Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 541: Which of the following findings is generally NOT seen in idiopathic thrombocytopenic purpura (ITP)?

A. More common in females
B. Petechiae, ecchymosis, and bleeding
C. Palpable splenomegaly (Correct Answer)
D. Increased megakaryocytes in bone marrow

Explanation: **Explanation:** **1. Why Palpable Splenomegaly is the Correct Answer:** In Idiopathic Thrombocytopenic Purpura (ITP), platelet destruction occurs via anti-platelet antibodies (IgG) in the reticuloendothelial system, primarily the spleen [1]. However, this process does not typically lead to splenic congestion or hyperplasia significant enough to cause organomegaly. **The presence of a palpable spleen in a patient with thrombocytopenia should prompt a search for alternative diagnoses**, such as leukemia, lymphoma, portal hypertension, or systemic lupus erythematosus (SLE) [3]. In ITP, the spleen is usually normal in size. **2. Analysis of Incorrect Options:** * **A. More common in females:** Chronic ITP is classically seen in young to middle-aged women (female-to-male ratio of approximately 3:1), making this a typical finding. * **B. Petechiae, ecchymosis, and bleeding:** These are the hallmark clinical manifestations of "mucocutaneous bleeding" caused by a low platelet count (thrombocytopenia) [2], [3]. * **D. Increased megakaryocytes in bone marrow:** Since ITP is a peripheral destruction disorder, the bone marrow responds by increasing platelet production. This results in a compensatory increase in the number and size of megakaryocytes. **3. Clinical Pearls for NEET-PG:** * **Diagnosis of Exclusion:** ITP is diagnosed only after ruling out other causes of thrombocytopenia [1]. * **First-line Treatment:** Corticosteroids (e.g., Prednisolone) or IVIG. * **Splenectomy:** Considered the most effective second-line treatment for chronic refractory ITP. * **Key Rule:** If a question mentions "massive splenomegaly" and "thrombocytopenia," think of Myelofibrosis or Malaria/Kala-azar, never ITP.

Question 542: Which of the following is NOT an intermediate grade Non-Hodgkin's Lymphoma (NHL)?

A. Diffuse small cell cleaved
B. Diffuse large cell
C. Follicular, predominantly small cleaved cell (Correct Answer)
D. Diffuse mixed

Explanation: This question is based on the **Working Formulation**, a clinical classification system that categorizes Non-Hodgkin’s Lymphomas (NHL) into Low, Intermediate, and High grades based on their survival patterns and aggressiveness. Clinically, the most important factor in classification is the grade, which reflects the proliferation rate [1]. ### Why the correct answer is right: **Option C (Follicular, predominantly small cleaved cell)** is classified as a **Low-grade NHL**. Follicular lymphomas are generally indolent (slow-growing) and characterized by a follicular (nodular) growth pattern [1]. While they are often incurable in advanced stages, patients can survive for many years without aggressive treatment. ### Why the other options are wrong: The Working Formulation classifies the following as **Intermediate-grade NHLs**, which are more aggressive than low-grade but often more responsive to intensive chemotherapy: * **Option A (Diffuse small cleaved cell):** Unlike its follicular counterpart, the diffuse pattern signifies a more aggressive clinical course. * **Option B (Diffuse large cell):** This is a classic intermediate-grade lymphoma (specifically, Diffuse Large B-Cell Lymphoma or DLBCL is the most common subtype) [1]. * **Option D (Diffuse mixed, small and large cell):** The presence of large cells and a diffuse architecture elevates this to the intermediate category. ### NEET-PG High-Yield Pearls: * **Most common NHL:** Diffuse Large B-Cell Lymphoma (DLBCL) – Intermediate grade [1]. * **Most common Indolent NHL:** Follicular Lymphoma – Low grade [1]. * **High-grade NHLs:** Include Small non-cleaved cell (Burkitt’s) and Lymphoblastic lymphoma [1]. * **Cytogenetics:** Follicular lymphoma is strongly associated with **t(14;18)**, leading to the overexpression of the **BCL-2** oncogene (anti-apoptotic). * **Clinical Rule:** Low-grade lymphomas are "indolent but incurable," while High-grade lymphomas are "aggressive but potentially curable" [1].

