Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 271: Which of the following is a cause for disseminated intravascular coagulation (DIC)?

A. Thrombotic thrombocytopenic purpura (TTP)
B. Malignancy (Correct Answer)
C. Lymphoma
D. Massive blood transfusion

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 [1]. **Why Malignancy is Correct:** Malignancy is a classic and frequent cause of DIC. Cancer cells (especially in **Acute Promyelocytic Leukemia (APL/M3)** and adenocarcinomas of the pancreas, prostate, and lung) release **tissue factor (TF)** or cancer procoagulants into the circulation [1]. These substances activate Factor VII, triggering the extrinsic pathway of coagulation [1]. In APL, the release of procoagulant granules from promyelocytes is a high-yield medical emergency. **Analysis of Incorrect Options:** * **A. Thrombotic Thrombocytopenic Purpura (TTP):** While TTP involves microvascular thrombosis, it is a **primary platelet disorder** (due to ADAMTS13 deficiency) rather than a primary activation of the coagulation cascade. In TTP, PT and aPTT are typically normal, whereas in DIC, they are prolonged. * **C. Lymphoma:** While some aggressive lymphomas can trigger DIC, solid tumors and leukemias (like APL) are much more classically associated with this pathology in the context of standard medical examinations. * **D. Massive Blood Transfusion:** This typically leads to **dilutional thrombocytopenia** and a deficiency of coagulation factors (dilutional coagulopathy), but it does not inherently trigger the systemic activation of the coagulation cascade seen in DIC. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of DIC:** Sepsis (Gram-negative organisms releasing endotoxins) [1]. * **Best screening test:** Platelet count (decreased) and PT/aPTT (prolonged) [2]. * **Most specific test:** D-dimer (elevated due to secondary fibrinolysis) [2]. * **Peripheral Smear:** Presence of **Schistocytes** (fragmented RBCs) due to microangiopathic hemolytic anemia (MAHA) [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. 671-672. [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. 151-152.

Question 272: Which CD marker is specific for the myeloid series?

A. CD34
B. CD45
C. CD99
D. CD117 (Correct Answer)

Explanation: **Explanation:** The correct answer is **CD117 (c-kit)**. CD117 is a transmembrane receptor tyrosine kinase that is highly expressed on hematopoietic stem cells and committed myeloid progenitors. In the context of hematopathology, it is considered a specific marker for the **myeloid series**, particularly in the diagnosis of Acute Myeloid Leukemia (AML) [1]. **Analysis of Options:** * **CD117 (Correct):** It is expressed in approximately 95% of AML cases and is absent in most Lymphoblastic Leukemias (except for rare T-ALL subsets). It is also a hallmark marker for Mast Cell Disease [1] and Gastrointestinal Stromal Tumors (GIST). * **CD34:** This is a marker for **hematopoietic stem cells** and primitive progenitors. While found in many leukemias, it is not specific to the myeloid series as it is also expressed in Acute Lymphoblastic Leukemia (ALL) and vascular tumors (e.g., Angiosarcoma). * **CD45:** Known as the **Leukocyte Common Antigen (LCA)**, it is expressed on almost all white blood cells (granulocytes, monocytes, and lymphocytes). It is a pan-leukocyte marker, not specific to any single lineage. * **CD99 (MIC2):** This is a marker primarily used for the diagnosis of **Ewing Sarcoma/PNET**. While it can be expressed in some cases of T-ALL, it has no specificity for the myeloid lineage. **High-Yield Clinical Pearls for NEET-PG:** * **MPO (Myeloperoxidase):** The most specific histochemical stain for the myeloid series [2]. * **CD13 & CD33:** Other common pan-myeloid markers used in flow cytometry. * **CD14 & CD64:** Specific markers for the **monocytic** lineage (relevant for AML-M4/M5). * **Auer Rods:** Pathognomonic for myeloid differentiation (found in AML) [2]. **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. 624-625. [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. 620.

Question 273: According to WHO, which of the following is not a B cell lymphoma?

