Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1141: Disseminated Intravascular Coagulation (DIC) is seen with all of the following conditions EXCEPT:

A. Accidental hemorrhage (Correct Answer)
B. Black water fever
C. Amniotic fluid embolism
D. Overdosage with Vitamin K

Explanation: **Explanation:** Disseminated Intravascular Coagulation (DIC) is a thrombohemorrhagic disorder characterized by the systemic activation of the coagulation cascade, leading to widespread fibrin deposition and subsequent consumption of platelets and clotting factors [4]. **Why Option D is the Correct Answer:** **Overdosage with Vitamin K** does not cause DIC. Vitamin K is a fat-soluble vitamin essential for the gamma-carboxylation (activation) of Clotting Factors II, VII, IX, and X, as well as Proteins C and S [2], [5]. An overdose of Vitamin K may lead to a hypercoagulable state or interfere with warfarin therapy, but it does not trigger the systemic, uncontrolled consumption of factors seen in DIC. **Why the other options are wrong (Causes of DIC):** * **Accidental Hemorrhage (Abruptio Placentae):** This is a classic trigger for DIC. The premature separation of the placenta releases massive amounts of **tissue thromboplastin** (Tissue Factor) into the maternal circulation, activating the extrinsic pathway [3]. * **Amniotic Fluid Embolism:** This is an obstetric emergency where amniotic fluid enters maternal circulation. The fluid contains procoagulant substances and tissue factor that trigger rapid, severe DIC [1], [3]. * **Black Water Fever:** This is a complication of *Plasmodium falciparum* malaria characterized by massive intravascular hemolysis. The release of erythrocyte stroma and procoagulant phospholipids acts as a trigger for DIC. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of DIC:** Gram-negative sepsis (due to Endotoxins/LPS) [3]. * **Best Screening Test:** Platelet count (decreased) and PT/aPTT (prolonged) [4]. * **Most Specific Test:** **D-dimer levels** (elevated), indicating fibrinolysis of cross-linked fibrin. * **Peripheral Smear:** Characterized by **Schistocytes** (fragmented RBCs) due to microangiopathic hemolytic anaemia (MAHA) [4]. **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. 151-152. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 671-672. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 624-625.

Question 1142: Which anticoagulant is used for chelating calcium?

A. EDTA
B. Oxalate
C. Sodium citrate
D. All of the above (Correct Answer)

Explanation: **Explanation:** The coagulation cascade is a calcium-dependent process; specifically, **Factor IV (Calcium)** is essential for several steps in the clotting pathway [1]. To prevent blood from clotting in vitro, anticoagulants must either remove or neutralize these calcium ions. **Mechanism of Action:** The correct answer is **"All of the above"** because EDTA, Oxalate, and Sodium Citrate all function by **chelating (binding) calcium**, thereby making it unavailable for the coagulation cascade. * **EDTA (Ethylenediamine Tetraacetic Acid):** The most common anticoagulant for routine hematology (CBC). It chelates calcium ions effectively, preserving cell morphology. * **Sodium Citrate:** Used for coagulation studies (PT/APTT) and blood transfusion bags. It binds calcium to form a soluble complex. It is preferred for coagulation tests because the process is reversible by adding back calcium. * **Oxalates:** (e.g., Potassium oxalate) These combine with calcium to form an insoluble precipitate of calcium oxalate, effectively removing it from the plasma. **Why other options are "wrong" as standalone answers:** While A, B, and C are all individually correct in their mechanism, the question asks which anticoagulant is used for this purpose. Since all three share the same fundamental mechanism of calcium chelation/removal, "All of the above" is the most accurate choice. **High-Yield Clinical Pearls for NEET-PG:** * **EDTA:** Best for morphology; however, it can cause "Platelet Satellitism" (an in-vitro artifact leading to pseudothrombocytopenia). * **Sodium Citrate:** The ratio for coagulation studies is **1:9** (anticoagulant to blood). For ESR (Westergren method), the ratio is **1:4**. * **Heparin:** Unlike the others, Heparin does **not** chelate calcium. It works by activating **Antithrombin III**, which inhibits Thrombin and Factor Xa [2]. It is the anticoagulant of choice for arterial blood gas (ABG) analysis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 126-130. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 583-584.

