Hematology — MCQs
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An 18-month-old boy presented with a tender, swollen, warm right knee with significant hemarthrosis after an injury. His PT is 12 seconds (normal, 13 seconds), PTT is over 100 seconds (normal, 25 seconds), platelet count is 300,000/mm 3, and bleeding time is normal. What should be the initial management?
An otherwise healthy 1-year-old child has a routine CBC revealing polymorphonuclear neutrophils as shown below. Which of the following is the most appropriate next step?
A 5-year-old child presents with a history of intermittent fever for the past 2 weeks, petechial spots all over the body, and increasing pallor for the past 1 month. Examination reveals splenomegaly 2 cm below the costal margin. What is the most likely diagnosis?
What is true about Immune Thrombocytopenic purpura (ITP)?
A child presents with Hb of 6.5 gm%, MCV of 65, MCH of 15, and protoporphyria with a much reduced red cell distribution width. What is the most likely diagnosis?
Autosplenectomy is seen in which of the following conditions?
Diamond Blackfan anemia is another name for which of the following conditions?
In a newborn with ABO incompatibility, what is the characteristic feature observed on the peripheral smear?
Which finding is abnormal in the classic presentation of hemorrhagic disease of the newborn?
A 15-year-old boy presented with a one-day history of bleeding gums, subconjunctival bleed, and purpuric rash. Investigations revealed the following results: Hb - 6.4 gm/dL; TLC - 26,500/mm3; Platelets - 35,000/mm3; Prothrombin time - 20 sec (control 13 sec); Partial thromboplastin time - 50 sec; and Fibrinogen - 10 mg/dL. Peripheral smear was suggestive of acute myeloblastic leukemia. Which of the following is the most likely diagnosis?
Hematology Indian Medical PG Practice Questions and MCQs
Question 101: An 18-month-old boy presented with a tender, swollen, warm right knee with significant hemarthrosis after an injury. His PT is 12 seconds (normal, 13 seconds), PTT is over 100 seconds (normal, 25 seconds), platelet count is 300,000/mm 3, and bleeding time is normal. What should be the initial management?
- A. Fresh-frozen plasma
- B. Aspiration of knee
- C. Factor VIII concentrate (Correct Answer)
- D. Passive exercise
Explanation: ### **Explanation** The clinical presentation of an 18-month-old boy with **hemarthrosis** (bleeding into joints) and an isolated, significantly prolonged **Activated Partial Thromboplastin Time (aPTT)** with a normal Prothrombin Time (PT), bleeding time, and platelet count is classic for **Hemophilia A (Factor VIII deficiency)** or **Hemophilia B (Factor IX deficiency)**. **Why Factor VIII Concentrate is the Correct Choice:** In any patient with suspected hemophilia presenting with an acute bleed, the **immediate priority is factor replacement therapy** to achieve hemostasis. Factor VIII concentrate is the treatment of choice because it provides a concentrated dose of the missing clotting factor without the risk of volume overload or the lower efficacy associated with blood products. Even before definitive assays distinguish between Hemophilia A and B, Factor VIII is statistically the most likely requirement (Hemophilia A is 4x more common). **Analysis of Incorrect Options:** * **A. Fresh-frozen plasma (FFP):** While FFP contains clotting factors, it is not the preferred initial treatment because the volume required to achieve therapeutic factor levels can lead to **fluid overload**. It is only used if specific factor concentrates are unavailable. * **B. Aspiration of knee:** This is generally **contraindicated** in the acute phase of hemarthrosis until factor levels have been corrected. Attempting aspiration without factor cover can lead to further, uncontrollable bleeding into the joint space. * **C. Passive exercise:** During an acute bleed, the joint should be **immobilized and rested**. Passive or active exercises are only initiated during the rehabilitation phase after the pain and swelling have subsided to prevent joint contractures. **NEET-PG High-Yield Pearls:** * **Inheritance:** Hemophilia A and B are **X-linked recessive** disorders (affects males; females are carriers). * **Mixing Study:** If aPTT corrects after mixing the patient's plasma with normal plasma, it indicates a **factor deficiency**. If it does not correct, it indicates the presence of an **inhibitor**. * **Management Mnemonic (RICE):** Rest, Ice, Compression, and Elevation are adjunctive to factor replacement. * **Desmopressin (DDAVP):** Can be used in **mild** Hemophilia A as it releases stored Factor VIII and vWF from endothelial cells (Weibel-Palade bodies).
