Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 41: A patient presented with splenomegaly, anemia, and reticulocytosis with increased bone marrow cellularity. What is the most likely diagnosis?

A. Pernicious anemia
B. Hemolytic anemia (Correct Answer)
C. Myelofibrosis
D. Hairy cell leukemia

Explanation: ### Explanation The clinical triad of **splenomegaly, anemia, and reticulocytosis** combined with a hypercellular bone marrow is a classic presentation of **Hemolytic Anemia**. [2] **Why Hemolytic Anemia is Correct:** In hemolytic anemia, there is premature destruction of red blood cells (RBCs). The body compensates for this loss through **erythroid hyperplasia** in the bone marrow (increased cellularity) and by releasing immature RBCs into the peripheral blood (**reticulocytosis**). [2] Splenomegaly occurs because the spleen is the primary site of extravascular hemolysis and becomes congested due to the increased workload of filtering abnormal or antibody-coated RBCs. [1] **Why the Other Options are Incorrect:** * **Pernicious Anemia:** This is a megaloblastic anemia characterized by **ineffective erythropoiesis**. While the marrow is hypercellular, the reticulocyte count is typically **low** because the cells cannot mature properly to enter circulation. * **Myelofibrosis:** This condition presents with a "dry tap" on bone marrow aspiration due to extensive fibrosis, not increased cellularity. While it causes massive splenomegaly, the peripheral smear would show **teardrop cells (dacrocytes)** and a leukoerythroblastic picture. * **Hairy Cell Leukemia:** While it causes massive splenomegaly, the bone marrow typically shows **interstitial infiltration** with a "fried egg" appearance and often results in a "dry tap." It presents with **pancytopenia** rather than isolated anemia with reticulocytosis. **NEET-PG High-Yield Pearls:** * **Reticulocyte Count:** The most reliable marker of bone marrow response to anemia. An elevated count (Reticulocyte Production Index >2%) always suggests hemolysis or acute blood loss. [2] * **Markers of Hemolysis:** Increased indirect bilirubin, increased LDH, and **decreased haptoglobin** (most sensitive for intravascular hemolysis). [2] * **Splenomegaly:** If absent in a suspected case of hemolysis, consider **intravascular** causes (e.g., PNH, G6PD deficiency crisis) or sickle cell anemia (due to autosplenectomy). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 640.

Question 42: Bence Jones proteins are associated with which of the following conditions?

A. Hodgkin's lymphoma
B. Multiple myeloma (Correct Answer)
C. Burkitt's Lymphoma
D. Infectious mononucleosis

Explanation: **Explanation:** **Multiple Myeloma (Option B)** is the correct answer. Multiple myeloma is a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells [1,5]. These cells produce excessive amounts of monoclonal (M) proteins. In many patients, there is an overproduction of **free monoclonal light chains** (either kappa or lambda) [1,2]. Due to their small molecular weight, these light chains are filtered by the renal glomeruli and excreted in the urine, where they are known as **Bence Jones proteins** [1,2]. A unique diagnostic feature of Bence Jones proteins is their thermal property: they **precipitate when heated to 40–60°C** and **redissolve upon boiling (100°C)**. **Why other options are incorrect:** * **Hodgkin’s Lymphoma (Option A):** Characterized by Reed-Sternberg cells and a reactive inflammatory background; it does not typically involve monoclonal light chain overproduction. * **Burkitt’s Lymphoma (Option C):** A high-grade B-cell lymphoma associated with c-MYC translocation; while it involves B-cells, it does not manifest with Bence Jones proteinuria. * **Infectious Mononucleosis (Option D):** A viral infection (EBV) causing reactive lymphocytosis (atypical Downey cells), not a plasma cell neoplasm [5]. **NEET-PG High-Yield Pearls:** * **Diagnosis:** Bence Jones proteins are **not detected by standard urine dipsticks** (which detect albumin). They require **Sulphosalicylic acid (SSA) test** or **Urine Protein Electrophoresis (UPEP)**. * **Renal Impact:** These proteins are nephrotoxic and lead to "Myeloma Kidney" (Cast Nephropathy), where waxy, eosinophilic casts obstruct the distal tubules [3,4]. * **CRAB Criteria:** Remember the hallmarks of Multiple Myeloma: **C**alcium (elevated), **R**enal failure, **A**nemia, and **B**one lesions (punched-out lytic lesions) [1,4]. **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. 608-609. [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. 607-608. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 618-619. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 606-607.