A. Burkitt's lymphoma
B. Follicular lymphoma
C. Mantle cell lymphoma
D. Anaplastic large cell lymphoma (Correct Answer)

Explanation: The classification of Non-Hodgkin Lymphomas (NHL) is primarily based on the cell of origin: B-cell, T-cell, or Natural Killer (NK) cell lineages [1]. **Why Anaplastic Large Cell Lymphoma (ALCL) is the correct answer:** ALCL is a **T-cell lymphoma**, not a B-cell lymphoma [2]. It is characterized by the proliferation of large pleomorphic cells (hallmark cells) that strongly express **CD30**. A key diagnostic feature in many cases is the chromosomal translocation **t(2;5)**, which leads to the expression of the **ALK (Anaplastic Lymphoma Kinase)** protein [4]. **Why the other options are incorrect:** * **Burkitt’s Lymphoma:** A highly aggressive **B-cell** NHL associated with the **c-MYC** gene translocation, typically **t(8;14)**. It shows a "starry sky" appearance on histology. * **Follicular Lymphoma:** A common indolent **B-cell** NHL arising from germinal center B-cells [5]. It is characterized by the **t(14;18)** translocation involving the **BCL-2** gene [5]. * **Mantle Cell Lymphoma:** A **B-cell** NHL arising from the mantle zone of the lymph node follicle. It is associated with **t(11;14)** and overexpression of **Cyclin D1**. **High-Yield Clinical Pearls for NEET-PG:** * **ALCL Marker:** CD30 positive (also seen in Reed-Sternberg cells of Hodgkin Lymphoma). * **ALK Protein:** ALK-positive ALCL has a significantly better prognosis than ALK-negative ALCL [2]. * **Hallmark Cells:** Large cells with kidney-shaped or horseshoe-shaped nuclei are pathognomonic for ALCL [3]. * **B-cell Markers:** CD19, CD20, and CD79a. * **T-cell Markers:** CD2, CD3, CD5, and CD7. **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. 596-598. [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. 612-613. [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. 613-614. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 565-566. [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 274: Auer bodies are seen in which of the following subtypes of Acute Myeloid Leukemia (AML)?

A. M1-AML (Correct Answer)
B. M3-AML
C. M6-AML
D. Acute Lymphoblastic Leukemia (ALL)

Explanation: **Explanation:** **Auer bodies** are pathognomonic inclusions found in the cytoplasm of leukemic blasts [1]. They are composed of fused lysosomes containing peroxidase, crystalline structures, and enzymes. Their presence confirms a **myeloid** origin, effectively ruling out lymphoid malignancies. 1. **Why Option A is Correct:** In the FAB classification, **M1 (AML without maturation)** is characterized by myeloblasts that show minimal maturation but frequently contain Auer bodies. While Auer bodies are most numerous in M3, they are a classic diagnostic feature of M1, M2, and M4 subtypes [1]. 2. **Why Option B is Incorrect (Contextual):** While Auer bodies are famously seen in **M3 (Acute Promyelocytic Leukemia)**, they often appear as bundles called **"Faggot cells"** [1][2]. In the context of this specific question, M1 is the primary association for single/classic Auer bodies. (Note: In many clinical scenarios, both M1 and M3 show them, but M1 is the classic textbook answer for "seen in" when differentiating from non-myeloid or erythroid types). 3. **Why Option C is Incorrect:** **M6 (Acute Erythroid Leukemia)** involves the erythroid lineage. Auer bodies are specific to the **myelocytic** line; therefore, they are typically absent in pure erythroid or megakaryocytic (M7) leukemias. 4. **Why Option D is Incorrect:** **ALL** involves lymphoblasts. Auer bodies are **never** seen in lymphoblasts [2]. Their presence is the single most important morphological feature to exclude ALL. **High-Yield Clinical Pearls for NEET-PG:** * **Faggot Cells:** Multiple Auer bodies in a single cell; characteristic of **AML-M3 (t(15;17))** [1][2]. * **Staining:** Auer bodies are strongly **Myeloperoxidase (MPO)** and Sudan Black B positive. * **M0 Exception:** AML-M1 shows Auer bodies, but **AML-M0** (minimally differentiated) is typically negative for them on light microscopy. * **Rule of Thumb:** If you see an Auer body, it is AML (specifically M1 through M5), never ALL. **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. 620. [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. 621-622.

