Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1031: Which tumor is most rapidly metastatic?

A. African Burkitt's jaw lymphoma (Correct Answer)
B. Hodgkin's lymphoma
C. Non-Hodgkin's lymphoma
D. None of the above

Explanation: **Explanation:** The correct answer is **African Burkitt's jaw lymphoma**. **Why it is correct:** Burkitt’s Lymphoma (BL) is recognized as one of the fastest-growing human tumors due to its extremely high proliferation rate. It is characterized by a **doubling time of approximately 24 to 48 hours**. This rapid growth is driven by the translocation of the **c-MYC proto-oncogene** (most commonly **t(8;14)**), which leads to constitutive activation of transcription and rapid cell cycle progression. The African (Endemic) variant typically presents as a mass involving the mandible of children and shows a predilection for extranodal involvement [1]. Its high mitotic index and aggressive nature make it the most rapidly metastatic/disseminating option among those listed [1], [2]. **Why the other options are incorrect:** * **Hodgkin’s Lymphoma (HL):** HL typically follows a predictable, orderly spread via contiguous lymph node chains. It is generally a slow-growing malignancy compared to high-grade Non-Hodgkin Lymphomas. * **Non-Hodgkin’s Lymphoma (NHL):** While BL is a subtype of NHL, the term "NHL" encompasses a broad spectrum of diseases, including many indolent (slow-growing) forms like Follicular Lymphoma. Therefore, "African Burkitt's" is the more specific and accurate answer for rapid growth. **NEET-PG High-Yield Pearls:** * **Morphology:** Classic **"Starry-sky appearance"** (tingible body macrophages containing apoptotic debris against a background of dark malignant B-cells) [2]. * **Genetics:** Overexpression of c-MYC; t(8;14) is the hallmark, though t(2;8) and t(8;22) can occur. * **Ki-67 Index:** Typically approaches **100%**, indicating that nearly every cell is in the division cycle. * **Tumor Lysis Syndrome:** Due to the rapid turnover and high sensitivity to chemotherapy, patients are at high risk for metabolic derangements upon starting treatment. **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] 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 1032: A single nucleotide change in a codon on chromosome 11 causes valine to replace glutamic acid at the sixth position of the beta chain of hemoglobin. What is the resulting condition?

A. Thalassemia
B. Hereditary spherocytosis
C. Paroxysmal nocturnal hemoglobinuria
D. Sickle cell anemia (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Sickle cell anemia** The question describes the classic molecular pathology of **Sickle Cell Anemia (HbS)**. This condition is caused by a **point mutation** (missense mutation) in the $\beta$-globin gene located on **chromosome 11** [2]. Specifically, a single nucleotide change (**GAG $\rightarrow$ GTG**) results in the substitution of the amino acid **Valine** (hydrophobic) for **Glutamic acid** (hydrophilic) at the **6th position** of the $\beta$-globin chain [1]. This substitution creates a "sticky patch" on the hemoglobin molecule, leading to polymerization under deoxygenated conditions, which causes the characteristic "sickling" of red blood cells [1], [2]. **Why other options are incorrect:** * **A. Thalassemia:** This is a **quantitative** defect characterized by the reduced or absent synthesis of globin chains (e.g., $\beta^0$ or $\beta^+$), rather than a structural (qualitative) change in the amino acid sequence. * **B. Hereditary spherocytosis:** This is a defect in the **RBC membrane proteins** (most commonly Ankyrin, followed by Spectrin or Band 3), not a hemoglobinopathy. * **C. Paroxysmal nocturnal hemoglobinuria (PNH):** This is an acquired clonal stem cell disorder caused by a mutation in the **PIGA gene**, leading to a deficiency of GPI-anchored proteins (CD55 and CD59) on the RBC surface. **High-Yield Facts for NEET-PG:** * **Inheritance:** Autosomal recessive [2]. * **HbS Protection:** Heterozygotes (Sickle cell trait) are protected against *Plasmodium falciparum* malaria. * **Metabisulfite test:** Used for screening (induces sickling). * **Electrophoresis:** HbS moves slower than HbA toward the anode because Valine is neutral, while Glutamic acid is negatively charged. * **Complications:** Vaso-occlusive crises, Autosplenectomy (Howell-Jolly bodies), and Acute Chest Syndrome [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 652-654.

Question 1033: Leukoreduced blood products have lower WBCs than normal by what fold?

