Hematopathology — MCQs
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Perioral pallor and Dennie's line are seen in which of the following conditions?
In thromboasthenia, what defect is present?
A 12-year-old girl who underwent a bone marrow transplant as part of therapy for ALL presents with pulmonary complaints and neurologic findings. Lung biopsy reveals a granulomatous vasculitis with associated atypical lymphocytes. Clonality studies reveal a monoclonal B cell population with associated polyclonal T cells. What infectious agent is related to this diagnosis?
The t(15;19) translocation is associated with which of the following conditions?
Cabot's rings are features of which condition?
The RBC morphology in a peripheral blood smear in thalassemia trait resembles that of which condition?
The Philadelphia chromosome is characteristically seen in which of the following conditions?
Cyclin D1/IgH gene rearrangement is associated with which of the following malignancies?
Sideroblasts are seen in all conditions except?
Neoplastic giant cells characteristically seen in Hodgkin's lymphoma are:
Hematopathology Indian Medical PG Practice Questions and MCQs
Question 501: Perioral pallor and Dennie's line are seen in which of the following conditions?
- A. Atopic dermatitis (Correct Answer)
- B. Chronic actinic dermatitis
- C. Blood dyscrasia
- D. Perioral contact dermatitis
Explanation: **Explanation:** **Atopic Dermatitis (AD)** is a chronic, relapsing inflammatory skin condition characterized by a defective skin barrier (often due to **Filaggrin mutations**) and Type I hypersensitivity [1]. The diagnosis is primarily clinical, based on the **Hanifin and Rajka criteria**. * **Why Option A is correct:** Perioral pallor and Dennie-Morgan lines are classic "minor criteria" for Atopic Dermatitis. * **Dennie-Morgan Line:** An infraorbital fold or wrinkle caused by chronic edema and inflammation of the lower eyelid. * **Perioral Pallor:** A characteristic paleness around the mouth, often contrasting with the erythematous, eczematous patches on the cheeks (especially in infants). * **Why other options are incorrect:** * **Chronic Actinic Dermatitis:** A photosensitive disorder occurring on sun-exposed areas; it does not typically present with infraorbital folds. * **Blood Dyscrasia:** While anemia (a dyscrasia) causes general pallor [1], it does not specifically cause localized perioral pallor or Dennie-Morgan lines. * **Perioral Contact Dermatitis:** This usually presents with erythema, scaling, and papules *around* the mouth, rather than a distinct zone of pallor. **High-Yield Clinical Pearls for NEET-PG:** * **Filaggrin (FLG) Gene:** The most common genetic association with AD. * **Atopic March:** The progression from Atopic Dermatitis → Food Allergy → Allergic Rhinitis → Asthma. * **Hertoghe’s Sign:** Thinning or loss of the lateral third of the eyebrows due to chronic rubbing (common in AD). * **Pityriasis Alba:** Hypopigmented, slightly scaly patches on the face; another minor criterion for AD. * **Serum IgE:** Typically elevated in the extrinsic type of Atopic Dermatitis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 634-636.
Question 502: In thromboasthenia, what defect is present?
- A. Platelet aggregation (Correct Answer)
- B. Platelet adhesion
- C. Decreased ADP release
- D. Disordered platelet secretion
Explanation: **Explanation:** **Glanzmann Thromboasthenia (GT)** is an autosomal recessive bleeding disorder characterized by a qualitative defect in platelets [1]. 1. **Why Option A is Correct:** The underlying defect in GT is a deficiency or dysfunction of the **Glycoprotein IIb/IIIa (GPIIb/IIIa)** complex [1], [2]. This receptor is essential for **platelet aggregation** because it binds to fibrinogen, which acts as a bridge between two adjacent platelets [2]. Without functional GPIIb/IIIa, platelets cannot clump together, leading to a primary hemostatic defect despite a normal platelet count [1]. 2. **Why Other Options are Incorrect:** * **Option B (Adhesion):** Platelet adhesion to the subendothelial matrix is mediated by **GPIb-IX-V** binding to von Willebrand Factor (vWF) [1], [2]. A defect here results in **Bernard-Soulier Syndrome**, not thromboasthenia [1]. * **Options C & D (Release/Secretion):** These refer to "Storage Pool Diseases" (e.g., Gray Platelet Syndrome or Delta-storage pool deficiency), where the defect lies in the alpha or dense granules, not the surface aggregation receptors [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Platelet Morphology:** In GT, platelets are normal in size and count (unlike Bernard-Soulier, where they are large and decreased). * **Platelet Aggregometry:** This is the gold standard diagnostic test. In GT, there is **failure of aggregation with all agonists** (ADP, Collagen, Epinephrine, Thrombin) **EXCEPT Ristocetin** [1]. * **Ristocetin Test:** Ristocetin-induced agglutination is **normal** in GT because it depends on GPIb and vWF, which are intact. (In Bernard-Soulier and vWD, Ristocetin agglutination is abnormal) [1], [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-670. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 128.