Question 543: Hypersplenism is characterized by all of the following EXCEPT:

A. Leukemoid reaction (Correct Answer)
B. Thrombocytopenia
C. Splenomegaly
D. Responds to splenectomy

Explanation: **Explanation:** **Hypersplenism** is a clinical syndrome characterized by the overactivity of the spleen, leading to the premature destruction and sequestration of blood cells [1]. **Why "Leukemoid Reaction" is the Correct Answer:** A leukemoid reaction is an exaggerated elevation in white blood cell count (typically >50,000/mm³), often seen in severe infections or malignancies. In contrast, hypersplenism is characterized by **cytopenias** (anemia, leukopenia, or thrombocytopenia) due to increased splenic pooling and destruction [1]. Therefore, a leukemoid reaction is physiologically opposite to the hematological findings of hypersplenism. **Analysis of Incorrect Options:** * **Splenomegaly (Option C):** This is a prerequisite for hypersplenism. An enlarged spleen increases the transit time of blood cells through the splenic cords, facilitating their destruction by macrophages. * **Thrombocytopenia (Option B):** The spleen normally stores about one-third of the body's platelets. In hypersplenism, this can increase to 90%, leading to significant peripheral thrombocytopenia [1]. * **Responds to Splenectomy (Option D):** Since the underlying pathology is the overactive spleen, surgical removal (splenectomy) typically corrects the cytopenias, provided the bone marrow is compensatory. **High-Yield Clinical Pearls for NEET-PG:** 1. **Dagnostic Criteria (Dacie’s Criteria):** 1) Splenomegaly, 2) Cytopenia (one or more cell lines), 3) Normal or hyperplastic bone marrow (compensatory), and 4) Correction by splenectomy. 2. **Most Common Cause:** In India, **Cirrhosis with Portal Hypertension** (leading to congestive splenomegaly) is the most frequent cause. 3. **Blood Picture:** Peripheral smear typically shows a "normocytic normochromic" anemia with reticulocytosis.

Question 544: All are true regarding Lupus anticoagulant, EXCEPT?

A. Increased aPTT
B. Arterial thrombosis
C. Rashes
D. Prolonged PT (Correct Answer)

Explanation: Lupus Anticoagulant (LA) is a misnomer; it is an **in vitro anticoagulant** but an **in vivo procoagulant**. It belongs to the family of antiphospholipid antibodies (aPL) that bind to phospholipid-binding proteins. **Why Option D is the Correct Answer:** The screening test for LA is the **activated Partial Thromboplastin Time (aPTT)**, which is prolonged because the antibodies interfere with the phospholipid surfaces required for the intrinsic pathway in the lab test tube [1]. However, the **Prothrombin Time (PT)** measures the extrinsic pathway and is typically **normal** in patients with Lupus Anticoagulant [1]. A prolonged PT in a patient with aPL usually suggests a co-existing factor deficiency (like Factor II deficiency in Lupus Anticoagulant-Hypoprothrombinemia Syndrome), but it is not a standard feature of LA itself. **Analysis of Other Options:** * **A. Increased aPTT:** This is the hallmark laboratory finding [1]. Despite the prolonged aPTT, the patient is at risk for clotting, not bleeding. * **B. Arterial thrombosis:** LA is a major component of Antiphospholipid Syndrome (APS), which characteristically causes both venous (e.g., DVT) and arterial (e.g., Stroke, MI) thrombosis. * **C. Rashes:** APS is strongly associated with Systemic Lupus Erythematosus (SLE), which presents with various rashes (malar rash, discoid rash). Additionally, **Livedo reticularis** is a specific vascular skin finding seen in patients with LA. **High-Yield Clinical Pearls for NEET-PG:** * **Mixing Study:** If aPTT is prolonged due to LA, it **will not correct** upon adding normal plasma (distinguishes it from factor deficiencies) [1]. * **Confirmatory Test:** Dilute Russell Viper Venom Test (dRVVT) is the most specific test for LA. * **Paradox:** LA causes a "prolonged clotting time" in the lab but "recurrent miscarriages and thrombosis" in the patient. * **Treatment:** Long-term anticoagulation with Warfarin (INR 2.0–3.0) is standard for thrombotic APS.

Question 545: A 23-year-old asymptomatic female presents with MCV of 70 fL, ferritin of 100 ng/mL, and Hb of 10 gm%. Which of the following is the most likely cause?