Question 43: Dohle bodies are seen in which of the following conditions?

A. Multiple myeloma
B. Burns (Correct Answer)
C. Waldenstrom macroglobulinemia
D. Lymphoma

Explanation: **Explanation:** **Dohle bodies** are small, light blue-gray, oval inclusions found in the periphery of the cytoplasm of **neutrophils**. They represent remnants of **rough endoplasmic reticulum (RER)** arranged in parallel rows. Their presence is a sign of "toxic change," indicating that the bone marrow is producing neutrophils rapidly, often in response to severe stress or inflammation. **Why Burns is correct:** Severe **burns** trigger a massive systemic inflammatory response, leading to the rapid release of neutrophils from the bone marrow [1]. This accelerated granulopoiesis results in cytoplasmic maturation defects, manifesting as Dohle bodies. Other conditions where they are commonly seen include severe bacterial infections (sepsis) [2], trauma, and pregnancy. **Why the other options are incorrect:** * **Multiple Myeloma & Waldenstrom Macroglobulinemia:** These are plasma cell dyscrasias. While they may show specific inclusions like **Russell bodies** (cytoplasmic) or **Dutcher bodies** (nuclear) in plasma cells, they do not typically present with Dohle bodies in neutrophils. * **Lymphoma:** This is a malignancy of lymphoid lineage. Dohle bodies are specific to the myeloid (neutrophil) lineage and are not a feature of lymphoma. **High-Yield Clinical Pearls for NEET-PG:** * **May-Hegglin Anomaly:** A rare autosomal dominant condition characterized by large, "Dohle-like" bodies, giant platelets, and thrombocytopenia. * **Toxic Granulation:** Often seen alongside Dohle bodies; these are dark, coarse granules representing abnormal primary granules (lysosomes). * **Chediak-Higashi Syndrome:** Characterized by giant peroxidase-positive lysosomal granules in neutrophils (not to be confused with Dohle bodies). **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.

Question 44: Splenic infarction is associated with which of the following conditions?

A. Typhoid fever
B. Infective endocarditis (Correct Answer)
C. Chronic myeloid leukemia
D. Paroxysmal nocturnal hemoglobinuria

Explanation: **Explanation:** Splenic infarction occurs when the splenic artery or its branches are occluded, leading to ischemic necrosis (typically **pale, wedge-shaped infarcts**) [1]. **1. Why Infective Endocarditis (IE) is correct:** The most common cause of splenic infarction is **systemic embolization** [3]. In IE, friable vegetations on the heart valves can break off and enter the systemic circulation [5]. Since the spleen receives a high volume of blood flow via the splenic artery, it is a frequent site for these "septic emboli," leading to infarction and potentially splenic abscess formation. **2. Analysis of Incorrect Options:** * **Typhoid Fever:** Characterized by **splenomegaly** (due to hyperplasia of the reticuloendothelial system) and "pea-soup" diarrhea, but it does not typically cause infarction. * **Chronic Myeloid Leukemia (CML):** While massive splenomegaly in CML *can* occasionally lead to "autoinfarction" due to the organ outgrowing its blood supply, it is not the classic association compared to the embolic nature of IE. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** PNH is associated with a high risk of **venous thrombosis** (e.g., Budd-Chiari syndrome or portal vein thrombosis) rather than arterial embolic infarction of the spleen. **Clinical Pearls for NEET-PG:** * **Morphology:** Splenic infarcts are classically **wedge-shaped**, subcapsular [2], and undergo **liquefactive necrosis** (unlike most organs which undergo coagulative necrosis) if they become infected. * **Pain:** Patients typically present with sharp **left upper quadrant (LUQ) pain** and referred pain to the left shoulder (Kehr’s sign) [4]. * **Sickle Cell Anemia:** A high-yield association where repeated micro-infarctions lead to **autosplenectomy** by adulthood [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 140. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology). Part 2 (Disease Mechanisms). Part 3 (Systemacy Pathology), pp. 148-149. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology). Part 2 (Disease Mechanisms). Part 3 (Systemacy Pathology), pp. 145-146. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 631-632. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 568.

