Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 941: Heterozygous sickle cell anemia provides protection against which of the following?

A. G6PD deficiency
B. Malaria (Correct Answer)
C. Thalassemia
D. Dengue fever

Explanation: **Explanation:** The correct answer is **Malaria**. Heterozygous sickle cell anemia (Sickle Cell Trait, HbAS) provides a selective survival advantage against severe malaria caused by *Plasmodium falciparum* [1]. This phenomenon is known as **balanced polymorphism**. **Why Malaria is correct:** The protection is mediated through several mechanisms: 1. **Reduced Parasite Proliferation:** Sickling occurs more readily in infected RBCs due to lower pH and oxygen tension. These sickled cells are prematurely cleared by the splenic macrophages, reducing the overall parasite load. 2. **Impaired Transport:** The polymerization of HbS disrupts the transport of parasite proteins (like PfEMP-1) to the RBC membrane, preventing the "knob" formation that causes infected cells to stick to blood vessels (cytoadherence). 3. **Oxidative Stress:** HbAS cells produce higher levels of reactive oxygen species (ROS), which are toxic to the parasite. **Why other options are incorrect:** * **G6PD deficiency & Thalassemia:** These are separate genetic hemoglobinopathies/enzymopathies. While they also offer some protection against malaria, they are not "protected against" by the sickle cell trait. In fact, they can co-exist with HbS. * **Dengue fever:** This is a viral infection transmitted by *Aedes* mosquitoes. Its pathogenesis involves immune-mediated mechanisms and capillary leak, which are unaffected by the hemoglobin variant. **High-Yield Clinical Pearls for NEET-PG:** * **Selective Advantage:** HbAS specifically protects against **cerebral malaria** and severe complications, not necessarily the initial infection [1]. * **Diagnosis:** Sickle cell trait is diagnosed via **Hb Electrophoresis** (HbA: 55-60%, HbS: 40-45%, HbF: <1%). * **Peripheral Smear:** Unlike Sickle Cell Disease (HbSS) [2], the peripheral smear in HbAS is typically **normal** unless the patient is under extreme hypoxic stress [2]. * **Screening:** The **Solubility test** and **Sodium metabisulfite test** will be positive in both HbAS and HbSS. **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. 50-51. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599.

Question 942: Which subtype of Acute Myeloid Leukemia (AML) is characterized by gum infiltration and hepatosplenomegaly?

A. Acute lymphoblastic leukemia (ALL)
B. M3 subtype
C. M2 subtype
D. M4 subtype (Correct Answer)

Explanation: **Explanation:** The correct answer is **M4 subtype (Acute Myelomonocytic Leukemia)**. In the FAB (French-American-British) classification of AML, subtypes with a **monocytic component** (M4 and M5) are uniquely associated with **extramedullary involvement**. This occurs because monoblasts and monocytes have a high propensity to migrate out of the bone marrow and infiltrate tissues [1]. Clinical manifestations of this tissue infiltration include **gum hypertrophy (gingival hyperplasia)**, skin involvement (leukemia cutis), and organomegaly (hepatosplenomegaly). **Analysis of Options:** * **A. Acute Lymphoblastic Leukemia (ALL):** While ALL commonly presents with hepatosplenomegaly and lymphadenopathy (especially in children), it is not typically associated with gum infiltration. * **B. M3 Subtype (Acute Promyelocytic Leukemia):** Characterized by the t(15;17) translocation and a high risk of **DIC (Disseminated Intravascular Coagulation)** due to the release of procoagulants from Auer rods [1]. It does not typically cause gum infiltration. * **C. M2 Subtype (AML with Maturation):** This is the most common subtype of AML. It is often associated with the t(8;21) translocation and the presence of **chloromas** (granulocytic sarcomas), but not specifically gum hypertrophy [1]. **High-Yield Clinical Pearls for NEET-PG:** * **M4 (Myelomonocytic):** Positive for both Myeloperoxidase (MPO) and Non-Specific Esterase (NSE). * **M5 (Monocytic):** Strongest association with gum hypertrophy; predominantly NSE positive. * **M3 (APL):** Associated with **Auer rods in faggot cells** and treated with ATRA (All-Trans Retinoic Acid). * **M0/M1/M2:** Primarily MPO positive. **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.