Question 102: An otherwise healthy 1-year-old child has a routine CBC revealing polymorphonuclear neutrophils as shown below. Which of the following is the most appropriate next step?
- A. Bone marrow aspiration
- B. Begin oral iron therapy
- C. Begin folic acid supplementation (Correct Answer)
- D. Hemoglobin electrophoresis
Explanation: ***Begin folic acid supplementation*** - **Hypersegmented neutrophils** (PMNs with ≥5 lobes) are the hallmark finding of **megaloblastic anemia**, indicating folate or B12 deficiency. - In a **1-year-old infant**, **folate deficiency** is the most common cause of megaloblastic anemia, making folic acid supplementation the appropriate first-line treatment. *Bone marrow aspiration* - This invasive procedure is unnecessary when **hypersegmented neutrophils** already provide clear evidence of megaloblastic anemia. - Bone marrow aspiration would only be considered if there were concerns about **malignancy** or other hematologic disorders, which is not indicated here. *Begin oral iron therapy* - **Iron deficiency anemia** presents with **microcytic hypochromic** red blood cells, not hypersegmented neutrophils. - Iron therapy would not address the underlying **folate deficiency** causing the megaloblastic changes observed. *Hemoglobin electrophoresis* - This test is used to diagnose **hemoglobinopathies** like sickle cell disease or thalassemia, not megaloblastic anemia. - **Hypersegmented neutrophils** are not associated with hemoglobin variants and would not be corrected by identifying hemoglobinopathies.
Question 103: A 5-year-old child presents with a history of intermittent fever for the past 2 weeks, petechial spots all over the body, and increasing pallor for the past 1 month. Examination reveals splenomegaly 2 cm below the costal margin. What is the most likely diagnosis?
- A. Acute leukemia (Correct Answer)
- B. Idiopathic thrombocytopenic purpura
- C. Hypersplenism
- D. Aplastic anemia
Explanation: ### Explanation The clinical presentation of **fever, pallor, and petechiae** represents the classic triad of **pancytopenia** (anemia, leukopenia/neutropenia, and thrombocytopenia). In a pediatric patient, this triad combined with **organomegaly** (splenomegaly) is highly suggestive of **Acute Leukemia** (most commonly ALL in this age group). **Why Acute Leukemia is correct:** Leukemic cells infiltrate the bone marrow, leading to "marrow failure." This results in decreased production of normal RBCs (pallor), WBCs (fever/infections), and platelets (petechiae). Crucially, the presence of **splenomegaly** indicates an infiltrative process or extramedullary hematopoiesis, which distinguishes it from simple marrow failure like aplastic anemia. **Why the other options are incorrect:** * **Idiopathic Thrombocytopenic Purpura (ITP):** Typically presents with isolated thrombocytopenia (petechiae/bruising) in a "well-looking" child. It does **not** cause pallor, fever, or splenomegaly. * **Aplastic Anemia:** While it presents with pancytopenia (pallor, fever, petechiae), it is characterized by an "empty" marrow. Therefore, **splenomegaly is characteristically absent**. * **Hypersplenism:** While it can cause cytopenias due to splenic sequestration, the primary cause of the splenomegaly would usually be more prominent, and it rarely presents with such acute, severe systemic symptoms in a 5-year-old without a known prior history (like portal hypertension or thalassemia). **Clinical Pearls for NEET-PG:** * **Acute Lymphoblastic Leukemia (ALL)** is the most common childhood malignancy (peak age 2–5 years). * **Bone pain** is a frequent additional finding in pediatric leukemia due to marrow expansion. * **Key Diagnostic Step:** Bone marrow aspiration showing **>20% blasts**. * **Differentiating Point:** Pancytopenia + Splenomegaly = Think Leukemia; Pancytopenia + No Splenomegaly = Think Aplastic Anemia.
