Hematopathology — MCQs
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A 24-year-old woman presents with a 4-day history of earache, increased urine production, a skin rash, bone pain on her scalp, otitis media, dermatitis, and exophthalmos. An X-ray of the scalp shows calvarial bone defects, and a fine-needle aspirate displays numerous eosinophils. Which of the following is the most likely diagnosis?
Which of the following does not indicate megaloblastic anemia?
A 6-year-old girl is brought into the emergency room after an automobile accident. Physical examination shows bleeding from multiple wounds, and a CBC reveals a normocytic, normochromic anemia. Which of the following indices is most helpful in defining this patient's anemia as normocytic?
In thrombocytopenic purpura, what is observed regarding the platelet count?
Which of the following may be seen in Multiple Myeloma?
A 67-year-old male presents with increasing fatigue and is found to be anemic. Physical examination reveals a hard 1-cm nodule in the left lobe of the prostate. The prostatic-specific antigen (PSA) level is found to be elevated. Examination of the peripheral blood reveals an occasional myelocyte. The erythrocytes are mainly normochromic and normocytic, and teardrop RBCs are not found. There are, however, about two nucleated red blood cells per 100 white cells. What is the best diagnosis for this patient's anemia?
Ring sideroblasts are characteristically seen in which condition?
Which of the following is absent in cryoprecipitate?
Microangiopathic hemolytic anemia is seen in all of the following diseases except?
All of the following statements about Hairy cell leukaemia are true, EXCEPT:
Hematopathology Indian Medical PG Practice Questions and MCQs
Question 331: A 24-year-old woman presents with a 4-day history of earache, increased urine production, a skin rash, bone pain on her scalp, otitis media, dermatitis, and exophthalmos. An X-ray of the scalp shows calvarial bone defects, and a fine-needle aspirate displays numerous eosinophils. Which of the following is the most likely diagnosis?
- A. Hodgkin lymphoma
- B. Langerhans cell histiocytosis (Correct Answer)
- C. Malignant melanoma
- D. Metastatic breast carcinoma
Explanation: **Explanation:** The clinical presentation describes the classic triad of **Hand-Schüller-Christian disease**, a multifocal unisystem variant of **Langerhans Cell Histiocytosis (LCH)**. This triad consists of: 1. **Calvarial bone defects** (punched-out lytic lesions) 2. **Diabetes Insipidus** (causing increased urine production/polyuria due to posterior pituitary involvement) 3. **Exophthalmos** (due to orbital bone involvement) LCH is a clonal proliferation of dendritic cells (Langerhans cells) [1]. In this case, the scalp lesions and otitis media are common manifestations of bone and skin involvement. Histologically, these lesions are characterized by a prominent infiltrate of **eosinophils** (hence the older name "Eosinophilic Granuloma"), along with characteristic Langerhans cells which are coffee-bean shaped with grooved nuclei [1]. **Why other options are incorrect:** * **Hodgkin Lymphoma:** Typically presents with painless lymphadenopathy and B-symptoms (fever, weight loss) [2]. While eosinophilia can occur, it does not cause the specific triad of lytic bone lesions, diabetes insipidus, and exophthalmos. * **Malignant Melanoma:** While it can metastasize to bone, it is highly unlikely in a 24-year-old with this specific systemic presentation and would not show a predominantly eosinophilic infiltrate. * **Metastatic Breast Carcinoma:** This is the most common cause of lytic lesions in older women, but it is extremely rare at age 24 and does not explain the diabetes insipidus or the eosinophilic aspirate. **NEET-PG High-Yield Pearls:** * **Electron Microscopy:** Look for **Birbeck Granules** (tennis-racket shaped pentalaminar structures) [1]. * **Immunohistochemistry (IHC):** LCH cells are characteristically positive for **CD1a, S100, and CD207 (Langerin)** [1]. * **BRAF Mutation:** Approximately 50% of cases harbor the **BRAF V600E** mutation [1]. * **Clinical Spectrum:** Ranges from Letterer-Siwe disease (multisystem, infants) to Eosinophilic Granuloma (unifocal, benign). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 629-630. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 618.