Question 943: Which one of the labeled boxes in the diagram below is most consistent with the expected findings for an individual with polycythemia rubra vera?

A. Box A
B. Box B
C. Box D
D. Box E (Correct Answer)

Explanation: ***Box E*** - Shows **markedly elevated RBC/Hct**, **elevated WBC**, and **elevated platelets** with **decreased EPO** - the classic triad of polycythemia rubra vera due to **JAK2 mutation** causing autonomous bone marrow proliferation. - **Normal oxygen saturation** with **low EPO** distinguishes primary polycythemia (PRV) from secondary causes where EPO would be elevated. *Box A* - Likely represents **normal values** with balanced RBC, WBC, platelets, and appropriate EPO levels. - Does not show the **panmyelosis** (increased RBC, WBC, and platelets) characteristic of polycythemia rubra vera. *Box B* - Probably shows **secondary polycythemia** with elevated RBC/Hct but **normal WBC and platelets** with **elevated EPO**. - Lacks the **autonomous proliferation** of all cell lines seen in PRV due to **JAK2 mutation**. *Box D* - May represent **relative polycythemia** or **dehydration** with elevated Hct but normal other parameters. - Missing the **clonal myeloproliferation** affecting multiple cell lines that defines polycythemia rubra vera.

Question 944: Defect in Bernard Soulier syndrome lies in which of the following?

A. Glycoprotein Ib-IX complex (Correct Answer)
B. Glycoprotein IIIa-IIb complex
C. Glycoprotein IIa-IIIb complex
D. Glycoprotein IIIb-IIa complex

Explanation: **Explanation:** **Bernard-Soulier Syndrome (BSS)** is an autosomal recessive bleeding disorder characterized by a defect in **platelet adhesion** [1]. 1. **Why Option A is Correct:** The primary defect in BSS is a deficiency or dysfunction of the **Glycoprotein Ib-IX-V (GpIb-IX-V) complex** on the platelet surface [1], [2]. This complex serves as the receptor for **von Willebrand Factor (vWF)** [3]. Under high shear stress (as seen in arterial circulation), vWF acts as a bridge between the subendothelial collagen and the GpIb receptor [2]. Without this complex, platelets cannot adhere to the damaged vessel wall, leading to a bleeding diathesis [1]. 2. **Why Other Options are Incorrect:** * **Option B (GpIIb-IIIa):** This complex is the receptor for **Fibrinogen** and is involved in **platelet aggregation** (platelet-to-platelet binding) [1], [3]. A deficiency in GpIIb-IIIa leads to **Glanzmann Thrombasthenia**, not BSS [1]. * **Options C and D:** These are distractors with transposed nomenclature. There are no major clinical bleeding syndromes associated with "GpIIa-IIIb" or "GpIIIb-IIa" in the context of primary hemostasis. **NEET-PG High-Yield Pearls:** * **Peripheral Smear:** Characterized by **Giant Platelets** (often the size of RBCs or larger) and **Thrombocytopenia**. * **Ristocetin Test:** Platelet aggregation is **absent/defective** with Ristocetin. Crucially, unlike von Willebrand Disease, the defect in BSS **cannot** be corrected by adding normal plasma (because the defect is in the platelet receptor, not the plasma factor). * **Bleeding Time:** Prolonged, while PT and aPTT remain normal. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 128. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 669-670.

Question 945: Which of the following conditions is characterized by an intrinsic cell wall defect of red blood cells?

A. Paroxysmal nocturnal hemoglobinuria (Correct Answer)
B. Sickle cell anemia
C. Hereditary spherocytosis
D. All of the above

