Hematology — MCQs
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Which of the following is NOT a feature of polycythemia vera?
Which enzyme is used in the treatment of Leukemia?
A 23-year-old man presents with prolonged nosebleeds. He has always noted easy bruising and ongoing bleeding after minor cuts. There is no prior history of surgery or dental procedures. His hemoglobin is 14.5 g/dL, platelets are 200,000/mL, and PT/PTT are normal. Further testing reveals that the bleeding time is elevated; the Factor VIII level is reduced, as is the ristocetin cofactor assay. What is the most likely diagnosis for this patient with a bleeding disorder?
Which action by a nursing assistant when caring for a patient who is pancytopenic indicates a need for the nurse to intervene?
Which of the following are causes of iron deficiency anemia?
What is the treatment of choice for aplastic anemia?
If a blood transfusion reaction develops due to incompatibility, what is the first immediate action to be taken?
A patient has Hb 6 gm%, folic acid 82 ng/ml, vitamin B12 60 pg/ml, serum iron 180 g/dL, and MCV of 104 fL. What is the most likely diagnosis?
What is the classification proposed by the International Lymphoma Study Group for non-Hodgkin's lymphoma?
Autoimmune hemolytic anemia is a feature of which of the following conditions?
Hematology Indian Medical PG Practice Questions and MCQs
Question 781: Which of the following is NOT a feature of polycythemia vera?
- A. Increased red cell mass
- B. Normal arterial oxygen saturation
- C. High leukocyte alkaline phosphatase score
- D. None of the above (Correct Answer)
Explanation: **Explanation:** Polycythemia Vera (PV) is a chronic myeloproliferative neoplasm characterized by the autonomous production of red blood cells, independent of erythropoietin levels. The correct answer is **None of the above** because all three options (A, B, and C) are classic features of the disease. 1. **Increased Red Cell Mass (Option A):** This is the hallmark of PV [1]. Unlike relative polycythemia (caused by dehydration), PV involves a true absolute increase in the total number of erythrocytes, leading to hyperviscosity. 2. **Normal Arterial Oxygen Saturation (Option B):** This is a crucial diagnostic differentiator. In secondary polycythemia (caused by chronic lung disease or high altitude), arterial oxygen saturation ($SaO_2$) is typically low ($<92\%$), triggering erythropoietin release. In PV, the $SaO_2$ remains normal ($>92\%$) because the erythropoiesis is primary and neoplastic. 3. **High Leukocyte Alkaline Phosphatase (LAP) Score (Option C):** PV is a panmyelosis. Along with red cells, there is often a reactive increase in mature granulocytes. This results in an elevated LAP score, which helps distinguish PV from Chronic Myeloid Leukemia (CML), where the LAP score is characteristically low. **High-Yield Clinical Pearls for NEET-PG:** * **JAK2 Mutation:** $>95\%$ of PV patients carry the **JAK2 V617F** mutation in exon 14 [1]. * **Erythropoietin (EPO) Levels:** Characteristically **low** in PV (negative feedback), whereas they are high in secondary polycythemia. * **Clinical Sign:** **Aquagenic pruritus** (itching after a warm bath) is a highly specific symptom [1]. * **Major Complications:** Thrombosis (Budd-Chiari syndrome) and transformation to myelofibrosis or Acute Myeloid Leukemia (AML) [1].
Question 782: Which enzyme is used in the treatment of Leukemia?
