Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 251: Which cells are characteristic of Hodgkin's disease?

A. Lacunar cells
B. Reed-Sternberg cells (Correct Answer)
C. Giant cells
D. Eosinophils

Explanation: **Explanation:** **Reed-Sternberg (RS) cells** are the diagnostic hallmark of Hodgkin Lymphoma (HL) [1]. These are large, multinucleated or polylobed B-cells, typically featuring a "mirror-image" nuclei with prominent, eosinophilic, owl-eye nucleoli. While they are the neoplastic component, they usually constitute only 1–5% of the total tumor mass, with the remainder being a reactive inflammatory background. **Analysis of Options:** * **Lacunar cells (Option A):** These are a specific *variant* of RS cells seen primarily in the **Nodular Sclerosis** subtype of HL. While characteristic of that subtype, the classic RS cell is the defining feature for Hodgkin’s disease as a whole. * **Giant cells (Option C):** This is a non-specific term. While RS cells are large, "giant cells" typically refer to Langhans giant cells (Tuberculosis) or Foreign Body giant cells, which are not diagnostic of HL. * **Eosinophils (Option D):** These are commonly found in the reactive background of HL (recruited by IL-5 secreted by RS cells), especially in the Mixed Cellularity subtype, but they are not the neoplastic or diagnostic cells. **High-Yield Pearls for NEET-PG:** * **Immunophenotype:** Classic RS cells are typically **CD15+ and CD30+**, but **CD20- and CD45-**. * **Popcorn Cells (L&H cells):** These are variants seen in **Nodular Lymphocyte Predominant HL**; they are CD20+ and CD45+, but CD15- and CD30-. * **Bimodal Age Distribution:** HL shows peaks in the 20s and again after age 50. * **EBV Association:** Most strongly linked with the Mixed Cellularity subtype.

Question 252: Combined autoimmune hemolytic anemia (AIHA) and immune thrombocytopenic purpura (ITP) is known as?

A. Evans syndrome (Correct Answer)
B. May-Hegglin anomaly
C. Fechtner syndrome
D. Rosenthal syndrome

Explanation: **Explanation:** **1. Correct Answer: Evans Syndrome** Evans syndrome is a rare autoimmune disorder characterized by the simultaneous or sequential development of **Immune Thrombocytopenic Purpura (ITP)** and **Autoimmune Hemolytic Anemia (AIHA)** (usually warm-type, Coombs positive) [2]. Occasionally, immune neutropenia may also be present. The underlying pathophysiology involves the production of autoantibodies against multiple lineages of blood cells (platelets and RBCs). It is often associated with other conditions like SLE, CLL, or Primary Immunodeficiency (e.g., CVID) [1]. **2. Analysis of Incorrect Options:** * **May-Hegglin Anomaly:** A rare autosomal dominant disorder characterized by the triad of **thrombocytopenia**, **giant platelets**, and the presence of **Döhle-like bodies** (basophilic inclusions) in the cytoplasm of neutrophils. It is caused by mutations in the *MYH9* gene. * **Fechtner Syndrome:** A variant of *MYH9*-related disease [1]. Like May-Hegglin, it features macrothrombocytopenia and leukocyte inclusions, but it is distinguished by additional clinical features: **Alport-like nephritis**, **sensorineural hearing loss**, and **cataracts**. * **Rosenthal Syndrome:** Also known as **Hemophilia C**, it is a deficiency of **Clotting Factor XI**. It is an autosomal recessive bleeding disorder, most common in the Ashkenazi Jewish population. **3. High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Requires a positive Direct Antiglobulin Test (DAT/Coombs test) for AIHA and exclusion of other causes of thrombocytopenia [2]. * **Treatment:** First-line therapy is typically **Corticosteroids** (Prednisolone) or IVIG. Rituximab or Splenectomy are considered for refractory cases. * **Association:** Always screen a patient with Evans syndrome for **Systemic Lupus Erythematosus (SLE)**, as it can be the presenting feature of connective tissue diseases [1].

Question 253: Non-immune hemolytic anemia occurs in which of the following conditions?