Explanation: **Explanation:** The correct answer is **Paroxysmal Nocturnal Hemoglobinuria (PNH)**. **1. Why PNH is the correct answer:** PNH is an acquired clonal hematopoietic stem cell disorder caused by a mutation in the **PIGA gene** [2]. This mutation leads to a deficiency in **GPI (Glycosylphosphatidylinositol) anchors**, which are essential components of the **red cell membrane (cell wall)**. Without these anchors, the RBC membrane lacks protective proteins like **CD55 (DAF)** and **CD59 (MIRL)**. This makes the RBC membrane intrinsically defective and hypersensitive to complement-mediated lysis [1]. **2. Why the other options are incorrect:** * **Sickle Cell Anemia:** This is a **hemoglobinopathy**, not a cell wall defect. It is caused by a qualitative defect in the globin chain (substitution of valine for glutamic acid at the 6th position of the ̢-chain). * **Hereditary Spherocytosis:** While this involves the RBC membrane, it is specifically a defect in the **membrane cytoskeleton proteins** (like Ankyrin, Spectrin, or Band 3), rather than an intrinsic biochemical defect of the cell wall/membrane anchor system itself. In the context of "cell wall/membrane anchor" questions, PNH is the classic example of an acquired intrinsic defect. **3. NEET-PG High-Yield Pearls:** * **Gold Standard Test:** Flow Cytometry (shows absence of CD55 and CD59) [1]. * **Classic Triad:** Hemolytic anemia, Pancytopenia, and Venous thrombosis (often in unusual sites like the Budd-Chiari syndrome) [1]. * **Screening Tests:** Ham’s test (Acidified serum test) and Sucrose Lysis test (now largely replaced by flow cytometry). * **Treatment:** Eculizumab (a monoclonal antibody against C5 complement). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-651. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 601-602.

Question 946: The cell mass in multiple myeloma is formed by?

A. Circulating B cells settling in bone marrow
B. Preformed B cells seen in the marrow
C. Circulating B cells settling in bone marrow
D. B-cells turning malignant and secreting light chains (Correct Answer)

Explanation: ### Explanation **Correct Option: D (B-cells turning malignant and secreting light chains)** Multiple myeloma is a **plasma cell dyscrasia** characterized by the neoplastic proliferation of a single clone of plasma cells [1]. These malignant plasma cells are derived from post-germinal center B-cells that have undergone somatic hypermutation and class-switch recombination. These cells secrete a monoclonal (M) protein, which can be a complete immunoglobulin or, frequently, **excess free light chains** (kappa or lambda) [1][2]. These light chains are small enough to be filtered by the glomerulus and excreted in the urine as **Bence-Jones proteins** [1][3]. **Why other options are incorrect:** * **Options A & C:** These options suggest that the primary pathology is simply the "settling" of normal circulating B-cells. In reality, the process involves a malignant transformation (often involving translocations of the IgH locus on chromosome 14) and homing to the bone marrow niche, where they proliferate uncontrollably [2]. * **Option B:** While the marrow is the site of proliferation, "preformed B cells" is a vague term that does not account for the essential malignant transformation and the characteristic secretory function (light chains) that defines the disease's clinical manifestations (like renal failure) [1][3]. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** Clinical features include **C**alcium elevation, **R**enal insufficiency, **A**nemia, and **B**one lesions (punched-out lytic lesions) [3]. * **Diagnosis:** Bone marrow biopsy showing **>10% clonal plasma cells**. * **Morphology:** Look for **Flame cells** (IgA myeloma), **Mott cells** (grape-like cytoplasmic droplets), and **Russell bodies** (cytoplasmic Ig inclusions). * **Blood Film:** **Rouleaux formation** due to increased serum proteins (decreased zeta potential) [3]. * **Prognosis:** Serum **Beta-2 microglobulin** is the most important prognostic marker. **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] 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. 606-607. [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. 607-609.

Question 947: Nuclear-cytoplasmic asynchrony is usually seen in:

