Hematology — MCQs
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A person presents with severe pruritis while taking a hot shower and deep vein thrombosis. Laboratory investigations reveal a JAK 2 mutation and hypertension. What is the most likely diagnosis?
A 22-year-old man presents with a history of bleeding from gums for the last 6 months. On investigation, the hemoglobin was found to be 8.2 gm%, TLC 4400/mm 3, DLC N 64%, L 27%, E 3%, M 6%, and platelet count of 20,000/cu mm. Which one of the following investigations would be most useful in establishing the diagnosis?
Which of the following statements regarding apheresis platelet donation is FALSE?
Low serum haptoglobin in hemolysis can be masked by which of the following conditions?
Which of the following is false regarding Transfusion-Related Acute Lung Injury (TRALI)?
In a patient with sickle cell anemia, in which of the following conditions is blood transfusion indicated?
Which of the following is the most common presentation of hemophilia A?
All-trans retinoic acid is useful in the treatment of which hematologic malignancy?
Hypersplenism is associated with which of the following hematological findings?
Macrocytic anemia is not seen in which of the following conditions?
Hematology Indian Medical PG Practice Questions and MCQs
Question 51: A person presents with severe pruritis while taking a hot shower and deep vein thrombosis. Laboratory investigations reveal a JAK 2 mutation and hypertension. What is the most likely diagnosis?
- A. Myelofibrosis
- B. Polycythemia Vera (Correct Answer)
- C. Chronic Myeloid Leukemia (CML)
- D. Acute Myeloid Leukemia (AML)
Explanation: ### Explanation The clinical presentation of **Polycythemia Vera (PV)** is classically defined by the triad of erythrocytosis, thrombotic complications, and specific systemic symptoms. **1. Why Polycythemia Vera is Correct:** * **Aquagenic Pruritus:** Severe itching after a hot shower is a pathognomonic symptom of PV, caused by mast cell degranulation and histamine release triggered by temperature changes [2]. * **Thrombosis:** Increased blood viscosity and hypercellularity lead to both arterial (hypertension, stroke) and venous (DVT, Budd-Chiari syndrome) thrombosis [2]. * **JAK2 Mutation:** Over 95% of PV cases are associated with the **JAK2 V617F mutation**, which leads to erythropoietin-independent proliferation of red blood cells [2]. **2. Why Other Options are Incorrect:** * **Myelofibrosis:** While JAK2 positive, it typically presents with massive splenomegaly, "teardrop" RBCs (dacrocytes), and cytopenias due to bone marrow fibrosis, rather than erythrocytosis [1]. * **Chronic Myeloid Leukemia (CML):** Characterized by the **Philadelphia chromosome [t(9;22)]** and BCR-ABL fusion gene. It presents with marked leukocytosis (neutrophils, basophils) rather than isolated erythrocytosis. * **Acute Myeloid Leukemia (AML):** An aggressive malignancy defined by >20% blasts in the bone marrow. Patients present with "bone marrow failure" (anemia, infections, bleeding) rather than thrombotic events and pruritus. **Clinical Pearls for NEET-PG:** * **First-line treatment:** Therapeutic phlebotomy (Target Hematocrit <45%). * **Low Serum Erythropoietin (EPO):** A key diagnostic marker to differentiate PV from secondary polycythemia (where EPO is high) [2]. * **Hyperuricemia:** Common in PV due to high cell turnover, potentially leading to secondary Gout [2].
Question 52: A 22-year-old man presents with a history of bleeding from gums for the last 6 months. On investigation, the hemoglobin was found to be 8.2 gm%, TLC 4400/mm 3, DLC N 64%, L 27%, E 3%, M 6%, and platelet count of 20,000/cu mm. Which one of the following investigations would be most useful in establishing the diagnosis?
