Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 541: Acute promyelocytic leukaemia (AML - M3) includes which of the following subtypes?

A. Hyper granular and hypo granular type
B. Hyper granular and hyper segmented
C. Hyper granular and micro granular type (Correct Answer)
D. Hypo granular and micro granular type

Explanation: **Explanation:** Acute Promyelocytic Leukaemia (APL), classified as **AML-M3** in the FAB classification, is characterized by the malignant proliferation of promyelocytes [1]. Morphologically, APL is divided into two distinct subtypes based on the appearance of the cytoplasm: 1. **Hypergranular Type (Typical/Classic):** This is the most common form. The cells contain numerous coarse, azurophilic granules and characteristic **Auer rods**, often found in bundles called **"Faggot cells"** [1]. 2. **Microgranular Type (Hypogranular/M3v):** In this variant, the granules are so small and fine that they are often invisible under a light microscope, giving the cytoplasm a "dust-like" or clear appearance [1]. A key diagnostic feature is the **bilobed or reniform (kidney-shaped) nucleus**, which can sometimes be mistaken for monocytes (AML-M5) [1]. **Analysis of Options:** * **Option A & D:** While "hypogranular" is often used interchangeably with "microgranular" in clinical practice, the formal morphological classification specifically uses the term **Microgranular** to describe the M3 variant. * **Option B:** "Hypersegmented" refers to neutrophils in megaloblastic anemia, not the morphology of promyelocytes in APL. **High-Yield Clinical Pearls for NEET-PG:** * **Cytogenetics:** Strongly associated with **t(15;17)**, involving the *PML-RARA* fusion gene [1]. * **Complication:** High risk of **Disseminated Intravascular Coagulation (DIC)** due to the release of procoagulants from granules [1]. * **Treatment:** Highly responsive to **All-Trans Retinoic Acid (ATRA)** and Arsenic Trioxide, which induce differentiation of the blast cells. * **Immunophenotype:** Typically **CD34 negative** and **HLA-DR negative**, but strongly positive for MPO. **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. 620-622.

Question 542: Which of the following laboratory tests is affected by platelet count?

A. Bleeding time (Correct Answer)
B. Prothrombin time
C. Partial thromboplastin time
D. Thrombin time

Explanation: **Explanation:** The laboratory evaluation of hemostasis is divided into tests for primary hemostasis (platelet plug formation) and secondary hemostasis (coagulation cascade). **Why Bleeding Time (BT) is correct:** Bleeding time is the classic screening test for **primary hemostasis**. It measures the time taken for a standardized skin puncture to stop bleeding. This process depends entirely on two factors: **platelet number (count)** and **platelet function**, along with vessel wall integrity [2]. If the platelet count falls below 50,000/µL (thrombocytopenia) or if the platelets are dysfunctional (e.g., aspirin use, Bernard-Soulier syndrome), the BT will be prolonged [4]. **Why the other options are incorrect:** * **Prothrombin Time (PT), Partial Thromboplastin Time (PTT), and Thrombin Time (TT):** These are tests of **secondary hemostasis** (the coagulation cascade). These tests are performed on **platelet-poor plasma**. During the laboratory process, the patient's platelets are removed via centrifugation, and exogenous phospholipids (platelet substitutes) are added to the reagent. Therefore, the patient’s own platelet count has no impact on these results [3]. * **PT** evaluates the Extrinsic and Common pathways. * **PTT** evaluates the Intrinsic and Common pathways. * **TT** evaluates the conversion of Fibrinogen to Fibrin. **High-Yield Clinical Pearls for NEET-PG:** * **Platelet Count vs. BT:** BT does not usually prolong until the platelet count is **<100,000/µL**. * **von Willebrand Disease (vWD):** This is a unique condition where **both** BT and PTT may be prolonged (due to deficient platelet adhesion and low Factor VIII levels, respectively). * **Standardization:** In modern clinical practice, the **Platelet Function Analyzer (PFA-100)** has largely replaced the manual Bleeding Time due to better reproducibility [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. 664-665. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 619-620. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 666-667. [4] 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 543: Which of the following are inherited coagulation disorders?

