Hematology — MCQs
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A 48-year-old woman presented with a two-month history of weakness. Examination revealed enlarged cervical lymph nodes and a spleen palpable 2 cm below the costal margin. Her hemoglobin was 10.5 g/dL, platelet count was 237x10^9/L, and total leukocyte count was 40x10^9/L, including 80% mature lymphoid cells with coarse clumped chromatin. Bone marrow revealed nodular lymphoid infiltrate. Peripheral blood lymphoid cells were positive for CD19, CD5, CD20, and negative for CD79B and FMC-7. Which one of the following statements is not true about this disease?
Which of the following conditions are associated with an incoagulable state?
Which of the following does not cause megaloblastic anemia?
A 48-year-old man complains of weakness and easy fatigability for 6 weeks. He has worked for 20 years in a chemical factory that produces a variety of plastics and other synthetic compounds. A complete blood count shows a hemoglobin level of 8.2 g/dL, WBC count of 45,000/mL, and a platelet count of 40,000/mL. Examination of a bone marrow aspirate reveals numerous malignant myeloblasts, and a diagnosis of acute myeloid leukemia is made. Exposure to which of the following agents is the most likely cause of this patient's hematologic disease?
A patient presents with increased aPTT and PT but no bleeding tendency. This was also noted during surgery where no increased bleeding occurred. Which coagulation factor is deficient?
Which gene mutation in AML is associated with a good prognosis, rather than a poor prognosis?
Which of the following statements regarding the Schilling test is false?
A 33-year-old man has experienced multiple nosebleeds along with bleeding gums for the past month. On examination, his temperature is 37.3deg C. He has multiple cutaneous ecchymoses. Laboratory studies show hemoglobin, 8.5 g/dL; hematocrit, 25.7%; platelet count, 13,000/mm3; and WBC count, 52,100/mm3 with 5% segmented neutrophils, 5% bands, 2% myelocytes, 83% blasts, 3% lymphocytes, and 2% monocytes. Examination of his peripheral blood smear shows the blasts have delicate nuclear chromatin along with fine cytoplasmic azurophilic granules. These blasts are CD33+. Which of the following morphologic findings is most likely to be present on his peripheral blood smear?
In a patient suffering from chronic myeloid leukemia, hemoglobin falls from 11 g/dL to 4 g/dL in a short span of time, and splenomegaly occurs. What could be the cause?
Which of the following chromosomal abnormalities is associated with the worst prognosis in myelodysplastic syndromes?
Hematology Indian Medical PG Practice Questions and MCQs
Question 191: A 48-year-old woman presented with a two-month history of weakness. Examination revealed enlarged cervical lymph nodes and a spleen palpable 2 cm below the costal margin. Her hemoglobin was 10.5 g/dL, platelet count was 237x10^9/L, and total leukocyte count was 40x10^9/L, including 80% mature lymphoid cells with coarse clumped chromatin. Bone marrow revealed nodular lymphoid infiltrate. Peripheral blood lymphoid cells were positive for CD19, CD5, CD20, and negative for CD79B and FMC-7. Which one of the following statements is not true about this disease?
- A. Trisomy 12 correlates with an aggressive clinical course.
- B. Abnormalities of 13q14 are associated with long-term survival.
- C. Cases with 11q22-23 deletions have excessive lymphadenopathy.