Question 332: Which of the following does not indicate megaloblastic anemia?
- A. Increased reticulocyte count (Correct Answer)
- B. Raised Bilirubin
- C. Mild splenomegaly
- D. Nucleated RBC
Explanation: **Explanation:** The hallmark of megaloblastic anemia is **ineffective erythropoiesis**. This means that while the bone marrow is hypercellular, the red blood cell precursors (megaloblasts) are defective due to impaired DNA synthesis (Vitamin B12 or Folate deficiency). These defective cells are destroyed within the marrow before they can mature and enter the circulation (intramedullary hemolysis) [1]. **Why Option A is correct:** In megaloblastic anemia, the **reticulocyte count is characteristically low** (or inappropriately normal). Because the marrow cannot successfully produce mature RBCs, the output of reticulocytes into the peripheral blood is decreased. An increased reticulocyte count would instead suggest a regenerative response, such as in acute blood loss or hemolytic anemia. **Why the other options are incorrect:** * **B. Raised Bilirubin:** Intramedullary hemolysis of megaloblasts releases hemoglobin, which is converted into unconjugated bilirubin, leading to mild indirect hyperbilirubinemia and jaundice. * **C. Mild Splenomegaly:** Chronic ineffective erythropoiesis and the sequestration of abnormal macrocytic cells can lead to modest enlargement of the spleen in some patients. * **D. Nucleated RBCs:** Due to the intense erythroid hyperplasia in the marrow, some immature nucleated RBCs (megaloblasts) may escape into the peripheral blood smear [1], [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Peripheral Smear:** Look for **hypersegmented neutrophils** (earliest sign) and macro-ovalocytes [1], [3]. * **Biochemical Markers:** Elevated **LDH** (often very high due to cell turnover) and elevated **Homocysteine** levels [2]. * **MCV:** Typically >100 fL. * **Pancytopenia:** Severe megaloblastic anemia can present with low WBC and platelet counts alongside anemia. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 654. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 654-655. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 593-594.
Question 333: A 6-year-old girl is brought into the emergency room after an automobile accident. Physical examination shows bleeding from multiple wounds, and a CBC reveals a normocytic, normochromic anemia. Which of the following indices is most helpful in defining this patient's anemia as normocytic?
- A. Hematocrit
- B. Hemoglobin
- C. Mean corpuscular hemoglobin concentration
- D. Mean corpuscular volume (Correct Answer)
Explanation: **Explanation:** The classification of anemia is primarily based on red blood cell (RBC) indices. To define an anemia as **normocytic, microcytic, or macrocytic**, we must look at the average size of the red blood cells [2]. **1. Why Mean Corpuscular Volume (MCV) is correct:** MCV measures the average volume (size) of a single red blood cell. It is the gold standard index for the morphological classification of anemia [2]. * **Normocytic:** MCV 80–100 fL (as seen in acute blood loss, like this patient) [1]. * **Microcytic:** MCV < 80 fL (e.g., Iron deficiency) [3]. * **Macrocytic:** MCV > 100 fL (e.g., B12/Folate deficiency). **2. Why other options are incorrect:** * **Hemoglobin (Hb) & Hematocrit (Hct):** These are used to **diagnose** the presence of anemia (decreased oxygen-carrying capacity), but they do not provide information about the size or morphology of the cells [2]. * **Mean Corpuscular Hemoglobin Concentration (MCHC):** This measures the average concentration of hemoglobin in a given volume of packed red cells. It defines whether an anemia is **normochromic** (32–36 g/dL) or **hypochromic** (e.g., Iron deficiency), not its size [3]. **Clinical Pearls for NEET-PG:** * **Acute Blood Loss:** Immediately after trauma, Hb/Hct may be normal due to proportionate loss of plasma and RBCs. Anemia becomes apparent after hemodilution (fluid shift from interstitium to vessels) [2]. * **Reticulocyte Count:** In normocytic anemia, a high reticulocyte count suggests hemolysis or acute hemorrhage, while a low count suggests bone marrow failure [1]. * **Mentzer Index:** (MCV/RBC count) is a high-yield formula to differentiate Iron Deficiency Anemia (<13) from Thalassemia trait (>13). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 638-639. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 590-591.