A. Systemic Lupus Erythematosus (SLE)
B. Plasmodium vivax infection (Correct Answer)
C. Chronic Lymphocytic Leukemia (CLL)
D. Chronic Myeloid Leukemia (CML)

Explanation: **Explanation:** Hemolytic anemia is broadly classified into **Immune** (mediated by antibodies) and **Non-immune** (mediated by mechanical, infectious, or metabolic factors). **Why Option B is Correct:** *Plasmodium vivax* (Malaria) causes **non-immune hemolytic anemia** through direct mechanical destruction of red blood cells (RBCs) [1]. The parasite invades the RBC, consumes hemoglobin, and eventually causes the cell to rupture (erythrocytic schizogony). Additionally, the spleen sequesters and destroys both parasitized and non-parasitized RBCs due to increased fragility and oxidative stress. Since this process is driven by the pathogen and not by autoantibodies, it is non-immune. **Why the Other Options are Incorrect:** * **A. SLE:** This is a classic cause of **Autoimmune Hemolytic Anemia (AIHA)**, typically mediated by IgG antibodies (Warm AIHA). It is a "Type II Hypersensitivity" reaction. * **C. CLL:** This is the most common malignancy associated with **Warm AIHA** [2]. The neoplastic B-cells produce autoantibodies against RBC antigens. * **D. CML:** While CML causes anemia, it is typically due to bone marrow infiltration (myelophthisis) or anemia of chronic disease, not primary hemolysis. It is not a classic cause of immune or non-immune hemolytic anemia. **NEET-PG High-Yield Pearls:** * **Direct Antiglobulin Test (Coombs Test):** Positive in immune hemolysis (SLE, CLL) and **negative** in non-immune hemolysis (Malaria, G6PD deficiency, HUS/TTP). * **Malaria & RBCs:** *P. vivax* and *P. ovale* selectively infect **reticulocytes** (young RBCs), whereas *P. falciparum* infects RBCs of all ages, leading to higher parasitemia. * **Microangiopathic Hemolytic Anemia (MAHA):** Another high-yield non-immune cause characterized by **schistocytes** on peripheral smear.

Question 254: Which of the following is NOT a cause of thrombocytopenia?

A. Disseminated intravascular coagulation (DIC)
B. Vitamin B12 and folate deficiency
C. Systemic lupus erythematosus (SLE)
D. Rheumatoid arthritis (Correct Answer)

Explanation: The correct answer is **Rheumatoid Arthritis (RA)**. In clinical practice, RA is typically associated with **thrombocytosis** (elevated platelet count) rather than thrombocytopenia [1]. This occurs because platelets act as acute-phase reactants; chronic inflammation in RA triggers the release of cytokines like IL-6, which stimulates the liver to produce thrombopoietin, leading to reactive thrombocytosis [2]. **Analysis of Options:** * **A. Disseminated Intravascular Coagulation (DIC):** This is a consumptive coagulopathy. Widespread activation of the coagulation cascade leads to the formation of microthrombi, which rapidly consumes platelets and clotting factors, resulting in profound thrombocytopenia [3]. * **B. Vitamin B12 and Folate Deficiency:** These vitamins are essential for DNA synthesis. Their deficiency leads to ineffective hematopoiesis (megaloblastic anemia). While anemia is most common, it often manifests as **pancytopenia**, where the production of all cell lines, including platelets, is decreased. * **C. Systemic Lupus Erythematosus (SLE):** Thrombocytopenia is a common hematologic manifestation of SLE, usually occurring via immune-mediated destruction (secondary ITP) where anti-platelet antibodies are produced [3]. **NEET-PG High-Yield Pearls:** * **Felty’s Syndrome:** A rare complication of RA characterized by the triad of **RA, Splenomegaly, and Neutropenia** [1]. While neutropenia is the hallmark, splenomegaly can occasionally lead to mild thrombocytopenia via sequestration, but RA itself is fundamentally a pro-thrombotic/thrombocytotic state. * **Reactive Thrombocytosis:** Always consider chronic inflammation (RA, IBD), iron deficiency anemia, or malignancy when you see an unexplained high platelet count. * **Drug-induced:** Remember that Methotrexate (used in RA) can cause bone marrow suppression, leading to thrombocytopenia as a side effect, but the disease process itself does not.