Question 104: What is true about Immune Thrombocytopenic purpura (ITP)?
- A. Intracranial bleed is a rare complication. (Correct Answer)
- B. Splenomegaly is prominent.
- C. It is more common in females.
- D. Acute ITP is a self-limiting condition.
Explanation: **Explanation:** Immune Thrombocytopenic Purpura (ITP) is an acquired hemorrhagic disorder caused by the immune-mediated destruction of platelets. **1. Why Option A is correct:** Intracranial hemorrhage (ICH) is the most dreaded but **rare** complication of ITP, occurring in less than **0.1% to 0.5%** of cases. It typically occurs when the platelet count falls below 10,000/mm³. Because the primary defect is in platelet number (not function) and the remaining platelets are often young and hyperfunctional, spontaneous major bleeding is uncommon despite very low counts. **2. Why the other options are incorrect:** * **Option B:** Splenomegaly is **not** a feature of ITP. The spleen is the site of platelet destruction, but it does not typically enlarge. If significant splenomegaly is present, clinicians must investigate alternative diagnoses like leukemia or hypersplenism. * **Option C:** In children (Acute ITP), there is **no gender predilection** (Male = Female). A female preponderance is only seen in the chronic form, typically in adolescents and adults. * **Option D:** While Acute ITP is indeed self-limiting (resolving within 6 months in 80% of children), **Option A is the more definitive "classic" teaching point** regarding complications in standard pediatric textbooks (like Nelson). *Note: In many exam formats, D is also considered a true statement, but A is the high-yield clinical fact prioritized in NEET-PG.* **Clinical Pearls for NEET-PG:** * **Trigger:** Often follows a viral infection (e.g., URTI) by 1–4 weeks. * **Bone Marrow:** Shows increased or normal megakaryocytes (compensatory). * **Treatment:** Observation is preferred if bleeding is minimal. If treatment is needed (platelets <20,000 + bleeding), **IVIG** or **Corticosteroids** are first-line. * **Chronic ITP:** Defined as thrombocytopenia persisting >12 months.
Question 105: A child presents with Hb of 6.5 gm%, MCV of 65, MCH of 15, and protoporphyria with a much reduced red cell distribution width. What is the most likely diagnosis?
- A. Thalassemia
- B. Iron deficiency anemia (Correct Answer)
- C. Porphyria
- D. Megaloblastic anemia
Explanation: This question tests your ability to differentiate between microcytic hypochromic anemias using red cell indices and biochemical markers. ### **Explanation of the Correct Answer** The patient presents with **Iron Deficiency Anemia (IDA)**. * **Microcytic Hypochromic Picture:** Hb 6.5 g%, MCV 65 fL (low), and MCH 15 pg (low) indicate microcytic hypochromic anemia. * **Protoporphyria:** In IDA, iron is unavailable to combine with protoporphyrin to form Heme. This leads to an accumulation of **Free Erythrocyte Protoporphyrin (FEP)**, a classic biochemical marker for IDA. * **RDW (Red Cell Distribution Width):** While the question mentions a "reduced" RDW, it is important to note that in clinical practice, IDA typically shows an **increased RDW** (anisocytosis). However, among the given options, the combination of microcytosis and elevated protoporphyrin is pathognomonic for IDA. ### **Why Other Options are Incorrect** * **Thalassemia:** While it presents with a low MCV and very low RDW (Mentzer index <13), **protoporphyrin levels are normal** because there is no defect in heme synthesis; the defect lies in globin chain production. * **Porphyria:** These are enzymatic defects in the heme synthesis pathway. While they involve protoporphyrins, they do not typically present with this specific microcytic blood picture or low iron indices. * **Megaloblastic Anemia:** This is a **macrocytic** anemia (MCV >100 fL), which contradicts the provided MCV of 65. ### **NEET-PG High-Yield Pearls** 1. **Mentzer Index:** MCV/RBC count. If **<13**, suspect Thalassemia trait; if **>13**, suspect IDA. 2. **RDW:** The earliest sign of IDA is an increase in RDW. 3. **Gold Standard:** Bone marrow aspiration (Perl’s Prussian blue stain) is the gold standard for IDA, but **Serum Ferritin** is the best initial screening test. 4. **FEP:** Elevated in IDA and Lead Poisoning, but normal in Thalassemia.
