Hematology — MCQs
On this page
Anemia of chronic disease is differentiated from iron deficiency anemia by the presence of?
Which of the following statements about coagulation factor VII is not true?
An 18-year-old man develops excessive bleeding 2 hours after wisdom tooth extraction. He has a history of easy bruising after playing sports, and of minor cuts that rebleed. His examination is normal, except for the tooth extraction site, which is still oozing blood. His hemoglobin is 14.8 g/dL, platelets 230,000 mL, PT is normal, and partial thromboplastin time (PTT) is elevated. A bleeding time is normal, factor VIII level is reduced, factor IX is normal, and ristocetin cofactor assay is normal. For the above patient with a bleeding disorder, select the most likely diagnosis?
Recurrent spontaneous hemarthrosis is commonly seen in patients with hemophilia when factor VIII levels are:
Which of the following is NOT true about Hemophilia A?
Anti-parietal cell antibodies are found in patients with?
A 39-year-old man with chronic alcoholism presents with a hemoglobin of 9.6 g/dL. His platelets and WBC are normal. Additional tests, including ferritin, vitamin B12, and folate levels, are also normal. Which of the following findings is most likely to be seen on his peripheral blood film?
Paroxysmal Nocturnal Hemoglobinuria (PNH) is associated with a deficiency of which of the following?
A 15-year-old boy presented with a 1-day history of bleeding gums, subconjunctival bleed, and purpuric rash. Investigations revealed: Hb 6.4 gm/dL; TLC-26,500/mm3; prothrombin time-20 sec with a control of 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 60-year-old man presented with fatigue, weight loss, and heaviness in the left hypochondrium for 6 months. The hemogram showed Hb 10 gm/dL, TLC 5 lakhs/mm3, platelet count 4 lakhs/mm3, and DLC showed neutrophils 55%, lymphocytes 4%, monocytes 2%, basophils 6%, metamyelocytes 10%, myelocytes 18%, promyelocytes 2%, and blasts 3%. What is the most likely cytogenetic abnormality in this case?
Hematology Indian Medical PG Practice Questions and MCQs
Question 431: Anemia of chronic disease is differentiated from iron deficiency anemia by the presence of?
- A. TIBC
- B. Low serum iron (Correct Answer)
- C. Serum ferritin
- D. Bone marrow iron store
Explanation: **Explanation:** The differentiation between **Anemia of Chronic Disease (ACD)** and **Iron Deficiency Anemia (IDA)** is a high-yield topic for NEET-PG. While both conditions can present as microcytic hypochromic anemia with low serum iron, the fundamental difference lies in iron utilization versus iron availability [3]. **Why "Low Serum Iron" is the Correct Answer (Contextualizing the Question):** In the context of this specific question, **Low Serum Iron** is the shared feature that often confuses the two; however, the question asks what differentiates them. In clinical practice, both have low serum iron, but the *mechanism* differs. In ACD, iron is trapped within macrophages due to high **Hepcidin** levels (an acute-phase reactant), leading to low circulating iron despite adequate stores [1], [2]. **Analysis of Options:** * **Serum Ferritin (Option C):** This is the **best non-invasive test** to differentiate the two. Ferritin is low in IDA (depleted stores) but normal or high in ACD (sequestration/inflammation) [3]. * **Bone Marrow Iron Store (Option D):** This is the **Gold Standard** for differentiation. In IDA, Prussian blue staining shows absent marrow iron; in ACD, marrow iron is abundant but trapped in macrophages [3]. * **TIBC (Option A):** Total Iron Binding Capacity is high in IDA (the body wants more iron) and low/normal in ACD. *Note: While Serum Ferritin and Bone Marrow stores are superior discriminators, "Low Serum Iron" is often used in older question banks to highlight that ACD is a "sideropenic" anemia despite normal stores." **NEET-PG High-Yield Pearls:** 1. **Hepcidin:** The key mediator in ACD; it degrades ferroportin, preventing iron release [2]. 2. **sTfR (Soluble Transferrin Receptor):** Elevated in IDA, but **normal** in ACD. This is an excellent marker when ACD and IDA coexist. 3. **Mentzer Index:** Used to differentiate IDA from Thalassemia (MCV/RBC count <13 suggests Thalassemia).
