Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 731: Which staining technique is used to detect coarse basophilic stippling?

A. Peripheral blood reticulocytes
B. Heinz bodies
C. Coarse basophilic stippling (Correct Answer)
D. Globin chain inclusions in severe thalassemia

Explanation: **Explanation:** **Basophilic stippling** (punctate basophilia) refers to the presence of numerous small, blue-purple granules distributed throughout the cytoplasm of red blood cells on a peripheral smear. These granules represent **precipitated ribosomes** and clusters of ribosomal RNA. **Why the Correct Answer is Right:** Basophilic stippling is visualized using standard Romanowsky stains (like **Leishman or Wright stain**). While "fine" stippling is often a non-specific finding in various anemias, **coarse basophilic stippling** is a hallmark of **Lead Poisoning** [1] (due to inhibition of the enzyme 5'-nucleotidase) and **Sideroblastic Anemia**. **Analysis of Incorrect Options:** * **Peripheral blood reticulocytes:** These are visualized using **Supravital stains** (e.g., New Methylene Blue or Brilliant Cresyl Blue). These stains cause the ribosomal RNA to clump into a linear "reticulum" or network, which is not visible on routine Romanowsky stains. * **Heinz bodies:** These represent denatured hemoglobin (common in G6PD deficiency). They are invisible on routine smears and require **Supravital stains** (Crystal Violet) to appear as purple round inclusions attached to the RBC membrane. * **Globin chain inclusions:** Seen in severe α-thalassemia (HbH disease), these "golf-ball" inclusions also require **Supravital staining** for visualization. **NEET-PG High-Yield Pearls:** 1. **Lead Poisoning Triad:** Coarse basophilic stippling + Microcytic hypochromic anemia + Burtonian lines (lead lines on gums) [1]. 2. **Basophilic Stippling vs. Reticulocytes:** Both contain RNA. Stippling is seen on **Leishman stain** (fixed smear); Reticulocytes are seen on **Supravital stain** (living cells). 3. **Pappenheimer Bodies:** These are iron-containing granules (Siderocytes) that can mimic stippling but are confirmed using **Prussian Blue (Perl’s) stain**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 418-419.

Question 732: The presence of Heinz bodies in erythrocytes indicates which of the following?

A. Malarial infection
B. Hemoglobin abnormalities
C. Oxidative stress (Correct Answer)
D. Degraded bacterial forms

Explanation: **Explanation:** Heinz bodies are inclusions within red blood cells (RBCs) composed of **denatured, precipitated hemoglobin**. The primary mechanism behind their formation is **oxidative stress**. When RBCs are exposed to oxidative damage (often due to drugs like dapsone, fava beans, or infections), the sulfhydryl groups on the globin chains are oxidized, causing the hemoglobin to lose its solubility and precipitate [1]. This is most commonly seen in **G6PD deficiency**, where the lack of NADPH prevents the regeneration of reduced glutathione, leaving the cell vulnerable to oxidative injury [1]. **Analysis of Options:** * **Option A (Malarial infection):** Malaria is characterized by intracellular parasites (ring forms, gametocytes) or Schüffner’s dots, not precipitated hemoglobin. * **Option B (Hemoglobin abnormalities):** While certain unstable hemoglobins (e.g., Hb Cologne) can cause Heinz bodies, "Oxidative stress" is the more fundamental physiological process that triggers the precipitation. * **Option D (Degraded bacterial forms):** Bacteria do not form intra-erythrocytic inclusions like Heinz bodies. **NEET-PG High-Yield Pearls:** 1. **Staining:** Heinz bodies are **not visible on routine Leishman or Wright-Giemsa stains**. they require **Supravital stains** (e.g., Crystal Violet, Brilliant Cresyl Blue, or Methylene Blue). 2. **Bite Cells (Degmacytes):** When RBCs containing Heinz bodies pass through the splenic sinusoids, splenic macrophages pluck out the inclusions, resulting in "Bite cells" seen on peripheral smears [1]. 3. **Differential:** Do not confuse Heinz bodies with **Howell-Jolly bodies** (DNA remnants seen in hyposplenism) or **Pappenheimer bodies** (iron granules seen in sideroblastic anemia). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 642-643.