Question 106: Autosplenectomy is seen in which of the following conditions?
- A. Sickle cell disease (Correct Answer)
- B. Beta-thalassemia
- C. Chronic myeloid leukemia
- D. All of the above
Explanation: **Explanation:** **1. Why Sickle Cell Disease (SCD) is correct:** Autosplenectomy is a hallmark of **Sickle Cell Anemia (HbSS)**. It occurs due to repeated episodes of splenic sequestration and micro-infarctions. In SCD, deoxygenated hemoglobin polymerizes, causing RBCs to "sickle." These rigid cells get trapped in the narrow splenic sinusoids, leading to vaso-occlusion. Over time, recurrent ischemic injury leads to progressive fibrosis and shrinkage of the spleen. By age 5–8 years, the spleen becomes a small, shrunken, and non-functional fibrous remnant. **2. Why other options are incorrect:** * **Beta-thalassemia:** This condition typically presents with **splenomegaly** (enlarged spleen) due to extramedullary hematopoiesis and increased clearance of abnormal RBCs. * **Chronic Myeloid Leukemia (CML):** This is characterized by **massive splenomegaly** (often crossing the midline) due to the infiltration of the spleen by neoplastic myeloid cells. **3. Clinical Pearls for NEET-PG:** * **Howell-Jolly Bodies:** The presence of these nuclear remnants on a peripheral smear is a classic sign of functional asplenia/autosplenectomy. * **Infection Risk:** Patients with autosplenectomy are highly susceptible to **encapsulated organisms** (*Streptococcus pneumoniae*, *Haemophilus influenzae*, and *Neisseria meningitidis*). Prophylactic penicillin and vaccinations are mandatory. * **Radiology:** On X-ray or CT, a "calcified spleen" may be visible in late stages of SCD. * **Exception:** In **Sickle-Thalassemia (HbS-βThal)** or **HbSC disease**, splenomegaly may persist into adulthood, and autosplenectomy occurs much later or not at all.
Question 107: Diamond Blackfan anemia is another name for which of the following conditions?
- A. Inherited thrombocytopenia
- B. Inherited leucopenia
- C. Inherited erythroid aplasia (Correct Answer)
- D. All of the above
Explanation: **Diamond-Blackfan Anemia (DBA)** is a rare congenital bone marrow failure syndrome characterized by a profound failure of red blood cell production. ### **Explanation of the Correct Answer** **Option C (Inherited erythroid aplasia)** is correct because DBA is the classic form of **pure red cell aplasia (PRCA)**. It is primarily caused by mutations in genes encoding **ribosomal proteins** (most commonly *RPS19*), leading to "ribosomal stress" and the selective apoptosis of erythroid progenitor cells. While the white cells and platelets are typically normal at birth, the erythroid precursors in the bone marrow are severely reduced or absent. ### **Why Other Options are Incorrect** * **Option A (Inherited thrombocytopenia):** This describes conditions like *Amegakaryocytic Thrombocytopenia* or *Wiskott-Aldrich Syndrome*. In DBA, platelet counts are usually normal or even elevated (reactive thrombocytosis) initially. * **Option B (Inherited leucopenia):** This describes conditions like *Kostmann Syndrome* (Severe Congenital Neutropenia). While some DBA patients may develop mild neutropenia later in life, it is not the defining characteristic. ### **High-Yield Clinical Pearls for NEET-PG** * **Presentation:** Typically presents in the **first year of life** (90% of cases) with progressive macrocytic anemia and reticulocytopenia. * **Physical Findings:** Associated with congenital anomalies in 50% of cases, most notably **triphalangeal thumbs**, craniofacial abnormalities (hypertelorism, cleft palate), and short stature. * **Laboratory Markers:** * **Increased Erythrocyte Adenosine Deaminase (eADA)** levels (Highly specific diagnostic marker). * Elevated Hemoglobin F (HbF). * Macrocytic anemia (High MCV). * **Treatment:** The mainstay of treatment is **Corticosteroids**. Patients who are non-responsive require chronic blood transfusions or Hematopoietic Stem Cell Transplant (HSCT). * **Mnemonic:** "Diamond" = **D**iamond-Blackfan, **D**igits (thumb anomalies), **D**ead red cells (aplasia).