A. Protein C deficiency
B. Protein S deficiency
C. Factor V Leiden
D. All of the above (Correct Answer)

Explanation: **Explanation:** The correct answer is **D (All of the above)**. Inherited coagulation disorders (thrombophilias) are genetic predispositions to thromboembolism caused by mutations in genes encoding coagulation factors or their regulators [1]. 1. **Factor V Leiden (Option C):** This is the **most common** inherited cause of hypercoagulability [1]. It involves a point mutation (G1691A) in the Factor V gene, making Factor Va resistant to cleavage by Activated Protein C (APC) [1]. This leads to a prothrombotic state. 2. **Protein C and Protein S Deficiencies (Options A & B):** Both are natural anticoagulants. Protein C, when activated, degrades Factors Va and VIIIa. Protein S acts as a necessary cofactor for Protein C. Inherited deficiencies in either (usually autosomal dominant) result in a failure to inhibit the clotting cascade, significantly increasing the risk of venous thromboembolism (VTE). **Clinical Pearls for NEET-PG:** * **Most Common Inherited Thrombophilia:** Factor V Leiden mutation [1]. * **Second Most Common:** Prothrombin G20210A mutation [1]. * **Warfarin-Induced Skin Necrosis:** Classically associated with **Protein C deficiency**. When starting Warfarin, Protein C levels drop faster than other factors (due to a short half-life), leading to a transient hypercoagulable state and microvascular thrombosis. * **Antithrombin III (ATIII) Deficiency:** Another major inherited disorder; patients may show **heparin resistance** because heparin requires ATIII to exert its anticoagulant effect. * **Screening:** These tests should generally not be performed during an acute thrombotic event or while the patient is on anticoagulants, as results may be falsely low. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 133-134.

Question 544: Which of the following is NOT a method of hemoglobin estimation?

A. Drabkin's method
B. Sahli's method
C. Spectrophotometric method
D. Wintrobe's method (Correct Answer)

Explanation: ### Explanation **1. Why Wintrobe’s Method is the Correct Answer:** Wintrobe’s method is used for the estimation of **Packed Cell Volume (PCV)** or Hematocrit and the **Erythrocyte Sedimentation Rate (ESR)** [1]. It involves centrifuging anticoagulated whole blood in a Wintrobe tube to measure the ratio of the volume of occupied erythrocytes to the total volume of blood. It is **not** a method used to directly estimate hemoglobin (Hb) concentration. **2. Analysis of Incorrect Options:** * **Drabkin’s Method (Cyanmethemoglobin Method):** This is the **gold standard** and the most accurate method for Hb estimation. It uses Drabkin’s reagent (containing potassium ferricyanide and potassium cyanide) to convert all forms of hemoglobin (except sulfhemoglobin) into stable cyanmethemoglobin, which is then measured colorimetrically. * **Sahli’s Method (Acid Hematin Method):** A visual comparative method where Hb is converted into brown-colored acid hematin by adding N/10 HCl. While simple and inexpensive, it is less accurate due to subjective visual errors. * **Spectrophotometric Method:** This is the underlying principle for most automated hematology analyzers. It measures light absorbance at specific wavelengths (usually 540 nm) to calculate Hb concentration rapidly and accurately. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Standard Wintrobe Tube:** Length is 110 mm with an internal diameter of 3 mm. It is graduated from 0–100 mm in both directions. * **ESR vs. PCV:** In the Wintrobe tube, ESR is read from top to bottom (0 at top), while PCV is read from bottom to top (0 at bottom). * **Drabkin’s Reagent:** It measures almost all variants of Hb, including **carboxyhemoglobin** and **methemoglobin**, but it **cannot** measure sulfhemoglobin. * **Specific Gravity Method:** Another method for Hb estimation (often used in blood donation camps) using **Copper Sulfate** solution. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 577-578.

Question 545: In sickle cell crisis, bone pain is primarily due to which of the following mechanisms?

