Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 181: Transient myeloproliferative disorder of the newborn is seen in association with which of the following conditions?

A. Turner's syndrome
B. Down's syndrome (Correct Answer)
C. Neurofibromatosis
D. Ataxia telangiectasia

Explanation: **Explanation:** **Transient Myeloproliferative Disorder (TMD)**, also known as Transient Abnormal Myelopoiesis (TAM), is a unique hematologic condition characterized by the clonal proliferation of megakaryoblasts. It occurs almost exclusively in neonates with **Down’s syndrome (Trisomy 21)** [1] or mosaicism for trisomy 21 [2]. **1. Why Down’s Syndrome is correct:** The pathogenesis involves a synergistic relationship between the extra copy of chromosome 21 and an acquired somatic mutation in the **GATA1 gene** (located on the X chromosome). This mutation leads to the production of a truncated protein (GATA1s) that impairs normal megakaryocyte differentiation. While TMD usually resolves spontaneously within the first 3 months of life, approximately 20-30% of these infants later develop **Acute Megakaryoblastic Leukemia (AML-M7)**. **2. Why other options are incorrect:** * **Turner’s Syndrome (45, XO):** Associated with coarctation of the aorta and dysgenetic gonads [1], but not specifically with neonatal myeloproliferative disorders. * **Neurofibromatosis (NF-1):** While NF-1 increases the risk of Juvenile Myelomonocytic Leukemia (JMML), it is not associated with TMD. * **Ataxia Telangiectasia:** This DNA repair defect predisposes patients to lymphomas and lymphoid leukemias (ALL), rather than transient myeloid proliferations. **High-Yield Clinical Pearls for NEET-PG:** * **GATA1 mutation** is the molecular hallmark of TMD and Down-associated AML. * **AML-M7** is the most common subtype of leukemia in children with Down syndrome under the age of 5. * Paradoxically, children with Down syndrome and AML-M7 have a **better prognosis** and superior response to low-dose Cytarabine compared to non-Down syndrome children. **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. 40-41. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 170-172.

Question 182: What is the normal myeloid:erythroid ratio?

A. 2:1
B. 1:1
C. 3:1 (Correct Answer)
D. 4:1

Explanation: **Explanation:** The **Myeloid:Erythroid (M:E) ratio** is a critical parameter in bone marrow aspiration analysis, representing the numerical ratio between granulocytic precursors (myeloid series) and nucleated red cell precursors (erythroid series). [1] **1. Why 3:1 is Correct:** In a healthy adult, the normal M:E ratio typically ranges from **2:1 to 4:1**, with **3:1** being the most widely accepted average. Although the lifespan of a Red Blood Cell (120 days) [2] is significantly longer than that of a White Blood Cell (hours to days), the bone marrow maintains a higher number of myeloid precursors to ensure a constant, rapid supply of leukocytes for the immune system. [1] **2. Analysis of Incorrect Options:** * **A (2:1):** While this is the lower limit of normal, it is less representative of the average physiological state than 3:1. * **B (1:1):** This indicates an **increased erythroid** component (Erythroid Hyperplasia) or **decreased myeloid** component. It is seen in conditions like hemolytic anemias or polycythemia. * **D (4:1):** This is the upper limit of normal. Ratios exceeding 4:1 suggest **Myeloid Hyperplasia** (e.g., infection, CML) or **Erythroid Hypoplasia** (e.g., Pure Red Cell Aplasia). **3. NEET-PG High-Yield Pearls:** * **Lymphocytes and Plasma Cells:** These are **not** included in the calculation of the M:E ratio. * **Increased M:E Ratio (>4:1):** Common in Chronic Myeloid Leukemia (CML) where it can reach 10:1 or higher, and in acute infections (leukemoid reaction). * **Decreased M:E Ratio (<2:1):** Seen in Megaloblastic anemia, Thalassemia, and Hemolytic anemias due to compensatory erythroid hyperplasia. * **Newborns:** The M:E ratio is naturally higher at birth (approx. 5:1) before settling to adult levels. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 588-590. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 577-578.

Question 183: Which subtype of Hodgkin lymphoma is characterized by the lymphohistiocytic variant of Reed-Sternberg cells?