Question 432: Which of the following statements about coagulation factor VII is not true?
- A. Deficiency is associated with prolonged APTT (Correct Answer)
- B. Deficiency can be managed by Fresh Frozen Plasma
- C. Deficiency is inherited as an Autosomal Recessive trait
- D. Has a short half-life in comparison to Hageman factor (XII)
Explanation: Factor VII (Proconvertin) is a vitamin K-dependent protease that plays a pivotal role in the Extrinsic Pathway of the coagulation cascade. 1. Why Option A is the Correct Answer (The False Statement): The Activated Partial Thromboplastin Time (APTT) measures the integrity of the Intrinsic and Common pathways (Factors XII, XI, IX, VIII, X, V, II, and I). Since Factor VII is uniquely part of the Extrinsic Pathway, its deficiency will result in a prolonged Prothrombin Time (PT) but a normal APTT [1]. Therefore, the statement that deficiency is associated with prolonged APTT is incorrect. 2. Analysis of Other Options: * Option B: Fresh Frozen Plasma (FFP) contains all coagulation factors, including Factor VII. It is a standard treatment for factor deficiencies when specific concentrates are unavailable. * Option C: Congenital Factor VII deficiency (Hypoconvertinemia) is a rare bleeding disorder inherited in an Autosomal Recessive pattern [2]. * Option D: Factor VII has the shortest half-life (approximately 4–6 hours) of all clotting factors. In contrast, Factor XII (Hageman factor) has a much longer half-life (approximately 48–52 hours). Clinical Pearls for NEET-PG: * Isolated PT prolongation with a normal APTT is the hallmark of Factor VII deficiency or early Vitamin K deficiency/Warfarin therapy (as Factor VII levels drop first) [1]. * Factor VII is the first factor to decrease in liver disease due to its short half-life, making PT a sensitive marker for acute liver protein synthesis. * Treatment: Recombinant activated Factor VII (rFVIIa) is the preferred treatment for severe bleeding or surgery in these patients.
Question 433: An 18-year-old man develops excessive bleeding 2 hours after wisdom tooth extraction. He has a history of easy bruising after playing sports, and of minor cuts that rebleed. His examination is normal, except for the tooth extraction site, which is still oozing blood. His hemoglobin is 14.8 g/dL, platelets 230,000 mL, PT is normal, and partial thromboplastin time (PTT) is elevated. A bleeding time is normal, factor VIII level is reduced, factor IX is normal, and ristocetin cofactor assay is normal. For the above patient with a bleeding disorder, select the most likely diagnosis?
- A. von Willebrand disease
- B. hemophilia A (Correct Answer)
- C. hemophilia B
- D. thrombotic thrombocytopenic purpura (TTP)
Explanation: ### Explanation **1. Why Hemophilia A is Correct:** The clinical presentation of delayed bleeding after a minor procedure (wisdom tooth extraction) and easy bruising is characteristic of a **coagulation factor deficiency** [1]. * **Laboratory Profile:** The patient has an isolated **elevated PTT** with a **normal PT** and **normal Platelet count**, which narrows the pathology to the intrinsic pathway (Factors VIII, IX, XI, or XII) [5]. * **Definitive Finding:** The **reduced Factor VIII level** combined with a **normal Ristocetin Cofactor Assay** (which measures von Willebrand Factor activity) confirms the diagnosis of Hemophilia A (Factor VIII deficiency). **2. Why Other Options are Incorrect:** * **von Willebrand Disease (vWD):** While vWD also presents with low Factor VIII and elevated PTT, it typically features a **prolonged Bleeding Time** and an **abnormal Ristocetin Cofactor Assay** [4]. * **Hemophilia B:** This is a deficiency of **Factor IX**. In this case, Factor IX levels were specifically noted as normal. * **Thrombotic Thrombocytopenic Purpura (TTP):** TTP is a microangiopathic hemolytic anemia characterized by thrombocytopenia (low platelets) and schistocytes. This patient has a normal platelet count and normal hemoglobin [2]. **3. NEET-PG High-Yield Pearls:** * **Inheritance:** Hemophilia A and B are **X-linked recessive** (mostly affecting males) [2], whereas most types of vWD are Autosomal Dominant. * **Bleeding Pattern:** Hemophilia typically presents with "deep" bleeding (hemarthrosis, hematomas, delayed post-surgical bleed), whereas vWD and platelet disorders present with "superficial" bleeding (epistaxis, petechiae, immediate mucosal bleed) [1]. * **Mixing Study:** If PTT is prolonged, a mixing study is the next step. If it corrects, it indicates a factor deficiency; if not, it suggests an inhibitor [5]. * **Treatment:** Recombinant Factor VIII is the mainstay for Hemophilia A; Desmopressin (DDAVP) can be used in mild cases to release stored Factor VIII/vWF [3].