- A. Asparaginase (Correct Answer)
- B. Lipase
- C. Amylase
- D. Transaminase
Explanation: **Explanation:** **L-Asparaginase** is a cornerstone enzyme therapy used primarily in the treatment of **Acute Lymphoblastic Leukemia (ALL)** [1]. **Mechanism of Action:** Normal cells can synthesize the amino acid **L-asparagine** from aspartate using the enzyme *asparagine synthetase*. However, leukemic lymphoblasts are deficient in this enzyme and rely entirely on exogenous (extracellular) sources of asparagine for protein synthesis. L-Asparaginase catalyzes the conversion of serum asparagine into aspartic acid and ammonia. By depleting the circulating pool of asparagine, the enzyme "starves" the leukemic cells, leading to inhibited protein synthesis and subsequent apoptosis. **Analysis of Incorrect Options:** * **B. Lipase:** An enzyme that breaks down dietary fats into fatty acids and glycerol. It is a diagnostic marker for acute pancreatitis but has no role in leukemia therapy. * **C. Amylase:** Responsible for the hydrolysis of starch into sugars. Like lipase, it is used to diagnose pancreatic pathology. * **D. Transaminase (AST/ALT):** These enzymes are involved in amino acid metabolism and serve as markers of hepatocellular injury; they are not therapeutic agents [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Indication:** Induction protocol of childhood ALL [1]. * **Unique Side Effects:** 1. **Hypofibrinogenemia & Thrombosis:** Due to decreased synthesis of clotting factors (Protein C, S, and Antithrombin III). 2. **Acute Pancreatitis:** A classic board-exam association. 3. **Anaphylaxis:** Since it is a bacterial product (derived from *E. coli* or *Erwinia*), it is highly immunogenic. * **Cell Cycle Specificity:** It is **G1 phase-specific**.
Question 783: A 23-year-old man presents with prolonged nosebleeds. He has always noted easy bruising and ongoing bleeding after minor cuts. There is no prior history of surgery or dental procedures. His hemoglobin is 14.5 g/dL, platelets are 200,000/mL, and PT/PTT are normal. Further testing reveals that the bleeding time is elevated; the Factor VIII level is reduced, as is the ristocetin cofactor assay. What is the most likely diagnosis for this patient with a bleeding disorder?
- A. von Willebrand's disease (Correct Answer)
- B. hemophilia A
- C. hemophilia B
- D. thrombotic thrombocytopenic purpura (TTP)
Explanation: ### Explanation **Correct Answer: A. von Willebrand's disease (vWD)** The patient presents with a classic **mucocutaneous bleeding pattern** (epistaxis, easy bruising, prolonged bleeding from minor cuts) [1]. The key to the diagnosis lies in the laboratory profile: 1. **Normal Platelet Count:** Rules out thrombocytopenia. 2. **Elevated Bleeding Time:** Indicates a defect in primary hemostasis (platelet adhesion) [2]. 3. **Reduced Ristocetin Cofactor Assay:** This is the most specific test for vWD; it measures the ability of von Willebrand Factor (vWF) to agglutinate platelets [1]. 4. **Reduced Factor VIII:** vWF acts as a carrier protein for Factor VIII, protecting it from degradation [1]. Therefore, a deficiency in vWF often leads to a secondary decrease in Factor VIII. **Why Incorrect Options are Wrong:** * **B & C (Hemophilia A & B):** These are disorders of secondary hemostasis (clotting factors). They typically present with deep-tissue bleeding (hemarthrosis, muscle hematomas) rather than mucosal bleeding [1]. In Hemophilia, the Bleeding Time is **normal**, but the **aPTT is prolonged**. * **D (TTP):** TTP is characterized by the pentad of microangiopathic hemolytic anemia, **thrombocytopenia** (which is absent here), neurological symptoms, fever, and renal failure. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** vWD is the most common inherited bleeding disorder (usually Autosomal Dominant). * **vWF Functions:** 1) Platelet-to-subendothelial adhesion (via GpIb receptor); 2) Carrier for Factor VIII [1]. * **Lab Findings:** Normal PT, Normal/Prolonged aPTT (depending on Factor VIII levels), and prolonged Bleeding Time/PFA-100. * **Treatment:** **Desmopressin (DDAVP)** is the drug of choice for Type 1 vWD as it releases stored vWF from Weibel-Palade bodies in endothelial cells [1].