A. Vitamin B12 deficiency
B. Iron deficiency
C. Folate deficiency
D. Thalassemia trait (Correct Answer)

Explanation: ### Explanation The correct answer is **Thalassemia trait**. **1. Why Thalassemia Trait is Correct:** The patient presents with **microcytic anemia** (MCV 70 fL, Hb 10 gm%). The key to distinguishing the cause lies in the **ferritin level (100 ng/mL)**, which is well within the normal range (normal: 15–150 ng/mL). * In **Thalassemia trait**, there is a genetic defect in globin chain synthesis, leading to microcytosis. However, iron stores remain normal or even slightly elevated because the pathology is not iron deficiency. * A classic NEET-PG clue is an **asymptomatic** patient with a disproportionately low MCV relative to a mild anemia, often accompanied by a Mentzer Index (MCV/RBC count) < 13. **2. Why Other Options are Incorrect:** * **Iron Deficiency (B):** This is the most common cause of microcytic anemia, but it is characterized by **low ferritin** (<15–30 ng/mL) [2]. A ferritin of 100 ng/mL effectively rules out iron deficiency in an uncomplicated case [1]. * **Vitamin B12 (A) and Folate (C) Deficiency:** Both are causes of **megaloblastic anemia**, which presents with a **high MCV (>100 fL)** (macrocytosis), contrary to the 70 fL seen here [1]. **3. NEET-PG High-Yield Pearls:** * **Mentzer Index:** MCV ÷ RBC count. If **< 13**, suspect Thalassemia; if **> 13**, suspect Iron Deficiency Anemia (IDA). * **Gold Standard Diagnosis:** For β-Thalassemia trait, the investigation of choice is **Hb Electrophoresis/HPLC**, showing elevated **HbA2 (>3.5%)**. * **RDW (Red Cell Distribution Width):** Usually normal in Thalassemia trait (homogenous cell population) but increased in IDA (anisocytosis). * **Ferritin** is the most sensitive initial lab test for diagnosing Iron Deficiency Anemia.

Question 546: Which of the following indicates the worst prognosis in Chronic Lymphocytic Leukemia (CLL) patients?

A. Presence of lymphadenopathy
B. Presence of hepatosplenomegaly
C. Hemoglobin level less than 10 g/dL (Correct Answer)
D. WBC count exceeding 1,00,000 cells/mL

Explanation: The prognosis of Chronic Lymphocytic Leukemia (CLL) is primarily determined by the extent of bone marrow failure and the total tumor burden, as defined by the Rai and Binet staging systems [1]. **Why Option C is Correct:** A hemoglobin level of **<10 g/dL** (or a platelet count <100,000/mm³) signifies **Rai Stage IV** or **Binet Stage C**. This indicates advanced disease where the bone marrow is heavily infiltrated by leukemic lymphocytes, leading to hematopoietic failure [1]. This stage carries the worst prognosis, with a median survival of approximately 1.5 to 3.5 years [1]. **Analysis of Incorrect Options:** * **Options A & B:** Lymphadenopathy (Rai Stage I) and Hepatosplenomegaly (Rai Stage II) represent intermediate-risk disease. While they indicate a higher tumor burden than isolated lymphocytosis (Stage 0), they do not signify bone marrow failure and thus have a significantly better prognosis than anemia or thrombocytopenia [1]. * **Option D:** While a very high White Blood Cell (WBC) count reflects a high tumor burden, the absolute lymphocyte count itself is not a primary staging criterion for prognosis in the Rai or Binet systems. Patients can have very high counts for years without clinical deterioration. **High-Yield Clinical Pearls for NEET-PG:** * **Rai Staging:** Stage 0 (Lymphocytosis only), Stage I (Nodes), Stage II (Spleen/Liver), Stage III (Anemia), Stage IV (Thrombocytopenia). * **Poor Prognostic Markers:** 17p deletion (TP53 mutation), 11q deletion, ZAP-70 expression, and unmutated IGHV. * **Good Prognostic Marker:** 13q deletion (isolated). * **Richter Transformation:** Sudden clinical worsening or rapid lymph node growth in a CLL patient suggests transformation into Diffuse Large B-cell Lymphoma (DLBCL).

Question 547: A pregnant lady in her second trimester has a hemoglobin level of 6 mg%. The gynecologist suggests IV transfusion of packed red cells. What is the most common oral change due to nutritional anemia?