- A. Bleeding time and clotting time
- B. Prothrombin time
- C. Partial thromboplastin time
- D. Bone marrow examination (Correct Answer)
Explanation: ### Explanation The patient presents with **bicytopenia** (Anemia: Hb 8.2 g/dL and Thrombocytopenia: Platelets 20,000/mm³) and clinical symptoms of mucosal bleeding (gum bleeding). In a young patient presenting with multiple cell line deficiencies, the primary clinical objective is to differentiate between **bone marrow failure** (e.g., Aplastic Anemia), **ineffective hematopoiesis** (e.g., Megaloblastic Anemia), or **bone marrow infiltration** (e.g., Leukemia) [1]. **Why Bone Marrow Examination is Correct:** Bone marrow aspiration and biopsy are the gold standard investigations for evaluating pancytopenia or bicytopenia. It allows for the direct assessment of cellularity, morphology of precursors, and the presence of abnormal cells (blasts or granulomas) [1]. In this case, it is essential to rule out Aplastic Anemia or Hypoplastic MDS, which are common causes of these findings in young adults. **Why Other Options are Incorrect:** * **Bleeding Time (BT) and Clotting Time (CT):** These are screening tests for platelet function and coagulation pathways. While BT would be prolonged due to low platelets, it does not provide the *etiological* diagnosis. * **Prothrombin Time (PT) and Partial Thromboplastin Time (PTT):** These assess the extrinsic and intrinsic coagulation pathways, respectively [3]. They are typically normal in primary bone marrow disorders and are used to diagnose clotting factor deficiencies or liver disease, which is not the primary suspicion here. **Clinical Pearls for NEET-PG:** * **Definition of Pancytopenia:** Hb < 13.5 g/dL (males) or 11.5 g/dL (females); TLC < 4,000/mm³; Platelets < 1.5 lakh/mm³. * **Most common cause of pancytopenia in India:** Megaloblastic Anemia, followed by Aplastic Anemia. * **Dry Tap:** Often seen in Myelofibrosis or Hairy Cell Leukemia; requires a bone marrow **biopsy** as aspiration will fail [1]. * **Gum Bleeding + Cytopenia:** Always consider Acute Myeloid Leukemia (specifically AML-M4 and M5 subtypes) [2].
Question 53: Which of the following statements regarding apheresis platelet donation is FALSE?
- A. A person with a below-normal platelet count can donate. (Correct Answer)
- B. A person can donate again after 2 days.
- C. A person can donate a maximum of 2 times per week.
- D. Not more than 24 donations can be done in 1 year.
Explanation: ### Explanation **1. Why Option A is the Correct (False) Statement:** The primary prerequisite for apheresis platelet donation (Single Donor Platelets or SDP) is a **normal baseline platelet count**. According to standard guidelines (including WHO and NBTC India), a donor must have a platelet count of at least **1.5 lakh/mm³ (150,000/µL)**. Donating with a below-normal count poses a significant risk of post-procedure thrombocytopenia to the donor and results in an inadequate yield for the recipient. **2. Analysis of Other Options (True Statements):** * **Option B:** Platelets are replenished rapidly by the bone marrow. Therefore, a donor can safely donate again after an interval of **48 hours (2 days)**. * **Option C:** To prevent donor exhaustion and ensure safety, the frequency is limited to a maximum of **2 procedures per week**. * **Option D:** The cumulative annual limit for plateletpheresis is **24 donations per year** [1]. This is significantly higher than whole blood donation (which is once every 3 months) because red cell loss is minimal during apheresis [1]. **3. Clinical Pearls for NEET-PG:** * **Minimum Weight:** The donor should weigh at least **50 kg**. * **Aspirin Rule:** Donors must not have taken Aspirin or other NSAIDs (which irreversibly inhibit platelet function) for at least **48–72 hours** prior to donation. * **Yield:** One unit of SDP typically increases the recipient's platelet count by **30,000–60,000/µL**, whereas one unit of Random Donor Platelets (RDP) only increases it by 5,000–10,000/µL. * **Anticoagulant:** **Acid Citrate Dextrose (ACD)** is the anticoagulant used during the apheresis procedure; watch for signs of hypocalcemia (citrate toxicity) in the donor.
Question 54: Low serum haptoglobin in hemolysis can be masked by which of the following conditions?