Question 334: In thrombocytopenic purpura, what is observed regarding the platelet count?
- A. Increase in platelet count
- B. Decrease in platelet count (Correct Answer)
- C. Normal platelet count
- D. Defective platelet function
Explanation: **Explanation:** **1. Understanding the Correct Answer (B):** The term **Thrombocytopenia** is derived from "thrombocyte" (platelet) and "penia" (deficiency). Therefore, by definition, thrombocytopenic purpura refers to a bleeding disorder characterized by a **decrease in the absolute platelet count** (typically below 150,000/µL) [1, 2]. When counts drop significantly (usually <20,000/µL), it leads to spontaneous capillary bleeding, manifesting as **purpura** (bruises) and **petechiae** (pinpoint hemorrhages) on the skin and mucous membranes [2]. **2. Analysis of Incorrect Options:** * **Option A (Increase):** An increase in platelets is termed **Thrombocytosis**, which is associated with myeloproliferative neoplasms (e.g., Essential Thrombocythemia) or reactive states, rather than purpura. * **Option C (Normal):** A normal platelet count with bleeding symptoms suggests a vascular disorder (e.g., Senile Purpura) or a qualitative platelet defect [2]. * **Option D (Defective Function):** This refers to **Thrombocytopathy**. While it causes similar bleeding symptoms, the platelet *count* remains normal. Examples include Bernard-Soulier Syndrome or Glanzmann Thrombasthenia [2]. **3. NEET-PG High-Yield Pearls:** * **Immune Thrombocytopenic Purpura (ITP):** The most common cause of isolated thrombocytopenia [1]. It is caused by anti-platelet antibodies (usually IgG) against GpIIb/IIIa or GpIb/IX. * **Bone Marrow Findings:** In peripheral destruction (like ITP), the bone marrow shows an **increased number of Megakaryocytes** (compensatory hyperplasia) [1]. * **Bleeding Time (BT):** In thrombocytopenic purpura, the BT is **prolonged**, while PT and aPTT remain **normal** (as coagulation factors are unaffected) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 665-667. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 619-621.
Question 335: Which of the following may be seen in Multiple Myeloma?
- A. Decreased Calcium
- B. Sclerotic bone lesion
- C. Bone deposition
- D. Renal failure (Correct Answer)
Explanation: **Explanation:** **Multiple Myeloma (MM)** is a plasma cell neoplasm characterized by the monoclonal proliferation of plasma cells in the bone marrow [1]. **Why Renal Failure is Correct:** Renal failure is a classic feature of Multiple Myeloma (the 'R' in the **CRAB** mnemonic) [2]. The primary cause is **Myeloma Kidney (Cast Nephropathy)**, where excess monoclonal light chains (Bence-Jones proteins) are filtered by the glomerulus and precipitate with Tamm-Horsfall protein in the distal tubules [3]. This forms dense, waxy, eosinophilic casts that cause intratubular obstruction and inflammation [3]. Other causes include hypercalcemia-induced nephrocalcinosis and AL amyloidosis [2]. **Why the other options are incorrect:** * **A. Decreased Calcium:** MM typically presents with **Hypercalcemia**. Myeloma cells secrete RANK-L and other cytokines (IL-6) that activate osteoclasts, leading to excessive bone resorption and release of calcium into the blood [5]. * **B & C. Sclerotic bone lesion / Bone deposition:** MM is characterized by **punched-out lytic lesions**, not sclerotic (blastic) ones [5]. The neoplastic plasma cells inhibit osteoblast activity (via DKK1) while stimulating osteoclasts, meaning there is bone destruction without new bone formation or deposition [1]. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** **C**alcium (High), **R**enal failure, **A**nemia (Normocytic), **B**one lesions (Lytic) [2], [5]. * **Peripheral Smear:** **Rouleaux formation** (due to high ESR/globulins) [4]. * **Diagnosis:** Bone marrow shows >10% clonal plasma cells; **M-spike** on serum protein electrophoresis (usually IgG) [1], [5]. * **Urine:** Bence-Jones proteins (detected by sulfosalicylic acid test, not by standard dipstick) [1], [4]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 618-619. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 942-943. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 607-608. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 617-618.