Question 784: Which action by a nursing assistant when caring for a patient who is pancytopenic indicates a need for the nurse to intervene?
- A. The nursing assistant assists the patient to use dental floss after eating. (Correct Answer)
- B. The nursing assistant makes an oral rinse using 1 teaspoon of salt in a liter of water.
- C. The nursing assistant adds baking soda to the patient’s saline oral rinses.
- D. The nursing assistant puts fluoride toothpaste on the patient’s toothbrush.
Explanation: **Explanation:** **Pancytopenia** is characterized by a simultaneous decrease in all three peripheral blood lineages: Red Blood Cells (anemia), White Blood Cells (leukopenia/neutropenia), and Platelets (thrombocytopenia). **Why Option A is the correct intervention:** In a pancytopenic patient, the risk of bleeding (due to thrombocytopenia) and infection (due to neutropenia) is significantly elevated. **Dental flossing** is a high-risk activity in this context because it can cause mechanical trauma to the gingiva, leading to gingival bleeding that is difficult to control. Furthermore, any break in the mucosal integrity provides a portal of entry for oral flora into the bloodstream, potentially causing life-threatening sepsis in an immunocompromised patient. Clinical examination of the mouth in hematological diseases often reveals gum hypertrophy, petechiae on the buccal mucosa, and signs of bleeding [1]. **Analysis of Incorrect Options:** * **Options B & C:** Saline and baking soda (sodium bicarbonate) oral rinses are safe, non-irritating methods to maintain oral hygiene. They help liquefy thick secretions and soothe the mucosa without the alcohol content found in commercial mouthwashes, which can cause drying and crusting. * **Option D:** Fluoride toothpaste is acceptable; however, the nurse should ensure the patient uses a **soft-bristled toothbrush** to prevent trauma. **Clinical Pearls for NEET-PG:** * **Thrombocytopenic Precautions:** Generally initiated when platelets <50,000/µL. Spontaneous bleeding risk increases significantly when platelets <10,000-20,000/µL. Petechiae and mucosal hemorrhages are hallmark findings [1]. * **Neutropenic Precautions:** Avoid rectal temperatures, suppositories, IM injections, and invasive procedures to prevent endogenous infection. Death in such cases can occur due to secondary infection following hematopoietic failure [2]. * **Oral Care:** In severe mucositis or extreme thrombocytopenia, even soft brushing may be replaced by sponge toothettes or rinses. * **Common Causes of Pancytopenia:** Aplastic anemia, Megaloblastic anemia (Vitamin B12/Folate deficiency), Myelodysplastic Syndromes (MDS), and Bone marrow infiltration (Leukemia/Lymphoma).
Question 785: Which of the following are causes of iron deficiency anemia?
- A. Chronic renal failure, Young male, Celiac sprue
- B. Chronic renal failure, Celiac sprue, Hookworm, Carcinoma of the cecum (Correct Answer)
- C. Chronic renal failure, Young male, Celiac sprue, Hookworm
- D. Chronic renal failure, Young male, Hookworm, Carcinoma of the cecum
Explanation: **Explanation:** Iron Deficiency Anemia (IDA) occurs when iron loss or demand exceeds intake/absorption [1]. The correct answer (Option B) identifies four distinct mechanisms of iron deficiency: 1. **Chronic Renal Failure (CRF):** Patients develop IDA due to frequent blood loss during hemodialysis, repeated blood sampling, and increased levels of **hepcidin** (which blocks iron absorption) [2]. Renal failure is recognized as a significant cause of decreased marrow production and anemia of chronic disease [3]. 2. **Celiac Sprue:** Iron is primarily absorbed in the **duodenum**. Celiac disease causes villous atrophy in the proximal small intestine, leading to primary malabsorption of iron [2]. 3. **Hookworm (*Ancylostoma duodenale*):** This is a classic cause of chronic occult GI blood loss in tropical regions; the worms attach to the intestinal mucosa and suck blood [1]. 4. **Carcinoma of the Cecum:** In elderly patients or post-menopausal women, IDA is **GI malignancy until proven otherwise** [1]. Right-sided colon cancers often present with chronic, occult bleeding rather than obstruction [3]. **Why other options are incorrect:** The presence of a **"Young male"** in options A, C, and D makes them less likely to be "standard" causes of IDA. In healthy young males, iron stores are usually stable because they lack the physiological blood loss seen in menstruating females [3]. If a young male has IDA, it is usually secondary to a pathological cause (like Hookworm or Celiac) rather than his demographic status itself. **NEET-PG High-Yield Pearls:** * **Gold Standard Diagnosis:** Bone marrow aspiration (Prussian blue staining) showing absent hemosiderin. * **Best Initial Test:** Serum Ferritin (Low ferritin is the most specific biochemical indicator). * **Plummer-Vinson Syndrome:** Triad of IDA, esophageal webs, and atrophic glossitis. * **Pica:** A specific sign of IDA involving the craving for non-nutritive substances (e.g., ice/pagophagia, dirt).