Question 733: “Checker board” histologic appearance of chromatin clumping is seen in which of the following conditions?

A. Plasmacytoma (Correct Answer)
B. Neutropenia
C. Neutrocytosis
D. All of the above

Explanation: **Explanation:** The "checkerboard" appearance (also described as **"clock-face"** or **"cartwheel"** appearance) is a classic histological hallmark of **plasma cells**. This pattern is created by the unique arrangement of chromatin, which clumps in dense masses against the inner aspect of the nuclear membrane, interspersed with lighter areas of euchromatin. **1. Why Plasmacytoma is Correct:** A plasmacytoma is a neoplastic proliferation of plasma cells [1]. In this condition, the biopsy reveals sheets of plasma cells exhibiting this characteristic eccentric nucleus with "checkerboard" chromatin [1]. The abundant basophilic cytoplasm and a prominent perinuclear Golgi zone (hof) are additional diagnostic features. This morphology is essential for identifying plasma cell dyscrasias, including Multiple Myeloma [1]. **2. Why Incorrect Options are Wrong:** * **Neutropenia:** This refers to a decreased absolute neutrophil count. Histologically, it involves a lack of cells rather than a specific nuclear chromatin pattern. * **Neutrocytosis:** This is an increase in the number of neutrophils (usually due to infection or inflammation). Neutrophils are characterized by multi-lobed nuclei with dense, clumped chromatin, but they do not exhibit the organized "checkerboard" or "clock-face" symmetry seen in plasma cells. **High-Yield NEET-PG Pearls:** * **Plasma Cell Morphology:** Eccentric nucleus + Clock-face/Checkerboard chromatin + Perinuclear clearing (Hof). * **Mnemonic:** "Plasma cells have a **C**lock-face nucleus and produce **C**omplementary antibodies." * **Russell Bodies:** Intracytoplasmic eosinophilic inclusions of immunoglobulins in plasma cells. * **Dutcher Bodies:** Intranuclear inclusions of immunoglobulins (seen more commonly in Waldenström Macroglobulinemia). **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. 606-608.

Question 734: What is the most common type of heavy chain disease?

A. Alpha chain disease (Correct Answer)
B. Gamma chain disease
C. Mu chain disease
D. Delta chain disease

Explanation: **Explanation:** Heavy chain diseases (HCDs) are rare B-cell proliferative disorders characterized by the synthesis and secretion of free monoclonal immunoglobulin heavy chains that lack associated light chains [1]. **Why Alpha Chain Disease is correct:** **Alpha chain disease (Seligmann’s disease)** is the **most common** type of heavy chain disease worldwide. It primarily involves the IgA-secreting B-cells in the mucosal-associated lymphoid tissue (MALT), most frequently in the small intestine. It is clinically characterized by severe malabsorption, chronic diarrhea, and abdominal pain. It is often associated with poor hygiene and chronic parasitic infections in Mediterranean and Middle Eastern regions. **Why the other options are incorrect:** * **Gamma chain disease (Franklin’s disease):** This is the second most common type. It clinically resembles a systemic lymphoma or chronic lymphocytic leukemia (CLL), presenting with lymphadenopathy, fever, and anemia. Unlike Alpha chain disease, it does not specifically target the gut. * **Mu chain disease:** This is very rare and is almost always associated with an underlying chronic lymphocytic leukemia (CLL). A key diagnostic feature is the presence of **vacuolated plasma cells** in the bone marrow. * **Delta chain disease:** This is extremely rare, with only a few cases reported in medical literature. It typically presents similarly to multiple myeloma. **High-Yield NEET-PG Pearls:** * **Alpha chain disease** is considered a precursor to **Immunoproliferative Small Intestinal Disease (IPSID)**, a type of MALT lymphoma. * **Diagnosis:** Serum protein electrophoresis (SPEP) often shows a broad "hump" rather than a sharp M-spike because the heavy chains tend to polymerize. * **Key Association:** Alpha chain disease is unique because it may respond to **antibiotics** (like tetracycline) in its early stages, suggesting an infectious trigger. **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. 606-607.

Question 735: In which of the following conditions does the Periodic Acid-Schiff (PAS) test show block positivity?