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

Explanation: **Explanation:** **Leukoreduction** is the process of removing white blood cells (WBCs) from whole blood or blood components (red cells and platelets) prior to transfusion. According to international standards (AABB and FDA), a blood product is considered "leukoreduced" if the residual WBC count is **less than 5 × 10⁶ per unit**. 1. **Why 3 log reduction is correct:** A standard unit of whole blood contains approximately $10^9$ WBCs. To reach the threshold of $<5 \times 10^6$, a **3 log reduction** (99.9% removal) is required. This level of depletion is clinically significant because it crosses the threshold necessary to prevent most leukocyte-mediated transfusion reactions. 2. **Analysis of Incorrect Options:** * **1 log (90%) and 2 log (99%) reduction:** These levels leave behind too many residual WBCs ($10^8$ and $10^7$ respectively), which are still sufficient to cause HLA sensitization and transmit CMV. * **4 log (99.99%) reduction:** While achievable with advanced filtration, it is not the standard requirement for labeling a product as leukoreduced. **Clinical Pearls for NEET-PG:** * **Indications for Leukoreduction:** 1. Prevention of **Febrile Non-Hemolytic Transfusion Reactions (FNHTR)** – the most common indication. 2. Prevention of **HLA Alloimmunization** (useful in patients requiring chronic transfusions). 3. Prevention of **CMV transmission** (as CMV resides within leukocytes). * **Note:** Leukoreduction does **NOT** prevent Graft-vs-Host Disease (GVHD). To prevent GVHD, **Gamma Irradiation** is required to inactivate T-lymphocytes. * **Timing:** "Pre-storage" leukoreduction (done within 48 hours of collection) is superior to "bedside" filtration as it prevents the release of inflammatory cytokines during storage.

Question 1034: Which of the following conditions is not typically associated with leucocytosis?

A. Typhoid fever (Correct Answer)
B. Myocardial infarction
C. Appendicitis
D. Measles

Explanation: **Explanation:** Leucocytosis refers to an increase in the total white blood cell (WBC) count above the normal range (usually >11,000/mm³). While most acute bacterial infections and tissue necrosis trigger a leucocytic response, certain specific infections are classic exceptions [1]. **1. Why Typhoid Fever is the Correct Answer:** Typhoid fever (Enteric fever), caused by *Salmonella typhi*, is characteristically associated with **leucopenia** (decreased WBC count) rather than leucocytosis [1]. This occurs due to the invasion of the bone marrow and the toxic effects of the bacteria on hematopoiesis. In clinical practice, a finding of leucopenia in a patient with sustained high fever and abdominal symptoms is a strong diagnostic clue for Typhoid. **2. Analysis of Incorrect Options:** * **Myocardial Infarction (MI):** Tissue necrosis (like an MI) triggers an acute inflammatory response. Neutrophilic leucocytosis typically appears within 24 hours of the infarct as the body responds to cell death [3,4]. * **Appendicitis:** This is a classic acute bacterial infection. The body releases neutrophils from the bone marrow (often with a "left shift" or increased band cells) to combat the localized infection, leading to significant leucocytosis [3,4]. * **Measles:** While many viral infections cause leucopenia [1], the question asks for the condition *not typically* associated with leucocytosis. However, in the context of NEET-PG, **Typhoid is the "classic" textbook answer** for leucopenia. (Note: Measles can cause leucopenia, but Typhoid is the higher-yield association for this specific question type). **High-Yield Clinical Pearls for NEET-PG:** * **Conditions causing Leucopenia:** Typhoid, Brucellosis, Kala-azar, Malaria, and viral infections like Influenza and Hepatitis [1]. * **Eosinophilia:** Classic in parasitic infections (e.g., Ascariasis) and allergic conditions (e.g., Bronchial Asthma) [3]. * **Basophilia:** Highly suggestive of Chronic Myeloid Leukemia (CML) [3]. * **Leukemoid Reaction:** A WBC count >50,000/mm³ mimicking leukemia, commonly seen in severe sepsis or perforated appendicitis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 110-111. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 580-581. [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. 592.

Question 1035: Which of the following is NOT an immunohistochemical marker of Langerhans cell histiocytosis?

