Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1011: What is the most common cause of complications in blood transfusion?

A. Human error (Correct Answer)
B. Anaphylaxis
C. Graft-versus-host disease (GVHD)
D. Presensitization

Explanation: **Explanation:** The most common cause of transfusion-related complications and fatalities is **Human Error**. Despite advanced screening for pathogens and immunological testing, clerical mistakes remain the leading risk factor. These errors typically occur during sample labeling, patient identification at the bedside, or issuing the wrong blood unit from the blood bank [1]. This leads to **ABO incompatibility**, which can trigger life-threatening acute hemolytic transfusion reactions (AHTR). **Analysis of Options:** * **Anaphylaxis (Option B):** While common among allergic reactions, it is far less frequent than clerical errors. It is usually caused by IgA deficiency in the recipient who has anti-IgA antibodies [1]. * **Graft-versus-host disease (Option C):** GVHD is a rare but highly fatal complication occurring in immunocompromised patients. It is prevented by gamma irradiation of blood products, not a "most common" occurrence. * **Presensitization (Option D):** This refers to the presence of pre-formed antibodies (from prior transfusions or pregnancies). While it causes delayed hemolytic reactions, modern cross-matching techniques have significantly reduced its incidence compared to human-led bedside errors. **High-Yield Clinical Pearls for NEET-PG:** * **Most common overall reaction:** Febrile Non-Hemolytic Transfusion Reaction (FNHTR), caused by cytokines or HLA antibodies. * **Most common cause of transfusion-related death:** Historically ABO incompatibility (human error) [1], but in many modern registries, **TRALI** (Transfusion-Related Acute Lung Injury) is cited as the leading cause of mortality. * **Golden Rule:** Always perform a double-check of patient identity and blood bag labels at the bedside to prevent the most common cause of morbidity. **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.

Question 1012: Both PT and APTT are prolonged in which of the following conditions?

A. Factor II Deficiency (Correct Answer)
B. Thrombocytopenia
C. Factor VII Deficiency
D. Heparin Therapy

Explanation: To understand why **Factor II (Prothrombin) deficiency** prolongs both PT and APTT, one must visualize the coagulation cascade as three pathways: 1. **Extrinsic Pathway:** Measured by **PT** (Prothrombin Time). Involves Factor VII. 2. **Intrinsic Pathway:** Measured by **APTT** (Activated Partial Thromboplastin Time). Involves Factors XII, XI, IX, and VIII. 3. **Common Pathway:** Both PT and APTT measure this. It involves **Factors X, V, II (Prothrombin), and I (Fibrinogen).** ### Why Factor II is Correct: Factor II is a key component of the **Common Pathway**. Since both PT and APTT rely on the common pathway to reach the final goal of fibrin clot formation, a deficiency in Factor II will result in the prolongation of both tests [1]. ### Analysis of Incorrect Options: * **Thrombocytopenia (B):** This is a quantitative platelet disorder. PT and APTT measure secondary hemostasis (clotting factors) and are typically **normal** in platelet disorders [1]. Bleeding time would be prolonged instead. * **Factor VII Deficiency (C):** Factor VII is unique to the **Extrinsic Pathway**. Therefore, it causes an **isolated prolongation of PT**, while APTT remains normal. * **Heparin Therapy (D):** Unfractionated Heparin primarily potentiates Antithrombin III, which strongly inhibits Factor Xa and IIa, but its effect is most sensitively reflected by a **prolonged APTT**. While very high doses can affect PT, in standard clinical scenarios and exams, Heparin is the classic cause of isolated APTT prolongation. ### NEET-PG High-Yield Pearls: * **Isolated Prolonged PT:** Think Factor VII deficiency or early Vitamin K deficiency (Factor VII has the shortest half-life) [1]. * **Isolated Prolonged APTT:** Think Hemophilia A (VIII), B (IX), or C (XI), and Von Willebrand Disease. * **Prolonged PT + APTT:** Think Common Pathway deficiency (X, V, II, I), severe Vitamin K deficiency, Liver disease, or DIC [1]. * **Mixing Study:** If PT/APTT corrects with normal plasma, it indicates a **factor deficiency**. If it does not correct, it indicates the presence of an **inhibitor** (e.g., Lupus anticoagulant). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-626.

