Low in both IDA and ACD, but usually much lower in IDA (<15%). * **Soluble Transferrin Receptor (sTfR):** Elevated in IDA but **Normal** in ACD; this is a key marker to differentiate the two when they coexist.

Question 654: A patient with A-negative blood group can receive blood from which of the following donor blood groups?

A. O positive
B. B negative
C. AB positive
D. A negative (Correct Answer)

Explanation: ### Explanation The fundamental principle of blood transfusion is that the recipient must not have antibodies against the donor’s red cell antigens [1]. **1. Why A negative is correct:** A patient with **A-negative** blood has: * **Antigens:** A antigen on the RBC surface [2]. * **Antibodies:** Naturally occurring anti-B antibodies in the plasma [1]. * **Rh status:** Absence of the D antigen (Rh-negative). These individuals will develop anti-D antibodies if exposed to Rh-positive blood. Therefore, an A-negative patient can safely receive blood that lacks the B antigen and lacks the Rh (D) antigen. **A-negative** and **O-negative** are the only compatible groups [1]. **2. Why the other options are incorrect:** * **O positive:** While O is the "universal donor" for ABO, the **positive** Rh status means it contains the D antigen. This would trigger a transfusion reaction (isoimmunization) in an Rh-negative recipient. * **B negative:** This blood contains the B antigen. The recipient’s naturally occurring **anti-B antibodies** would cause immediate hemolytic transfusion reaction [1]. * **AB positive:** This blood contains both the B antigen and the Rh (D) antigen, both of which are incompatible with an A-negative recipient [1]. **3. Clinical Pearls for NEET-PG:** * **Universal Donor (RBCs):** O negative (lacks A, B, and D antigens) [1]. * **Universal Recipient (RBCs):** AB positive (lacks anti-A, anti-B, and anti-D antibodies). * **Universal Donor (Plasma):** AB (lacks anti-A and anti-B antibodies). * **Rh Incompatibility:** In emergencies, Rh-negative females of childbearing age **must** receive Rh-negative blood to prevent Rh isoimmunization and future Hemolytic Disease of the Newborn (HDN).

Question 655: A patient presented with painless proptosis. What is the next investigation to diagnose it as chloroma?

A. Blood haemoglobin
B. Peripheral smear (Correct Answer)
C. Platelets
D. Bone marrow biopsy

Explanation: **Explanation:** **Chloroma**, also known as **Myeloid Sarcoma** or Granulocytic Sarcoma, is an extramedullary collection of immature myeloid cells. In the pediatric population, it classically presents as **painless proptosis** due to orbital involvement. **Why Peripheral Smear is the Correct Next Step:** Chloroma is most commonly associated with **Acute Myeloid Leukemia (AML)**, particularly the **M2 (AML with maturation)** and **M4/M5** subtypes [1]. When a patient presents with a clinical suspicion of chloroma, the immediate priority is to look for systemic involvement of leukemia. A **Peripheral Smear** is the most rapid, cost-effective, and non-invasive "next step" to identify circulating myeloblasts, Auer rods, or abnormal cell counts that point toward a primary hematologic malignancy [1]. **Analysis of Incorrect Options:** * **A & C (Hemoglobin/Platelets):** While these may show cytopenias (anemia or thrombocytopenia) in leukemia, they are non-specific and do not provide a definitive morphological diagnosis of the underlying disease. * **D (Bone Marrow Biopsy):** While this is the *gold standard* for confirming and subtyping leukemia, it is a more invasive procedure [1]. In the diagnostic algorithm, a peripheral smear always precedes a bone marrow biopsy. **High-Yield Clinical Pearls for NEET-PG:** * **Color:** The name "Chloroma" comes from the Greek *chloros* (green), due to the presence of the enzyme **Myeloperoxidase (MPO)**, which gives the tumor a greenish hue upon exposure to light. * **Common Site:** The orbit is a classic site in children; other sites include the skin (leukemia cutis), lymph nodes, and gingiva [2]. * **Cytogenetics:** Frequently associated with **t(8;21)** [1]. * **Management:** Treatment involves systemic chemotherapy (as for AML), even if the bone marrow appears uninvolved at presentation.

Question 656: Which of the following is used to irradiate blood products?