Question 786: What is the treatment of choice for aplastic anemia?
- A. Blood transfusion
- B. Oxymethalone
- C. Bone marrow transplantation (Correct Answer)
- D. Azathioprine
Explanation: **Explanation:** Aplastic anemia is characterized by pancytopenia resulting from bone marrow failure and fatty replacement of the marrow. The treatment strategy is dictated primarily by the patient's age and the availability of a donor. **Why Bone Marrow Transplantation (BMT) is the Correct Choice:** Allogeneic Hematopoietic Stem Cell Transplantation (HSCT/BMT) is the **treatment of choice** for young patients (typically <40-50 years) who have a human leukocyte antigen (HLA)-matched sibling donor [1]. It is the only curative modality as it replaces the defective stem cell pool with healthy cells. For patients over 50 or those without a matched donor, Immunosuppressive Therapy (IST) with Anti-Thymocyte Globulin (ATG) and Cyclosporine is the preferred alternative. **Analysis of Incorrect Options:** * **A. Blood Transfusion:** This is a **supportive measure**, not a definitive treatment. While it manages symptoms of anemia and prevents bleeding (platelets), chronic transfusion leads to iron overload and sensitization, which can complicate future transplantation [1]. * **B. Oxymetholone:** This is an androgen. Androgens were historically used to stimulate erythropoiesis, but they are now considered **second or third-line therapy** due to low efficacy and significant side effects (virilization, liver toxicity). * **D. Azathioprine:** This is an immunosuppressant used in conditions like SLE or RA, but it has **no proven role** in the treatment of aplastic anemia and may further worsen cytopenias. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Investigation:** Bone marrow aspiration and biopsy (shows "dry tap" and fatty marrow). * **Severity Criteria (Camitta Criteria):** Severe Aplastic Anemia (SAA) is defined by marrow cellularity <25% plus two of the following: Neutrophils <500/µL, Platelets <20,000/µL, or Reticulocytes <1%. * **First-line for >50 years:** Triple therapy (ATG + Cyclosporine + Eltrombopag). * **Drug of choice for PNH-associated aplastic anemia:** Eculizumab.
Question 787: If a blood transfusion reaction develops due to incompatibility, what is the first immediate action to be taken?