Question 503: A 12-year-old girl who underwent a bone marrow transplant as part of therapy for ALL presents with pulmonary complaints and neurologic findings. Lung biopsy reveals a granulomatous vasculitis with associated atypical lymphocytes. Clonality studies reveal a monoclonal B cell population with associated polyclonal T cells. What infectious agent is related to this diagnosis?
- A. CMV
- B. EBV (Correct Answer)
- C. HPV
- D. HHV-8
Explanation: ### Explanation The clinical presentation describes **Post-Transplant Lymphoproliferative Disorder (PTLD)**, specifically a subtype resembling **Lymphomatoid Granulomatosis**. **1. Why EBV is the Correct Answer:** PTLD is a serious complication following hematopoietic stem cell or solid organ transplantation. It occurs due to the therapeutic suppression of T-cell immunity, which allows for the uncontrolled proliferation of B-cells infected with the **Epstein-Barr Virus (EBV)** [1]. * **Pathology:** The "granulomatous vasculitis" and "atypical lymphocytes" in the lung are classic features of Lymphomatoid Granulomatosis, an EBV-associated B-cell proliferation. * **Clonality:** The presence of a **monoclonal B-cell population** (driven by EBV) surrounded by reactive **polyclonal T-cells** is a hallmark of this condition [3]. EBV proteins (like LMP-1) mimic CD40 signaling, driving B-cell survival and expansion [2]. **2. Why Other Options are Incorrect:** * **CMV (Cytomegalovirus):** While common post-transplant, it typically causes interstitial pneumonitis with characteristic "owl’s eye" intranuclear inclusions, not monoclonal B-cell proliferation or granulomatous vasculitis [4]. * **HPV (Human Papillomavirus):** Associated with squamous cell carcinomas (cervix, oropharynx) and warts, not post-transplant lymphoproliferative disorders. * **HHV-8 (Human Herpesvirus 8):** Associated with Kaposi Sarcoma, Primary Effusion Lymphoma, and Multicentric Castleman Disease. While it causes malignancy in immunosuppressed patients, it does not typically present as granulomatous vasculitis in the lungs [1]. **3. NEET-PG High-Yield Pearls:** * **PTLD Spectrum:** Ranges from early polyclonal hyperplasia to monomorphic B-cell or T-cell lymphomas. * **Lymphomatoid Granulomatosis:** An "angiocentric and angiodestructive" EBV-positive B-cell lesion. It primarily affects the lungs, followed by the kidney, skin, and CNS. * **Treatment:** Often involves reduction of immunosuppression and Rituximab (anti-CD20). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 181-182. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 368-369. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 369-370. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 367-368.
Question 504: The t(15;19) translocation is associated with which of the following conditions?
- A. Chronic myelogenous leukemia
- B. Chronic neutrophilic leukemia (Correct Answer)
- C. Chronic eosinophilic leukemia
- D. Essential thrombocytosis
Explanation: ### Explanation **Correct Answer: B. Chronic neutrophilic leukemia** **1. Why the correct answer is right:** Chronic Neutrophilic Leukemia (CNL) is a rare BCR-ABL1-negative myeloproliferative neoplasm (MPN). While the most common molecular driver in CNL is the **CSF3R T618I mutation** (present in >80% of cases), specific cytogenetic abnormalities are also associated with the disease. The **t(15;19)(q13;p13.3)** translocation is a characteristic, albeit rare, cytogenetic marker for CNL. This translocation involves the *BRD4* gene on chromosome 19 and the *NUT* gene on chromosome 15, though in the context of CNL, it is specifically recognized as a diagnostic clue when CSF3R mutations are absent. **2. Why the incorrect options are wrong:** * **A. Chronic Myelogenous Leukemia (CML):** CML is defined by the **t(9;22)** translocation [2], resulting in the *BCR-ABL1* fusion gene (Philadelphia chromosome) [1]. * **C. Chronic Eosinophilic Leukemia (CEL):** CEL is frequently associated with rearrangements involving **PDGFRα** (4q12), **PDGFRβ** (5q32), or **FGFR1** (8p11) [1]. The most common is the *FIP1L1-PDGFRA* fusion [1]. * **D. Essential Thrombocytosis (ET):** ET is characterized by mutations in **JAK2 V617F** (~55%), **CALR** (~25%), or **MPL** (~4%) [1]. It does not have a specific diagnostic translocation like t(15;19). **3. Clinical Pearls for NEET-PG:** * **CSF3R T618I:** This is the "hallmark" mutation for CNL and is a high-yield fact for recent exams. * **Diagnostic Criteria:** CNL requires a sustained peripheral blood white cell count ≥ 25 x 10⁹/L, with >80% neutrophils and <10% immature myeloid cells (blasts are rarely seen). * **Splenomegaly:** Almost all CNL patients present with significant splenomegaly [3]. * **Differentiate from Leukemoid Reaction:** Unlike a leukemoid reaction, CNL will show clonal markers (like CSF3R or t(15;19)) and a low/absent LAP (Leukocyte Alkaline Phosphatase) score is not reliable here; molecular testing is gold standard. **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. 624. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 225-226. [3] 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. 625-626.