A. Nodular sclerosis
B. Lymphocyte rich
C. Lymphocyte predominant (Correct Answer)
D. Lymphocyte depleted

Explanation: **Explanation:** The correct answer is **Lymphocyte Predominant** (specifically, Nodular Lymphocyte Predominant Hodgkin Lymphoma - NLPHL). **1. Why it is correct:** In NLPHL, the characteristic neoplastic cell is the **Lymphohistiocytic (L&H) variant** [1] of the Reed-Sternberg (RS) cell. These are also known as **"Popcorn cells"** [1] because their nuclei are multi-lobed and resemble exploded kernels of corn. Unlike classical RS cells, L&H cells are CD15 and CD30 negative but **CD20 positive** [1], reflecting their B-cell origin. **2. Why other options are incorrect:** * **Nodular Sclerosis:** This is the most common subtype. It is characterized by **Lacunar cells** [1] (RS cells in clear spaces caused by formalin fixation) and collagen bands dividing the lymph node into nodules. * **Lymphocyte Rich:** This subtype features **Classical RS cells** (CD15+, CD30+) against a background of small lymphocytes [2]. It has the best prognosis among classical types. * **Lymphocyte Depleted:** This is the rarest and most aggressive form. It shows numerous **Pleomorphic/Anaplastic RS cells** with very few background lymphocytes [2]. **3. High-Yield Pearls for NEET-PG:** * **NLPHL vs. Classical HL:** NLPHL is considered a distinct entity. It is often **EBV-negative** [1] and presents with localized peripheral lymphadenopathy (cervical/axillary). * **Immunophenotype:** Classical HL is CD15+, CD30+, CD20-, and CD45-. NLPHL is **CD20+, CD45+, CD15-, and CD30-**. * **Prognosis:** NLPHL generally has an excellent long-term prognosis [1] but carries a risk of transformation into Diffuse Large B-cell Lymphoma (DLBCL) [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. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 559-560.

Question 184: For a thalassemic patient requiring recurrent transfusions who develops fever and chills after transfusion, what modification of the blood product can decrease the incidence of transfusion reactions?

A. Leukocyte depletion (Correct Answer)
B. Antibiotics
C. Irradiation
D. Washed RBCs

Explanation: ### Explanation The patient is experiencing a **Febrile Non-Hemolytic Transfusion Reaction (FNHTR)**, characterized by fever and chills shortly after transfusion. This is the most common transfusion reaction in multi-transfused patients like those with Thalassemia. **1. Why Leukocyte Depletion is Correct:** FNHTRs are primarily caused by two mechanisms: * **Host antibodies** (HLA antibodies) reacting against donor white blood cells (WBCs). * **Cytokines** (e.g., IL-1, IL-6, TNF-̑) that accumulate in the blood bag during storage, released by donor leukocytes. [1] **Leukoreduction** (Leukocyte depletion) removes >99.9% of WBCs from the blood product, significantly reducing the incidence of FNHTR, HLA alloimmunization, and CMV transmission. **2. Why Other Options are Incorrect:** * **Antibiotics:** These are used to treat bacterial sepsis (a rare, severe complication) but do not prevent the immunological cytokine release responsible for FNHTR. [1] * **Irradiation:** This is used to prevent **Transfusion-Associated Graft-Versus-Host Disease (TA-GVHD)** by inactivating donor T-lymphocytes. It does not prevent febrile reactions. * **Washed RBCs:** Washing removes plasma proteins. This is specifically indicated for patients with **IgA deficiency** [2] or those with a history of severe **allergic/anaphylactic reactions**, not standard FNHTR. [2] **Clinical Pearls for NEET-PG:** * **Definition of FNHTR:** A rise in temperature of $\geq 1^\circ\text{C}$ during or shortly after transfusion with no other explanation. * **Universal Leukoreduction:** Many centers now perform "Pre-storage leukoreduction" to prevent cytokine buildup. * **CMV Prevention:** Leukoreduction is considered "CMV-safe" because the virus resides within leukocytes. * **Management:** For an active FNHTR, stop the transfusion and administer antipyretics (Acetaminophen). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 110-111. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 673-674.

Question 185: Which of the following is not a feature of disseminated intravascular coagulation (DIC)?