Question 434: Recurrent spontaneous hemarthrosis is commonly seen in patients with hemophilia when factor VIII levels are:
- A. < 36%
- B. < 10%
- C. < 5% (Correct Answer)
- D. < 1%
Explanation: **Explanation:** The severity of Hemophilia (A or B) is directly correlated with the plasma concentration of the deficient clotting factor (Factor VIII or IX). This classification is crucial for predicting clinical manifestations and determining treatment protocols. **1. Why < 5% is the correct answer:** Hemophilia is categorized into three clinical grades: * **Severe (< 1% activity):** Characterized by frequent spontaneous bleeds into joints (hemarthrosis) and muscles [1]. * **Moderate (1% to 5% activity):** Patients experience bleeding after minor trauma, but **recurrent spontaneous hemarthrosis** is a hallmark of this group and those below it [1]. * **Mild (> 5% to 40% activity):** Bleeding usually occurs only after significant trauma or surgery; spontaneous hemarthrosis is rare. Therefore, the threshold for recurrent spontaneous joint bleeds is generally seen when factor levels fall **below 5%** (encompassing both moderate and severe categories). **2. Analysis of Incorrect Options:** * **Option A (< 36%):** This is near the lower limit of normal (50-150%). Patients with 36% activity are usually asymptomatic or only bleed during major surgery. * **Option B (< 10%):** While patients with 10% activity have "Mild Hemophilia," they typically do not experience *spontaneous* hemarthrosis. * **Option D (< 1%):** While spontaneous bleeding definitely occurs at < 1%, this option is too restrictive. The clinical threshold for recurrent spontaneous bleeds includes the "Moderate" range (up to 5%). **High-Yield Clinical Pearls for NEET-PG:** * **Most common joint involved:** Knee (followed by elbow and ankle) [1]. * **Target Joint:** A joint that has had $\geq$ 3 spontaneous bleeds within 6 months. * **Treatment of choice:** Recombinant factor replacement [1]. * **Mixing Study:** In Hemophilia, the prolonged aPTT **corrects** upon mixing with normal plasma (distinguishes it from factor inhibitors).
Question 435: Which of the following is NOT true about Hemophilia A?