Question 505: Cabot's rings are features of which condition?
- A. Pernicious anaemia (Correct Answer)
- B. Multiple myeloma
- C. Burkitt's lymphoma
- D. All of the above
Explanation: **Explanation:** **Cabot’s rings** are thin, red-purple, thread-like strands found inside erythrocytes. They typically appear in the shape of a loop or a "figure-of-eight." Morphologically, they are remnants of the **mitotic spindle** (microtubules) or fragments of the nuclear membrane, indicating a defect in erythrocyte production. **Why Pernicious Anaemia is correct:** Cabot’s rings are most characteristically seen in conditions of **severe dyserythropoiesis** (abnormal RBC formation). Pernicious anaemia, a form of Megaloblastic anaemia caused by Vitamin B12 deficiency, leads to significant maturation defects in the bone marrow [1]. Other conditions where they may be seen include lead poisoning and homozygous thalassemia. **Why other options are incorrect:** * **Multiple Myeloma:** This is a plasma cell dyscrasia. The classic peripheral smear finding is **Rouleaux formation** (stacking of RBCs) due to high paraprotein levels, not nuclear remnants. * **Burkitt’s Lymphoma:** This is a high-grade B-cell lymphoma. The hallmark is the **"Starry sky appearance"** on lymph node biopsy and "hand-mirror" cells or vacuolated blasts on a blood film, rather than Cabot's rings. **High-Yield Clinical Pearls for NEET-PG:** * **Howell-Jolly Bodies:** DNA remnants (seen in post-splenectomy/hyposplenism). * **Basophilic Stippling:** Ribosomal RNA precipitates (seen in Lead poisoning and Thalassemia). * **Pappenheimer Bodies:** Siderotic (iron) granules (seen in Sideroblastic anaemia). * **Heinz Bodies:** Denatured hemoglobin (seen in G6PD deficiency; visualized with supra-vital stains like Crystal Violet). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 592-593.
Question 506: The RBC morphology in a peripheral blood smear in thalassemia trait resembles that of which condition?
- A. Vitamin B12 deficiency anemia
- B. Folate deficiency anemia
- C. Hereditary spherocytosis
- D. Iron deficiency anemia (Correct Answer)
Explanation: **Explanation:** The correct answer is **Iron Deficiency Anemia (IDA)**. Both Thalassemia trait and IDA are characterized by a **microcytic hypochromic** blood picture [1]. **1. Why Iron Deficiency Anemia is correct:** In both conditions, there is a defect in hemoglobin synthesis—IDA due to lack of iron and Thalassemia due to reduced globin chain production [1]. This results in small (microcytic) and pale (hypochromic) RBCs. Morphological similarities include the presence of **target cells** (codocytes), though they are typically more numerous in Thalassemia. **2. Why other options are incorrect:** * **Vitamin B12 and Folate Deficiency (Options A & B):** These are **megaloblastic anemias** characterized by **macrocytic** (large) RBCs and hypersegmented neutrophils [3]. This is the morphological opposite of the microcytic cells seen in Thalassemia. * **Hereditary Spherocytosis (Option C):** This condition presents with **spherocytes**—small, dark-staining RBCs that lack central pallor due to a membrane defect [2]. In contrast, Thalassemia cells have increased central pallor (hypochromia). **NEET-PG High-Yield Pearls:** * **Mentzer Index:** Used to differentiate IDA from Thalassemia trait. * **MCV/RBC count < 13** suggests Thalassemia trait (high RBC count relative to MCV). * **MCV/RBC count > 13** suggests Iron Deficiency Anemia. * **RDW (Red Cell Distribution Width):** Usually **normal** in Thalassemia trait (uniform cell size) but **elevated** in IDA (anisocytosis). * **Confirmatory Test:** Hb Electrophoresis is the gold standard for Thalassemia (showing raised HbA2 >3.5%), while Serum Ferritin is the best initial test for IDA. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 590-591. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 594-595.