- A. Stop the transfusion (Correct Answer)
- B. Administer hydrocortisone injection
- C. Administer chlorpheniramine maleate injection
- D. Administer furosemide injection
Explanation: ### Explanation **1. Why "Stop the Transfusion" is Correct:** The most critical step in managing any suspected transfusion reaction—whether it is a simple febrile reaction or a life-threatening acute hemolytic reaction—is to **immediately stop the transfusion** [1]. This prevents further exposure to the offending antigen or antibody, limiting the severity of the immune response. Following this, the IV line must be maintained with normal saline using a new administration set to ensure vascular access for emergency medications [1]. **2. Analysis of Incorrect Options:** * **B & C (Hydrocortisone and Chlorpheniramine):** These are secondary treatments. Antihistamines (Chlorpheniramine) are used for allergic reactions (Urticaria), and steroids (Hydrocortisone) are used for severe allergic or febrile reactions. However, they should never be administered before stopping the offending agent. * **D (Furosemide):** This is indicated in cases of Transfusion-Associated Circulatory Overload (TACO) to reduce fluid volume or to maintain renal blood flow in hemolytic reactions. It is a supportive measure, not the primary immediate action. **3. NEET-PG High-Yield Clinical Pearls:** * **Acute Hemolytic Transfusion Reaction (AHTR):** Most commonly due to **ABO incompatibility** (clerical error). Classic triad: Fever, chills, and flank pain [1]. * **First Step:** Stop transfusion $\rightarrow$ Check vitals $\rightarrow$ Maintain IV access with NS $\rightarrow$ Notify blood bank [1]. * **Investigation:** Perform a **Direct Antiglobulin Test (DAT/Coombs test)** on the post-transfusion sample and check for hemoglobinuria [1]. * **Febrile Non-Hemolytic Reaction (FNHRT):** The most common reaction overall; caused by cytokines released from donor leukocytes. Prevented by **leukoreduction** [1].
Question 788: A patient has Hb 6 gm%, folic acid 82 ng/ml, vitamin B12 60 pg/ml, serum iron 180 g/dL, and MCV of 104 fL. What is the most likely diagnosis?
- A. Iron deficiency anaemia
- B. Vitamin B12 deficiency (Correct Answer)
- C. Folic acid deficiency
- D. Pyridoxine deficiency
Explanation: ### Explanation The correct diagnosis is **Vitamin B12 deficiency**, based on the integration of hematological indices and biochemical markers. **1. Why Vitamin B12 Deficiency is Correct:** * **Macrocytosis:** The MCV is 104 fL (Normal: 80–100 fL), indicating a macrocytic anemia. [1] * **Low Vitamin B12:** The level is 60 pg/ml, which is significantly below the normal range (Normal: 200–900 pg/ml). Blood levels of vitamin B12 provide a reasonable indication of tissue stores and are usually diagnostic of deficiency. [1] * **High Serum Iron:** In megaloblastic anemias, erythropoiesis is ineffective. Since iron is not being utilized for hemoglobin synthesis, serum iron levels often rise (180 µg/dL is high-normal to elevated). * **Normal/High Folate:** The folic acid level (82 ng/ml) is well above the normal range (Normal: 2–20 ng/ml), ruling out folate deficiency. Serum folate is very sensitive to dietary intake. [1] **2. Why Other Options are Incorrect:** * **Iron Deficiency Anemia (IDA):** IDA typically presents with **microcytic hypochromic** indices (low MCV, low MCH) and low serum iron levels. * **Folic Acid Deficiency:** While this also causes macrocytic anemia, the patient’s folate levels are high, and B12 is specifically low. * **Pyridoxine (B6) Deficiency:** This is a cause of **sideroblastic anemia**, which is usually microcytic. While it can cause high serum iron, the MCV and specific B12 level provided point directly to B12 deficiency. **3. NEET-PG High-Yield Pearls:** * **Megaloblastic Anemia:** Characterized by "nuclear-cytoplasmic asynchrony" (nucleus matures slower than cytoplasm). [1] * **Peripheral Smear:** Look for **hypersegmented neutrophils** (>5 lobes) and macro-ovalocytes. * **Biochemical Markers:** In B12 deficiency, both **Methylmalonic Acid (MMA)** and **Homocysteine** are elevated. In Folate deficiency, only Homocysteine is elevated. * **Neurological Symptoms:** Subacute Combined Degeneration (SCD) of the spinal cord is specific to B12 deficiency, not Folate deficiency.