Question 1143: Which of the following conditions predisposes to leukemia?

A. Ionizing radiation
B. Myelofibrosis
C. Infectious mononucleosis (Correct Answer)
D. Polycythemia vera

Explanation: **Explanation:** The question asks for the condition that **predisposes** to leukemia. While several factors are associated with leukemogenesis, the correct answer in this context is **Infectious Mononucleosis (IM)**. **1. Why Infectious Mononucleosis is the Correct Answer:** Infectious Mononucleosis is caused by the **Epstein-Barr Virus (EBV)**. EBV is a potent oncogenic virus that infects B-lymphocytes via the CD21 receptor [3]. It drives B-cell proliferation and is strongly associated with the development of various hematological malignancies, most notably **Burkitt Lymphoma** (a high-grade B-cell leukemia/lymphoma) and Hodgkin Lymphoma [1]. In the context of "predisposing to leukemia," EBV’s ability to immortalize B-cells is the key underlying mechanism [4]. **2. Analysis of Incorrect Options:** * **Ionizing Radiation (A):** While radiation is a known risk factor for AML and CML [2], it is considered an **extrinsic etiological agent** rather than a predisposing clinical "condition" or disease state [5]. * **Myelofibrosis (B) & Polycythemia Vera (D):** These are Myeloproliferative Neoplasms (MPNs). While they can *transform* into Acute Myeloid Leukemia (Blast Crisis), they are technically already considered "pre-leukemic" or chronic malignant states themselves. In standard MCQ patterns, viral triggers like EBV are frequently highlighted as predisposing biological factors. **High-Yield Clinical Pearls for NEET-PG:** * **EBV Associations:** Burkitt Lymphoma (t(8;14)), Nasopharyngeal Carcinoma, and Primary CNS Lymphoma in HIV patients. * **Atypical Lymphocytes:** In IM, the "Downey cells" seen on peripheral smear are actually **CD8+ T-cells** reacting against infected B-cells. * **Other Predisposing Conditions:** Down Syndrome (increased risk of ALL and AML-M7), Fanconi Anemia, and Bloom Syndrome. **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. 219-220. [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. 595-596. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 368-369. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 335-336. [5] 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. 220-221.

Question 1144: Which organ is most commonly affected in the disorder characterized by the given peripheral blood smear findings?

A. Lungs
B. Kidney
C. Spleen (Correct Answer)
D. Liver

Explanation: ***Spleen*** - The spleen is the **most commonly affected organ** in sickle cell disease due to **vaso-occlusive crises** causing repeated infarction and congestion. - Early in the disease, the spleen undergoes **sequestration crises**, and later develops **autosplenectomy** from repeated sickling episodes. *Lungs* - While **acute chest syndrome** can occur in sickle cell disease, it is not the most commonly affected organ overall. - Pulmonary complications are **episodic** rather than the primary site of chronic organ damage. *Kidney* - **Nephropathy** can develop in sickle cell disease due to chronic hypoxia and sickling in renal medulla. - However, renal involvement typically occurs **later in the disease course** and is less frequent than splenic complications. *Liver* - **Hepatic sequestration** and cholestasis can occur but are **less common** than splenic involvement. - Liver complications are usually **secondary** to hemolysis and transfusion-related iron overload rather than primary sickling effects.

Question 1145: In leucopenia, which white blood cell type is predominantly involved?