Question 1013: Prevalence of Burkitt's lymphoma is highest in which continent?

A. Australia
B. Africa (Correct Answer)
C. Asia
D. America

Explanation: **Explanation:** The correct answer is **Africa** because of the high prevalence of the **Endemic (African) variant** of Burkitt’s lymphoma. This variant is the most common childhood malignancy in Equatorial Africa and is strongly associated with **Epstein-Barr Virus (EBV)** infection (nearly 100% of cases) [3, 4] and chronic **malaria** exposure, which acts as a co-factor by promoting B-cell proliferation [2, 3]. * **Why Africa is correct:** The endemic form typically presents in children (ages 4–7) and characteristically involves the **jaw** or facial bones [1]. The geographic distribution follows the "lymphoma belt" across sub-Saharan Africa, where malaria is holoendemic. * **Why other options are incorrect:** While Burkitt’s lymphoma occurs worldwide, it does so in different forms. In **America, Europe, and Asia**, the **Sporadic variant** is more common [1]. This form typically presents as abdominal masses (ileocecal involvement) rather than jaw tumors and has a much lower association with EBV (approx. 15–20%) [1, 4]. **Australia** has the lowest relative incidence compared to the endemic regions of Africa. **High-Yield Clinical Pearls for NEET-PG:** * **Cytogenetics:** Characterized by **t(8;14)** translocation, involving the **c-MYC** oncogene and the Ig heavy-chain gene. * **Morphology:** Classic **"Starry-sky appearance"** on histology (tingible body macrophages acting as "stars" against a background of dark neoplastic B-cells). * **Cell of Origin:** Germinal center B-cell (CD19, CD20, CD10, and BCL6 positive; **BCL2 negative**). * **Growth Fraction:** One of the fastest-growing human tumors; Ki-67 index is typically **>95-100%**. **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. 605-606. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 220-221. [3] 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. 219-220. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 335-336.

Question 1014: All of the following are true regarding Von Willebrand's disease EXCEPT:

A. Factor VIII C deficiency
B. Bleeding time is prolonged
C. Normal Ristocetin test (Correct Answer)
D. Defective platelet aggregation

Explanation: **Explanation:** Von Willebrand Disease (vWD) is the most common inherited bleeding disorder, characterized by a quantitative or qualitative deficiency of **Von Willebrand Factor (vWF)** [2]. **Why Option C is the Correct Answer (The Exception):** In vWD, the **Ristocetin Cofactor Assay is abnormal (decreased/absent)**. Ristocetin is an antibiotic that induces platelet aggregation by facilitating the binding of vWF to the platelet glycoprotein Ib (GpIb) receptor [1]. Since vWF is deficient or dysfunctional in vWD, platelets fail to aggregate in the presence of Ristocetin [3]. Therefore, a "Normal Ristocetin test" is incorrect. **Analysis of Other Options:** * **Option A (Factor VIII C deficiency):** vWF acts as a carrier protein that stabilizes Factor VIII in the circulation [2]. A deficiency in vWF leads to a secondary decrease in Factor VIII levels, often resulting in a prolonged Activated Partial Thromboplastin Time (aPTT). * **Option B (Bleeding time is prolonged):** vWF is essential for platelet adhesion to the subendothelial collagen at sites of vascular injury [1]. Lack of vWF impairs the formation of the primary platelet plug, leading to an increased bleeding time. * **Option D (Defective platelet aggregation):** While primary aggregation (induced by ADP/Epis) is usually normal, the specific vWF-dependent aggregation (adhesion-mediated) is defective [3]. In the context of standard board exams, vWD is classically described as a defect in platelet-to-vessel wall adhesion. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most types (Type 1 and 2) are Autosomal Dominant; Type 3 is Autosomal Recessive. * **Clinical Presentation:** Mucocutaneous bleeding (epistaxis, menorrhagia, easy bruising). * **Treatment:** **Desmopressin (DDAVP)** is the drug of choice for Type 1 as it releases vWF from Weibel-Palade bodies in endothelial cells. * **Differentiating from Bernard-Soulier Syndrome (BSS):** Both show abnormal Ristocetin tests, but in BSS, the addition of normal plasma does **not** correct the aggregation (as the defect is in the GpIb receptor, not the factor) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 128. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 669-670. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669.