A. Prolonged prothrombin time (PT) and activated partial thromboplastin time (aPTT)
B. Increased fibrin degradation products
C. Thrombocytopenia
D. Platelet function defect (Correct Answer)

Explanation: ### Explanation **Disseminated Intravascular Coagulation (DIC)** is a systemic thrombohemorrhagic disorder characterized by the widespread activation of the coagulation cascade, leading to the formation of microthrombi and the subsequent consumption of clotting factors and platelets (consisting of **consumptive coagulopathy**) [1], [2]. **Why "Platelet function defect" is the correct answer:** In DIC, the primary issue is a **quantitative** deficiency of platelets (thrombocytopenia) due to their rapid consumption in microthrombi [2]. It is not a **qualitative** defect (intrinsic functional failure) of the platelets themselves. Platelet function defects are typically seen in conditions like Bernard-Soulier Syndrome, Glanzmann Thrombasthenia, or uremia. **Analysis of Incorrect Options:** * **Option A (Prolonged PT and aPTT):** Correct feature. DIC consumes clotting factors (especially V, VIII, and Fibrinogen) [2]. Since both the extrinsic and intrinsic pathways are depleted, both PT and aPTT are characteristically prolonged [2]. * **Option B (Increased FDPs):** Correct feature. As microthrombi form, the fibrinolytic system is activated to break them down. This results in elevated levels of Fibrin Degradation Products (FDPs) [1], [2] and **D-dimers** (the most specific marker). * **Option C (Thrombocytopenia):** Correct feature. Platelets are trapped and used up in the widespread formation of fibrin clots throughout the microvasculature [2]. **NEET-PG High-Yield Pearls:** * **Blood Smear:** Look for **Schistocytes** (fragmented RBCs) indicating Microangiopathic Hemolytic Anemia (MAHA) [2]. * **Best Screening Test:** Platelet count and PT/aPTT. * **Most Specific Test:** D-dimer assay. * **Common Triggers:** Sepsis (Gram-negative), Obstetric complications (Abruptio placentae), and Acute Promyelocytic Leukemia (M3). * **Fibrinogen:** Low levels are a sensitive indicator of severity in DIC [2]. **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. 625-626.

Question 186: What is the most common cause of hereditary spherocytosis?

A. Spectrin
B. Glycophorin
C. Ankyrin (Correct Answer)
D. Band 4

Explanation: **Explanation:** Hereditary Spherocytosis (HS) is an autosomal dominant (most common) or recessive disorder caused by defects in the red blood cell (RBC) membrane skeleton [1]. These defects lead to a loss of membrane surface area, resulting in the characteristic spherical shape of the cells [1]. **Why Ankyrin is Correct:** The most common molecular defect in Hereditary Spherocytosis is a deficiency or abnormality in **Ankyrin** (approximately 50-60% of cases). Ankyrin is a critical protein that anchors the spectrin-based cytoskeleton to the lipid bilayer via Band 3 [1]. A defect here destabilizes the membrane, leading to the formation of microvesicles and subsequent splenic sequestration. **Analysis of Other Options:** * **Spectrin (Option A):** While mutations in $\alpha$-spectrin or $\beta$-spectrin are the second most common cause of HS (and the most common cause of Hereditary Elliptocytosis), they are less frequent than Ankyrin mutations in HS patients [1]. * **Glycophorin (Option B):** Glycophorins are integral membrane proteins that carry RBC antigens (like the MN system) [1]. They are not typically implicated as a primary cause of Hereditary Spherocytosis. * **Band 4 (Option C):** Specifically Band 4.1 or 4.2. While Band 4.2 deficiency can cause HS (especially in Japanese populations), it is significantly less common globally than Ankyrin defects [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Triad:** Anemia, Jaundice, and Splenomegaly. * **Diagnosis:** The gold standard screening test is the **Eosin-5-maleimide (EMA) binding test** (Flow cytometry). The Osmotic Fragility Test is also used but is less specific [3]. * **Peripheral Smear:** Shows spherocytes (small, dark red cells lacking central pallor) and increased reticulocytes [2]. * **Lab Marker:** Characteristically high **MCHC** (>36 g/dL). * **Complication:** Risk of aplastic crisis (Parvovirus B19) and pigment gallstones (calcium bilirubinate) [2], [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. 640-641. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 641-642. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598.

Question 187: All of the following are poor prognostic markers of multiple myeloma, except?