A. S-100
B. CD1a
C. CD207
D. None of the above (Correct Answer)

Explanation: **Explanation:** Langerhans Cell Histiocytosis (LCH) is a clonal proliferation of Langerhans cells, which are specialized antigen-presenting cells [2]. The diagnosis relies heavily on identifying specific immunohistochemical (IHC) markers that distinguish these cells from other histiocytic disorders. **Why "None of the above" is correct:** All three options listed (S-100, CD1a, and CD207) are positive markers for LCH. Since the question asks which is **NOT** a marker, and all are indeed markers, "None of the above" is the correct choice. **Analysis of Markers:** * **CD1a (Option B):** This is a highly sensitive and specific surface marker for Langerhans cells. It is considered a gold standard for diagnosis. * **CD207 / Langerin (Option C):** This is the **most specific** marker for LCH [1]. Langerin is a protein associated with the formation of **Birbeck granules** (the characteristic "tennis-racket" shaped organelles seen on electron microscopy) [1]. * **S-100 (Option A):** While not specific (as it also stains melanocytes, neural tissue, and chondrocytes), it is characteristically positive in LCH and is used as a screening marker. **High-Yield Clinical Pearls for NEET-PG:** * **Electron Microscopy:** The pathognomonic finding is the **Birbeck Granule** (tennis-racket appearance) [1]. * **BRAF V600E Mutation:** This mutation is found in approximately 50-60% of LCH cases, highlighting its neoplastic nature [2]. * **Clinical Triad (Hand-Schüller-Christian disease):** Calvarial bone defects, diabetes insipidus, and exophthalmos. * **Letterer-Siwe Disease:** The aggressive, multisystem form seen in infants (<2 years) involving skin rash, hepatosplenomegaly, and bone lesions. **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. 630. [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. 629-630.

Question 1036: At autopsy, the spleen of a patient is noted to have a thickened capsule and many small, scarred areas. Microscopic examination of the scarred areas reveals fibrosis with hemosiderin and calcium deposition. This type of spleen is usually seen in conjunction with which of the following disorders?

A. Hepatic cirrhosis (Correct Answer)
B. Hodgkin’s disease
C. Rheumatoid arthritis
D. Sickle cell anemia

Explanation: ### Explanation The pathological findings described—thickened capsule, fibrosis, and small scarred areas containing hemosiderin and calcium—are characteristic of **Gamna-Gandy bodies** (siderofibrotic nodules). **1. Why Hepatic Cirrhosis is Correct:** Gamna-Gandy bodies are most commonly associated with **congestive splenomegaly**, which occurs secondary to **portal hypertension** (most frequently caused by **hepatic cirrhosis**) [1]. In portal hypertension, chronic venous congestion leads to focal hemorrhages within the splenic parenchyma. Over time, these hemorrhages organize, resulting in deposits of **hemosiderin** (from degraded RBCs) and **calcium** on a background of **fibrosis**. Grossly, these appear as firm, tobacco-brown or rust-colored nodules. Long-standing splenic congestion produces marked enlargement where the organ is firm and the capsule is usually thickened and fibrous [1]. **2. Analysis of Incorrect Options:** * **Hodgkin’s Disease:** Typically presents with "Marmorated spleen" (hard-bake appearance) due to white tumor nodules infiltrating the red pulp, not siderofibrotic nodules. * **Rheumatoid Arthritis:** Associated with **Felty Syndrome** (Splenomegaly + Neutropenia + RA). The spleen shows follicular hyperplasia but lacks the characteristic siderofibrotic nodules of chronic congestion. * **Sickle Cell Anemia:** While the spleen undergoes infarction and fibrosis (autosplenectomy), the specific constellation of Gamna-Gandy bodies in a *congestive* setting is the hallmark of portal hypertension [2]. In Sickle Cell, the spleen eventually becomes shrunken and non-functional, rather than showing the congestive features of cirrhosis [2]. **3. NEET-PG High-Yield Pearls:** * **Gamna-Gandy Bodies:** Also known as Siderofibrotic nodules. * **Stain:** They stain positive with **Prussian Blue** (for iron) and **Von Kossa** (for calcium). * **Common Causes:** Portal hypertension (Cirrhosis), Splenic lymphoma, and Sickle cell anemia (less common than in cirrhosis). * **Splenomegaly in Cirrhosis:** This is a "passive" congestion; the spleen can weigh up to 1000g [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. 632-634. [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. 631-632.

Question 1037: A child with prolonged aPTT, who underwent laparotomy without bleeding complications, is most likely to have a deficiency in which clotting factor?