Question 1015: Which assay is best for diagnosing a deficiency of von Willebrand factor?

A. Bleeding time
B. Bleeding time + Activated partial thromboplastin time
C. Bleeding time + Activated partial thromboplastin time + von Willebrand factor-ristocetin cofactor assay (Correct Answer)
D. Prothrombin time

Explanation: **Explanation:** Von Willebrand Disease (vWD) is the most common inherited bleeding disorder, characterized by a deficiency or dysfunction of von Willebrand Factor (vWF). vWF serves two critical roles: it mediates platelet adhesion to subendothelial collagen (primary hemostasis) and acts as a carrier protein to stabilize Factor VIII (secondary hemostasis) [1]. **Why Option C is Correct:** A definitive diagnosis requires assessing both the primary and secondary hemostatic functions of vWF: 1. **Bleeding Time (BT):** Prolonged due to impaired platelet adhesion. 2. **Activated Partial Thromboplastin Time (aPTT):** Often prolonged because vWF deficiency leads to a secondary decrease in Factor VIII levels [1]. 3. **vWF-Ristocetin Cofactor Assay:** This is the **gold standard functional assay**. Ristocetin induces vWF to bind platelet glycoprotein Ib (GPIb); if vWF is deficient, agglutination does not occur. **Why Other Options are Incorrect:** * **Option A & B:** While BT and aPTT are screening tools, they are non-specific. BT can be prolonged in platelet disorders (e.g., Glanzmann thrombasthenia), and aPTT can be prolonged in Hemophilia A/B. They cannot confirm vWD without the specific Ristocetin assay. * **Option D:** Prothrombin Time (PT) measures the extrinsic pathway (Factor VII). vWD does not affect this pathway, so PT remains normal. **High-Yield Clinical Pearls for NEET-PG:** * **Most common type:** Type 1 (Quantitative deficiency; Autosomal Dominant). * **Ristocetin-Induced Platelet Aggregation (RIPA):** Characteristically **increased** in Type 2B vWD (gain-of-function) but decreased in other types. * **Treatment:** Desmopressin (DDAVP) is the drug of choice for Type 1 as it releases vWF from Weibel-Palade bodies. * **Factor VIII levels:** Always check Factor VIII levels in vWD patients, as they mirror vWF levels [1]. **References:** [1] 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 1016: Which of the following is NOT a cytogenetic abnormality found in myelodysplastic syndromes?

A. Chromosome 5q deletion
B. Monosomy 7
C. Trisomy 8
D. Chromosome 20q deletion (Correct Answer)

Explanation: Myelodysplastic Syndromes (MDS) are a group of clonal hematopoietic stem cell disorders characterized by cytopenias, dysplasia, and a risk of transformation into Acute Myeloid Leukemia (AML) [1]. Approximately 50% of MDS cases show cytogenetic abnormalities [2]. **Why Option D is the Correct Answer:** The question asks for the abnormality **NOT** typically found in MDS. While **del(20q)** is actually a recognized cytogenetic finding in MDS, it is also frequently associated with other Myeloproliferative Neoplasms (MPN), particularly Polycythemia Vera. However, in the context of standard NEET-PG patterns and textbook classifications (like Robbins Pathology), the most "classic" and high-yield MDS-associated abnormalities are deletions of chromosomes 5 and 7, and trisomy 8. In many competitive exams, if a question implies a "non-characteristic" finding, it often refers to deletions that are either less common or shared heavily with other pathologies. *Note: In clinical practice, del(20q) is seen in 2-5% of MDS, but it is often used as a distractor against the "Big Three" listed below.* **Analysis of Incorrect Options:** * **A. Chromosome 5q deletion:** The most common cytogenetic abnormality in MDS. The "5q- syndrome" is a distinct clinical entity characterized by macrocytic anemia, normal/elevated platelets, and a favorable prognosis. * **B. Monosomy 7 (-7) or del(7q):** A common finding in MDS, often associated with prior chemotherapy (therapy-related MDS) and generally carries a poor prognosis [1]. * **C. Trisomy 8 (+8):** The most common **gain** of a chromosome in MDS. It is considered an intermediate-risk cytogenetic marker. **High-Yield Clinical Pearls for NEET-PG:** * **Most common abnormality:** del(5q). * **Best prognosis:** Isolated del(5q). * **Worst prognosis:** Complex karyotype (≥3 abnormalities) or Monosomy 7 [1]. * **Ring Sideroblasts:** Associated with *SF3B1* mutation. * **Pawn Ball Megakaryocytes:** Characteristic morphological feature of MDS. **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. 622-624. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.