Question 507: The Philadelphia chromosome is characteristically seen in which of the following conditions?
- A. Chronic Myeloid Leukemia (CML)
- B. Acute Lymphoblastic Leukemia (ALL)
- C. Both CML and ALL (Correct Answer)
- D. Neither CML nor ALL
Explanation: **Explanation:** The Philadelphia (Ph) chromosome is a hallmark cytogenetic abnormality resulting from a reciprocal translocation between chromosomes 9 and 22, denoted as **t(9;22)(q34;q11)** [1]. This translocation fuses the *ABL1* gene on chromosome 9 with the *BCR* gene on chromosome 22, creating the **BCR-ABL1 fusion gene** [2]. This gene encodes a chimeric protein with constitutive tyrosine kinase activity, driving uncontrolled cellular proliferation [2]. **Why Option C is Correct:** * **Chronic Myeloid Leukemia (CML):** The Ph chromosome is the diagnostic hallmark of CML, present in **>95%** of cases [2]. It is typically associated with the **p210** protein isoform. * **Acute Lymphoblastic Leukemia (ALL):** The Ph chromosome is also found in approximately **25-30% of adult ALL** cases and **3-5% of pediatric ALL** cases. In ALL, it is often associated with the **p190** protein isoform and signifies a poor prognosis. **Why other options are incorrect:** * **Option A & B:** While the Ph chromosome is most famously associated with CML, selecting only one leukemia is incomplete. Because it serves as a major diagnostic and prognostic marker in both conditions, "Both" is the most accurate answer. **NEET-PG High-Yield Pearls:** 1. **Molecular Weight:** CML is usually associated with **p210** (Major breakpoint), while Ph+ ALL is more commonly associated with **p190** (Minor breakpoint). 2. **Prognosis:** In ALL, the presence of t(9;22) is a **poor prognostic indicator**. 3. **Targeted Therapy:** The discovery of the Ph chromosome led to the development of **Imatinib (Gleevec)**, a tyrosine kinase inhibitor (TKI) that revolutionized the treatment of these malignancies [3]. 4. **Detection:** Gold standard methods include Conventional Karyotyping, FISH (Fluorescence In Situ Hybridization), and RT-PCR [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 225-226. [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. 624. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612.
Question 508: Cyclin D1/IgH gene rearrangement is associated with which of the following malignancies?
- A. Mantle cell lymphoma (Correct Answer)
- B. Hairy cell leukemia
- C. Follicular lymphoma
- D. Diffuse large B-cell lymphoma
Explanation: **Mantle Cell Lymphoma (MCL)** is characterized by the pathognomonic chromosomal translocation **t(11;14)(q13;q32)** [1]. This translocation involves the **CCND1 gene** (encoding Cyclin D1) on chromosome 11 and the **Immunoglobulin Heavy chain (IgH) locus** on chromosome 14 [2]. The juxtaposition leads to the overexpression of Cyclin D1, a protein that promotes the transition from the G1 to the S phase of the cell cycle by phosphorylating the Retinoblastoma (Rb) protein [2]. Immunohistochemistry (IHC) typically shows positivity for **Cyclin D1 and CD5**, while being negative for CD23 [2]. **Analysis of Incorrect Options:** * **Hairy Cell Leukemia:** Associated with the **BRAF V600E** mutation. It typically presents with massive splenomegaly and "dry tap" on bone marrow aspiration. * **Follicular Lymphoma:** Characterized by **t(14;18)**, involving the **BCL-2** gene [4,5]. This leads to the overexpression of BCL-2, an anti-apoptotic protein [4,5]. * **Diffuse Large B-cell Lymphoma (DLBCL):** A heterogeneous group; however, it is most commonly associated with rearrangements of **BCL-6** (30% of cases) or t(14;18) [3]. **High-Yield Pearls for NEET-PG:** * **MCL Marker:** CD5 positive, CD23 negative (helps differentiate from CLL/SLL which is CD5+ and CD23+). * **Morphology:** Presence of "centrocyte-like" cells [2]. * **Clinical:** Often presents at an advanced stage; may involve the GI tract as **lymphomatous polyposis** [1]. * **Translocation Mnemonic:** "Mantle" has 11 letters (if you count carefully or use it as a hook) → t(11;14). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 562-563. [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. 610-612. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 563-564. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 561-562. [5] 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. 602-604.