A. Erythrocytes
B. Granulocytes (Correct Answer)
C. Eosinophils
D. Monocytes

Explanation: **Explanation:** **Leucopenia** is defined as a decrease in the total white blood cell (WBC) count below the normal range (typically <4,000/mm³). While a decrease in any WBC subtype can contribute to leucopenia, it is **predominantly caused by a reduction in granulocytes**, specifically **neutrophils** (neutropenia) [2]. Since neutrophils are the most abundant leucocytes in the peripheral blood (50-70%), their fluctuation has the most significant impact on the total WBC count [2]. **Analysis of Options:** * **B. Granulocytes (Correct):** This category includes neutrophils, eosinophils, and basophils. Neutropenia is the most common clinical cause of leucopenia, often resulting from reduced production (e.g., drug-induced bone marrow suppression) or increased peripheral destruction [1]. * **A. Erythrocytes:** These are red blood cells (RBCs). A decrease in erythrocytes is termed **anemia**, not leucopenia. * **C. Eosinophils:** While a decrease in eosinophils (eosinopenia) can occur (e.g., in Cushing syndrome or acute stress), they constitute only 1-4% of the total WBC count. Their reduction does not significantly lower the total leucocyte count compared to granulocytes. * **D. Monocytes:** Monocytopenia is rare and typically associated with specific conditions like hairy cell leukemia or MAC infections, but it is not the primary driver of general leucopenia. **High-Yield Clinical Pearls for NEET-PG:** * **Agranulocytosis:** A severe form of neutropenia where the count drops below **500 cells/mm³**, making the patient highly susceptible to fulminant bacterial and fungal infections. * **Common Causes:** Drugs are a frequent culprit (e.g., Clozapine, Antithyroid drugs like Methimazole, and Chemotherapy) [1]. * **Morphology:** In drug-induced agranulocytosis, the bone marrow may show a "maturation arrest" at the promyelocyte stage [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 590-592. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 578-579.

Question 1146: Which cell is not seen in Hodgkin lymphoma?

A. Reed-Sternberg cell
B. Lacunar cell
C. L&H cell
D. Langerhans cell (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Langerhans cell**. This question tests the ability to distinguish between the specific neoplastic cells of Hodgkin Lymphoma (HL) and cells belonging to the dendritic cell lineage. **1. Why Langerhans cell is the correct answer:** Langerhans cells are specialized antigen-presenting dendritic cells normally found in the stratum spinosum of the epidermis [1]. In pathology, they are the hallmark of **Langerhans Cell Histiocytosis (LCH)**, characterized by Birbeck granules (tennis-racket shape) on electron microscopy and CD1a/S100/Langerin positivity [1]. They have no primary role in the pathogenesis or diagnosis of Hodgkin Lymphoma. **2. Why the other options are incorrect:** * **Reed-Sternberg (RS) cell:** The diagnostic hallmark of Classical Hodgkin Lymphoma (CHL). It is a large, multinucleated cell with prominent "owl-eye" nucleoli [2], [3]. * **Lacunar cell:** A variant of the RS cell seen specifically in **Nodular Sclerosis HL**. During formalin fixation, the cytoplasm retracts, leaving the nucleus in a clear space or "lacuna" [2]. * **L&H cell (Lymphocytic and Histiocytic cell):** Also known as the **"Popcorn cell,"** this is the characteristic neoplastic cell of **Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLPHL)** [4]. Unlike classical RS cells, these are CD20 positive and CD15/CD30 negative [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Classical HL Markers:** CD15+, CD30+, CD45–. * **NLPHL (Popcorn cell) Markers:** CD20+, CD45+, CD15–, CD30– [4]. * **Most common subtype:** Nodular Sclerosis (often presents with mediastinal mass in young females). * **Best prognosis:** Lymphocyte Rich; **Worst prognosis:** Lymphocyte Depleted. * **EBV Association:** Highest in Mixed Cellularity subtype. **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. 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. 614-616. [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.