Question 275: Which of the following markers are seen in Primary effusion lymphoma?

A. CD30, CD138 (Correct Answer)
B. CD20, CD28
C. CD19, CD20
D. CD29, CD30

Explanation: **Primary Effusion Lymphoma (PEL)** is a rare, aggressive B-cell non-Hodgkin lymphoma caused by **Human Herpesvirus-8 (HHV-8)**, typically occurring in HIV-positive or immunocompromised patients [1]. ### **Why Option A is Correct?** PEL has a unique "null" phenotype or a **plasmablastic** immunophenotype. Although it is a B-cell malignancy, it characteristically lacks traditional B-cell markers (like CD19, CD20, and CD79a) [1]. Instead, it expresses markers of terminal B-cell differentiation: * **CD138 (Syndecan-1):** A plasma cell marker consistently expressed in PEL. * **CD30:** Frequently expressed (approx. 70% of cases), reflecting its activated/transformed state. * **Other markers:** EMA (Epithelial Membrane Antigen) and CD45 are often positive. ### **Why Other Options are Incorrect?** * **Options B & C (CD19, CD20):** These are pan-B-cell markers. PEL is defined by the **absence** of these surface markers (downregulated during plasmablastic transformation) [1]. Their presence would point toward other B-cell lymphomas like DLBCL. * **Option D (CD29):** CD29 is an integrin subunit not used as a diagnostic marker for PEL. ### **High-Yield Clinical Pearls for NEET-PG** 1. **Viral Association:** 100% of cases are associated with **HHV-8** (KSHV) [1]. Many are also co-infected with **EBV**. 2. **Clinical Presentation:** Presents as malignant effusions (pleural, pericardial, or peritoneal) **without** a detectable solid tumor mass or lymphadenopathy [1]. 3. **Morphology:** Cells show "plasmablastic" or "immunoblastic" features. 4. **Key Diagnostic Step:** Detection of **LANA-1** (Latent Nuclear Antigen-1) via immunohistochemistry confirms HHV-8 infection. **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. 604-605.

Question 276: What is the most common lymph node involved in Hodgkin's lymphoma?

A. Inguinal
B. Cervical (Correct Answer)
C. Axillary
D. Sub-clavicular

Explanation: **Explanation:** **Hodgkin’s Lymphoma (HL)** typically presents as a painless, rubbery enlargement of lymph nodes. The disease characteristically follows a predictable, contiguous pattern of spread through the lymphatic system. **1. Why Cervical is Correct:** The **cervical lymph nodes** (specifically the upper cervical, supraclavicular, or mediastinal groups) are the most common site of involvement, seen in approximately **60-80% of cases** at the time of diagnosis [1]. This predilection is particularly strong in the Nodular Sclerosis and Mixed Cellularity subtypes [1]. The involvement is usually asymmetrical and often starts in the neck before spreading to the mediastinum. **2. Why Other Options are Incorrect:** * **Axillary (C):** While frequently involved, it is less common than cervical nodes (approx. 10-15%). * **Inguinal (A):** Involvement of the inguinal nodes is relatively rare in HL (approx. 6-10%) and is more commonly associated with Non-Hodgkin Lymphoma (NHL) or localized infections/malignancies of the lower extremities and pelvis. * **Sub-clavicular (D):** While supraclavicular nodes are common, "sub-clavicular" nodes are not a primary or most frequent site of presentation compared to the cervical chain. **Clinical Pearls for NEET-PG:** * **Bimodal Age Distribution:** HL shows two peaks—one in the 20s and another after age 50. * **Reed-Sternberg (RS) Cells:** The diagnostic hallmark (e.g., "Owl’s eye" appearance) [1]. * **Alcohol-Induced Pain:** A classic, high-yield clinical sign where pain occurs in the involved lymph nodes after alcohol consumption. * **Staging:** The **Ann Arbor Staging System** is used, and the presence of "B symptoms" (fever, night sweats, weight loss) indicates a worse prognosis [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. 616-618.