Question 45: Reed Sternberg cells are characteristic of which type of cell?

A. B cells (Correct Answer)
B. T cells
C. Natural killer cells
D. All of the above

Explanation: **Explanation:** **1. Why B cells is the correct answer:** Reed-Sternberg (RS) cells are the hallmark neoplastic cells of **Classical Hodgkin Lymphoma (cHL)** [1]. Molecular studies, specifically single-cell PCR and microdissection, have demonstrated that in almost all cases of cHL, the RS cells are derived from **germinal center or post-germinal center B cells** [1]. Although these cells often fail to express typical B-cell markers (like CD20) due to the downregulation of the B-cell gene expression program, they possess rearranged and somatically mutated immunoglobulin (Ig) genes. This confirms their B-cell lineage, even if they are "crippled" and cannot produce functional antibodies. **2. Why other options are incorrect:** * **T cells & Natural Killer (NK) cells:** While some rare peripheral T-cell lymphomas can show "RS-like" morphology (e.g., Angioimmunoblastic T-cell Lymphoma), true Reed-Sternberg cells defining Hodgkin Lymphoma are not derived from T or NK lineages. In cHL, the T cells present in the lymph node are reactive background cells, not the neoplastic component [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Immunophenotype of RS Cells (Classical HL):** They are typically **CD15+**, **CD30+**, and **CD45–** (LCA negative). * **The "Owl’s Eye" Appearance:** Classic RS cells are large, multinucleated (or have a bilobed nucleus) with prominent, eosinophilic, inclusion-like nucleoli [1]. * **L&H Cells (Popcorn Cells):** Found in Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLPHL) [2]. Unlike classical RS cells, these are **CD20+** and **CD45+**, but CD15– and CD30–. * **Pax-5:** This is a B-cell transcription factor that is weakly but consistently expressed in RS cells, further proving their B-cell origin. **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. 614-616. [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. 618.

Question 46: What is Franklin disease?

A. Heavy chain disease
B. alpha-heavy chain disease
C. gamma-heavy chain disease (Correct Answer)
D. mu-heavy chain disease

Explanation: **Explanation:** **Franklin disease** is the eponym for **$\gamma$-heavy chain disease ($\gamma$-HCD)**. It is a rare B-cell lymphoproliferative disorder characterized by the production of a truncated monoclonal immunoglobulin heavy chain (gamma) that lacks associated light chains [1]. 1. **Why Option C is correct:** Franklin disease specifically refers to the $\gamma$-heavy chain variant. It typically presents in older adults and clinically mimics a malignant lymphoma rather than multiple myeloma. Patients often present with systemic symptoms (fever, weight loss), lymphadenopathy, and hepatosplenomegaly. A classic diagnostic sign is **palatal edema** due to involvement of Waldeyer’s ring. 2. **Why other options are incorrect:** * **Option A:** "Heavy chain disease" is a general category that includes alpha, gamma, and mu types; Franklin disease is specifically the gamma subtype [1]. * **Option B:** **$\alpha$-heavy chain disease (Seligmann disease)** is the most common HCD. It primarily involves the gastrointestinal tract (immunoproliferative small intestinal disease - IPSID) and is often associated with *Campylobacter jejuni* infections. * **Option D:** **$\mu$-heavy chain disease** is the rarest form, usually associated with Chronic Lymphocytic Leukemia (CLL). It is unique because it often shows vacuolated plasma cells in the bone marrow. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Serum protein electrophoresis (SPEP) shows a broad "M-spike" (often in the beta region), but unlike Myeloma, **Bence-Jones proteinuria is absent** because no light chains are produced. * **Classic Sign:** Palatal erythema/edema (Waldeyer’s ring involvement) is a high-yield physical finding for Franklin disease. * **Pathology:** The heavy chains in HCD are structurally abnormal (deleted constant regions), which prevents them from binding to light chains. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 606-607.

Question 47: All are true about iron deficiency anemia EXCEPT?