Question 509: Sideroblasts are seen in all conditions except?
- A. Thalassemia (Correct Answer)
- B. Myelofibrosis
- C. Alcoholism
- D. Iron overload
Explanation: **Explanation:** The presence of **sideroblasts** (nucleated erythroblasts with iron granules in the cytoplasm) is a hallmark of disorders where iron utilization is impaired despite adequate iron stores. **Why Thalassemia is the correct answer:** In **Thalassemia**, the primary defect is a quantitative deficiency in globin chain synthesis [1]. While iron overload can occur due to repeated transfusions or increased absorption, the iron is typically deposited in the reticuloendothelial system or as diffuse ferritin [3]. Thalassemia is characterized by **target cells** and microcytic hypochromic anemia, but it is not classically associated with the formation of ring sideroblasts in the bone marrow, which require a defect in the heme synthesis pathway itself [2]. **Analysis of other options:** * **Alcoholism:** Alcohol is a mitochondrial toxin that inhibits several enzymes in the heme synthesis pathway (like ferrochelatase), leading to the formation of ring sideroblasts. * **Iron Overload:** Conditions like primary or secondary hemochromatosis lead to excessive iron deposition within developing erythroblasts. * **Myelofibrosis:** Sideroblasts can be seen in various myeloproliferative and myelodysplastic syndromes (MDS). Specifically, Refractory Anemia with Ring Sideroblasts (RARS) is a subtype of MDS where sideroblasts are a defining feature. **NEET-PG High-Yield Pearls:** * **Ring Sideroblasts:** Defined as having $\geq$ 5 iron granules covering at least one-third of the nuclear circumference. * **Stain used:** **Prussian Blue (Perl’s stain)** is essential to visualize siderotic granules. * **Common Causes of Sideroblastic Anemia:** Remember the mnemonic **LEAD**: **L**ead poisoning, **E**thanol (Alcohol), **A**INH (Isoniazid), and **D**eficiency of Vitamin B6 (Pyridoxine). * **Key Enzyme:** The most common congenital cause is a defect in **ALAS-2** (delta-aminolevulinate synthase). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 600-601. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 590-591. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 648.
Question 510: Neoplastic giant cells characteristically seen in Hodgkin's lymphoma are:
- A. Warthin-Finkeldey cells
- B. Russell bodies
- C. Reed-Sternberg cells (Correct Answer)
- D. Mikulicz cells
Explanation: **Explanation:** **Correct Answer: C. Reed-Sternberg (RS) cells** Reed-Sternberg cells are the hallmark neoplastic cells of Hodgkin’s Lymphoma (HL) [1]. They are derived from germinal center B-cells [1]. Morphologically, a classic RS cell is a large cell (15–45 µm) with abundant cytoplasm and at least two nuclear lobes or nuclei [2]. These nuclei possess large, acidophilic, "owl-eye" nucleoli surrounded by a clear halo [2]. Their presence in a characteristic reactive inflammatory background is essential for the diagnosis of HL [1]. **Analysis of Incorrect Options:** * **A. Warthin-Finkeldey cells:** These are multinucleated giant cells with "grape-like" nuclear clusters found in hyperplastic lymph nodes during the prodromal stage of **Measles**. * **B. Russell bodies:** These are eosinophilic, homogeneous cytoplasmic inclusions representing accumulated immunoglobulin within **Plasma cells**. They are seen in conditions like Multiple Myeloma or chronic inflammation. * **D. Mikulicz cells:** These are large, foamy macrophages containing *Klebsiella rhinoscleromatis*, characteristic of **Rhinoscleroma** (a chronic granulomatous condition of the nose). **High-Yield Clinical Pearls for NEET-PG:** * **Immunophenotype:** Classic RS cells are typically **CD15+ and CD30+**, but **CD20- and CD45-**. * **Variants:** * *L&H Cells (Popcorn cells):* Seen in Nodular Lymphocyte Predominant HL (CD20+, CD15-, CD30-) [4]. * *Lacunar cells:* Characteristic of the Nodular Sclerosis variant [2]. * **Bimodal Age Distribution:** HL shows peaks in the 20s and after age 50 [1]. * **EBV Association:** Most commonly associated with the Mixed Cellularity subtype [3]. **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. 614-616. [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. 616. [3] 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. 616-618. [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, p. 618.
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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
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Chronic Leukemias
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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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