A. Alpha rays
B. Beta rays
C. Gamma rays (Correct Answer)
D. X-rays

Explanation: ### Explanation **Correct Answer: C. Gamma rays** **Medical Concept:** Blood irradiation is performed to prevent **Transfusion-Associated Graft-Versus-Host Disease (TA-GVHD)**. This fatal complication occurs when donor T-lymphocytes engraft and attack the recipient’s tissues (skin, liver, and bone marrow). Irradiation induces cross-linking of DNA in the donor lymphocytes, rendering them incapable of proliferation without affecting the function of erythrocytes, platelets, or granulocytes. **Gamma rays** (typically from Cesium-137 or Cobalt-60 sources) are the gold standard and most commonly used method in blood banks to deliver the required dose (standard 25 Gy). [1] **Analysis of Options:** * **A & B (Alpha and Beta rays):** These are particulate radiations with very low penetration power. [1] They cannot penetrate the plastic blood bags or the volume of the blood product effectively to reach all lymphocytes. * **D (X-rays):** While linear accelerators can produce X-rays for irradiation, they are less commonly used than Gamma sources in traditional blood banking. [1] However, in the context of standard NEET-PG questions, **Gamma rays** are the primary answer as they are the conventional source for standalone blood irradiators. **High-Yield Clinical Pearls for NEET-PG:** 1. **Indications for Irradiated Blood:** Immunodeficient patients (SCID, DiGeorge), Hodgkin lymphoma, patients receiving purine analogs (Fludarabine), intrauterine transfusions, and **directed donations from first-degree relatives**. 2. **Shelf Life:** Irradiation damages the red cell membrane, leading to potassium leakage. Therefore, the shelf life of irradiated RBCs is reduced to **28 days** (or the original expiry, whichever is earlier). 3. **Dose:** The central dose required is **25 Gray (Gy)**, with no less than 15 Gy delivered to any part of the bag. 4. **Leukoreduction vs. Irradiation:** Leukoreduction (filtering) reduces CMV transmission and febrile reactions but **does not** prevent TA-GVHD; only irradiation is definitive for TA-GVHD prevention.

Question 657: Pancytopenia with massive/moderate splenomegaly is seen in which of the following conditions?

A. Myelofibrosis
B. Thalassemia (Correct Answer)
C. Polycythemia Rubra Vera (PRV)
D. Hairy cell leukemia

Explanation: **Explanation:** The correct answer is **Thalassemia**. This question tests the ability to differentiate causes of pancytopenia associated with significant splenomegaly. **1. Why Thalassemia is Correct:** In severe forms of Thalassemia (like Thalassemia Major), chronic hemolysis and ineffective erythropoiesis lead to massive expansion of the erythron. This results in **extramedullary hematopoiesis**, primarily in the spleen and liver, causing massive splenomegaly. Pancytopenia occurs due to **hypersplenism**, where the enlarged spleen sequesters and destroys circulating RBCs, WBCs, and platelets [1]. **2. Analysis of Incorrect Options:** * **Myelofibrosis:** While it causes massive splenomegaly and anemia/thrombocytopenia in late stages, the classic peripheral smear finding is **leukoerythroblastic picture** (teardrop cells) rather than a simple pancytopenia [2]. * **Polycythemia Rubra Vera (PRV):** This is a myeloproliferative neoplasm characterized by **pancytosis** (increased RBCs, WBCs, and platelets), not pancytopenia. Splenomegaly is common, but the cell counts are elevated. * **Hairy Cell Leukemia:** This is a classic cause of pancytopenia with massive splenomegaly. However, in the context of standard medical examinations, if Thalassemia is an option, it is often prioritized due to the sheer scale of hypersplenism seen in chronic hemolytic states. *Note: In many clinical scenarios, Hairy Cell Leukemia is also a correct answer; however, Thalassemia is the traditional textbook answer for this specific MCQ pattern.* **Clinical Pearls for NEET-PG:** * **Massive Splenomegaly (Spleen >8cm or crossing midline):** Remember the mnemonic **"M-C-H"**: **M**yelofibrosis, **C**hronic Myeloid Leukemia (CML), **H**airy Cell Leukemia, **H**ydatid Cyst, **H**eavy chain disease, and **M**alarial big spleen (Hyperreactive Malarial Splenomegaly). * **Pancytopenia + Small Spleen:** Think of Aplastic Anemia. * **Pancytopenia + Massive Spleen:** Think of Hypersplenism (Thalassemia, Portal Hypertension) or Hairy Cell Leukemia.

Question 658: What is the most appropriate investigation for a 40-year-old female presenting with anemia, jaundice, and spherocytosis?

A. Osmotic fragility
B. Coomb's test (Correct Answer)
C. Electrophoresis
D. RBC Enzyme analysis

Explanation: ### Explanation The clinical triad of **anemia, jaundice, and spherocytosis** in a 40-year-old female strongly suggests a diagnosis of **Autoimmune Hemolytic Anemia (AIHA)**. **1. Why Coomb's Test is the Correct Answer:** In clinical practice, the most common cause of acquired spherocytosis is AIHA. The **Direct Antiglobulin Test (Coomb’s test)** is the gold standard investigation to confirm this [1]. It detects antibodies (IgG) or complement (C3) bound to the surface of red blood cells. In AIHA, splenic macrophages partially "nibble" the antibody-coated RBC membrane, reducing the surface-area-to-volume ratio and transforming the cells into **spherocytes** [1]. **2. Why Other Options are Incorrect:** * **Osmotic Fragility (A):** While increased in both Hereditary Spherocytosis (HS) and AIHA, it is a non-specific test. In a 40-year-old presenting acutely, AIHA must be ruled out first before considering a congenital condition like HS [1]. * **Electrophoresis (C):** This is used to diagnose hemoglobinopathies (e.g., Thalassemia, Sickle Cell Anemia), which typically present with microcytic or sickle cells, not primary spherocytosis. * **RBC Enzyme Analysis (D):** Used for G6PD deficiency or Pyruvate Kinase deficiency. These conditions present with bite cells or echinocytes, respectively, rather than predominant spherocytosis [2]. **Clinical Pearls for NEET-PG:** * **Hereditary Spherocytosis (HS) vs. AIHA:** Both show spherocytes. However, HS usually presents in childhood with a positive family history and a **negative** Coomb’s test. AIHA is usually acquired in adulthood and is **Coomb’s positive** [1]. * **MCHC:** Spherocytosis is the only condition where the Mean Corpuscular Hemoglobin Concentration (MCHC) is typically **increased** (>36 g/dL). * **Confirmatory Test for HS:** The Eosin-5-maleimide (EMA) binding test via flow cytometry is now preferred over osmotic fragility.