A. Cobalamin Deficiency Anemia (Correct Answer)
B. Myelophthisic Anemia
C. Aplastic Anemia
D. Iron deficiency Anemia

Explanation: **Explanation:** **1. Why Cobalamin Deficiency Anemia is Correct:** Nuclear-cytoplasmic asynchrony is the hallmark of **Megaloblastic Anemias**, most commonly caused by Cobalamin (Vitamin B12) or Folate deficiency [1], [2]. The underlying mechanism is an **impairment of DNA synthesis** (due to decreased thymidine production), while RNA synthesis and protein (hemoglobin) synthesis remain unaffected. * **Result:** The nucleus remains immature and "lacey" (delayed maturation), while the cytoplasm matures and expands normally [1], [2]. This leads to the characteristic large cells (macrocytes) with immature nuclei seen in the bone marrow. **2. Why the Other Options are Incorrect:** * **Myelophthisic Anemia:** This is a "space-occupying" lesion in the bone marrow (e.g., metastatic cancer, fibrosis). It is characterized by a **leukoerythroblastic blood picture** (teardrop cells and immature precursors) rather than maturational asynchrony. * **Aplastic Anemia:** This involves a primary failure of hematopoietic stem cells leading to **pancytopenia and a hypocellular marrow**. The cells that are present typically show normal maturation patterns. * **Iron Deficiency Anemia (IDA):** IDA is a cytoplasmic maturation defect. Here, DNA synthesis is normal, but **hemoglobin synthesis is impaired**. This results in small, pale cells (microcytic hypochromic), which is the opposite of the megaloblastic process. **High-Yield NEET-PG Pearls:** * **Hypersegmented Neutrophils:** The earliest peripheral blood sign of megaloblastic anemia (defined as >5% neutrophils with 5 lobes or a single neutrophil with 6 lobes) [4]. * **Howell-Jolly Bodies:** Nuclear remnants seen in RBCs due to dysfunctional erythropoiesis. * **MCV:** Typically >100 fL in megaloblastic states. * **Pernicious Anemia:** The most common cause of B12 deficiency, caused by autoimmune destruction of parietal cells (Intrinsic Factor deficiency) [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. 654-655. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 592-595. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 592-593. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 654.

Question 948: Bone marrow showing positive staining with Periodic Acid Schiff. What is the likely diagnosis?

A. Acute Myeloid Leukemia - M2 (AML-M2)
B. Acute Myeloid Leukemia - M3 (AML-M3)
C. Acute Myeloid Leukemia - M6 (AML-M6) (Correct Answer)
D. Acute Lymphoblastic Leukemia

Explanation: ### Explanation The correct answer is **C. Acute Myeloid Leukemia - M6 (AML-M6)**, also known as Erythroleukemia. **1. Why AML-M6 is correct:** Periodic Acid Schiff (PAS) stains glycogen and related mucopolysaccharides. In normal hematopoiesis, early erythroid precursors (normoblasts) are PAS-negative. However, in **AML-M6 (Erythroleukemia)** and certain cases of myelodysplastic syndrome, the malignant erythroid precursors exhibit **globular or chunky PAS positivity**. This is a classic diagnostic hallmark used to identify abnormal erythroid maturation in the bone marrow. **2. Why the other options are incorrect:** * **AML-M2 & AML-M3:** These are myeloid leukemias (granulocytic). They are typically characterized by positivity for **Myeloperoxidase (MPO)** and Sudan Black B (SBB) [1]. While they may show faint, diffuse background staining with PAS, they do not show the characteristic chunky/granular positivity seen in M6 or ALL. Specifically, AML-M3 (Acute Promyelocytic Leukemia) is identified by coarse azurophilic granules and Auer rods [1], [2]. * **Acute Lymphoblastic Leukemia (ALL):** While ALL is famously **PAS positive** (showing a "block-like" or "necklace" pattern), the question specifically asks for a diagnosis within the context of the provided options where AML-M6 is the most specific "myeloid" association for erythroid PAS positivity. If the question implies a myeloid context or focuses on erythroid precursors, M6 is the classic answer. **3. High-Yield Clinical Pearls for NEET-PG:** * **MPO/SBB:** Best stains for Myeloid cells (AML M1-M5). * **Non-Specific Esterase (NSE):** Strongly positive in Monocytic lineages (**AML-M4 and M5**); inhibited by Sodium Fluoride [1]. * **PAS Pattern:** * **ALL:** Block-like/Granular positivity. * **AML-M6:** Chunky/Globular positivity in erythroid precursors. * **AML-M3 (APML):** Associated with t(15;17), Auer rods (Faggot cells), and risk of DIC [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. 621-622. [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 949: Dohle bodies are seen in which of the following conditions?