Question 336: A 67-year-old male presents with increasing fatigue and is found to be anemic. Physical examination reveals a hard 1-cm nodule in the left lobe of the prostate. The prostatic-specific antigen (PSA) level is found to be elevated. Examination of the peripheral blood reveals an occasional myelocyte. The erythrocytes are mainly normochromic and normocytic, and teardrop RBCs are not found. There are, however, about two nucleated red blood cells per 100 white cells. What is the best diagnosis for this patient's anemia?
- A. Fanconi's anemia
- B. Microangiopathic hemolytic anemia
- C. Myelophthisic anemia (Correct Answer)
- D. Autoimmune hemolytic anemia
Explanation: ### Explanation **Correct Answer: C. Myelophthisic anemia** **Mechanism:** Myelophthisic anemia occurs when the bone marrow is infiltrated by non-hematopoietic tissue, most commonly **metastatic carcinoma** (as seen in this patient with a prostatic nodule and elevated PSA), granulomas, or fibrosis [1]. This infiltration disrupts the "blood-bone marrow barrier," allowing immature cells to escape into the peripheral circulation. This classic peripheral blood finding is known as a **leukoerythroblastic picture** (presence of nucleated RBCs and immature white cells like myelocytes) [1]. While teardrop cells (dacrocytes) are often associated with this condition (especially in myelofibrosis), their absence does not rule out early metastatic infiltration [1]. **Why Incorrect Options are Wrong:** * **A. Fanconi's anemia:** This is a hereditary form of aplastic anemia characterized by pancytopenia and physical anomalies (e.g., thumb defects, short stature). It typically presents in childhood, not in a 67-year-old with a prostatic mass. * **B. Microangiopathic hemolytic anemia (MAHA):** This would show **schistocytes** (fragmented RBCs) on a peripheral smear. It is caused by mechanical destruction of RBCs in small vessels (e.g., DIC, TTP, HUS). * **D. Autoimmune hemolytic anemia (AIHA):** This typically presents with **spherocytes** and a positive Coombs test. It does not explain the presence of immature myeloid cells (myelocytes) in the periphery. **NEET-PG High-Yield Pearls:** * **Leukoerythroblastic Picture:** Defined as the presence of nucleated RBCs + immature myeloid cells in the peripheral smear [1]. It is the hallmark of **Myelophthisic Anemia**. * **Common Causes:** Metastatic cancers (Prostate, Breast, Lung), Myelofibrosis, and Gaucher’s disease. * **Dacrocytes (Teardrop cells):** Classically seen when RBCs are "squeezed" out of a fibrotic or infiltrated marrow [1]. * **Prostate Cancer:** Often spreads to the bone (osteoblastic lesions), making it a frequent cause of myelophthisic anemia in elderly males. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 628-629.
Question 337: Ring sideroblasts are characteristically seen in which condition?