A. Acute lymphoblastic leukemia (ALL) (Correct Answer)
B. Acute myeloid leukemia (AML)
C. Chronic myeloid leukemia (CML)
D. Hodgkin's lymphoma

Explanation: **Explanation:** The **Periodic Acid-Schiff (PAS)** stain is a cytochemical stain used to detect glycogen and mucopolysaccharides. In hematopathology, it is primarily used to differentiate between various types of leukemias. **1. Why Acute Lymphoblastic Leukemia (ALL) is correct:** In ALL, the lymphoblasts often contain large aggregates of glycogen. When stained with PAS, these appear as coarse granules or thick "chunks" of magenta-colored material against a clear cytoplasm [4]. This characteristic pattern is known as **"block positivity"** or "globular positivity." It is most commonly seen in the L1 and L2 subtypes (FAB classification) of ALL [1]. **2. Analysis of Incorrect Options:** * **Acute Myeloid Leukemia (AML):** Most AML subtypes (M1, M2, M3) are typically PAS negative or show faint, diffuse cytoplasmic staining. An exception is **AML-M6 (Erythroleukemia)**, which can show intense PAS positivity in the proerythroblasts, but "block positivity" is the classic hallmark of ALL [2]. * **Chronic Myeloid Leukemia (CML):** CML is a myeloproliferative neoplasm where the mature neutrophils show a decrease in **Leukocyte Alkaline Phosphatase (LAP)** score. PAS is not the diagnostic stain of choice here. * **Hodgkin’s Lymphoma:** The diagnostic cells are Reed-Sternberg (RS) cells. While they may show some staining, they are not characterized by PAS block positivity; they are typically identified by IHC markers like **CD30 and CD15** [3]. **High-Yield Clinical Pearls for NEET-PG:** * **ALL:** PAS (+) block pattern, Myeloperoxidase (MPO) (-), TdT (+). * **AML:** MPO (+) (except M0), Sudan Black B (+), Auer rods present. * **AML-M4/M5:** Non-specific Esterase (NSE) positive. * **Pure Erythroid Leukemia (M6):** Shows diffuse or granular PAS positivity in erythroid precursors. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 560-561. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 609-611. [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. 635-636. [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, pp. 599-600.

Question 736: What is the most common type of Hodgkin's lymphoma?

A. Lymphocyte predominant
B. Lymphocyte depletion
C. Nodular sclerosis (Correct Answer)
D. Mixed cellularity

Explanation: **Explanation:** Hodgkin’s Lymphoma (HL) is histologically divided into Classical HL (95%) and Nodular Lymphocyte Predominant HL (5%). Among the classical subtypes, **Nodular Sclerosis** is the most common, accounting for approximately **60–70% of all cases** [2]. **Why Nodular Sclerosis is correct:** It is characterized by the presence of broad collagen bands that divide the lymphoid tissue into nodules and the presence of **Lacunar cells** [5] (a variant of Reed-Sternberg cells). It has a unique clinical profile, frequently affecting young adults (especially females) and typically presenting with a mediastinal mass [1]. **Analysis of incorrect options:** * **Mixed Cellularity:** This is the second most common subtype (20–25%) [2]. It is strongly associated with the **Epstein-Barr Virus (EBV)** and is more common in older men and immunocompromised patients [3]. * **Lymphocyte Predominant:** This refers to Nodular Lymphocyte Predominant HL (NLPHL). It is rare (5%) and characterized by **"Popcorn cells"** (L&H cells) which are CD20 positive, unlike classical HL [4]. * **Lymphocyte Depletion:** This is the rarest and most aggressive subtype. It is associated with advanced-stage disease, HIV infection, and a poor prognosis [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Bimodal Age Distribution:** HL shows peaks at 15–35 years and >50 years. * **RS Cell Markers:** In Classical HL, Reed-Sternberg cells are typically **CD15+ and CD30+**, but CD45– and CD20–. * **Prognosis:** Lymphocyte Rich has the best prognosis among classical types; Lymphocyte Depletion has the worst [3]. * **Staging:** The **Ann Arbor Staging System** is used, and the most important prognostic factor is the stage of the disease. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 558-559. [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. 616-618. [3] 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. [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. [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, p. 616.

Question 737: All of the following are B cell markers except?