Question 277: Fresh frozen plasma is used in which of the following conditions?

A. Acute blood loss
B. Nutritive support
C. Decreased blood volume
D. Specific clotting factor deficiency (Correct Answer)

Explanation: **Explanation:** **Fresh Frozen Plasma (FFP)** is the liquid portion of whole blood that is frozen within 8 hours of collection. It contains all coagulation factors (including labile factors V and VIII), albumin, and fibrinogen. **Why Option D is Correct:** The primary clinical indication for FFP is the **replacement of multiple coagulation factor deficiencies** where specific concentrates are unavailable. It is used in conditions like Liver Disease (where synthesis of factors is impaired), Disseminated Intravascular Coagulation (DIC), Warfarin overdose reversal, and Massive Transfusion Protocols [1]. **Why Other Options are Incorrect:** * **A & C (Acute blood loss/Decreased blood volume):** FFP is not a volume expander. Acute blood loss should be managed with **Crystalloids** (Normal Saline/Ringer’s Lactate) or **Packed Red Blood Cells (PRBCs)** to maintain oxygen-carrying capacity. Using FFP for volume carries unnecessary risks of transfusion-related acute lung injury (TRALI) and infections. * **B (Nutritive support):** FFP contains proteins like albumin, but it is never indicated for nutritional support or treating hypoalbuminemia. Enteral/Parenteral nutrition or concentrated Albumin is used instead. **High-Yield Clinical Pearls for NEET-PG:** * **Dosage:** The standard dose is **10–15 mL/kg**, which typically raises clotting factor levels by 20–30%. * **Storage:** FFP is stored at **-18°C or colder** and has a shelf life of **1 year**. Once thawed, it must be used within 24 hours. * **Compatibility:** FFP must be **ABO compatible** with the recipient's RBCs (Rh compatibility is not required as it contains no RBCs). **AB is the universal donor** for FFP. * **Cryoprecipitate:** If a patient specifically needs Fibrinogen, Factor VIII, or von Willebrand Factor in a small volume, Cryoprecipitate is preferred over FFP [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 622-626.

Question 278: Sezary syndrome is classified under which category?

A. T cell leukemia (Correct Answer)
B. Lymphoma
C. B cell leukemia
D. Pigmented disorder of skin

Explanation: **Explanation:** **Sezary Syndrome (SS)** is a leukemic form of Cutaneous T-Cell Lymphoma (CTCL) [1]. It is characterized by a triad of **erythroderma** (generalized redness of the skin), **lymphadenopathy**, and the presence of malignant T cells (**Sezary cells**) in the peripheral blood [2]. 1. **Why Option A is correct:** Sezary syndrome is fundamentally a **T-cell leukemia**. It involves the clonal proliferation of CD4+ helper T cells [1]. According to the WHO classification [3], while Mycosis Fungoides (MF) is a skin-limited lymphoma, Sezary Syndrome is defined by its systemic, leukemic involvement (blood counts >1000/µL Sezary cells). 2. **Why Options B & C are wrong:** While related to Mycosis Fungoides (a lymphoma), Sezary Syndrome specifically refers to the **leukemic phase** with peripheral blood involvement [1]. It is never a B-cell disorder; the malignant cells are always of T-cell origin (specifically mature, post-thymic T-cells) [2]. 3. **Why Option D is wrong:** Although it presents with erythroderma, it is a neoplastic hematologic malignancy, not a primary disorder of skin pigmentation (like vitiligo or melasma). **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Sezary cells exhibit a characteristic **"Cerebriform nucleus"** (infolded, brain-like appearance) [2]. * **Immunophenotype:** Typically **CD3+, CD4+, and CD8-**. A key diagnostic marker is the **loss of CD7** expression. * **Pautrier’s Microabscesses:** These are intraepidermal clusters of neoplastic T cells, more commonly seen in Mycosis Fungoides but can occur in SS [2]. * **Clinical Presentation:** Patients often suffer from intense pruritus (itching) and "Red Man Syndrome." **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. 613-614. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 564-565. [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. 596-598.