A. Multiple myeloma
B. May-Hegglin anomaly (Correct Answer)
C. Waldenstrom macroglobulinemia
D. Lymphoma

Explanation: **Explanation:** **Dohle bodies** are small, light blue-grey, oval inclusions found in the periphery of the cytoplasm of neutrophils. They represent **remnants of rough endoplasmic reticulum (RER)** arranged in parallel rows. 1. **Why May-Hegglin Anomaly is correct:** This is a rare, autosomal dominant disorder caused by a mutation in the **MYH9 gene**. It is characterized by a classic triad: **thrombocytopenia, giant platelets, and large Dohle-like bodies** in all types of granulocytes (neutrophils, eosinophils, basophils, and monocytes). While "true" Dohle bodies are typically seen in reactive states (infections, burns, inflammation), the inclusions in May-Hegglin are larger and more prominent. 2. **Why the other options are incorrect:** * **Multiple Myeloma:** Characterized by malignant plasma cells, bone marrow plasmacytosis, and "M-spike" on electrophoresis. Characteristic inclusions include **Russell bodies** (cytoplasmic) and **Dutcher bodies** (nuclear). * **Waldenstrom Macroglobulinemia:** A lymphoplasmacytic lymphoma producing IgM. It typically shows Dutcher bodies but not Dohle bodies. * **Lymphoma:** This is a broad category of lymphoid malignancies. While some may show specific inclusions (like Auer rods in AML, though not a lymphoma), Dohle bodies are markers of myeloid/neutrophilic activation or specific genetic defects, not primary lymphoid neoplasia. **High-Yield Pearls for NEET-PG:** * **Dohle bodies** are also seen in **"Toxic Granulation"** during severe bacterial infections, burns, and pregnancy. [1], [2] * **Chediak-Higashi Syndrome:** Characterized by giant lysosomal granules in neutrophils. * **Alder-Reilly Anomaly:** Large, coarse purple granules (mucopolysaccharidosis). * **Pelger-Huet Anomaly:** Hyposegmented neutrophils (spectacle-shaped/Pince-nez nuclei). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 580-581. [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. 592.

Question 950: Acquired mutations in the PIGA gene give rise to which condition?

A. Paroxysmal Nocturnal Hemoglobinuria (Correct Answer)
B. Hereditary Spherocytosis
C. Isoimmune hemolytic anemia
D. Fanconi’s anemia

Explanation: ### Explanation **Correct Answer: A. Paroxysmal Nocturnal Hemoglobinuria (PNH)** **Mechanism:** Paroxysmal Nocturnal Hemoglobinuria is an acquired clonal hematopoietic stem cell disorder [2]. It is caused by a somatic mutation in the **PIGA (Phosphatidylinositol Glycan class A)** gene located on the X chromosome [2]. This gene is essential for the synthesis of **GPI (Glycosylphosphatidylinositol) anchors**. These anchors normally tether specific proteins to the cell membrane, most notably **CD55 (Decay Accelerating Factor)** and **CD59 (Membrane Inhibitor of Reactive Lysis)**. In PNH, the absence of these protective proteins makes red blood cells hypersensitive to **complement-mediated lysis**, leading to intravascular hemolysis [1]. **Why the other options are incorrect:** * **B. Hereditary Spherocytosis:** This is an inherited (autosomal dominant) defect in red cell membrane proteins like **Ankyrin** (most common), Spectrin, or Band 3, leading to extravascular hemolysis. * **C. Isoimmune Hemolytic Anemia:** This occurs when antibodies from one individual react with antigens on the RBCs of another (e.g., Rh incompatibility or transfusion reactions), not due to a genetic mutation. * **D. Fanconi’s Anemia:** This is an autosomal recessive DNA repair defect (mutations in FANC genes) leading to progressive bone marrow failure and physical anomalies; it is not a GPI-anchor defect. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Flow cytometry showing absence of CD55 and CD59 on RBCs and WBCs [1]. * **Classic Triad:** Hemolytic anemia, Pancytopenia, and Venous thrombosis (often in unusual sites like the portal or hepatic veins—Budd-Chiari syndrome) [1]. * **Screening Test:** Ham’s Test (Acidified serum test) or Sucrose Lysis test (now largely replaced by flow cytometry). * **Treatment:** **Eculizumab**, a monoclonal antibody against complement protein C5. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-651. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 601-602.

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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