- A. Fibrinogen-to-thrombin time (FIT) is increased
- B. Prothrombin time (PT) is increased (Correct Answer)
- C. Clotting time is increased
- D. Serum levels of Factor VIII are decreased
Explanation: **Explanation:** Hemophilia A is an X-linked recessive bleeding disorder caused by a deficiency or dysfunction of **Coagulation Factor VIII** [1]. To answer this question, one must understand the coagulation cascade and which laboratory tests evaluate specific pathways [2]. **Why Option B is the Correct Answer (The False Statement):** Prothrombin Time (PT) measures the **Extrinsic** and **Common pathways** (Factors VII, X, V, II, and I) [2]. Since Factor VIII is part of the **Intrinsic pathway**, its deficiency does not affect the PT. Therefore, PT remains **normal** in Hemophilia A [2]. **Analysis of Other Options:** * **Option A (Fibrinogen-to-thrombin time/Clotting dynamics):** While "FIT" is a less common term, in the context of hemophilia, any deficiency in the intrinsic pathway delays the generation of thrombin, which is essential for converting fibrinogen to fibrin. * **Option C (Clotting Time):** Clotting time is a global measure of the time required for blood to coagulate. In Hemophilia A, the defect in the intrinsic pathway significantly prolongs the clotting time. * **Option D (Factor VIII levels):** This is the hallmark of the disease [1]. Hemophilia A is defined by decreased serum levels of Factor VIII. **High-Yield Clinical Pearls for NEET-PG:** * **Lab Profile:** Prolonged aPTT (Activated Partial Thromboplastin Time) + Normal PT + Normal Bleeding Time + Normal Platelet Count [2]. * **Mixing Study:** If aPTT corrects after mixing the patient's plasma with normal plasma, it indicates a factor deficiency (like Hemophilia) [2]. If it does not correct, it suggests an inhibitor (like Lupus Anticoagulant). * **Clinical Presentation:** Characterized by deep tissue bleeding, **hemarthrosis** (bleeding into joints), and postsurgical bleeding. * **Treatment:** Recombinant Factor VIII concentrate; Desmopressin (DDAVP) can be used in mild cases to release stored Factor VIII from endothelial cells [3].
Question 436: Anti-parietal cell antibodies are found in patients with?
- A. Good-pasture syndrome.
- B. Primary biliary cirrhosis
- C. Wegener granulomatosis.
- D. Pernicious anemia (Correct Answer)
Explanation: Pernicious anemia is an autoimmune condition characterized by the destruction of gastric parietal cells or the neutralization of Intrinsic Factor (IF). [1] **Anti-parietal cell antibodies (APCA)** are found in approximately 90% of these patients. These antibodies target the H+/K+ ATPase pump in the parietal cells of the gastric fundus and body, leading to chronic atrophic gastritis (Type A), achlorhydria, and vitamin B12 malabsorption. Analysis of Incorrect Options: Goodpasture Syndrome: This is characterized by anti-GBM antibodies targeting the alpha-3 chain of Type IV collagen in the glomerular and alveolar basement membranes, leading to pulmonary hemorrhage and glomerulonephritis. Primary Biliary Cirrhosis (PBC): The hallmark diagnostic marker is Anti-mitochondrial antibodies (AMA). It involves autoimmune destruction of the small intrahepatic bile ducts. Wegener Granulomatosis (GPA): This small-vessel vasculitis is strongly associated with c-ANCA (PR3-ANCA), not anti-parietal antibodies.
Question 437: A 39-year-old man with chronic alcoholism presents with a hemoglobin of 9.6 g/dL. His platelets and WBC are normal. Additional tests, including ferritin, vitamin B12, and folate levels, are also normal. Which of the following findings is most likely to be seen on his peripheral blood film?
- A. Macrocytosis (Correct Answer)
- B. Basophilia
- C. Red cell fragments
- D. Increased platelet adhesiveness
Explanation: The correct answer is **Macrocytosis (Option A)**. In a patient with chronic alcoholism and anemia, macrocytosis (increased Mean Corpuscular Volume or MCV) is the most common hematologic finding [1]. While macrocytosis is often associated with Vitamin B12 or Folate deficiency (megaloblastic anemia), it frequently occurs in alcoholics even when these levels are **normal** [1]. **The underlying mechanism:** Alcohol has a direct toxic effect on the bone marrow and interferes with erythrocyte membrane lipid metabolism, leading to an increased surface area-to-volume ratio. This results in "non-megaloblastic" macrocytosis, characterized by round macrocytes rather than the oval macrocytes seen in B12/Folate deficiency [2]. **Why other options are incorrect:** * **Basophilia (Option B):** Associated with myeloproliferative disorders (e.g., CML) or lead poisoning, not typically seen in chronic alcoholism. * **Red cell fragments (Option C):** These (schistocytes) are markers of microangiopathic hemolytic anemia (MAHA) or mechanical heart valve destruction, not alcohol toxicity. * **Increased platelet adhesiveness (Option D):** Alcohol actually **decreases** platelet aggregation and function, often leading to a mild bleeding tendency despite normal platelet counts. **High-Yield Clinical Pearls for NEET-PG:** 1. **Most common cause of Macrocytosis:** Alcohol consumption (even in the absence of anemia) [1]. 2. **MCV in Alcoholism:** Usually ranges between 100–110 fL. 3. **Target Cells:** May also be seen in alcoholic liver disease due to increased cholesterol deposition in the RBC membrane. 4. **Sideroblastic Anemia:** Chronic alcohol use can also cause ringed sideroblasts in the bone marrow due to interference with heme synthesis [2].