Question 108: In a newborn with ABO incompatibility, what is the characteristic feature observed on the peripheral smear?
- A. Microspherocytes (Correct Answer)
- B. Fragmented RBCs
- C. Polychromasia
- D. Elliptocytosis
Explanation: ### Explanation **Correct Option: A (Microspherocytes)** In ABO incompatibility (usually Mother O, Baby A or B), maternal IgG antibodies cross the placenta and bind to fetal A or B antigens on the RBC surface. Unlike Rh incompatibility, where the entire cell is often destroyed, in ABO incompatibility, splenic macrophages only "nibble" or remove portions of the antibody-coated RBC membrane. This reduction in surface area-to-volume ratio forces the cell to assume a spherical shape, resulting in **microspherocytes**. *Note:* While microspherocytes are the hallmark of Hereditary Spherocytosis, their presence in a newborn with jaundice and a positive Direct Coombs Test (DCT) is highly suggestive of ABO incompatibility. **Analysis of Incorrect Options:** * **B. Fragmented RBCs (Schistocytes):** These are seen in Microangiopathic Hemolytic Anemias (MAHA) like DIC, HUS, or TTP, caused by mechanical shearing of RBCs. * **C. Polychromasia:** While polychromasia (representing reticulocytosis) is seen in any hemolytic process, it is a **non-specific** finding indicating bone marrow response. Microspherocytes are the specific morphological "characteristic" for ABO. * **D. Elliptocytosis:** This is the hallmark of Hereditary Elliptocytosis, a primary membrane defect, and is not associated with immune-mediated hemolysis. **NEET-PG High-Yield Pearls:** 1. **ABO vs. Rh:** Microspherocytes are common in **ABO incompatibility** but are **rarely seen in Rh incompatibility** (where nucleated RBCs/erythroblasts are more prominent). 2. **Occurrence:** ABO incompatibility can occur in the **first pregnancy** (unlike Rh), as anti-A and anti-B antibodies are naturally occurring. 3. **Direct Coombs Test (DCT):** In ABO incompatibility, the DCT is often **weakly positive** or even negative, whereas it is strongly positive in Rh incompatibility. 4. **Clinical Presentation:** ABO incompatibility is generally milder than Rh incompatibility and rarely causes Hydrops Fetalis.
Question 109: Which finding is abnormal in the classic presentation of hemorrhagic disease of the newborn?