A. t(1;14) (Correct Answer)
B. t(14;16)
C. 1q gain
D. t(14;20)

Explanation: **Explanation:** In Multiple Myeloma (MM), cytogenetic abnormalities are the strongest predictors of prognosis. These are broadly categorized into **High-Risk (Poor Prognosis)** and **Standard-Risk (Good/Intermediate Prognosis)**. **1. Why t(1;14) is the correct answer:** Translocation **t(1;14)** involves the *BCL9* gene and the immunoglobulin heavy chain (*IGH*) locus. Unlike other translocations involving chromosome 14, t(1;14) is considered a **standard-risk** cytogenetic marker. Patients with this translocation generally have outcomes similar to those with standard-risk disease, making it the "exception" among the poor prognostic markers listed. **2. Analysis of Incorrect Options (Poor Prognostic Markers):** * **t(14;16):** Involves the *MAF* gene. It is a classic high-risk translocation associated with aggressive disease and shorter survival. * **1q gain:** Gain of the long arm of chromosome 1 (1q21) is one of the most common high-risk features. It is associated with disease progression and resistance to standard therapies. * **t(14;20):** Involves the *MAFB* gene. Similar to t(14;16), it is categorized as a high-risk cytogenetic abnormality. **High-Yield Clinical Pearls for NEET-PG:** * **High-Risk Markers (Poor Prognosis):** del(17p) [TP53 mutation], t(4;14), t(14;16), t(14;20), and 1q gain. * **Standard-Risk Markers:** t(11;14), t(6;14), and hyperdiploidy. * **Revised ISS (R-ISS):** Prognosis is now determined by combining Serum Albumin, Beta-2 Microglobulin, LDH levels, and High-risk Cytogenetics (FISH) [1]. * **Most common translocation in MM:** t(11;14). (Note: While the provided literature discusses the clinical features and protein types in Multiple Myeloma [1], it confirms that renal failure is a significant poor prognostic indicator [1].) **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 618-619.

Question 188: Which one of the following is the cause of non-cardiogenic pulmonary edema seen in immunologic blood transfusion reactions?

A. Antibody to IgA in donor plasma
B. Antibody to donor leukocyte antigen
C. Donor antibody to leukocyte of patient (Correct Answer)
D. RBC incompatibility

Explanation: The question describes **TRALI (Transfusion-Related Acute Lung Injury)**, which is the leading cause of transfusion-related fatalities. ### **Explanation of the Correct Answer** The primary mechanism of TRALI involves a **"Two-Hit Hypothesis."** The "second hit" is typically the infusion of **donor antibodies** (usually HLA or human neutrophil-specific antibodies) that react against the **recipient's (patient's) leukocytes**. This interaction causes neutrophils to sequester in the pulmonary microvasculature, where they release inflammatory mediators and reactive oxygen species. This leads to endothelial damage, capillary leak, and the development of **non-cardiogenic pulmonary edema** within 6 hours of transfusion [2]. ### **Why Other Options are Incorrect** * **Option A:** Antibodies to IgA in the recipient (not donor) reacting against donor IgA cause **Anaphylaxis**, not pulmonary edema [1]. * **Option B:** Recipient antibodies against donor leukocytes cause **Febrile Non-Hemolytic Transfusion Reactions (FNHTR)**. * **Option D:** RBC incompatibility (ABO/Rh) leads to **Acute Hemolytic Transfusion Reactions**, characterized by fever, hypotension, and hemoglobinuria, rather than primary pulmonary edema [1]. ### **NEET-PG High-Yield Pearls** * **Definition:** TRALI is defined as new-onset Acute Lung Injury (ALI) during or within **6 hours** of transfusion [2]. * **Clinical Presentation:** Sudden dyspnea, hypoxia (SpO2 <90%), and bilateral infiltrates on CXR, notably **without** signs of heart failure (normal PCWP) [2]. * **Prevention:** Using "male-only" plasma or plasma from nulliparous women reduces risk, as multiparous women have a higher prevalence of anti-HLA antibodies. * **Management:** Immediate cessation of transfusion and aggressive **respiratory support**. Diuretics are generally not indicated (unlike in TACO). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 673-674. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, p. 679.