Question 659: What is the commonest mode of inheritance of Von Willebrand's disease?

A. Codominant
B. Autosomal recessive
C. Autosomal dominant (Correct Answer)
D. X-linked recessive

Explanation: **Explanation:** **1. Why Autosomal Dominant is Correct:** Von Willebrand Disease (vWD) is the most common inherited bleeding disorder worldwide. It is primarily caused by quantitative or qualitative defects in Von Willebrand Factor (vWF) [3]. The gene for vWF is located on **Chromosome 12**. The vast majority of clinical cases (approximately 70-80%) fall under **Type 1** (quantitative deficiency) and **Type 2** (qualitative defect), both of which are inherited in an **Autosomal Dominant** fashion. Because it is autosomal, it affects males and females equally, distinguishing it from Hemophilia. **2. Why the Other Options are Incorrect:** * **Codominant:** While some blood group systems (like ABO) exhibit codominance, vWD does not follow this pattern. * **Autosomal Recessive:** This is the mode of inheritance for **Type 3 vWD** (the most severe form with near-total absence of vWF) and certain rare subtypes of Type 2 (like 2N). However, these represent a very small percentage of total cases. * **X-linked Recessive:** This is the classic inheritance pattern for **Hemophilia A (Factor VIII deficiency) and Hemophilia B (Factor IX deficiency)**. vWD is specifically known for being the "autosomal" alternative to Hemophilia [2]. **3. NEET-PG High-Yield Pearls:** * **Most Common Type:** Type 1 (Autosomal Dominant). * **Clinical Presentation:** Mucocutaneous bleeding (epistaxis, menorrhagia, gingival bleeding) [4]. * **Lab Findings:** Prolonged Bleeding Time (BT) and often a prolonged aPTT (since vWF stabilizes Factor VIII). Platelet count is usually normal (except in Type 2B). * **Screening Test:** Ristocetin Cofactor Activity (decreased) [3]. * **Treatment of Choice:** Desmopressin (DDAVP) for Type 1 [1]; Factor VIII concentrates containing vWF for severe cases.

Question 660: Which one of the following findings is NOT consistent with the diagnosis of aplastic anemia?

A. Hematopoietic cells occupying less than 25% of marrow space
B. Hematopoietic cells morphology should be normal
C. Normocytic normochromic anemia
D. Splenomegaly (Correct Answer)

Explanation: **Explanation:** Aplastic anemia is a bone marrow failure syndrome characterized by **pancytopenia** and a **hypocellular bone marrow**. **Why Splenomegaly is the Correct Answer:** The hallmark of aplastic anemia is the replacement of hematopoietic tissue with fat. Because the primary pathology is a failure of production (stem cell depletion) rather than peripheral destruction or infiltration, **splenomegaly is characteristically absent**. If a patient presents with pancytopenia and an enlarged spleen, clinicians should instead suspect conditions like portal hypertension (cirrhosis), hypersplenism, hairy cell leukemia, or myelofibrosis [1]. **Analysis of Other Options:** * **Option A:** According to the **Camitta Criteria** for severe aplastic anemia, the bone marrow must show cellularity <25% (or <50% if less than 30% of remaining cells are hematopoietic). * **Option B:** In true aplastic anemia, the few remaining hematopoietic cells should appear **morphologically normal**. The presence of significant dysplasia (abnormal morphology) would point toward Myelodysplastic Syndrome (MDS) rather than aplastic anemia. * **Option C:** The anemia is typically **normocytic normochromic**, though a mild macrocytosis (increased MCV) is sometimes seen due to stressed erythropoiesis. **NEET-PG High-Yield Pearls:** * **Most common cause:** Idiopathic (Autoimmune T-cell mediated destruction of stem cells). * **Drug triggers:** Chloramphenicol (most famous), Carbamazepine, Sulfonamides, and Gold salts. * **Viral triggers:** Hepatitis (Non-A, Non-B, Non-C, Non-G), Parvovirus B19 (usually causes pure red cell aplasia or aplastic crisis in hemolytic states). * **Treatment of choice:** Allogeneic Bone Marrow Transplant (for young patients) or Immunosuppressive Therapy (Antithymocyte globulin + Cyclosporine).

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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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