Question 789: What is the classification proposed by the International Lymphoma Study Group for non-Hodgkin's lymphoma?
- A. Kiel classification
- B. REAL classification (Correct Answer)
- C. WHO classification
- D. Rappapo classification
Explanation: The **REAL (Revised European-American Lymphoma) classification** was proposed in 1994 by the **International Lymphoma Study Group (ILSG)**. This classification marked a paradigm shift in hematopathology by defining lymphomas as distinct clinico-pathologic entities based on a combination of morphology, immunophenotype, genetic features, and clinical presentation, rather than just histological patterns. **Analysis of Options:** * **REAL Classification (Correct):** It was specifically developed by the ILSG to resolve discrepancies between previous systems and forms the foundational basis for the current WHO classification. * **Kiel Classification:** Developed by Lennert in Europe, this system focused primarily on the cytology (cell of origin) and divided lymphomas into low-grade and high-grade based on the presence of "blasts." * **WHO Classification:** While the WHO classification is the current "gold standard," it is actually an **extension and update** of the REAL classification [1]. It was not the original proposal by the ILSG but a subsequent international consensus. * **Rappaport Classification:** This is an older, obsolete system (1956) based purely on architectural patterns (nodular vs. diffuse) and cell size, which failed to account for B-cell or T-cell lineage. **NEET-PG High-Yield Pearls:** * The **REAL classification** was the first to recognize that lymphomas are distinct diseases, not just different grades of the same process. * The **Working Formulation** (1982) was another historical system used primarily for clinical trials, categorizing lymphomas by prognosis (Low, Intermediate, High grade). * **Current Standard:** The 5th edition of the **WHO Classification of Haematolymphoid Tumours (2022)** is the most recent update used in clinical practice today [1].
Question 790: Autoimmune hemolytic anemia is a feature of which of the following conditions?
- A. ALL
- B. CML
- C. Burkitt's Lymphoma
- D. Lymphoma (Correct Answer)
Explanation: Autoimmune Hemolytic Anemia (AIHA), specifically the **Warm-antibody type (IgG)**, is a well-recognized paraneoplastic manifestation of B-cell malignancies [1]. **1. Why Lymphoma is Correct:** Lymphoproliferative disorders, particularly **Chronic Lymphocytic Leukemia (CLL)** and **Non-Hodgkin Lymphomas (NHL)** (such as Small Lymphocytic Lymphoma), are the most common neoplastic causes of AIHA [1]. The underlying mechanism involves the production of autoantibodies by dysfunctional B-lymphocytes against Rh antigens on the red blood cell surface, leading to extravascular hemolysis in the spleen [1]. In NEET-PG contexts, "Lymphoma" is the classic association for secondary AIHA. **2. Analysis of Incorrect Options:** * **ALL (Acute Lymphoblastic Leukemia):** While it involves lymphoid cells, AIHA is exceptionally rare in ALL. The primary hematological issues here are bone marrow failure (anemia, thrombocytopenia) due to blast crowding. * **CML (Chronic Myeloid Leukemia):** This is a myeloproliferative neoplasm. Anemia in CML is typically due to marrow replacement or hypersplenism, not autoimmune destruction. * **Burkitt’s Lymphoma:** Although a B-cell lymphoma, it is characterized by extremely rapid cell turnover and "starry sky" morphology. It is not classically associated with AIHA compared to indolent B-cell lymphomas [2]. **Clinical Pearls for NEET-PG:** * **CLL** is the single most common leukemia associated with AIHA (up to 10% of patients) [1]. * **Evans Syndrome:** The combination of AIHA and Immune Thrombocytopenic Purpura (ITP). * **Diagnosis:** The **Direct Antiglobulin Test (Direct Coombs Test)** is the gold standard for diagnosing AIHA [1]. * **Other Associations:** Systemic Lupus Erythematosus (SLE) is the most common non-malignant cause of secondary warm AIHA.
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
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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