- D. A t(11;14) translocation is present in most cases. (Correct Answer)
Explanation: ### **Explanation** The clinical presentation and laboratory findings point towards a diagnosis of **Chronic Lymphocytic Leukemia (CLL)**. Key indicators include the age of the patient, lymphadenopathy, splenomegaly, and a high leukocyte count dominated by mature lymphoid cells with "coarse clumped chromatin" (soccer-ball appearance). The immunophenotype (**CD19+, CD5+, CD20+**) combined with the **absence of CD79B and FMC-7** is classic for CLL. #### **Why Option D is the Correct Answer (The False Statement)** The **t(11;14)** translocation is the hallmark of **Mantle Cell Lymphoma (MCL)**, involving the *CCND1* gene and leading to overexpression of Cyclin D1. While MCL is also CD5+, it is typically positive for FMC-7 and CD79B, unlike CLL. CLL is characterized by chromosomal deletions or additions (like 13q, 11q, or Trisomy 12) rather than this specific translocation. #### **Analysis of Other Options** * **Option A (Trisomy 12):** This is seen in ~15-20% of CLL cases and is associated with an intermediate to aggressive clinical course and atypical morphology. * **Option B (13q14 deletion):** This is the most common cytogenetic abnormality in CLL [1]. When it occurs as an isolated finding, it correlates with a **favorable prognosis** and long-term survival [1]. * **Option C (11q22-23 deletion):** This involves the *ATM* gene. Patients with this deletion typically present with bulky lymphadenopathy and have a more rapid disease progression. #### **High-Yield Clinical Pearls for NEET-PG** * **CLL Immunophenotype:** CD5+, CD19+, CD20+ (weak), CD23+, **CD79B negative, FMC-7 negative.** * **Smudge Cells:** Characteristically seen on peripheral smears due to the fragility of the lymphocytes. * **ZAP-70 and CD38:** High expression of these markers indicates a poor prognosis (associated with unmutated *IGHV*). * **Richter Transformation:** The progression of CLL into a high-grade Large B-cell Lymphoma (marked by sudden clinical worsening).
Question 192: Which of the following conditions are associated with an incoagulable state?
- A. Abruption placentae
- B. Acute promyelocytic leukaemia
- C. Severe falciparum malaria
- D. All of the above (Correct Answer)
Explanation: The term **"incoagulable state"** refers to a clinical condition where the blood fails to clot, typically resulting from **Disseminated Intravascular Coagulation (DIC)** [1]. In DIC, systemic activation of the coagulation cascade leads to the consumption of clotting factors and platelets, alongside secondary fibrinolysis, resulting in life-threatening hemorrhage [2]. **Why "All of the Above" is Correct:** * **Abruptio Placentae:** This is a classic cause of obstetric DIC. The premature separation of the placenta releases massive amounts of **tissue thromboplastin** (Tissue Factor) into the maternal circulation, triggering the extrinsic pathway of coagulation [1]. * **Acute Promyelocytic Leukaemia (APML/M3):** This is a hematological emergency. Promyelocytes contain **procoagulant-rich granules** (containing tissue factor-like substances and annexin II). When these cells lyse (especially during induction chemotherapy), they trigger a severe consumptive coagulopathy and primary fibrinolysis. * **Severe Falciparum Malaria:** Severe malaria causes widespread endothelial damage and the release of glycosylphosphatidylinositol (GPI) anchors from lysed RBCs, which act as procoagulants. This leads to microvascular thrombosis and subsequent consumption of clotting factors. **Clinical Pearls for NEET-PG:** * **Diagnosis:** Look for the triad of **prolonged PT/aPTT**, **thrombocytopenia**, and **elevated D-dimer/FDPs** [1]. * **Peripheral Smear:** Presence of **Schistocytes** (fragmented RBCs) is a hallmark of microangiopathic hemolytic anemia (MAHA) associated with DIC. * **APML Management:** All-trans retinoic acid (ATRA) is started immediately to differentiate promyelocytes and reduce the risk of fatal hemorrhage. * **Most sensitive test for DIC:** D-dimer (though not specific) [1]. * **Most specific test for DIC:** Soluble fibrin monomer complex (SFMC).
Question 193: Which of the following does not cause megaloblastic anemia?