A. Bone infarction (Correct Answer)
B. Osteoporosis
C. Osteomalacia
D. Periosteal reaction

Explanation: **Explanation:** **Mechanism of Bone Pain (Correct Answer: A):** The hallmark of a sickle cell vaso-occlusive crisis (VOC) is the polymerization of deoxygenated Hemoglobin S (HbS), which causes red blood cells to become rigid and sickle-shaped [1]. These sickled cells obstruct the microvasculature (capillaries and post-capillary venules), leading to tissue hypoxia and ischemia [1]. In the skeletal system, this results in **bone marrow infarction** and intraosseous hypertension [4]. The resulting inflammatory response and release of nociceptive mediators are the primary cause of the intense, acute bone pain characteristic of the crisis. **Analysis of Incorrect Options:** * **B. Osteoporosis:** While chronic sickle cell disease can lead to low bone mineral density due to marrow hyperplasia and nutritional deficiencies, it is a chronic process and does not cause the acute, severe pain seen in a crisis [3]. * **C. Osteomalacia:** This refers to impaired mineralization of the bone matrix (usually due to Vitamin D deficiency). It is not a primary feature or the cause of pain in sickle cell crises. * **D. Periosteal reaction:** This is a radiographic finding (new bone formation) that may occur secondary to healing after an infarct or in cases of osteomyelitis, but it is a consequence rather than the primary mechanism of the pain itself. **High-Yield Clinical Pearls for NEET-PG:** * **Hand-Foot Syndrome (Dactylitis):** The earliest manifestation of sickle cell disease in infants, caused by symmetrical infarcts of the small bones of the hands and feet [2]. * **Avascular Necrosis (AVN):** Chronic bone infarction commonly affects the **femoral head** due to its retrograde blood supply [4]. * **Osteomyelitis:** Patients are uniquely susceptible to *Salmonella* osteomyelitis, though *Staphylococcus aureus* remains a common cause. * **Radiology:** Look for "H-shaped vertebrae" (Codfish vertebrae) due to central endplate infarction. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 652-654. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 645-646. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 644-645. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1196-1197.

Question 546: Which of the following conditions is NOT typically associated with a lymphatic leukemoid reaction?

A. Tuberculosis
B. Pertussis
C. Lobar Pneumonia (Correct Answer)
D. Viral infections

Explanation: A **leukemoid reaction** is defined as a reactive increase in the white blood cell (WBC) count exceeding 50,000/µL, mimicking leukemia but occurring in response to an underlying infection or inflammatory process. **Why Lobar Pneumonia is the Correct Answer:** Lobar pneumonia, typically caused by *Streptococcus pneumoniae*, is a classic cause of a **myeloid (neutrophilic) leukemoid reaction** [1], [2]. In this condition, the bone marrow releases immature precursors (shifts to the left), but the cells are predominantly neutrophils, not lymphocytes [3]. Therefore, it is not associated with a lymphatic leukemoid reaction. **Analysis of Incorrect Options:** * **Pertussis (*Bordetella pertussis*):** This is the classic cause of a lymphatic leukemoid reaction. The bacteria produce "Lymphocytosis Promoting Factor," which prevents lymphocytes from extravasating into tissues, leading to a massive accumulation in the blood. * **Tuberculosis:** While often associated with a monocytic or neutrophilic response [1], chronic granulomatous infections like TB can occasionally trigger a significant reactive lymphocytosis, mimicking chronic lymphocytic leukemia (CLL) [4]. * **Viral Infections:** Infections such as Infectious Mononucleosis (EBV), Cytomegalovirus (CMV), and infectious lymphocytosis are hallmark causes of reactive lymphocytosis [2]. **NEET-PG High-Yield Pearls:** 1. **Leukemoid vs. Leukemia:** Leukemoid reactions show **high Leukocyte Alkaline Phosphatase (LAP) scores**, whereas Chronic Myeloid Leukemia (CML) shows a low LAP score. 2. **Differentiating Feature:** The presence of toxic granulations and Dohle bodies in neutrophils suggests a leukemoid reaction over malignancy. 3. **Pertussis Exception:** It is one of the few bacterial infections that causes a **lymphocytic** rather than a neutrophilic response. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 592. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 580-581. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 317-318. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360.

Question 547: Which of the following statements is not true regarding Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma (CLL/SLL)?

A. The tumor cells are positive for CD5 and CD20.
B. Transformation to Richter syndrome is commonly seen. (Correct Answer)
C. ZAP-70 expression is a poor prognostic marker.
D. Proliferation centers in lymph nodes are pathognomonic.