Question 1147: Lupus anticoagulants may cause all of the following except:

A. Recurrent abortion
B. False positive VDRL results
C. Increased prothrombin time (Correct Answer)
D. Arterial thrombosis

Explanation: **Explanation:** Lupus Anticoagulant (LA) is a misnomer. While it acts as an anticoagulant *in vitro*, it is a potent prothrombotic agent *in vivo*. It belongs to the Antiphospholipid Antibody Syndrome (APS) spectrum. **Why "Increased Prothrombin Time" is the correct answer:** Lupus anticoagulants are antibodies directed against phospholipids and phospholipid-binding proteins. In laboratory testing, they interfere with phospholipid-dependent coagulation assays [1], [2]. This characteristically causes a **prolonged Activated Partial Thromboplastin Time (aPTT)**, not Prothrombin Time (PT). PT remains typically normal because the concentration of phospholipids used in the PT reagent (thromboplastin) is high enough to override the inhibitory effect of the antibodies. **Analysis of Incorrect Options:** * **Recurrent abortion:** APS is a leading cause of pregnancy morbidity. LA causes placental infarction and spiral artery thrombosis, leading to recurrent miscarriages (usually after 10 weeks) [1]. * **False positive VDRL:** The VDRL/RPR test uses cardiolipin as an antigen. Since LA patients often have anti-cardiolipin antibodies, they may show a "biological false positive" for syphilis [2]. * **Arterial thrombosis:** Despite the name "anticoagulant," LA promotes a hypercoagulable state leading to both venous (DVT/PE) and arterial (stroke/MI) thrombosis [1], [2]. **High-Yield Clinical Pearls for NEET-PG:** * **The Paradox:** LA causes a **prolonged aPTT** in the lab but **thrombosis** in the patient [1]. * **Mixing Study:** If aPTT is prolonged due to LA, it **will not correct** upon mixing with normal plasma (unlike factor deficiencies). * **Confirmatory Test:** Dilute Russell Viper Venom Time (dRVVT) is the most sensitive screening test for LA. * **Diagnostic Criteria:** Requires at least one clinical criteria (thrombosis or pregnancy loss) and one laboratory criteria (LA, anti-cardiolipin, or anti-β2-glycoprotein I antibodies) positive on two occasions 12 weeks apart [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 626-627. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 134-135.

Question 1148: Reticulocytes are stained with which of the following reagents?

A. Methyl violet
B. Brilliant Cresyl blue (Correct Answer)
C. Sudan black
D. Indigo carmine

Explanation: **Explanation:** Reticulocytes are immature red blood cells that contain residual ribosomal RNA (rRNA). Because these cells lack a nucleus, they cannot be identified on a standard Leishman or Wright stain (where they appear as polychromatic cells). To visualize the characteristic "reticulum" or network of RNA, **Supravital Staining** is required [1]. **1. Why Brilliant Cresyl Blue is correct:** Supravital stains are applied to living, unfixed cells. Reagents like **Brilliant Cresyl Blue** or **New Methylene Blue** penetrate the living cell membrane and cause the acidic ribosomal RNA to aggregate and precipitate into a visible blue-stained network or granules [1]. This allows for an accurate reticulocyte count, which is the best indicator of bone marrow erythropoietic activity. **2. Analysis of Incorrect Options:** * **Methyl Violet:** Used primarily to visualize **Heinz bodies** (denatured hemoglobin) in conditions like G6PD deficiency. * **Sudan Black:** A lipid-soluble stain used to identify myeloblasts in **Acute Myeloid Leukemia (AML)**; it stains the phospholipid membranes of primary granules. * **Indigo Carmine:** A dye used primarily in surgery and urology to highlight urinary tract patency or as a marker for chromoendoscopy; it has no role in hematological cell staining. **3. NEET-PG High-Yield Pearls:** * **Supravital Stains:** Remember the duo—**New Methylene Blue** (preferred/more stable) and **Brilliant Cresyl Blue**. * **Reticulocyte Index (RI):** In anemia, always look for the "Corrected Reticulocyte Count." An RI > 2-3% indicates a brisk marrow response (e.g., hemolysis or acute blood loss). * **Miller Disc:** An optical tool used in the eyepiece of a microscope to standardize the manual counting of reticulocytes. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 578-579.

Question 1149: Which of the viruses is not commonly implicated in the pathogenesis of Non-Hodgkin's lymphomas?