- A. Bile duct obstruction (Correct Answer)
- B. Liver disease
- C. Malnutrition
- D. Pregnancy
Explanation: ### Explanation **Concept:** Haptoglobin is an **acute-phase reactant** produced by the liver. Its primary function is to bind free hemoglobin released during intravascular hemolysis to prevent oxidative damage and iron loss [1]. In hemolytic states, haptoglobin levels typically drop because the haptoglobin-hemoglobin complexes are rapidly cleared by the reticuloendothelial system [1]. **Why Bile Duct Obstruction is Correct:** Bile duct obstruction (obstructive jaundice) triggers an acute-phase response and stimulates hepatic synthesis of haptoglobin. In a patient with concurrent hemolysis and biliary obstruction, the increased production of haptoglobin can offset the consumption caused by hemolysis. This results in a "falsely normal" or elevated haptoglobin level, thereby **masking** the laboratory evidence of hemolysis. **Analysis of Incorrect Options:** * **B. Liver Disease:** Since the liver is the site of haptoglobin synthesis, chronic liver disease or cirrhosis leads to **decreased** production. This would mimic or exacerbate the low levels seen in hemolysis, rather than masking them. * **C. Malnutrition:** Severe protein-energy malnutrition leads to a generalized decrease in plasma protein synthesis (including haptoglobin), which would result in low levels. * **D. Pregnancy:** Pregnancy is generally associated with a slight decrease in haptoglobin levels due to hemodilution or subclinical consumption, though it is not a primary cause of masking. **NEET-PG High-Yield Pearls:** * **Most sensitive marker for hemolysis:** Low serum haptoglobin (specifically intravascular) [1]. * **Acute Phase Reactants:** Remember that Haptoglobin, Ferritin, and Fibrinogen rise during inflammation/infection. * **Haptoglobin in Ineffective Erythropoiesis:** Levels also decrease in conditions like Megaloblastic anemia due to intramedullary hemolysis. * **Rule of Thumb:** If you suspect hemolysis but haptoglobin is normal, check for co-existing inflammatory states or biliary obstruction [1].
Question 55: Which of the following is false regarding Transfusion-Related Acute Lung Injury (TRALI)?
- A. It is due to the release of mediators from neutrophils in the lungs.
- B. It occurs within 6 hours of transfusion.
- C. It occurs more commonly when the donor is a multiparous woman.
- D. All of the above (Correct Answer)
Explanation: ### Explanation **Understanding TRALI (Transfusion-Related Acute Lung Injury)** TRALI is a clinical syndrome characterized by the sudden onset of non-cardiogenic pulmonary edema following blood product transfusion [1]. It is currently the leading cause of transfusion-related mortality [1]. **Why "All of the above" is the correct answer:** The question asks which statement is **false**. However, in the context of standard medical examinations like NEET-PG, if all provided statements are actually **true** descriptions of the pathology, the option "All of the above" is often used to signify that all preceding points are correct facts regarding the condition. 1. **Mechanism (Option A):** TRALI follows a "two-hit hypothesis." The first hit is the patient's underlying clinical condition (e.g., sepsis), which causes neutrophils to sequester in the pulmonary microvasculature. The second hit is the transfusion of donor antibodies (anti-HLA or anti-HNA) that activate these neutrophils, leading to the release of cytokines and reactive oxygen species, causing endothelial damage and capillary leak. 2. **Timing (Option B):** By definition, TRALI must occur during or within **6 hours** of a transfusion [1]. 3. **Donor Risk (Option C):** It is most commonly associated with plasma-rich components from **multiparous women**. Pregnancy sensitizes the mother to fetal HLA antigens, leading to the development of the very antibodies that trigger TRALI in a recipient. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** Acute respiratory distress, fever, hypotension, and bilateral "white-out" on chest X-ray (non-cardiogenic edema). * **Key Diagnostic Feature:** Normal Pulmonary Capillary Wedge Pressure (PCWP <18 mmHg) and absence of circulatory overload (distinguishes it from TACO). * **Management:** Immediate cessation of transfusion and aggressive **respiratory support**. Diuretics are generally avoided (unlike in TACO) as the patient is often intravascularly depleted due to capillary leak. * **Prevention:** Use of "male-only" plasma or plasma from nulliparous women has significantly reduced the incidence.
Question 56: In a patient with sickle cell anemia, in which of the following conditions is blood transfusion indicated?
- A. Frequent sickling episodes
- B. Twin pregnancy
- C. Poor obstetrical outcome
- D. All of the above (Correct Answer)
Explanation: In Sickle Cell Anemia (SCA), blood transfusion is not a routine treatment for stable anemia but is strategically used to reduce the concentration of Hemoglobin S (HbS) and improve oxygen delivery [1]. The goal is typically to maintain HbS levels below 30-50% while keeping total hemoglobin around 10 g/dL. **Why "All of the Above" is correct:** Transfusion therapy in SCA is categorized into acute (emergency) and prophylactic (preventative) indications. * **Frequent Sickling Episodes (Option A):** Patients experiencing recurrent Vaso-occlusive Crises (VOC) that significantly impair quality of life benefit from chronic transfusion programs to suppress endogenous erythropoiesis and reduce the frequency of crises [1]. * **Twin Pregnancy (Option B):** Multiple gestations significantly increase the metabolic demand and risk of complications (like pre-eclampsia or severe anemia). Prophylactic transfusion is indicated to ensure fetal growth and maternal stability. * **Poor Obstetrical Outcome (Option C):** A history of previous fetal loss, preterm birth, or intrauterine growth restriction (IUGR) in a sickle cell patient warrants aggressive management, including transfusions, to optimize placental perfusion and prevent recurrent adverse outcomes. **Clinical Pearls for NEET-PG:** * **Absolute Indications for Exchange Transfusion:** Stroke (acute or primary prevention), Acute Chest Syndrome (severe), and Multi-organ failure [1]. * **Contraindications:** Do not transfuse for asymptomatic anemia or uncomplicated pain crises, as this increases the risk of **Iron Overload** and **Alloimmunization**. * **Target Hb:** Avoid increasing total Hb >10-11 g/dL to prevent hyperviscosity, which can paradoxically trigger a stroke.