Question 438: Paroxysmal Nocturnal Hemoglobinuria (PNH) is associated with a deficiency of which of the following?
- A. DAF (Decay Accelerating Factor)
- B. MIRL (Membrane Inhibitor of Ribonucleic acid synthesis)
- C. GPI anchored protein
- D. All of the above (Correct Answer)
Explanation: **Explanation:** **Paroxysmal Nocturnal Hemoglobinuria (PNH)** is an acquired clonal hematopoietic stem cell disorder caused by a somatic mutation in the **PIGA (Phosphatidylinositol Glycan class A) gene**. This mutation leads to a deficiency in the **GPI (Glycosylphosphatidylinositol) anchor**, which is essential for attaching various protective proteins to the cell membrane of red blood cells, leukocytes, and platelets. * **Option C (GPI anchored protein):** This is the fundamental defect. Without the GPI anchor, cells cannot express specific surface proteins that protect them from the body's own complement system. * **Option A (DAF/CD55):** Decay Accelerating Factor is a GPI-anchored protein. Its absence prevents the inactivation of C3 convertase, leading to increased complement activation. * **Option B (MIRL/CD59):** Membrane Inhibitor of Reactive Lysis is also a GPI-anchored protein. It normally inhibits the formation of the **Membrane Attack Complex (MAC)**. Its deficiency is the primary cause of the intravascular hemolysis seen in PNH. Since both DAF and MIRL are specific types of GPI-anchored proteins that are deficient in this condition, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Flow Cytometry (shows absence of CD55 and CD59 on RBCs/WBCs). * **Classic Triad:** Hemolytic anemia, Pancytopenia, and Venous thrombosis (often in unusual sites like the Budd-Chiari syndrome). * **Screening Test:** Ham’s Test (Acidified Serum Test) or Sucrose Lysis Test (Historical; largely replaced by flow cytometry). * **Treatment:** Eculizumab (a monoclonal antibody against C5) is the drug of choice. * **Complications:** PNH has a known risk of transforming into **Acute Myeloid Leukemia (AML)** or Aplastic Anemia.
Question 439: A 15-year-old boy presented with a 1-day history of bleeding gums, subconjunctival bleed, and purpuric rash. Investigations revealed: Hb 6.4 gm/dL; TLC-26,500/mm3; prothrombin time-20 sec with a control of 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) combined with a high white cell count and profound coagulopathy is classic for **Acute Promyelocytic Leukemia (APL)**, formerly classified as FAB M3 [1], [3]. **1. Why Promyelocytic Leukemia is Correct:** The hallmark of APL is the association with **Disseminated Intravascular Coagulation (DIC)** [2]. This is evidenced in the question by the prolonged PT (20s), prolonged PTT (50s), and critically low fibrinogen (10 mg/dL; normal: 200–400 mg/dL). In APL, the primary granules of the malignant promyelocytes contain procoagulants and fibrinolytic enzymes (like annexin II) that trigger a massive consumptive coagulopathy upon release. **2. Why Other Options are Incorrect:** * **A & B (M1 & M2):** While these are common subtypes of AML, they typically present with signs of bone marrow failure (anemia, infections) [1]. While they can cause thrombocytopenia, they rarely present with such severe, primary DIC at the time of diagnosis. * **D (M4):** Myelomonocytic leukemia is often associated with extramedullary involvement (e.g., gingival hyperplasia or CNS involvement) rather than the severe consumptive coagulopathy seen here [3]. **3. High-Yield Pearls for NEET-PG:** * **Cytogenetics:** Associated with **t(15;17)**, involving the **PML-RARA** fusion gene. * **Morphology:** Characterized by **Auer rods** (often in bundles called **Faggot cells**). * **Treatment:** Medical emergency! Start **ATRA (All-trans retinoic acid)** or Arsenic Trioxide immediately to differentiate the blasts and resolve DIC. * **Complication:** Watch for **Differentiation Syndrome** (fever, dyspnea, pulmonary infiltrates) during treatment.