A. Enlarged tongue
B. Atrophic glossitis (Correct Answer)
C. Generalized osteolysis
D. Focal marrow expansion

Explanation: The patient presents with severe anemia (Hb 6 g/dL) during pregnancy, which is most commonly due to **Iron Deficiency Anemia (IDA)** [1] or megaloblastic anemia (folate/B12 deficiency) [2]. **Why Atrophic Glossitis is correct:** Nutritional anemias lead to a high turnover rate of the oral mucosal cells. In iron deficiency, there is a depletion of iron-dependent intracellular enzymes, leading to the atrophy of the **filiform papillae** (and later fungiform papillae) on the dorsum of the tongue. This results in **Atrophic Glossitis**, characterized by a smooth, red, and "glazed" appearance of the tongue. It is often accompanied by angular cheilitis and burning sensations (glossodynia). **Analysis of Incorrect Options:** * **A. Enlarged tongue (Macroglossia):** This is typically seen in conditions like amyloidosis, hypothyroidism (myxedema), or acromegaly, rather than nutritional anemia. * **C. Generalized osteolysis:** This refers to bone destruction, commonly seen in Multiple Myeloma or metastatic bone disease, not anemia. * **D. Focal marrow expansion:** While chronic hemolytic anemias (like Thalassemia) cause marrow hyperplasia leading to "crew-cut" appearance on X-ray, it is not a common *oral* mucosal change of nutritional anemia. **High-Yield Clinical Pearls for NEET-PG:** * **Plummer-Vinson Syndrome (Paterson-Kelly Syndrome):** A classic triad of Iron deficiency anemia, Atrophic glossitis, and Esophageal webs. It carries an increased risk of post-cricoid carcinoma. * **Pernicious Anemia:** Often presents with **Hunter’s glossitis** (beefy red tongue). * **Oral manifestations of IDA:** Atrophic glossitis, angular cheilitis, and oral candidiasis.

Question 548: Which of the following statements is false regarding pernicious anemia?

A. Severe lack of intrinsic factor
B. Autoimmune disorder against parietal cells of the stomach
C. Atrophy of all layers of the body and fundus
D. Serum gastrin level is decreased (Correct Answer)

Explanation: Pernicious anemia is an autoimmune condition characterized by the destruction of gastric parietal cells, leading to a profound deficiency of **Intrinsic Factor (IF)** and gastric acid (achlorhydria). [1, 2] **1. Why Option D is the correct (False) statement:** In pernicious anemia, the destruction of parietal cells leads to **achlorhydria** (absence of hydrochloric acid). Under normal physiological conditions, gastric acid provides negative feedback to G-cells in the antrum. In the absence of acid, this feedback loop is lost, resulting in **hypergastrinemia** (increased serum gastrin levels) as the body attempts to stimulate non-existent parietal cells. [1] Therefore, saying gastrin is decreased is incorrect. **2. Analysis of incorrect (True) options:** * **Option A:** True. The hallmark of the disease is a severe lack of IF, which is essential for Vitamin B12 absorption in the terminal ileum. * **Option B:** True. It is an autoimmune Type IV hypersensitivity reaction involving autoantibodies against parietal cells and intrinsic factor. [2] * **Option C:** True. Chronic inflammation leads to **Type A (Autoimmune) Gastritis**, causing diffuse atrophy of the acid-secreting mucosa in the **body and fundus**, while the antrum is typically spared. [2] **Clinical Pearls for NEET-PG:** * **Diagnostic Markers:** Anti-parietal cell antibodies (sensitive) and Anti-intrinsic factor antibodies (highly specific). * **Peripheral Smear:** Hypersegmented neutrophils and macro-ovalocytes. * **Schilling Test:** Historically used to diagnose B12 malabsorption (now largely replaced by antibody testing). * **Malignancy Risk:** Patients have a 3x increased risk of **Gastric Adenocarcinoma** and **Gastric Carcinoid tumors** due to chronic hypergastrinemia.