Question 255: All are true about the clinical features of hereditary spherocytosis, EXCEPT?

A. Gallstones
B. Severe anemia during childhood (Correct Answer)
C. Splenomegaly
D. Jaundice

Explanation: Hereditary Spherocytosis (HS) is the most common inherited erythrocyte membrane defect, typically caused by mutations in proteins like Ankyrin (most common), Spectrin, or Band 3 [2]. This leads to a loss of membrane surface area, resulting in spherical, rigid RBCs that are prematurely destroyed in the splenic sinusoids [1]. **Why Option B is the correct answer:** In HS, the anemia is typically mild to moderate, not severe [2]. The bone marrow is usually able to compensate for the extravascular hemolysis by increasing erythropoiesis. Severe anemia in HS is rare and usually only occurs during "crises" (e.g., Aplastic crisis triggered by Parvovirus B19 or Megaloblastic crisis due to folate deficiency). **Analysis of Incorrect Options:** * **A. Gallstones:** Chronic extravascular hemolysis [3] leads to increased production of indirect bilirubin. This results in the formation of pigment (calcium bilirubinate) gallstones, which can be seen even in young children. * **C. Splenomegaly:** Since the spleen is the primary site of destruction for the rigid spherocytes [1], it undergoes work hypertrophy, making splenomegaly a hallmark clinical feature. * **D. Jaundice:** Intermittent unconjugated hyperbilirubinemia (acholuric jaundice) is common due to the continuous breakdown of RBCs. **NEET-PG High-Yield Pearls:** * **Inheritance:** Most cases are Autosomal Dominant. * **Diagnosis:** The gold standard is the **EMA Binding Test** (Flow cytometry). The Osmotic Fragility Test is also used but is less specific. * **Peripheral Smear:** Shows spherocytes (small, dark cells lacking central pallor) and reticulocytosis. * **Lab Marker:** Characteristically high **MCHC** (>36 g/dL) [1]. * **Treatment:** Splenectomy is the definitive treatment for symptomatic cases (usually deferred until age 6 to reduce sepsis risk) [2].

Question 256: Low TIBC is seen in which of the following conditions?

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

Explanation: Explanation: Total Iron Binding Capacity (TIBC) is a functional measurement of the amount of Transferrin available to bind iron. It is generally inversely proportional to body iron stores. 1. Why Anemia of Chronic Disease (ACD) is correct: In ACD, the body produces high levels of Hepcidin (an acute-phase reactant) in response to inflammation. [1] Hepcidin sequesters iron within macrophages and hepatocytes, leading to low serum iron. [2] Simultaneously, the liver decreases the production of Transferrin to "starve" potential pathogens of iron. Since TIBC measures Transferrin levels, a decrease in Transferrin results in a Low TIBC. 2. Why the other options are incorrect: * Iron Deficiency Anemia (IDA): This is the classic "opposite" of ACD. [1] When iron stores are depleted, the liver compensates by increasing Transferrin production to maximize iron transport. Thus, IDA is characterized by a High TIBC. * Fanconi Anemia & Aplastic Anemia: These are bone marrow failure syndromes. They involve a primary defect in stem cells (pancytopenia) rather than a defect in iron metabolism. In these conditions, TIBC is usually normal or decreased (due to iron overload from multiple transfusions), but they are not the classic textbook examples for TIBC differentiation like ACD. [3] High-Yield Clinical Pearls for NEET-PG: * Ferritin: The most sensitive indicator for IDA (Low Ferritin). In ACD, Ferritin is Normal or High (as it is an acute-phase reactant). * Transferrin Saturation: Low in both IDA and ACD. * Soluble Transferrin Receptor (sTfR): Elevated in IDA but Normal in ACD. This is the best test to differentiate the two when they coexist. * Summary Table: * IDA: ↓ Iron, ↑ TIBC, ↓ Ferritin. * ACD: ↓ Iron, ↓ TIBC, ↑ Ferritin. [3]

Question 257: Serum alkaline phosphatase is normal in which of the following conditions?