- A. Myelodysplastic syndrome (MDS) (Correct Answer)
- B. Acute Lymphoid Leukemia (ALL)
- C. Acute Myeloid Leukemia (AML)
- D. Anemia of chronic disease
Explanation: **Explanation:** **Ring sideroblasts** are erythroid precursors (erythroblasts) characterized by the presence of five or more iron granules encircling at least one-third of the nucleus. This occurs due to **mitochondrial iron overload**, where iron accumulates in the mitochondria because of defective heme synthesis. 1. **Why MDS is correct:** In Myelodysplastic Syndromes (specifically subtypes like MDS-RS), there is an acquired mutation in the **SF3B1 gene** (most common) or defects in mitochondrial enzymes [1], [2]. This leads to ineffective erythropoiesis and the characteristic "ring" appearance on a **Perls’ Prussian Blue stain**. 2. **Why other options are incorrect:** * **ALL:** This is a lymphoid malignancy involving lymphoblasts; it does not typically involve the iron-loading pathways of the erythroid lineage. * **AML:** While some MDS cases can transform into AML, ring sideroblasts are the hallmark of the dysplastic phase (MDS) rather than the blast-heavy phase of AML [1]. * **Anemia of Chronic Disease:** This is characterized by trapped iron within macrophages (increased storage iron) but **decreased** iron availability for erythroid precursors. Therefore, sideroblasts are usually absent or reduced. **High-Yield Clinical Pearls for NEET-PG:** * **Stain of choice:** Perls’ Prussian Blue (not H&E). * **Genetic Marker:** **SF3B1 mutation** is highly specific for MDS with ring sideroblasts [2]. * **Other causes:** Sideroblastic anemia can also be caused by **Lead poisoning**, **Alcoholism**, and drugs like **Isoniazid** (which inhibits Vitamin B6, a cofactor for ALA synthase). * **Morphology:** The "ring" represents iron-laden mitochondria arranged around the nucleus. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 622-624.
Question 338: Which of the following is absent in cryoprecipitate?
- A. von Willebrand factor
- B. Factor XIII
- C. Factor VIIIc
- D. Protein C (Correct Answer)
Explanation: **Explanation:** Cryoprecipitate is the cold-insoluble fraction of plasma obtained by thawing Fresh Frozen Plasma (FFP) at 1–6°C. It is a concentrated source of specific coagulation proteins. **Why Protein C is the correct answer:** Protein C is a vitamin K-dependent natural anticoagulant [1]. Unlike the high-molecular-weight clotting factors that precipitate in the cold, Protein C remains in the supernatant (the "cryo-poor" plasma) during the production process. Therefore, it is **absent** (or present in negligible amounts) in cryoprecipitate. **Analysis of Incorrect Options:** * **Factor VIIIc:** Cryoprecipitate was historically developed as a treatment for Hemophilia A because it is highly enriched with Factor VIII [1]. * **von Willebrand factor (vWF):** It contains significant amounts of vWF, making it a secondary treatment option for von Willebrand disease when concentrates are unavailable. * **Factor XIII:** It is the only concentrated source of Factor XIII available for transfusion, used in cases of congenital or acquired deficiency [1]. * *Note:* **Fibrinogen (Factor I)** is the most abundant component of cryoprecipitate and is its most common clinical indication today. **High-Yield Clinical Pearls for NEET-PG:** * **Contents of Cryoprecipitate (The "Big 5"):** Fibrinogen, Factor VIII, Factor XIII, vWF, and Fibronectin. * **Storage:** Stored at -18°C or colder for up to 1 year. Once thawed, it must be used within 6 hours (or 4 hours if pooled). * **Primary Indication:** Hypofibrinogenemia (e.g., in DIC or massive hemorrhage). One unit of cryoprecipitate typically raises fibrinogen levels by 5–10 mg/dL. * **Dosage:** Usually administered as a "pool" of 10 units for an adult. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-584.
Question 339: Microangiopathic hemolytic anemia is seen in all of the following diseases except?