A. CD 22
B. CD 19
C. CD 20
D. CD 34 (Correct Answer)

Explanation: **Explanation:** The correct answer is **CD 34** because it is a marker of **hematopoietic stem cells (HSCs)** and early progenitor cells, rather than a lineage-specific B-cell marker. **1. Why CD 34 is the correct answer:** CD 34 is a cell surface glycoprotein expressed on pluripotent stem cells and early precursor cells in the bone marrow. As these cells mature and differentiate into specific lineages (like B-cells, T-cells, or myeloid cells), they lose CD 34 expression. In clinical pathology, CD 34 is primarily used to identify **blasts** in Acute Leukemias (AML and B-ALL) and to quantify stem cells for bone marrow transplantation. **2. Why the other options are incorrect (B-cell Markers):** * **CD 19:** This is the earliest and most specific pan-B-cell marker [2]. It is expressed from the pro-B cell stage until terminal differentiation into plasma cells (where it is lost). * **CD 20:** A widely used pan-B-cell marker expressed on mature B-cells [2]. It is the target for the monoclonal antibody **Rituximab**. It is not expressed on plasma cells. * **CD 22:** Another specific B-cell marker appearing shortly after CD 19. It is highly expressed in the cytoplasm of early B-cells and on the surface of mature B-cells. **High-Yield Clinical Pearls for NEET-PG:** * **Pan-B markers:** CD 19, CD 20, CD 22, CD 79a, and PAX-5 (the most specific lineage marker) [1], [2]. * **Plasma Cell Markers:** CD 138 (Syndecan-1) and CD 38. Note that plasma cells typically lose CD 19 and CD 20 [2]. * **Pre-B Cell Marker:** TdT (Terminal deoxynucleotidyl transferase) is a marker for lymphoblasts (both B and T). * **CD 34** is also expressed on vascular endothelial cells (useful for identifying vascular tumors like Angiosarcoma). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 199-200. [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. 598.

Question 738: Bleeding in Disseminated Intravascular Coagulation (DIC) is most closely related to which of the following?

A. Raised fibrin degradation products level in blood
B. Prolonged prothrombin time
C. Low serum fibrinogen level (Correct Answer)
D. Raised thrombin time

Explanation: **Explanation:** Disseminated Intravascular Coagulation (DIC) is a complex thrombo-hemorrhagic disorder characterized by the systemic activation of the coagulation cascade [1]. This leads to widespread microvascular thrombosis, which consumes clotting factors and platelets [2]. **Why Option C is Correct:** The primary mechanism behind the bleeding diathesis in DIC is **Consumption Coagulopathy** [1]. As thrombin is generated uncontrollably, it converts fibrinogen into fibrin clots throughout the microcirculation. This leads to a critical depletion (consumption) of circulating **fibrinogen** (Factor I), platelets, and other clotting factors (V and VIII) [2]. When fibrinogen levels fall below a critical threshold, the blood loses its ability to form stable clots at sites of injury, leading to profuse bleeding. Therefore, low serum fibrinogen is the most direct cause of the bleeding tendency [2]. **Analysis of Incorrect Options:** * **Option A:** Raised Fibrin Degradation Products (FDPs) are a result of secondary fibrinolysis [1]. While FDPs have a mild anticoagulant effect, they are a *marker* of the process rather than the primary cause of the hemorrhage [2]. * **Option B & D:** Prolonged Prothrombin Time (PT) and Thrombin Time (TT) are diagnostic findings in DIC reflecting the deficiency of coagulation factors [2]. However, these are *tests* that indicate a state of deficiency; the actual clinical bleeding is physically due to the lack of the substrate (fibrinogen) and platelets. **NEET-PG High-Yield Pearls:** * **Best Screening Test:** Platelet count (usually low) [2]. * **Most Sensitive/Specific Test:** D-dimer (indicates cross-linked fibrin degradation). * **Blood Film:** Presence of **Schistocytes** (fragmented RBCs) due to microangiopathic hemolytic anemia (MAHA) [2]. * **Common Triggers:** Sepsis (most common), Obstetric complications (Abruptio placentae), and Acute Promyelocytic Leukemia (M3). **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 739: Down syndrome is a known predisposing factor for which type of cancer?