A. Factor VII
B. Factor X
C. Factor XII (Correct Answer)
D. Factor XIII

Explanation: The clinical scenario describes a "paradoxical" laboratory finding: a significantly prolonged **activated Partial Thromboplastin Time (aPTT)** in a patient who clinically exhibits **no bleeding tendency**, even during invasive procedures like a laparotomy. [1] **1. Why Factor XII is correct:** Factor XII (Hageman factor) is the initiator of the **intrinsic pathway** of the coagulation cascade *in vitro*. A deficiency in Factor XII leads to a marked prolongation of aPTT because the laboratory test relies on this pathway. However, in the human body (*in vivo*), Factor XII is not required for physiological hemostasis; thrombin generation is primarily initiated via the Tissue Factor/Factor VIIa (extrinsic) pathway [1]. Therefore, patients with Factor XII deficiency do not bleed clinically but show abnormal lab results. **2. Why the other options are incorrect:** * **Factor VII:** Deficiency affects the **extrinsic pathway**, leading to a prolonged Prothrombin Time (PT), not aPTT. It is associated with clinical bleeding. * **Factor X:** This is part of the **common pathway**. Deficiency would prolong both PT and aPTT and cause significant bleeding. * **Factor XIII:** This factor stabilizes the fibrin clot. Deficiency results in severe bleeding (e.g., umbilical cord stump bleeding), but because it acts after the formation of fibrin, both **PT and aPTT remain normal**. **Clinical Pearls for NEET-PG:** * **The "No-Bleed" Trio:** Deficiencies in **Factor XII**, **Pre-kallikrein (Fletcher factor)**, and **High Molecular Weight Kininogen (HMWK/Fitzgerald factor)** all cause a prolonged aPTT without clinical bleeding. * Factor XII deficiency is actually associated with a theoretical increased risk of **thrombosis** (due to its role in activating the fibrinolytic system), though this is rarely clinically significant [1]. * Always suspect Factor XII deficiency in an asymptomatic preoperative patient with an incidentally discovered high aPTT. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 128-132.

Question 1038: A child is diagnosed with Burkitt's Lymphoma. The presence of which of the following translocations confirms the diagnosis?

A. t (11:22)
B. t (8:14) (Correct Answer)
C. t (15:17)
D. t (9:22)

Explanation: **Explanation:** **Burkitt’s Lymphoma** is a highly aggressive B-cell non-Hodgkin lymphoma characterized by the rapid proliferation of B-lymphocytes [2]. The hallmark of this condition is the **t(8;14)** translocation, which occurs in approximately 85% of cases [1]. * **Why t(8;14) is correct:** This translocation involves the **c-MYC proto-oncogene** on chromosome 8 and the **Immunoglobulin Heavy chain (IgH) gene** on chromosome 14 [1]. When c-MYC is moved adjacent to the highly active IgH promoter, it leads to the constitutive overexpression of the MYC protein, a potent transcription factor that drives rapid cell cycle progression and cell growth [1]. **Analysis of Incorrect Options:** * **t(11;22):** Associated with **Ewing Sarcoma** and PNET. It involves the EWS-FLI1 gene fusion. * **t(15;17):** Pathognomonic for **Acute Promyelocytic Leukemia (AML-M3)**. It involves the PML-RARA fusion, making the disease responsive to All-Trans Retinoic Acid (ATRA). * **t(9;22):** Known as the **Philadelphia Chromosome**, characteristic of **Chronic Myeloid Leukemia (CML)** and some cases of ALL. It creates the BCR-ABL1 fusion protein with tyrosine kinase activity. **High-Yield NEET-PG Pearls:** 1. **Morphology:** Classic **"Starry-sky appearance"** (tingible body macrophages against a sea of dark neoplastic B-cells) [3]. 2. **Variants:** Endemic (African/Jaw involvement, 100% EBV association), Sporadic (Abdominal involvement), and Immunodeficiency-associated [2]. 3. **Immunophenotype:** CD19+, CD20+, CD10+, and **BCL-6+**. Notably, it is **BCL-2 negative**. 4. **Ki-67 index:** Typically approaches **100%**, reflecting the extremely high proliferation rate [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 605-606. [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 1039: Which one of the following statements about thalassemia is not true?