- A. Antiphospholipid antibody syndrome
- B. Thrombotic thrombocytopenic purpura
- C. Microscopic polyangiitis
- D. Metallic cardiac valves (Correct Answer)
Explanation: **Explanation:** Microangiopathic Hemolytic Anemia (MAHA) is a subcategory of fragmentation hemolysis characterized by the formation of **schistocytes** (helmet cells) due to the mechanical destruction of RBCs as they pass through narrowed or fibrin-clotted **small blood vessels (microvasculature).** [1] **Why "Metallic cardiac valves" is the correct answer:** While metallic cardiac valves do cause mechanical hemolysis and schistocyte formation, this occurs in the **macrovasculature** (large vessels/heart). This specific condition is termed **Macroangiopathic Hemolytic Anemia** (or Cardiac Hemolytic Anemia). In MAHA, the pathology is localized to arterioles and capillaries, whereas in prosthetic valves, the trauma occurs due to high-shear stress across a large mechanical device. **Analysis of Incorrect Options (Causes of MAHA):** * **Antiphospholipid Antibody Syndrome (APS):** Can lead to catastrophic APS, characterized by widespread microvascular thrombosis, resulting in MAHA. * **Thrombotic Thrombocytopenic Purpura (TTP):** A classic cause of MAHA where ADAMTS13 deficiency leads to von Willebrand factor multimers, causing microthrombi that shear RBCs. [2] * **Microscopic Polyangiitis:** This is a small-vessel vasculitis. Inflammation of the microvasculature leads to luminal narrowing and fibrin deposition, causing RBC fragmentation. **NEET-PG High-Yield Pearls:** 1. **Hallmark Finding:** Schistocytes on a peripheral blood smear (must be >1% to be clinically significant for MAHA). 2. **The "Pentad" of TTP:** Microangiopathic hemolytic anemia, Thrombocytopenia, Fever, Renal failure, and Neurological symptoms. [2] 3. **Lab Profile:** Elevated LDH, decreased haptoglobin, and indirect hyperbilirubinemia (standard for intravascular hemolysis). 4. **Differential:** Always distinguish MAHA (micro) from mechanical trauma due to aortic stenosis or prosthetic valves (macro). [3] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 667-668. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 946-948. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 540-541.
Question 340: All of the following statements about Hairy cell leukaemia are true, EXCEPT:
- A. Splenomegaly is conspicuous
- B. Results from an expansion of neoplastic T lymphocytes (Correct Answer)
- C. Cells are positive for Tartrate Resistant Acid Phosphatase
- D. The cells express CD25 consistently
Explanation: ### Explanation **Hairy Cell Leukaemia (HCL)** is a rare, chronic lymphoproliferative disorder characterized by the proliferation of mature **B-lymphocytes**, not T-lymphocytes [1]. #### Why Option B is the Correct Answer (The False Statement) HCL is a **B-cell neoplasm**. The "hairy" cells are derived from post-germinal center memory B-cells. They express pan-B-cell markers such as **CD19, CD20, and CD22**. Therefore, the statement that it results from an expansion of T-lymphocytes is immunologically incorrect [1]. #### Analysis of Other Options * **Option A (Splenomegaly is conspicuous):** This is a hallmark clinical feature. Massive splenomegaly occurs due to the infiltration of the splenic **red pulp** by leukemic cells [1]. Notably, lymphadenopathy is usually absent. * **Option C (TRAP Positive):** Hairy cells contain the isoenzyme 5 of acid phosphatase. The **Tartrate-Resistant Acid Phosphatase (TRAP)** stain shows strong positivity in these cells, serving as a classic diagnostic marker (though flow cytometry is now the gold standard). * **Option D (CD25 Expression):** Hairy cells consistently express a specific set of markers: **CD25** (IL-2 receptor), **CD11c, CD103, and Annexin A1**. Annexin A1 is considered the most specific marker for HCL. --- ### High-Yield Clinical Pearls for NEET-PG * **BRAF V600E Mutation:** Present in nearly 100% of classic HCL cases; it is a defining molecular feature. * **"Dry Tap" on Bone Marrow:** Infiltration leads to increased reticulin fibers (fibrosis), making marrow aspiration difficult [1]. * **Fried Egg Appearance:** On bone marrow biopsy, cells show abundant pale cytoplasm with distinct cell borders. * **Monocytopenia:** A highly characteristic laboratory finding in HCL. * **Treatment:** Highly sensitive to purine analogues like **Cladribine** (2-CdA) and Pentostatin. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 612.
Practice by Chapter
Anemias: Classification and Approach
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Hemolytic Anemias
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Myeloproliferative Neoplasms
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Myelodysplastic Syndromes
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Acute Leukemias
Practice Questions
Chronic Leukemias
Practice Questions
Lymphomas and Lymphoid Neoplasms
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Plasma Cell Disorders
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Bleeding Disorders
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Thrombotic Disorders
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