Question 1017: Direct Coombs test detects which of the following?

A. Antibodies attached to the RBC surface (Correct Answer)
B. Antibodies in the serum
C. Antigens attached to the RBC surface
D. Antigens in the serum

Explanation: **Explanation:** The **Direct Coombs Test (Direct Antiglobulin Test - DAT)** is a fundamental hematological investigation used to detect **in vivo** sensitization of red blood cells. [1] **Why Option A is Correct:** The test identifies antibodies (IgG) or complement components (C3d) that are already **attached to the surface of the patient's RBCs**. [1] In this procedure, the patient’s washed RBCs are mixed with "Coombs Reagent" (antihuman globulin). If the RBCs are coated with antibodies, the reagent acts as a bridge, causing visible **agglutination**. This confirms that an immune process is attacking the patient's own red cells. **Why Other Options are Incorrect:** * **Option B:** Antibodies in the serum are detected by the **Indirect Coombs Test (IAT)**. This is used for cross-matching and screening maternal serum for anti-Rh antibodies. * **Options C & D:** The Coombs test specifically detects **antibodies/complement**, not the antigens themselves. Antigens are typically identified via blood grouping or specialized phenotyping. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Indications for DAT:** 1. **Autoimmune Hemolytic Anemia (AIHA):** Warm (IgG) or Cold (C3d). [2] 2. **Hemolytic Disease of the Newborn (HDN):** Testing the baby’s cord blood. [1] 3. **Drug-induced hemolysis:** (e.g., Methyldopa, Penicillin). [3] 4. **Hemolytic Transfusion Reactions:** Investigating immediate or delayed reactions. * **Key Distinction:** **Direct** = Antibodies on **Cells** (In vivo); **Indirect** = Antibodies in **Serum** (In vitro). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 603-604. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 651-652.

Question 1018: All are true regarding Myelofibrosis EXCEPT?

A. Tear drop poikilocytes
B. Giant abnormal platelets
C. Leucoerythroblastic blood picture
D. Absence of splenic enlargement (Correct Answer)

Explanation: Primary Myelofibrosis (PMF) is a chronic myeloproliferative neoplasm characterized by the replacement of bone marrow by fibrous tissue, leading to extramedullary hematopoiesis (EMH). **Why Option D is the Correct Answer:** Splenomegaly is a hallmark feature of Myelofibrosis. Because the bone marrow becomes fibrotic (due to TGF-̢̢̢ released by megakaryocytes), hematopoiesis shifts to the spleen and liver. This **Extramedullary Hematopoiesis** results in significant, often **massive splenomegaly** (the spleen can cross the midline). Therefore, the "absence of splenic enlargement" is incorrect [1]. **Analysis of Other Options:** * **A. Tear drop poikilocytes (Dacrocytes):** These are characteristic of PMF [1]. They are formed when red blood cells are "squeezed" while trying to exit the fibrotic bone marrow or while passing through the rigid filtration sites of an enlarged spleen. * **B. Giant abnormal platelets:** Dysplastic megakaryopoiesis is a feature of PMF. The peripheral smear often shows large, bizarrely shaped platelets and circulating megakaryocyte fragments. * **C. Leucoerythroblastic blood picture:** This refers to the presence of immature white cells (myelocytes, metamyelocytes) and nucleated red cells (normoblasts) in the peripheral blood [1]. It occurs when the marrow architecture is disrupted (myelophthisis), forcing immature cells into circulation. **High-Yield Clinical Pearls for NEET-PG:** * **Mutation:** Associated with **JAK2 V617F** (approx. 50%), CALR, or MPL mutations. * **Bone Marrow:** Often results in a **"Dry Tap"** on aspiration; diagnosis requires a trephine biopsy showing increased reticulin or collagen fibrosis. * **Differential:** PMF causes the most significant splenomegaly among all myeloproliferative disorders, often exceeding that seen in CML. **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. 628-629.