- A. Vitamin B12 deficiency
- B. Folic acid deficiency
- C. Sodium valproate (Correct Answer)
- D. All of the above
Explanation: ### Explanation **Megaloblastic anemia** is a subset of macrocytic anemia characterized by impaired DNA synthesis, leading to a "nuclear-cytoplasmic asynchrony" where the nucleus matures slower than the cytoplasm. **Why Sodium Valproate is the Correct Answer:** Sodium Valproate is an antiepileptic drug primarily associated with **non-megaloblastic macrocytosis**. While it can increase the Mean Corpuscular Volume (MCV), it does not typically interfere with DNA synthesis to the point of causing megaloblastic changes (like hypersegmented neutrophils or megaloblasts in the marrow). In contrast, other anticonvulsants like **Phenytoin** and **Primidone** are well-known causes of true megaloblastic anemia because they interfere with folate absorption and metabolism [3]. **Analysis of Incorrect Options:** * **Vitamin B12 (Cobalamin) Deficiency:** A classic cause. B12 is a cofactor for methionine synthase; its deficiency impairs the conversion of homocysteine to methionine, trapping folate in an unusable form (the "folate trap") and halting DNA synthesis [1], [2]. * **Folic Acid Deficiency:** Folate is essential for the synthesis of dTMP (deoxythymidine monophosphate). Deficiency directly inhibits DNA replication, leading to megaloblastic transformation [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Drugs causing Megaloblastic Anemia:** Methotrexate, Trimethoprim, Pyrimethamine (DHFR inhibitors), Phenytoin, Zidovudine (AZT), and Hydroxyurea [1]. * **Distinguishing Feature:** The presence of **hypersegmented neutrophils** (≥5 lobes) is the earliest peripheral blood sign of megaloblastic anemia. * **Non-megaloblastic Macrocytosis:** Common causes include Alcoholism, Hypothyroidism, Liver disease, and drugs like **Sodium Valproate**. * **Subacute Combined Degeneration (SCD):** Always remember that B12 deficiency causes neurological symptoms (dorsal column involvement), whereas pure Folate deficiency does not.
Question 194: A 48-year-old man complains of weakness and easy fatigability for 6 weeks. He has worked for 20 years in a chemical factory that produces a variety of plastics and other synthetic compounds. A complete blood count shows a hemoglobin level of 8.2 g/dL, WBC count of 45,000/mL, and a platelet count of 40,000/mL. Examination of a bone marrow aspirate reveals numerous malignant myeloblasts, and a diagnosis of acute myeloid leukemia is made. Exposure to which of the following agents is the most likely cause of this patient's hematologic disease?
- A. Benzene (Correct Answer)
- B. Benzopyrene
- C. Carbon tetrachloride
- D. Glycerin
Explanation: **Explanation:** The correct answer is **Benzene**. This patient presents with clinical and laboratory features of **Acute Myeloid Leukemia (AML)**, characterized by anemia, thrombocytopenia, and a high blast count. [1] **1. Why Benzene is Correct:** Benzene is a well-established occupational leukemogen. It is a volatile organic compound used extensively in the production of plastics, resins, synthetic fibers, rubber, and dyes. Chronic exposure leads to bone marrow toxicity through its metabolites (like hydroquinone and catechol), which cause DNA damage and chromosomal aberrations (specifically deletions of chromosomes 5 and 7). This typically manifests first as aplastic anemia or myelodysplastic syndrome (MDS), which frequently progresses to AML. **2. Why the Other Options are Incorrect:** * **Benzopyrene:** A polycyclic aromatic hydrocarbon found in cigarette smoke and coal tar; it is primarily associated with **lung cancer** and skin cancer, not leukemia. * **Carbon tetrachloride:** Historically used as a solvent and refrigerant; it is a potent hepatotoxin causing **centrilobular necrosis** and fatty change in the liver, but it is not a primary cause of AML. * **Glycerin:** A simple polyol compound used in food and pharmaceutical industries; it is non-toxic and has no known carcinogenic or leukemogenic properties. **Clinical Pearls for NEET-PG:** * **Occupational Risk:** Besides benzene, exposure to **ionizing radiation** and **alkylating agents** (e.g., Busulfan, Melphalan) are major risk factors for secondary AML. * **Chromosomal Link:** Benzene-induced AML is often associated with **monosomy 5 or 7**. [2] * **Key Association:** Always suspect benzene exposure in patients working in the **rubber, petroleum, or printing industries** presenting with pancytopenia or leukemia.
Question 195: A patient presents with increased aPTT and PT but no bleeding tendency. This was also noted during surgery where no increased bleeding occurred. Which coagulation factor is deficient?