Question 549: Hess's (Tourniquet) test is a feature of -

A. Idiopathic Thrombocytopenic Purpura (ITP) (Correct Answer)
B. Secondary thrombocytopenia
C. Allergic purpura
D. Senile purpura

Explanation: ### Explanation **Hess’s Test (Tourniquet Test)** is a clinical assessment used to evaluate **capillary fragility** and **platelet function**. It involves inflating a blood pressure cuff to a point midway between systolic and diastolic pressure for 5 minutes. A positive result is defined by the appearance of 10–20 or more petechiae in a 1-inch square area distal to the cuff. #### Why the Correct Answer is Right: * **Idiopathic Thrombocytopenic Purpura (ITP):** In ITP, there is a significant reduction in platelet count due to immune-mediated destruction [1]. Since platelets are essential for maintaining the integrity of the capillary endothelium, their deficiency leads to increased capillary fragility. Therefore, the mechanical stress of the tourniquet causes micro-hemorrhages (petechiae), making the test positive [1]. #### Analysis of Incorrect Options: * **Secondary Thrombocytopenia:** While the test *can* be positive in any severe thrombocytopenia, ITP is the classic textbook association for this test in the context of primary platelet disorders. However, in many exams, if ITP is an option, it is the preferred answer for "feature of." * **Allergic Purpura (Henoch-Schönlein Purpura):** This is a small-vessel vasculitis. While it involves skin lesions, the primary pathology is IgA deposition rather than a simple mechanical fragility of the vessel wall or platelet deficiency. * **Senile Purpura:** This occurs due to age-related atrophy of dermal collagen and connective tissue supporting the blood vessels [1]. It typically presents as ecchymoses on the forearms rather than a positive Hess’s test triggered by pressure. #### NEET-PG High-Yield Pearls: * **Dengue Fever:** Hess’s test is a crucial bedside tool for the early diagnosis of Dengue Hemorrhagic Fever (WHO criteria). * **Vitamin C Deficiency (Scurvy):** Also shows a positive Hess’s test due to defective collagen synthesis leading to fragile capillary walls. * **Rumple-Leede Phenomenon:** Another name for a positive tourniquet test, often used interchangeably in clinical vignettes.

Question 550: A patient presents with microcytic hypochromic anemia. Serum iron levels and TIBC are decreased. What is the likely diagnosis?

A. Iron deficiency anemia
B. Anemia of chronic disease (Correct Answer)
C. Thalassemia
D. Sideroblastic anemia

Explanation: ### Explanation The key to solving this question lies in the **Iron Profile**. While microcytic hypochromic anemia is common to all four options, the combination of **decreased Serum Iron** and **decreased Total Iron Binding Capacity (TIBC)** is classic for **Anemia of Chronic Disease (ACD)**. [1] #### 1. Why Anemia of Chronic Disease is Correct In ACD, chronic inflammation leads to an increase in **Hepcidin** (an acute-phase reactant). [1] Hepcidin inhibits **ferroportin**, trapping iron inside macrophages and hepatocytes. [2] * **Serum Iron decreases** because iron cannot be released into the blood. [2] * **TIBC (Transferrin) decreases** because the body downregulates transferrin production in response to inflammation (unlike IDA, where it increases to "search" for iron). * **Ferritin** is typically normal or increased (reflecting trapped storage iron). [3] #### 2. Why Other Options are Incorrect * **Iron Deficiency Anemia (IDA):** While serum iron is low, **TIBC is increased** as the body compensates by producing more transferrin to maximize transport. [1] Ferritin is always low in IDA. * **Thalassemia:** This is a defect in globin chain synthesis. Iron studies are typically **normal or show iron overload** (increased Ferritin/Serum Iron) due to ineffective erythropoiesis. * **Sideroblastic Anemia:** Characterized by a defect in heme synthesis. It typically presents with **increased Serum Iron** and high Ferritin due to iron loading in the mitochondria (ringed sideroblasts). #### 3. High-Yield NEET-PG Pearls * **Gold Standard for ACD:** Bone marrow biopsy showing increased iron in macrophages (Prussian blue stain) but absent iron in erythroid precursors. [3] * **Hepcidin:** The "Master Regulator" of iron metabolism. [2] * **Differentiation Rule:** * Low Iron + High TIBC = **IDA** * Low Iron + Low TIBC = **ACD** * **Mentzer Index (MCV/RBC count):** <13 suggests Thalassemia; >13 suggests IDA.

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Hemoglobinopathies

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Thalassemias

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Platelet Disorders

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Coagulation Disorders

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Thrombotic Disorders

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Leukemias

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Lymphomas

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Multiple Myeloma and Plasma Cell Disorders

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Myeloproliferative Neoplasms

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Transfusion Medicine

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Hematopoietic Stem Cell Transplantation

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Hematology — MCQs

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