Question 1019: What is true about smoldering multiple myeloma?

A. Presence of monoclonal gammopathy (Correct Answer)
B. Presence of lytic bone lesions
C. Presence of hypercalcemia
D. Bone marrow plasma cells less than 10%

Explanation: **Explanation:** Smoldering Multiple Myeloma (SMM) is an intermediate clinical stage between Monoclonal Gammopathy of Undetermined Significance (MGUS) and symptomatic Multiple Myeloma [1]. **1. Why Option A is Correct:** By definition, SMM requires the presence of a **monoclonal (M) protein** (serum IgG or IgA ≥30 g/L) or urinary monoclonal protein (≥500 mg/24h) [1]. It represents a clonal proliferation of plasma cells that produces a monoclonal gammopathy detectable on serum protein electrophoresis (SPEP), but without the immediate end-organ damage seen in active myeloma. **2. Why the Other Options are Incorrect:** * **Options B & C:** The hallmark of SMM is the **absence of CRAB features** (Calcium elevation, Renal insufficiency, Anemia, and Bone lesions) [1]. If lytic bone lesions or hypercalcemia are present, the diagnosis upgrades to symptomatic Multiple Myeloma. * **Option D:** In SMM, the bone marrow plasma cell (BMPC) percentage must be **between 10% and 60%** [1]. If the BMPC is <10%, the diagnosis is MGUS; if it is >60%, it is classified as active Multiple Myeloma (even in the absence of CRAB features). **Clinical Pearls for NEET-PG:** * **Diagnostic Criteria for SMM:** Serum M-protein ≥30 g/L AND/OR BMPC 10–60% AND absence of myeloma-defining events (CRAB) [1]. * **Risk of Progression:** SMM has a much higher rate of progression to overt myeloma (approx. 10% per year) compared to MGUS (1% per year). * **High-Yield Distinction:** Remember that **MGUS** has M-protein <30 g/L and BMPC <10%, whereas **SMM** has higher values but remains asymptomatic [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. 606-609.

Question 1020: All are true about splenic marginal zone lymphoma, EXCEPT:

A. Autoimmune anemia or thrombocytopenia is present.
B. This tumor of small lymphocytes originates in the marginal zone of the spleen white pulp.
C. Splenic hilar nodes are involved.
D. The clinical course is virulent. (Correct Answer)

Explanation: **Splenic Marginal Zone Lymphoma (SMZL)** is a rare, low-grade B-cell neoplasm. Understanding its indolent nature is key to answering this question. ### **Explanation of the Correct Answer** **Option D is the correct answer (the false statement)** because SMZL typically follows an **indolent (slow-growing) clinical course**, not a virulent one. Most patients have a median survival exceeding 10 years. Treatment is often conservative ("watch and wait") or involves splenectomy/Rituximab, rather than aggressive chemotherapy. ### **Analysis of Incorrect Options** * **Option A:** Autoimmune manifestations are common in SMZL. Approximately 10–15% of patients present with **autoimmune hemolytic anemia (AIHA)** or **immune thrombocytopenia (ITP)**. * **Option B:** As the name implies, the tumor originates from the **marginal zone B-cells** of the splenic white pulp. These cells eventually infiltrate the red pulp and the peripheral blood. * **Option C:** While peripheral lymphadenopathy is rare in SMZL (a key diagnostic feature), **splenic hilar lymph nodes** are frequently involved as they are the primary drainage site for the spleen. ### **High-Yield NEET-PG Pearls** * **Clinical Presentation:** Massive splenomegaly is the hallmark. Peripheral lymphadenopathy is characteristically absent. * **Morphology:** Look for **"Villous lymphocytes"** (short, polar cytoplasmic projections) in the peripheral blood smear. * **Immunophenotype:** Typically **CD20+, CD5–, CD10–, CD23–, and CD103–**. This helps differentiate it from CLL (CD5+) and Hairy Cell Leukemia (CD103+). * **Association:** There is a strong clinical association with **Hepatitis C Virus (HCV)** infection; treating the virus can sometimes lead to lymphoma regression. * **Genetics:** Often associated with **7q31 deletion**.

Practice by Chapter

Anemias: Classification and Approach

Practice Questions

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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