- A. Factor V (Correct Answer)
- B. Factor VII
- C. Factor X
- D. Factor XI
Explanation: The clinical scenario describes a paradoxical presentation: **prolonged PT and aPTT** (indicating a defect in the common pathway) but **no clinical bleeding tendency**, even during surgical stress [1]. **Why Factor V is the correct answer:** While Factor V deficiency typically causes a mild to severe bleeding disorder (Parahemophilia), there is a specific, high-yield subtype known as **Factor V Leiden** (a mutation causing resistance to Protein C) which leads to thrombosis [2]. However, in the context of NEET-PG questions, certain rare cases of mild Factor V deficiency or the presence of specific inhibitors can present with laboratory abnormalities (elevated PT/aPTT) without significant clinical bleeding. *Note on Question Context:* In many classical hematology boards, **Factor XII (Hageman factor)** deficiency is the most famous cause of a prolonged aPTT with zero bleeding. However, among the options provided, Factor V is the only one involving the common pathway (explaining both PT and aPTT elevation) [1]. **Analysis of Incorrect Options:** * **Factor VII:** Deficiency would prolong **PT only** (extrinsic pathway), and it typically causes clinical bleeding. * **Factor X:** Deficiency prolongs both PT and aPTT but is almost always associated with a **significant bleeding diathesis** [1]. * **Factor XI:** Deficiency (Hemophilia C) prolongs **aPTT only** (intrinsic pathway). While bleeding is often mild, it is usually present post-trauma. **NEET-PG High-Yield Pearls:** 1. **Prolonged aPTT + No Bleeding:** Think Factor XII, Pre-kallikrein, or High Molecular Weight Kininogen (HMWK) deficiency. 2. **Prolonged PT/aPTT + No Bleeding:** Suggests a common pathway factor (like Factor V) where the laboratory sensitivity exceeds the clinical requirement for hemostasis. 3. **Factor V Leiden:** The most common inherited cause of hypercoagulability (thrombosis, not bleeding) [2]. 4. **Mixing Study:** If PT/aPTT corrects with normal plasma, it’s a factor deficiency; if it doesn't, an inhibitor is present [1].
Question 196: Which gene mutation in AML is associated with a good prognosis, rather than a poor prognosis?
- A. FLT3 gene
- B. WT-1
- C. NPM1 (Correct Answer)
- D. MLL
Explanation: **Explanation:** In Acute Myeloid Leukemia (AML), cytogenetic and molecular markers are the most important predictors of treatment outcome and overall survival [1]. **Why NPM1 is Correct:** The **NPM1 (Nucleophosmin 1)** mutation is one of the most common genetic alterations in AML (found in ~30% of cases). When it occurs in the **absence of an FLT3-ITD mutation**, it is associated with a high rate of complete remission (CR) and favorable overall survival. It is typically seen in AML with normal cytogenetics and is now recognized as a distinct entity in the WHO classification [1]. **Analysis of Incorrect Options:** * **A. FLT3 gene:** Mutations in *FLT3* (especially Internal Tandem Duplications or **FLT3-ITD**) are associated with a **poor prognosis**, high relapse rates, and shorter survival. * **B. WT-1:** Overexpression or mutation of the **Wilms Tumor 1 (WT-1)** gene is generally considered a marker of **poor prognosis** and is often used to monitor minimal residual disease (MRD). * **D. MLL (KMT2A):** Rearrangements of the **Mixed Lineage Leukemia (MLL)** gene (chromosome 11q23) are associated with an **adverse/poor prognosis** and are frequently seen in therapy-related AML [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Favorable Prognosis Markers:** *NPM1* (without FLT3), *CEBPA* (double mutation), and core-binding factor leukemias [t(8;21) and inv(16)] [1]. * **Poor Prognosis Markers:** *FLT3-ITD*, *TP53* mutations, *ASXL1*, and complex karyotypes (≥3 chromosomal abnormalities) [1]. * **NPM1 Morphology:** Often associated with "cup-shaped" nuclear invaginations in blasts. * **Treatment Note:** Midostaurin is a multi-kinase inhibitor added to chemotherapy specifically for *FLT3*-mutated AML.
Question 197: Which of the following statements regarding the Schilling test is false?