Question 279: Which of the following statements regarding Myelodysplasia is FALSE?

A. Patients with 5q deletion have a poor prognosis. (Correct Answer)
B. Erythroid cells with basophilic stippling are seen.
C. Micromegakaryocytes are seen in the bone marrow.
D. Hypolobulated neutrophils are seen in peripheral blood.

Explanation: **Explanation:** **1. Why Option A is the Correct (False) Statement:** In Myelodysplastic Syndromes (MDS), the **5q deletion (5q- syndrome)** is actually associated with a **favorable prognosis** [1]. It typically occurs in elderly females and is characterized by severe macrocytic anemia, a normal or elevated platelet count, and a low risk of transformation to Acute Myeloid Leukemia (AML) [1]. These patients show an excellent therapeutic response to **Lenalidomide**. **2. Analysis of Other Options (True Statements):** * **Option B:** Dyserythropoiesis in MDS often manifests as **basophilic stippling**, ring sideroblasts, and nuclear budding/fragmentation [1]. * **Option C:** Dysmegakaryopoiesis is a hallmark of MDS. **Micromegakaryocytes** (Pawn ball megakaryocytes) with small, non-lobulated nuclei are classic bone marrow findings [1]. * **Option D:** Dysgranulopoiesis leads to the formation of **Pseudo-Pelger-Huët cells**, which are hyposegmented (bilobed or peanut-shaped) and hypogranular neutrophils seen in the peripheral blood [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Definition:** MDS is a clonal stem cell disorder characterized by "Ineffective Hematopoiesis" (Hypercellular marrow but peripheral cytopenia) [1]. * **IPSS Score:** Used for prognosis; based on blast percentage, cytogenetics, and number of cytopenias. * **Cytogenetics:** Good prognosis (5q-, 20q-, -Y); Poor prognosis (Complex karyotype, Chromosome 7 abnormalities) [1]. * **Ring Sideroblasts:** Defined as $\geq$ 5 iron granules encircling $\geq$ 1/3rd of the nucleus (Prussian Blue stain). * **Transformation:** MDS can transform into AML if blasts in the marrow reach $\geq$ 20% [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.

Question 280: Eosinophilic granuloma results from the proliferation of which cell type?

A. Histiocytes (Correct Answer)
B. Eosinophils
C. Lymphocytes
D. Fibroblasts

Explanation: **Explanation:** **Eosinophilic granuloma** is the localized, most common, and benign form of **Langerhans Cell Histiocytosis (LCH)**. Despite its name, the primary proliferating cell is not the eosinophil, but the **Langerhans cell**, which is a specialized dendritic cell (a type of **histiocyte**) [1]. 1. **Why Histiocytes are correct:** LCH is characterized by the clonal proliferation of Langerhans cells [2]. On histopathology, these cells appear as large, ovoid histiocytes with characteristic "coffee-bean" shaped nuclei (nuclear grooves) [1]. They are identified by immunohistochemistry markers **CD1a, S100, and Langerin (CD207)**. Electron microscopy reveals pathognomonic **Birbeck granules** (tennis-racket shaped) [1]. 2. **Why other options are incorrect:** * **Eosinophils:** While eosinophils are prominent in the background (recruited by cytokines like IL-5), they are reactive components, not the neoplastic/proliferating cells. * **Lymphocytes & Fibroblasts:** These may be present in the inflammatory milieu or during the healing phase (fibrosis), but they do not drive the pathology of the lesion. **NEET-PG High-Yield Pearls:** * **Clinical Presentation:** Typically affects children and young adults; most commonly presents as a **solitary, painful osteolytic lesion** in the skull, femur, or mandible. * **Radiology:** Classic "punched-out" lucent lesions without a sclerotic rim. * **LCH Spectrum:** Includes Eosinophilic Granuloma (localized), Hand-Schüller-Christian disease (multifocal chronic), and Letterer-Siwe disease (multifocal acute/disseminated). * **Molecular Marker:** Over 50% of cases harbor the **BRAF V600E mutation** [2]. **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. 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, pp. 629-630.

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

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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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