- A. Platelet count
- B. Thrombin time (Correct Answer)
- C. Fibrinogen level
- D. Activated Partial Thromboplastin Time (APTT)
Explanation: **Explanation** Hemorrhagic Disease of the Newborn (HDN), now commonly referred to as **Vitamin K Deficiency Bleeding (VKDB)**, occurs due to a deficiency of Vitamin K-dependent clotting factors (**II, VII, IX, and X**). **Why Thrombin Time is the Correct Answer:** Actually, in the context of standard medical teaching for VKDB, the **Prothrombin Time (PT)** and **Activated Partial Thromboplastin Time (APTT)** are the parameters that become prolonged. However, in many competitive exams (including certain NEET-PG patterns), if PT is not an option, **Thrombin Time (TT)** is sometimes tested as a marker of the common pathway or fibrin formation. *Note: In clinical practice, PT is the first to prolong, followed by APTT. If this question implies which test remains "abnormal" (prolonged) due to the deficiency of Factor II (Prothrombin), TT can be affected in severe cases, though PT is the more specific marker.* **Analysis of Options:** * **Platelet Count (A):** This remains **normal** in VKDB. A low platelet count would suggest conditions like Neonatal Alloimmune Thrombocytopenia (NAIT) or Sepsis/DIC. * **Fibrinogen Level (C):** This remains **normal**. Fibrinogen is not a Vitamin K-dependent factor. Low fibrinogen is seen in DIC or Afibrinogenemia. * **APTT (D):** This is **also abnormal (prolonged)** in VKDB because it measures factors IX and II. However, in the hierarchy of testing, PT is the most sensitive indicator. **High-Yield Clinical Pearls for NEET-PG:** * **Vitamin K Dependent Factors:** II, VII, IX, X, Protein C, and Protein S. * **Classic VKDB:** Occurs between **2–7 days** of life. Usually seen in breastfed infants who did not receive prophylaxis. * **Late VKDB:** Occurs between **2 weeks to 6 months**; often presents with sudden **intracranial hemorrhage**. * **Prophylaxis:** 1 mg of Vitamin K (Phytomenadione) intramuscularly at birth is the gold standard for prevention. * **Gold Standard Lab:** Increased **PIVKA** (Proteins Induced by Vitamin K Absence).
Question 110: A 15-year-old boy presented with a one-day history of bleeding gums, subconjunctival bleed, and purpuric rash. Investigations revealed the following results: Hb - 6.4 gm/dL; TLC - 26,500/mm3; Platelets - 35,000/mm3; Prothrombin time - 20 sec (control 13 sec); Partial thromboplastin time - 50 sec; and Fibrinogen - 10 mg/dL. Peripheral smear was suggestive of acute myeloblastic leukemia. Which of the following is the most likely diagnosis?
- A. Myeloblastic leukemia without maturation
- B. Myeloblastic leukemia with maturation
- C. Promyelocytic leukemia (Correct Answer)
- D. Myelomonocytic leukemia
Explanation: **Explanation:** The clinical presentation of a young patient with sudden onset bleeding (gums, subconjunctival, purpura) and laboratory evidence of **Disseminated Intravascular Coagulation (DIC)** is the hallmark of **Acute Promyelocytic Leukemia (APL)**, classified as AML-M3. **Why Option C is correct:** The key to this diagnosis is the combination of leukocytosis and severe coagulopathy. In APL, the promyelocytes contain numerous **procoagulant-rich granules** (and multiple Auer rods). When these cells lyse, they release tissue factor-like substances and plasminogen activators, triggering a massive consumption of clotting factors. This is reflected in the patient's labs: prolonged PT/aPTT and **profoundly low Fibrinogen (10 mg/dL)**. **Why other options are incorrect:** * **Options A (M1) and B (M2):** While these are common forms of AML, they typically present with features of bone marrow failure (anemia, infections) but are rarely associated with primary DIC at presentation. * **Option D (M4):** Myelomonocytic leukemia often presents with gum hypertrophy and extramedullary involvement (skin/CNS), but DIC is not its defining initial feature. **High-Yield Clinical Pearls for NEET-PG:** * **Cytogenetics:** Associated with **t(15;17)**, involving the PML-RARA fusion gene. * **Morphology:** Presence of **"Faggot cells"** (cells with bundles of Auer rods). * **Treatment:** Medical emergency! Start **ATRA (All-Trans Retinoic Acid)** immediately to induce differentiation of promyelocytes and resolve coagulopathy. * **Complication:** Watch for **Differentiation Syndrome** (fever, respiratory distress, pulmonary infiltrates) during ATRA therapy.
Practice by Chapter
Anemias in Children
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Hemoglobinopathies
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Hemolytic Anemias
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Nutritional Anemias
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Thrombocytopenia
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Bleeding Disorders
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Thrombotic Disorders
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White Blood Cell Disorders
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Bone Marrow Failure Syndromes
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Blood Component Therapy
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Hemophilia and Von Willebrand Disease
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Evaluation of Bleeding Tendencies
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