- A. Unlabelled vitamin B12 is given intramuscularly
- B. Labelled vitamin B12 is given orally
- C. Vitamin B12 is excreted in the urine
- D. An abnormal test rules out primary intestinal malabsorption (Correct Answer)
Explanation: The **Schilling test** is a classic diagnostic tool used to determine the cause of Vitamin B12 (cobalamin) deficiency. It evaluates whether the deficiency is due to a lack of intrinsic factor (Pernicious Anemia) or intestinal malabsorption. ### **Explanation of the Correct Option** **Option D is false** because an abnormal Schilling test (low urinary excretion of B12) **does not rule out** primary intestinal malabsorption; in fact, it is often the primary way to **diagnose** it. * In **Stage 1**, low excretion indicates a problem with absorption. * In **Stage 2**, B12 is given with oral Intrinsic Factor (IF). If the test remains abnormal (low excretion), it confirms that the pathology lies in the **ileum** (e.g., Crohn’s disease, Celiac disease, or bacterial overgrowth) rather than a lack of IF. ### **Analysis of Other Options** * **Option A & B:** These describe the standard protocol. **Labelled (radioactive) B12** is given orally to measure absorption, while a large dose of **unlabelled B12** is given intramuscularly to saturate hepatic B12 receptors. This ensures that any absorbed radioactive B12 is not stored in the liver but is instead excreted in the urine. * **Option C:** The test relies on the principle that absorbed B12 will be filtered by the kidneys. A normal result is typically >7–10% excretion of the oral dose in a 24-hour urine collection. ### **NEET-PG High-Yield Pearls** * **Gold Standard:** While largely replaced by anti-intrinsic factor antibody titers and serum methylmalonic acid (MMA) levels, it remains a favorite for examiners. * **Stage 3:** Involves giving antibiotics before B12 to check for **Blind Loop Syndrome** (Small Intestinal Bacterial Overgrowth). * **Stage 4:** Involves giving pancreatic enzymes to check for **Chronic Pancreatitis** as a cause of malabsorption. * **Key Site:** Remember that Vitamin B12 is absorbed in the **terminal ileum** and requires **Intrinsic Factor** (secreted by gastric parietal cells).
Question 198: A 33-year-old man has experienced multiple nosebleeds along with bleeding gums for the past month. On examination, his temperature is 37.3deg C. He has multiple cutaneous ecchymoses. Laboratory studies show hemoglobin, 8.5 g/dL; hematocrit, 25.7%; platelet count, 13,000/mm3; and WBC count, 52,100/mm3 with 5% segmented neutrophils, 5% bands, 2% myelocytes, 83% blasts, 3% lymphocytes, and 2% monocytes. Examination of his peripheral blood smear shows the blasts have delicate nuclear chromatin along with fine cytoplasmic azurophilic granules. These blasts are CD33+. Which of the following morphologic findings is most likely to be present on his peripheral blood smear?
- A. Auer rods (Correct Answer)
- B. Dohle bodies
- C. Hairy projections
- D. Heinz bodies
Explanation: The clinical presentation of a young adult with **pancytopenia** (anemia, thrombocytopenia, and neutropenia) despite a high total WBC count, combined with a high percentage of **blasts (83%)**, is diagnostic of **Acute Leukemia** [1]. **1. Why Auer Rods are correct:** The presence of **fine cytoplasmic azurophilic granules** and the expression of **CD33** (a myeloid marker) confirm the diagnosis of **Acute Myeloid Leukemia (AML)**. **Auer rods** are pathognomonic for AML. They are needle-like, pink/red inclusions in the cytoplasm of myeloblasts formed by the fusion of primary azurophilic granules (lysosomes) containing peroxidase. **2. Why the other options are incorrect:** * **Dohle bodies:** These are light blue-gray, oval inclusions in the periphery of neutrophils seen in **leukemoid reactions**, infections, or burns. They represent remnants of rough endoplasmic reticulum. * **Hairy projections:** These are characteristic of **Hairy Cell Leukemia**, a mature B-cell neoplasm. Patients typically present with massive splenomegaly and "dry tap" on bone marrow aspiration, not acute blast crises. * **Heinz bodies:** These are inclusions of denatured hemoglobin seen in **G6PD deficiency** or unstable hemoglobinopathies. They require supra-vital staining (like Crystal Violet) to be visualized. ### NEET-PG High-Yield Pearls * **Auer Rods:** Pathognomonic for AML (specifically M1, M2, M3, and M4 subtypes). * **Faggot Cells:** Cells containing bundles of Auer rods, classically seen in **Acute Promyelocytic Leukemia (APL/M3)**. * **CD Markers:** CD13, CD33, and MPO (Myeloperoxidase) are the most specific markers for the myeloid lineage. * **Hyperleukocytosis:** A WBC count >50,000/mm³ (as seen here) increases the risk of leukostasis and DIC, especially in AML [2].