Question 440: A 60-year-old man presented with fatigue, weight loss, and heaviness in the left hypochondrium for 6 months. The hemogram showed Hb 10 gm/dL, TLC 5 lakhs/mm3, platelet count 4 lakhs/mm3, and DLC showed neutrophils 55%, lymphocytes 4%, monocytes 2%, basophils 6%, metamyelocytes 10%, myelocytes 18%, promyelocytes 2%, and blasts 3%. What is the most likely cytogenetic abnormality in this case?
- A. t(1;21)
- B. t(9;22) (Correct Answer)
- C. t(15;17)
- D. Trisomy 21
Explanation: ### Explanation **Diagnosis: Chronic Myeloid Leukemia (CML) - Chronic Phase** The clinical presentation of a 60-year-old male with massive splenomegaly (heaviness in the left hypochondrium) and a massive leukocytosis (TLC 5 lakhs/mm³) is classic for CML. The differential leukocyte count (DLC) shows a "myelocyte bulge" (predominance of myelocytes and metamyelocytes) and a "left shift" to the level of blasts, but with a blast count <10%, confirming the **Chronic Phase** of CML [2]. Increased basophils (6%) are also a hallmark of myeloproliferative neoplasms. **Why t(9;22) is correct:** The cytogenetic hallmark of CML is the **Philadelphia (Ph) chromosome**, resulting from a reciprocal translocation between chromosomes 9 and 22, **t(9;22)(q34;q11)**. This creates the *BCR-ABL1* fusion gene, which encodes a constitutively active tyrosine kinase responsible for uncontrolled myeloid proliferation [2]. **Analysis of Incorrect Options:** * **A. t(1;21):** This is not a standard translocation associated with a specific leukemia. (Note: t(8;21) is associated with AML-M2) [1]. * **C. t(15;17):** This is the hallmark of **Acute Promyelocytic Leukemia (AML-M3)** [3]. It involves the *PML-RARA* fusion and presents with high blast counts and DIC, not chronic massive splenomegaly [1]. * **D. Trisomy 21:** Associated with Down Syndrome, which carries an increased risk of AML (specifically Megakaryoblastic M7) and ALL, but is not the primary driver of CML. **High-Yield Clinical Pearls for NEET-PG:** * **Leukocyte Alkaline Phosphatase (LAP) Score:** Characteristically **decreased** in CML (helps differentiate from a Leukemoid reaction where LAP is high). * **Basophilia:** An increase in basophils is a sensitive indicator of CML and may herald the onset of an accelerated phase. * **Treatment:** The first-line treatment is **Imatinib** (a Tyrosine Kinase Inhibitor) [2]. * **Splenomegaly:** CML is one of the most common causes of "Massive Splenomegaly" (crossing the midline/reaching the right iliac fossa).
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
Practice Questions
Thalassemias
Practice Questions
Platelet Disorders
Practice Questions
Coagulation Disorders
Practice Questions
Thrombotic Disorders
Practice Questions
Leukemias
Practice Questions
Lymphomas
Practice Questions
Multiple Myeloma and Plasma Cell Disorders
Practice Questions
Myeloproliferative Neoplasms
Practice Questions
Transfusion Medicine
Practice Questions
Hematopoietic Stem Cell Transplantation
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free