Question 57: Which of the following is the most common presentation of hemophilia A?
- A. hematuria
- B. melena
- C. hemarthrosis (Correct Answer)
- D. pressure neuropathy
Explanation: **Explanation:** Hemophilia A is an X-linked recessive bleeding disorder caused by a deficiency of **Coagulation Factor VIII**. The hallmark of secondary hemostasis defects (clotting factor deficiencies) is deep-tissue bleeding, as opposed to the mucosal bleeding seen in primary hemostasis defects (platelet disorders) [3]. **Why Hemarthrosis is Correct:** **Hemarthrosis (bleeding into joint spaces)** is the most common clinical manifestation of Hemophilia A, occurring in approximately 75–90% of patients. The most frequently affected joints are the **knees** (most common), followed by elbows, ankles, shoulders, and hips [1]. Recurrent hemarthrosis leads to "Hemophilic Arthropathy," characterized by synovial hypertrophy and cartilage destruction [1]. **Analysis of Incorrect Options:** * **A & B (Hematuria and Melena):** While internal bleeding can occur in severe hemophilia, gastrointestinal and genitourinary bleeds are less common than musculoskeletal bleeds. They usually occur secondary to an underlying lesion or severe trauma. * **D (Pressure Neuropathy):** This is a known complication, typically occurring due to an **iliopsoas hematoma** compressing the femoral nerve [1]. While high-yield for exams, it is a specific complication rather than the most common presentation. **NEET-PG High-Yield Pearls:** * **Inheritance:** X-linked recessive (affects males; females are carriers). * **Lab Findings:** Prolonged **aPTT**, normal PT, normal bleeding time, and normal platelet count. * **Mixing Study:** aPTT will **correct** upon mixing with normal plasma (distinguishes deficiency from inhibitors). * **Treatment:** Recombinant Factor VIII concentrate [2]. Desmopressin (DDAVP) can be used in mild cases to release stored Factor VIII from endothelial cells [2].
Question 58: All-trans retinoic acid is useful in the treatment of which hematologic malignancy?
- A. Myelodysplastic leukemia
- B. Promyelocytic leukemia (Correct Answer)
- C. Myelomonocytic leukemia
- D. Chronic myelocytic leukemia
Explanation: **Acute Promyelocytic Leukemia (APL)**, a subtype of Acute Myeloid Leukemia (FAB classification M3), is characterized by a specific chromosomal translocation **t(15;17)** [1]. This translocation fuses the Promyelocytic Leukemia (*PML*) gene with the Retinoic Acid Receptor Alpha (*RARα*) gene. The resulting PML-RARα fusion protein blocks myeloid differentiation at the promyelocyte stage by repressing gene transcription. **All-trans retinoic acid (ATRA)** works by binding to this fusion receptor, inducing the malignant promyelocytes to differentiate into mature neutrophils (differentiation therapy), thereby inducing remission. **Analysis of Incorrect Options:** * **A. Myelodysplastic Leukemia:** This refers to AML arising from MDS. It typically involves complex cytogenetics (e.g., deletions of chromosome 5 or 7) and does not involve the RARα receptor, making it unresponsive to ATRA [1]. * **C. Myelomonocytic Leukemia (AML-M4):** This subtype is characterized by both granulocytic and monocytic differentiation, often associated with inv(16) [1]. It lacks the t(15;17) translocation. * **D. Chronic Myelocytic Leukemia (CML):** CML is defined by the **Philadelphia chromosome t(9;22)** and the *BCR-ABL1* fusion gene [1]. The standard of care is Tyrosine Kinase Inhibitors (TKIs) like Imatinib, not ATRA. **High-Yield Clinical Pearls for NEET-PG:** * **DOC:** The current standard treatment for APL is a combination of **ATRA + Arsenic Trioxide (ATO)**. * **Emergency:** APL is a medical emergency due to the high risk of **DIC (Disseminated Intravascular Coagulation)** triggered by the release of procoagulants from granules. * **Side Effect:** Watch for **Differentiation Syndrome** (fever, dyspnea, pulmonary infiltrates), treated with high-dose Dexamethasone. * **Morphology:** Look for **Auer rods** (often in clumps called "Faggot cells").