A. Human T-cell leukemia virus-1 (HTLV-1)
B. Epstein-Barr virus (EBV)
C. Human herpesvirus-8 (HHV-8)
D. Cytomegalovirus (CMV) (Correct Answer)

Explanation: **Explanation:** The pathogenesis of Non-Hodgkin’s Lymphoma (NHL) is frequently linked to oncogenic viruses that drive malignant transformation through chronic inflammation or direct integration into the host genome. **Cytomegalovirus (CMV)** is the correct answer because, while it is a significant cause of morbidity in immunocompromised patients (causing retinitis, pneumonitis, or colitis), it is **not** an oncogenic virus and is not implicated in the development of lymphomas. **Analysis of Incorrect Options:** * **HTLV-1:** A retrovirus strongly associated with **Adult T-cell Leukemia/Lymphoma (ATLL)** [4]. It utilizes the *Tax* protein to stimulate cell proliferation and inhibit DNA repair. * **EBV (HHV-4):** One of the most common oncogenic viruses [2]. It is implicated in **Burkitt Lymphoma** (especially the endemic variant), Hodgkin Lymphoma, and **Diffuse Large B-cell Lymphoma (DLBCL)**, particularly in HIV patients [3], [5]. * **HHV-8 (KSHV):** This virus is the primary causative agent of **Primary Effusion Lymphoma (PEL)** and Multicentric Castleman Disease, in addition to Kaposi Sarcoma [1], [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Hepatitis C Virus (HCV):** Associated with **Splenic Marginal Zone Lymphoma** and Lymphoplasmacytic Lymphoma [4]. * ***H. pylori*:** Though a bacterium, it is a high-yield association for **Gastric MALToma**. * **Burkitt Lymphoma:** Look for the "Starry Sky" appearance on histology and the **t(8;14)** translocation involving the *c-myc* gene [5]. * **HTLV-1** is endemic in parts of Japan, the Caribbean, and Africa; look for "flower cells" on peripheral smears [4]. **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. 595-596. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 261-262. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 262-263. [4] 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. 219-220. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 335-336.

Question 1150: Histiocytosis X is a spectrum of disorders that includes which of the following conditions?

A. Eosinophilic granuloma
B. Hand-Schüller-Christian disease
C. Letterer-Siwe disease
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Histiocytosis X**, now more commonly known as **Langerhans Cell Histiocytosis (LCH)**, is a group of idiopathic disorders characterized by the abnormal proliferation of Langerhans cells (dendritic cells) [1]. These cells are identified by their characteristic "coffee-bean" nuclei and **Birbeck granules** (tennis-racket shaped) on electron microscopy [1]. The spectrum of Histiocytosis X includes three distinct clinical entities based on the extent of involvement and age of onset: 1. **Letterer-Siwe Disease (Option C):** The most severe form, typically seen in infants (<2 years). it is a **multifocal, multisystem** disorder involving the skin (seborrheic-like rash), organs (hepatosplenomegaly), and bone marrow. It carries a poor prognosis. 2. **Hand-Schüller-Christian Disease (Option B):** A **multifocal, unisystem** variant usually seen in children. It is classically defined by a high-yield triad: **Calvarial bone defects, Exophthalmos, and Diabetes Insipidus** (due to pituitary involvement). 3. **Eosinophilic Granuloma (Option A):** The mildest and most common form, usually **unifocal**. It typically presents as a solitary osteolytic lesion in the skull, ribs, or femur in older children or young adults. Since all three conditions are part of the Histiocytosis X spectrum, **Option D** is the correct answer. **High-Yield NEET-PG Pearls:** * **Immunohistochemistry (IHC):** LCH cells are characteristically positive for **CD1a, S100, and CD207 (Langerin)** [1]. Langerin is the most specific marker. * **Radiology:** Bone lesions are typically "punched-out" lytic lesions without a sclerotic rim. * **Morphology:** On H&E stain, look for "grooved" or "folded" nuclei resembling coffee beans [1]. **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.

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