A. Acute Myeloid Leukemia (AML)
B. Chronic Myeloid Leukemia (CML)
C. Acute Lymphoblastic Leukemia (ALL)
D. All of the above (Correct Answer)

Explanation: Explanation: Down Syndrome (Trisomy 21) is associated with a significantly increased risk (approximately 10–20 fold) of developing both myeloid and lymphoid malignancies. This is primarily due to the extra copy of the RUNX1 gene on chromosome 21, which regulates hematopoiesis, and GATA1 mutations. * Acute Myeloid Leukemia (AML): Children with Down Syndrome have a unique predisposition to AML-M7 (Acute Megakaryoblastic Leukemia), especially before the age of 3. They often present with a precursor condition called Transient Myeloproliferative Disorder (TMD). * Acute Lymphoblastic Leukemia (ALL): While AML-M7 is more specific to younger children with Down Syndrome, ALL is actually the most common leukemia in individuals with Down Syndrome over the age of 3 [2]. * Chronic Myeloid Leukemia (CML): Although much rarer than acute leukemias, there is a documented increased incidence of CML and other myeloproliferative neoplasms in the Down Syndrome population compared to the general public [1]. Why "All of the above" is correct: While textbooks often emphasize AML-M7 due to its unique association, epidemiological data confirms that Trisomy 21 increases the risk across the entire spectrum of leukemias (AML, ALL, and CML). High-Yield Clinical Pearls for NEET-PG: 1. AML-M7 is the most common leukemia in Down Syndrome patients <3 years old. 2. ALL is the most common leukemia in Down Syndrome patients >3 years old [3]. 3. GATA1 mutation is a hallmark of Down Syndrome-associated TMD and AML-M7. 4. Down Syndrome patients with AML generally have a better prognosis and better response to chemotherapy (especially Cytarabine) compared to non-Down Syndrome patients. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 605-607. [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. 598-599. [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, p. 606.

Question 740: Which of the following conditions is characterized by CD5+ lymphocytes?

A. Hairy cell leukemia
B. Burkitt lymphoma
C. Follicular cell lymphoma
D. Mantle cell lymphoma (Correct Answer)

Explanation: **Explanation:** The correct answer is **Mantle Cell Lymphoma (MCL)**. In hematopathology, CD5 is a T-cell marker; however, its expression on B-cells is a defining feature of two specific B-cell malignancies: **Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma (CLL/SLL)** and **Mantle Cell Lymphoma** [1]. MCL arises from the pre-germinal center B-cells of the mantle zone [2]. It is characterized by the translocation **t(11;14)**, which leads to the overexpression of **Cyclin D1**, a protein that promotes cell cycle progression from G1 to S phase. Immunophenotypically, MCL cells are **CD5+, CD19+, CD20+, and Cyclin D1+**, but notably **CD23 negative** (which distinguishes it from CLL/SLL) [1]. **Analysis of Incorrect Options:** * **A. Hairy Cell Leukemia:** Characterized by "hairy" cytoplasmic projections and markers like **CD11c, CD25, CD103, and Annexin A1**. It is CD5 negative. * **B. Burkitt Lymphoma:** A highly aggressive B-cell lymphoma associated with **c-MYC** translocation t(8;14). It expresses germinal center markers like **CD10 and Bcl-6**, but is CD5 negative. * **C. Follicular Lymphoma:** Arises from germinal center B-cells, characterized by **t(14;18)** and **Bcl-2** overexpression [3]. It is typically **CD10+ and CD5 negative**. **High-Yield Pearls for NEET-PG:** * **CD5+ B-cell Rule:** Always think of CLL/SLL (CD23+) vs. Mantle Cell Lymphoma (CD23-). * **MCL Hallmark:** t(11;14) involving the *CCND1* gene. * **Clinical Presentation:** Often presents with painless lymphadenopathy and may involve the GI tract as **lymphomatous polyposis**. **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. 610-612. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 562-563. [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. 602-604.

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Anemias: Classification and Approach

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Hemolytic Anemias

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Myeloproliferative Neoplasms

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Myelodysplastic Syndromes

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Acute Leukemias

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Chronic Leukemias

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Lymphomas and Lymphoid Neoplasms

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Plasma Cell Disorders

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Bleeding Disorders

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Thrombotic Disorders

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