Question 189: The c-myc oncogene is located on chromosome 8. Which of the following hematologic malignancies is characteristically associated with a translocation involving the c-myc gene?

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

Explanation: **Explanation:** The **c-myc oncogene**, located on **chromosome 8q24**, is a transcription factor that plays a critical role in cell cycle progression and apoptosis. Its dysregulation leads to uncontrolled cell proliferation [1]. **1. Why Burkitt’s Lymphoma is Correct:** Burkitt’s lymphoma is characteristically defined by the translocation **t(8;14)**, which involves the **c-myc** gene on chromosome 8 and the **Immunoglobulin Heavy chain (IgH)** locus on chromosome 14 [1]. This translocation places c-myc under the control of the highly active IgH promoter, leading to constitutive overexpression of the MYC protein. This results in the "starry sky" appearance seen on histology due to a very high proliferation index (Ki-67 ~100%). **2. Why the other options are incorrect:** * **Follicular Lymphoma:** Associated with **t(14;18)**, involving the **BCL-2** gene [2]. This leads to the overexpression of BCL-2, an anti-apoptotic protein, preventing programmed cell death [3]. * **Mantle Cell Lymphoma:** Associated with **t(11;14)**, involving the **CCND1 (Cyclin D1)** gene. Overexpression of Cyclin D1 promotes the transition from G1 to S phase in the cell cycle. * **Body Cavity Lymphoma (Primary Effusion Lymphoma):** This is a rare B-cell lymphoma associated with **HHV-8** infection, typically occurring in HIV-positive patients. It does not have a characteristic c-myc translocation. **High-Yield Clinical Pearls for NEET-PG:** * **Burkitt’s Lymphoma variants:** While t(8;14) is most common (80%), variant translocations include **t(2;8)** (kappa light chain) and **t(8;22)** (lambda light chain) [1]. * **Starry Sky Appearance:** The "stars" are tingible body macrophages ingesting apoptotic debris, while the "sky" is the sheet of dark, small non-cleaved B-cells. * **EBV Association:** The endemic (African) form is 100% associated with the Epstein-Barr Virus. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325. [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. 602-604. [3] 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.

Question 190: Increased levels of hemoglobin A2 is characteristic of which condition?

A. Sickle cell trait
B. Beta-thalassemia trait (Correct Answer)
C. Glucose-6-phosphate dehydrogenase deficiency
D. Alpha-thalassemia

Explanation: **Explanation:** **Why Beta-thalassemia trait is correct:** In Beta-thalassemia trait (minor), there is a partial deficiency in the production of $\beta$-globin chains. To compensate for this deficit, the body increases the production of alternative globin chains. Specifically, there is an increase in $\delta$-chain synthesis, which combines with $\alpha$-chains to form **Hemoglobin A2 ($\alpha_2\delta_2$)**. [1] * **Diagnostic Hallmark:** An HbA2 level **>3.5%** (typically 4–8%) on Hb electrophoresis is the gold standard for diagnosing Beta-thalassemia trait. HbF levels may also be slightly elevated (1–5%). **Why the other options are incorrect:** * **Sickle cell trait (HbAS):** Characterized by the presence of HbA and HbS. HbA2 levels remain within the normal range (2–3%). * **G6PD deficiency:** This is an enzyme deficiency affecting the hexose monophosphate shunt, leading to episodic hemolysis. It does not involve globin chain synthesis defects; thus, the hemoglobin profile remains normal. * **Alpha-thalassemia:** Since HbA2 ($\alpha_2\delta_2$) requires $\alpha$-chains, a decrease in $\alpha$-globin production leads to **low or normal** HbA2 levels. [1] In severe forms (HbH disease), one sees $\beta_4$ tetrads instead. **NEET-PG High-Yield Pearls:** 1. **Mentzer Index:** (MCV/RBC count) <13 suggests Thalassemia; >13 suggests Iron Deficiency Anemia (IDA). 2. **Differentiating IDA from Thalassemia:** HbA2 is **decreased** in IDA and **increased** in Beta-thalassemia trait. 3. **Peripheral Smear:** Look for microcytic hypochromic anemia with **target cells** and basophilic stippling. 4. **Silent Carrier:** Alpha-thalassemia minima (one gene deletion) usually has a completely normal electrophoresis. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 650.

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Hemolytic Anemias

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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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