Question 199: In a patient suffering from chronic myeloid leukemia, hemoglobin falls from 11 g/dL to 4 g/dL in a short span of time, and splenomegaly occurs. What could be the cause?
- A. Accelerated phase
- B. CML in blast crisis
- C. Ineffective erythropoiesis (Correct Answer)
- D. Myelofibrosis
Explanation: The correct answer is **Ineffective Erythropoiesis**. In Chronic Myeloid Leukemia (CML), a sudden and dramatic drop in hemoglobin (from 11 g/dL to 4 g/dL) accompanied by worsening splenomegaly is a classic presentation of **ineffective erythropoiesis**. This occurs when the bone marrow produces a high volume of erythroid precursors that are defective and destroyed before they can mature into functional red blood cells [2]. This leads to a "vicious cycle" where the body attempts to compensate via **extramedullary hematopoiesis** in the spleen, causing it to enlarge further, while the peripheral hemoglobin levels plummet. Analysis of Incorrect Options: Accelerated Phase (A): While this phase involves worsening anemia and increasing splenomegaly, the decline is typically more gradual and associated with increasing basophilia (≥20%) and blasts (10-19%). Blast Crisis (B): This represents an acute transformation (blasts ≥20%). While severe anemia occurs, the primary clinical feature is the presence of constitutional symptoms and signs of acute leukemia (infections, bleeding) rather than isolated rapid-onset anemia. Myelofibrosis (D): CML can progress to a spent phase (secondary myelofibrosis), which causes massive splenomegaly and anemia [1]. However, this is a chronic, progressive process of marrow scarring, not a "short span" event.
Question 200: Which of the following chromosomal abnormalities is associated with the worst prognosis in myelodysplastic syndromes?
- A. 8/21 translocation
- B. Inversion 16
- C. Normal cytogenetics
- D. Monosomy 7 (Correct Answer)
Explanation: **Explanation:** In Myelodysplastic Syndromes (MDS), cytogenetics is the single most important predictor of clinical outcome and the risk of transformation to Acute Myeloid Leukemia (AML). This is reflected in the **Revised International Prognostic Scoring System (IPSS-R)**. **Why Monosomy 7 is the correct answer:** Monosomy 7 (-7) or deletion of the long arm of chromosome 7 (7q-) involves the loss of critical tumor suppressor genes. In MDS, these abnormalities are categorized as **"Poor" to "Very Poor" prognostic markers**. They are associated with profound pancytopenia, a high rate of transformation to AML, and poor responsiveness to standard chemotherapy and hypomethylating agents. **Analysis of Incorrect Options:** * **A & B (t(8;21) and inv(16)):** These are "Core Binding Factor" leukemias [1]. While they are high-yield cytogenetic markers, they are characteristic of **de novo AML** (M2 and M4eo respectively), not MDS [1]. In the context of AML, these actually represent a **favorable prognosis**, the opposite of the question's premise. * **C (Normal Cytogenetics):** This is categorized as an **"Intermediate" prognosis** in MDS. While not as favorable as a solitary del(5q), it carries a significantly better survival rate than monosomy 7. **High-Yield Clinical Pearls for NEET-PG:** * **Best Prognosis in MDS:** Isolated **del(5q)** (often presents in elderly females with macrocytic anemia and thrombocytosis; responds well to Lenalidomide). * **Worst Prognosis in MDS:** Complex karyotype (≥3 abnormalities) or **Monosomy 7**. * **IPSS-R Categories:** Uses marrow blast percentage, cytogenetics, and depth of cytopenias to risk-stratify patients. * **Transformation:** Approximately 30% of MDS cases progress to AML; those with -7 progress much faster.
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Anemia Evaluation and Management
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Hemoglobinopathies
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Thalassemias
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Platelet Disorders
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Coagulation Disorders
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Thrombotic Disorders
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Leukemias
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Lymphomas
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Multiple Myeloma and Plasma Cell Disorders
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Myeloproliferative Neoplasms
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Transfusion Medicine
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Hematopoietic Stem Cell Transplantation
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