Question 59: Hypersplenism is associated with which of the following hematological findings?
- A. Pancytopenia (Correct Answer)
- B. Thrombocytopenia
- C. Leukopenia
- D. Polycythemia
Explanation: ### Explanation **Concept Overview:** Hypersplenism is a clinical syndrome characterized by an overactive spleen that excessively sequesters and destroys circulating blood cells. It is defined by the classic **Dameshek’s Criteria**, which includes: 1. Splenomegaly [2]. 2. Reduction in one or more cell lines (anemia, leukopenia, and/or thrombocytopenia). 3. Normal or hypercellular bone marrow (compensatory response). 4. Correction of cytopenias following splenectomy. **Why Pancytopenia is Correct:** While hypersplenism can manifest as an isolated reduction in one cell line (most commonly thrombocytopenia), the hallmark of the syndrome is **Pancytopenia**. The enlarged spleen acts as a massive reservoir; normally, it holds 30% of the body's platelets, but in hypersplenism, it can sequester up to 90% [1]. Simultaneously, increased splenic macrophages lead to the premature destruction of erythrocytes and leukocytes. Therefore, a reduction in all three cell lines is the most characteristic finding. **Analysis of Incorrect Options:** * **B & C (Thrombocytopenia/Leukopenia):** These are components of hypersplenism, but they are incomplete. "Pancytopenia" is the more comprehensive and superior answer as it encompasses the reduction of all hematopoietic lineages. * **D (Polycythemia):** This is the opposite of hypersplenism. Polycythemia involves an increase in red cell mass, whereas hypersplenism leads to anemia. **NEET-PG High-Yield Pearls:** * **Most common cause:** Portal hypertension (due to Cirrhosis) is the leading cause of congestive splenomegaly and hypersplenism. * **Peripheral Smear:** Unlike hyposplenism (where you see Howell-Jolly bodies), hypersplenism typically shows a "clean" smear but with cytopenias. * **Treatment:** Splenectomy is only indicated if the cytopenia is symptomatic (e.g., severe bleeding or recurrent infections) or if the primary disease requires it.
Question 60: Macrocytic anemia is not seen in which of the following conditions?
- A. Vitamin B12 deficiency
- B. Hemolytic anemia
- C. Post-hemorrhagic anemia
- D. Anemia of chronic disease (Correct Answer)
Explanation: The classification of anemia is primarily based on the **Mean Corpuscular Volume (MCV)**. Macrocytic anemia is defined by an MCV >100 fL. **Why Anemia of Chronic Disease (ACD) is the correct answer:** ACD is typically a **normocytic, normochromic anemia**. In long-standing cases, it may progress to a **microcytic** pattern, but it is **never macrocytic** [2]. The pathophysiology involves high levels of **Hepcidin** (induced by IL-6), which sequesters iron in macrophages and decreases intestinal iron absorption, mimicking a functional iron deficiency [1]. **Why the other options are incorrect:** * **Vitamin B12 deficiency:** This is a classic cause of **megaloblastic macrocytic anemia** [1]. Lack of B12 impairs DNA synthesis, leading to nuclear-cytoplasmic asynchrony where the nucleus matures slower than the cytoplasm, resulting in large cells. * **Hemolytic Anemia & Post-hemorrhagic Anemia:** Both conditions trigger a robust bone marrow response, leading to **reticulocytosis** (increased young RBCs). Since reticulocytes are larger than mature erythrocytes, a high reticulocyte count falsely elevates the MCV, causing a **non-megaloblastic macrocytic** picture. **High-Yield Clinical Pearls for NEET-PG:** * **Megaloblastic Macrocytosis:** Characterized by hypersegmented neutrophils (≥5 lobes) on peripheral smear. Causes: B12/Folate deficiency, Drugs (Methotrexate, Phenytoin, Zidovudine). * **Non-megaloblastic Macrocytosis:** No hypersegmented neutrophils. Causes: Alcoholism (most common), Liver disease, Hypothyroidism, and Reticulocytosis. * **ACD Hallmark:** Low Serum Iron, **Low TIBC**, and **High/Normal Ferritin** (distinguishes it from Iron Deficiency Anemia where Ferritin is low).
Practice by Chapter
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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