A. Osteosarcoma
B. Osteomalacia
C. Multiple myeloma (Correct Answer)
D. Malnutrition

Explanation: **Explanation:** The correct answer is **Multiple Myeloma**. **1. Why Multiple Myeloma is the correct answer:** In Multiple Myeloma (MM), bone destruction is primarily mediated by **osteoclast-activating factors** (like RANKL and IL-6), which lead to purely **lytic lesions** [1]. Unlike other bone pathologies, there is a characteristic **lack of osteoblastic activity** (bone formation). Since Serum Alkaline Phosphatase (ALP) is a marker of osteoblastic activity, it remains **normal** in MM despite extensive bone destruction [2]. This is a classic "negative" finding used to differentiate MM from other bone-metastasizing cancers. **2. Why the other options are incorrect:** * **Osteosarcoma:** This is a bone-forming tumor. Increased osteoblastic activity leads to significantly **elevated** ALP levels, which also serve as a prognostic marker. * **Osteomalacia:** Characterized by defective mineralization of the osteoid [3]. The body attempts to compensate for weak bones by increasing osteoblastic activity, resulting in **elevated** ALP [4]. * **Malnutrition:** Severe malnutrition, specifically Vitamin D or Calcium deficiency, leads to secondary hyperparathyroidism and increased bone turnover, typically causing an **elevation** in ALP [4]. **Clinical Pearls for NEET-PG:** * **The "Punch-out" Rule:** MM presents with "punched-out" lytic lesions on X-ray [2]. Because there is no reactive bone formation, a **Bone Scan** (which relies on osteoblastic activity) is often **falsely negative** in MM; Skeletal Surveys or MRI are preferred. * **Hypercalcemia in MM:** High serum calcium with normal ALP is a strong diagnostic clue for Multiple Myeloma. * **ALP in Healing:** ALP is also elevated during the healing phase of fractures and in Paget’s disease (where it is markedly high).

Question 258: A patient presented with skin pigmentation, hyperglycemia, and a serum ferritin level of 900 mcg/L. What is the possible diagnosis?

A. Atransferrinemia
B. Atransferrinemia (Correct Answer)
C. Hereditary spherocytosis
D. Thalassemia

Explanation: The clinical triad of **skin pigmentation** (bronzing), **hyperglycemia** (diabetes mellitus), and **elevated serum ferritin** (iron overload) is characteristic of **Secondary Hemochromatosis**. [1] ### **Explanation of the Correct Answer** **Atransferrinemia** is a rare autosomal recessive disorder characterized by a deficiency of transferrin. Without transferrin to transport iron to the bone marrow for erythropoiesis, iron remains "free" in the plasma. This leads to: 1. **Iron Overload:** Excess iron deposits in parenchymal organs (liver, pancreas, skin), causing the "Bronze Diabetes" presentation described in the question. [1], [2] 2. **Microcytic Anemia:** Despite high systemic iron, the bone marrow lacks iron for hemoglobin synthesis. ### **Why Other Options are Incorrect** * **Hereditary Spherocytosis:** This is a red cell membrane defect (e.g., ankyrin deficiency) leading to extravascular hemolysis. While chronic hemolysis can cause mild iron elevation, it does not typically present with the full triad of bronze diabetes unless the patient is heavily transfused. * **Thalassemia:** While Thalassemia Major causes significant iron overload (due to ineffective erythropoiesis and repeated transfusions), the primary presentation in NEET-PG vignettes usually emphasizes severe anemia, hepatosplenomegaly, and "chipmunk facies." Atransferrinemia is a more specific cause of "transferrin-deficient" iron overload. ### **NEET-PG High-Yield Pearls** * **Bronze Diabetes:** Refers to the combination of skin hyperpigmentation and diabetes mellitus due to iron deposition in the pancreas. [1] * **Classic Triad of Hemochromatosis:** Cirrhosis, Diabetes, and Skin Pigmentation. * **Diagnosis:** The most sensitive initial test for iron overload is **Transferrin Saturation** (>45-50%), while **Serum Ferritin** reflects total body iron stores. [3] * **Treatment of Atransferrinemia:** Plasma infusions (to provide transferrin) and iron chelation.