Explanation: **Explanation:** **1. Why Option B is the correct answer (False statement):** While Richter syndrome (transformation of CLL/SLL into a high-grade aggressive lymphoma, usually Diffuse Large B-Cell Lymphoma) is a well-known complication, it is **not common**. It occurs in only **2–8%** of patients. The question asks for the "not true" statement; since the transformation is infrequent rather than common, this is the correct choice. **2. Analysis of Incorrect Options (True statements):** * **Option A:** CLL/SLL cells characteristically express B-cell markers (**CD19, CD20, CD23**) along with **CD5**, a T-cell marker [1]. This "aberrant" expression of CD5 on B-cells is a hallmark of CLL and Mantle Cell Lymphoma. * **Option C:** Molecular markers are vital for prognosis. Expression of **ZAP-70** and **CD38**, or the presence of **unmutated IgVH genes**, are indicators of a **poor prognosis** and more aggressive disease course [2]. * **Option D:** In lymph node biopsies of SLL, the presence of **Proliferation Centers** (pale areas containing prolymphocytes and paraimmunoblasts) is considered **pathognomonic** (diagnostic) for this condition [3]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Peripheral Smear:** Look for **Smudge cells** (basket cells) due to increased fragility of lymphocytes [1]. * **Morphology:** Small, mature-looking lymphocytes with "block-type" or **"soccer-ball" chromatin** [1]. * **Hypogammaglobulinemia:** Common in late stages, leading to increased susceptibility to bacterial infections. * **Autoimmunity:** Patients may develop Autoimmune Hemolytic Anemia (AIHA) or Thrombocytopenia [1]. * **Most common** leukemia of adults in the Western world [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 602. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 612-613. [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. 610-612.

Question 548: Which of the following is NOT included in chronic myeloproliferative disorders?

A. Chronic myeloid leukemia (CML)
B. Polycythemia vera
C. Essential thrombocytosis
D. Erythroleukemia (Correct Answer)

Explanation: **Explanation:** Chronic Myeloproliferative Neoplasms (MPNs) are a group of clonal hematopoietic stem cell disorders characterized by the proliferation of one or more myeloid lineages (granulocytic, erythroid, or megakaryocytic) with relatively normal differentiation, leading to increased peripheral blood counts [1]. **Why Erythroleukemia is the correct answer:** Erythroleukemia (formerly FAB M6) is a subtype of **Acute Myeloid Leukemia (AML)**. Unlike MPNs, which are chronic and show mature cell proliferation, AML is characterized by a "maturation arrest" resulting in the accumulation of immature **blasts** (≥20% in bone marrow). Therefore, it is classified under Acute Leukemias, not Chronic Myeloproliferative Disorders. **Analysis of incorrect options:** * **Chronic Myeloid Leukemia (CML):** The prototype MPN, characterized by the Philadelphia chromosome $t(9;22)$ and the *BCR-ABL1* fusion gene, leading to predominant granulocytic proliferation [1]. * **Polycythemia Vera (PV):** An MPN characterized by autonomous erythropoiesis, resulting in increased red cell mass. Over 95% of cases are associated with the *JAK2 V617F* mutation [1], [2]. * **Essential Thrombocytosis (ET):** An MPN involving primary proliferation of megakaryocytes leading to persistent thrombocytosis [1]. Common mutations include *JAK2*, *CALR*, and *MPL* [1]. **NEET-PG High-Yield Pearls:** 1. **Classic MPNs:** CML, Polycythemia Vera, Essential Thrombocytosis, and Primary Myelofibrosis [1]. 2. **Common Feature:** All MPNs carry a risk of transforming into **Acute Myeloid Leukemia** (Blast Crisis) or **Myelofibrosis** (Spent Phase) [1], [3]. 3. **JAK2 Mutation:** Present in almost all PV cases but only ~50-60% of ET and Primary Myelofibrosis cases [1], [2]. 4. **Erythroleukemia (AML-M6):** Often associated with complex karyotypes and a poor prognosis; it must be distinguished from pure erythroid leukemia. **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. 624-625. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615. [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. 626-627.