A. Increase in the number of globulin chains (Correct Answer)
B. Erythrocyte fragility and hemolysis are present
C. Hypochromic microcytic anemia is present
D. Severe anemia and thrombocytopenia are present

Explanation: ### Explanation **1. Why Option A is the Correct Answer (The False Statement):** Thalassemia is characterized by a **quantitative deficiency** in the synthesis of globin chains, not an increase [1]. It is caused by mutations or deletions in the globin genes ($\alpha$ or $\beta$), leading to a **decreased or absent production** of normal globin chains. This imbalance results in the precipitation of the unaffected chains, causing damage to the red cell membrane [1]. **2. Analysis of Other Options:** * **Option B (Erythrocyte fragility and hemolysis):** The precipitation of excess globin chains (e.g., $\alpha$-tetramers in $\beta$-thalassemia) causes oxidative damage to the RBC membrane [1]. This leads to **extravascular hemolysis** in the spleen and premature destruction of erythroid precursors in the bone marrow (ineffective erythropoiesis). * **Option C (Hypochromic microcytic anemia):** Since hemoglobin synthesis is impaired due to the lack of globin chains, the RBCs produced are small (microcytic, low MCV) and pale (hypochromic, low MCH/MCHC) [1]. This is a hallmark morphological feature of thalassemia. * **Option D (Severe anemia and thrombocytopenia):** In Thalassemia Major, severe anemia is common [1]. Chronic hemolysis and ineffective erythropoiesis lead to massive **splenomegaly**. A large, overactive spleen (hypersplenism) often sequesters platelets, leading to secondary **thrombocytopenia**. **3. NEET-PG High-Yield Pearls:** * **Mentzer Index:** (MCV/RBC count) < 13 suggests Thalassemia; > 13 suggests Iron Deficiency Anemia. * **Peripheral Smear:** Look for **Target cells** (codocytes) and basophilic stippling. * **Diagnosis:** **Hb Electrophoresis** is the gold standard (shows increased HbA2 and HbF in $\beta$-thalassemia). * **X-ray Findings:** "Crew-cut" or "Hair-on-end" appearance of the skull due to compensatory extramedullary hematopoiesis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 646-650.

Question 1040: A patient presents with bone pain. X-ray reveals destructive lesions. Laboratory investigations show hypercalcemia. Serum electrophoresis shows M spike, while bone marrow shows 35% plasma cells. What is your diagnosis?

A. Monoclonal gammopathy of undetermined significance (MGUS)
B. Smoldering multiple myeloma
C. Multiple myeloma (Correct Answer)
D. Plasma cell leukemia

Explanation: This question tests the diagnostic criteria for Plasma Cell Dyscrasias, a high-yield topic for NEET-PG. [1] ### **Explanation of the Correct Answer** The diagnosis is **Multiple Myeloma (MM)** based on the **IMWG (International Myeloma Working Group) criteria**. MM is defined by the presence of clonal bone marrow plasma cells **≥10%** (this patient has 35%) AND the presence of **CRAB** features (End-organ damage): [2] * **C**alcium elevation (>11 mg/dL) [2] * **R**enal insufficiency [1] * **A**nemia * **B**one lesions (lytic lesions/bone pain) [1], [2] The presence of an **M-spike** on electrophoresis confirms a monoclonal gammopathy, and the combination of 35% plasma cells with hypercalcemia and lytic lesions confirms symptomatic Multiple Myeloma. [1] ### **Why Other Options are Incorrect** * **MGUS:** Characterized by an M-protein <3 g/dL, bone marrow plasma cells **<10%**, and **no** CRAB features. * **Smoldering Multiple Myeloma:** Characterized by M-protein ≥3 g/dL or marrow plasma cells **10–60%**, but critically, there is **no** end-organ damage (no CRAB features). [3] * **Plasma Cell Leukemia:** A rare, aggressive variant defined by an absolute plasma cell count of **>2,000/µL** in the peripheral blood or >20% of the differential white cell count. [2] ### **NEET-PG High-Yield Pearls** * **Most common** bone malignancy in adults: Multiple Myeloma. * **Peripheral Smear:** Characterized by **Rouleaux formation** (due to high ESR/globulins). [2] * **Urine:** Bence-Jones proteins (detected by the heat coagulation test, not dipstick). [1] * **X-ray:** "Punched-out" lytic lesions (Skull X-ray is classic). [2] * **Biomarker:** Beta-2 microglobulin is the most important prognostic marker. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617. [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. 607-609. [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. 606-607.

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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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