Question 259: Which of the following complications is likely to result after several units of blood have been transfused?

A. Metabolic acidosis
B. Metabolic alkalosis (Correct Answer)
C. Respiratory alkalosis
D. Respiratory acidosis

Explanation: Explanation: The correct answer is **Metabolic Alkalosis**. **Why it is correct:** Stored blood contains **sodium citrate** as an anticoagulant. When a patient receives a massive blood transfusion (typically defined as >10 units in 24 hours or >4 units in 1 hour), the liver metabolizes the citrate into **bicarbonate** ($HCO_3^-$). The accumulation of bicarbonate in the bloodstream leads to an increase in blood pH, resulting in metabolic alkalosis. This is a classic "post-transfusion" metabolic derangement. **Why other options are incorrect:** * **Metabolic Acidosis:** While stored blood is slightly acidic due to the accumulation of lactic acid and pyruvic acid during storage, the body’s metabolic conversion of citrate to bicarbonate usually overrides this, leading to alkalosis rather than acidosis in the post-transfusion period. * **Respiratory Alkalosis/Acidosis:** These conditions are primarily driven by changes in $CO_2$ levels due to ventilation abnormalities (hyperventilation or hypoventilation). Blood transfusion does not directly alter the respiratory drive or $CO_2$ exchange in a way that consistently produces these states. **High-Yield Clinical Pearls for NEET-PG:** * **Citrate Toxicity:** Citrate not only causes alkalosis but also binds to ionized calcium, leading to **Hypocalcemia**. Look for signs like Tetany or QTc prolongation on ECG. * **Hyperkalemia:** Stored RBCs leak potassium over time. Massive transfusion can lead to transient hyperkalemia, especially in patients with renal failure. * **Hypothermia:** Rapid infusion of cold blood can lead to cardiac arrhythmias. * **2,3-DPG Deficiency:** Stored blood has low 2,3-DPG, which shifts the Oxygen-Dissociation Curve to the **Left**, meaning hemoglobin holds onto oxygen more tightly, potentially reducing tissue oxygenation.

Question 260: In Thrombotic Thrombocytopenic Purpura (TTP), all of the following are seen except?

A. Renal failure
B. Hemolytic anemia
C. Thrombocytosis (Correct Answer)
D. Neurological features

Explanation: Explanation: Thrombotic Thrombocytopenic Purpura (TTP) is a life-threatening microangiopathic hemolytic anemia (MAHA) caused by a deficiency of the enzyme ADAMTS13. This deficiency leads to the accumulation of ultra-large von Willebrand factor (vWF) multimers, which cause spontaneous platelet aggregation and microthrombi formation throughout the circulation. Why Thrombocytosis is the correct answer: In TTP, there is massive consumption of platelets to form these microthrombi [2]. This results in thrombocytopenia (low platelet count), not thrombocytosis (high platelet count). Therefore, Option C is the "except" statement. Analysis of other options: * Hemolytic Anemia (Option B): This is a hallmark of TTP. As RBCs pass through vessels partially occluded by platelet thrombi, they are sheared, leading to microangiopathic hemolytic anemia (MAHA) characterized by schistocytes on peripheral smear [1]. * Neurological features (Option D): Microthrombi in the cerebral circulation lead to fluctuating neurological deficits, such as confusion, seizures, or focal deficits. * Renal failure (Option A): While more prominent in Hemolytic Uremic Syndrome (HUS), renal involvement (elevated creatinine, proteinuria) occurs in about 50% of TTP cases due to microthrombi in the renal vasculature [1]. NEET-PG High-Yield Pearls: 1. The Classic Pentad (FAT RN): Fever, Anemia (MAHA), Thrombocytopenia, Renal failure, and Neurological symptoms. 2. Diagnosis: Decreased ADAMTS13 activity (<10%). 3. Treatment: Emergency Plasmapheresis (Plasma Exchange) is the gold standard. Never delay treatment for lab confirmation. 4. Contraindication: Platelet transfusion is generally contraindicated as it may "fuel the fire" by promoting further thrombosis.

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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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Hematology — MCQs

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