Question 549: What is the most common malignancy affecting the spleen?

A. Angiosarcoma
B. Hamartoma
C. Secondaries
D. Lymphoma (Correct Answer)

Explanation: **Explanation:** The spleen is the largest lymphoid organ in the body, making it a primary site for hematological malignancies. **Lymphoma** is the most common malignancy involving the spleen [1]. It can present either as a primary splenic lymphoma (rare) or, more commonly, as part of systemic involvement in Non-Hodgkin Lymphoma (NHL) or Hodgkin Lymphoma [1]. In systemic lymphoma, the spleen is involved in approximately 30-40% of cases. **Analysis of Options:** * **A. Angiosarcoma:** This is the most common **primary non-lymphoid** malignant tumor of the spleen. However, it is extremely rare in absolute terms compared to lymphoma. * **B. Hamartoma:** This is a benign, non-neoplastic vascular malformation (composed of disorganized splenic red pulp). It is not a malignancy. * **C. Secondaries (Metastasis):** While the spleen is highly vascular, solid tumor metastases (e.g., from lung or breast) are relatively **uncommon**. This is attributed to the spleen’s sharp rhythmic contractions, the inhibitory effect of the high concentration of lymphoid cells, and the splenic microenvironment which is hostile to solid tumor seeding. **High-Yield Clinical Pearls for NEET-PG:** * **Most common benign tumor of the spleen:** Hemangioma. * **Most common primary malignancy of the spleen:** Lymphoma (specifically Splenic Marginal Zone Lymphoma is a classic primary type) [1]. * **Most common primary non-lymphoid malignancy:** Angiosarcoma (associated with high risk of spontaneous rupture). * **Gaucher Disease:** The most common cause of massive splenomegaly among storage disorders. * **Gamna-Gandy Bodies:** Siderofibrotic nodules (calcium and iron deposits) seen in the spleen in portal hypertension. **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. 569-570.

Question 550: Post-transfusion hepatitis is most commonly associated with which component?

A. Packed red blood cells (Correct Answer)
B. Platelets
C. Whole blood
D. Albumin

Explanation: **Explanation:** The risk of post-transfusion hepatitis (PTH) is primarily determined by the frequency of use and the presence of residual plasma or leukocytes in the blood component. **Why Packed Red Blood Cells (PRBCs) is correct:** PRBCs are the **most commonly transfused blood component** in clinical practice. Because hepatitis viruses (HBV, HCV) are primarily transmitted through blood and blood products, the sheer volume of PRBC units administered globally makes them the most frequent vehicle for transmission [1]. While modern nucleic acid testing (NAT) has drastically reduced the risk, PRBCs remain the leading cause due to their high utilization rate compared to other components. **Analysis of Incorrect Options:** * **Platelets:** While platelets carry a higher risk of **bacterial contamination** (due to storage at room temperature), they are transfused less frequently than PRBCs, making them a less common cause of PTH overall. * **Whole Blood:** Although whole blood contains all infectious elements, its clinical use has significantly declined in favor of component therapy. Therefore, it is not the "most common" source in modern medicine. * **Albumin:** This is considered **safe**. Albumin undergoes heat treatment (pasteurization at 60°C for 10 hours) during preparation, which inactivates hepatitis viruses and HIV. **NEET-PG High-Yield Pearls:** * **Most common infection** transmitted via blood transfusion: **Hepatitis B** (in developing countries) or **HCV** (historically, before NAT) [1]. * **Most common bacterial contaminant:** *Staphylococcus epidermidis* (Platelets); *Yersinia enterocolitica* (PRBCs). * **Screening:** Mandatory screening in India includes HIV I & II, HBV (HBsAg), HCV, Syphilis, and Malaria. * **Window Period:** The risk of PTH persists mainly due to the "window period" where the donor is infectious but tests are negative. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 391-392.

Practice by Chapter

Anemias: Classification and Approach

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Hemolytic Anemias

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Myeloproliferative Neoplasms

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Myelodysplastic Syndromes

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Acute Leukemias

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Chronic Leukemias

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Lymphomas and Lymphoid Neoplasms

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Plasma Cell Disorders

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Bleeding Disorders

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Thrombotic Disorders

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