A. Hypochromic microcytic red blood cells
B. Presence of sideroblasts (Correct Answer)
C. Serum ferritin as a marker
D. Anisocytosis and poikilocytosis

Explanation: In Iron Deficiency Anemia (IDA), the body lacks sufficient iron to complete the heme ring. This leads to characteristic morphological changes and specific biochemical markers. ### **Why "Presence of sideroblasts" is the correct answer (The Exception):** Sideroblasts are erythroblasts with iron granules in their cytoplasm. In a healthy state, 20-40% of bone marrow erythroblasts are sideroblasts. In **Iron Deficiency Anemia, sideroblasts are absent or significantly decreased** because there is no available iron to be incorporated into the developing red cells. *Note:* "Ringed sideroblasts" (where iron accumulates in mitochondria) are a hallmark of **Sideroblastic Anemia**, not IDA. ### **Explanation of Other Options:** * **A. Hypochromic microcytic RBCs:** Due to deficient hemoglobin synthesis, the cells become smaller (Microcytic: MCV <80 fL) and pale (Hypochromic: MCHC <30 g/dL) [1]. * **C. Serum ferritin as a marker:** Serum ferritin reflects total body iron stores. It is the **most sensitive and specific initial lab test** for diagnosing IDA (levels <15-30 ng/mL) [2]. * **D. Anisocytosis and poikilocytosis:** IDA typically shows a high **RDW (Red Cell Distribution Width)**, reflecting variation in cell size (anisocytosis) and shape (poikilocytosis), such as pencil cells [1]. ### **NEET-PG High-Yield Pearls:** * **Gold Standard Diagnosis:** Absence of stainable iron (Prussian Blue/Perl’s stain) in the bone marrow. * **First Lab Change:** Decreased Serum Ferritin [2]. * **First Peripheral Blood Change:** Increased RDW [1]. * **Classic Morphology:** Pencil cells (elliptocytes) and target cells [1]. * **Key Differential:** In Anemia of Chronic Disease (ACD), ferritin is normal or high, while in IDA, it is always low [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 590-591. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 658-659.

Question 48: Which one of the following lymphomas is associated with HTLV-virus infection?

A. Burkitt's lymphoma
B. B-cell lymphoma
C. Adult T-cell leukemia and lymphoma (Correct Answer)
D. Hodgkin's disease

Explanation: **Explanation:** **Adult T-cell Leukemia/Lymphoma (ATLL)** is the correct answer because it is directly caused by the **Human T-lymphotropic virus type 1 (HTLV-1)**, a retrovirus [1]. The virus encodes the **Tax protein**, which activates host cell transcription factors (like NF-κB), leading to the proliferation of CD4+ T-cells and eventual malignant transformation. **Analysis of Options:** * **Burkitt’s Lymphoma:** Strongly associated with the **Epstein-Barr Virus (EBV)**, particularly the endemic (African) form [1]. It is characterized by the c-MYC translocation t(8;14). * **B-cell Lymphoma:** This is a broad category. While some subtypes (like Diffuse Large B-cell Lymphoma) can be associated with EBV or HHV-8 [2], they are not associated with HTLV-1. * **Hodgkin’s Disease:** Frequently associated with **EBV** (especially the Mixed Cellularity subtype), but has no link to HTLV-1. **High-Yield NEET-PG Pearls for ATLL:** 1. **Clinical Presentation:** Patients often present with generalized lymphadenopathy, hepatosplenomegaly, and **lytic bone lesions** with **hypercalcemia** (mimicking Multiple Myeloma). 2. **Morphology:** The pathognomonic finding on a peripheral blood smear is the presence of **"Flower cells"** (leukemic cells with highly indented, multilobulated nuclei). 3. **Immunophenotype:** Typically **CD4+ positive** T-cells. 4. **Epidemiology:** Endemic in Japan, the Caribbean, and parts of Central Africa [1]. 5. **Prognosis:** Generally aggressive with a poor prognosis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 219-220. [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. 595-596.

Question 49: Prognosis of lymphoma depends on all of the following except:

A. Number of lymph node sites
B. Tumour size
C. Tumour stage
D. Associated symptoms (Correct Answer)

Explanation: The prognosis of lymphoma is primarily determined by the anatomical extent of the disease and the biological aggressiveness of the tumor cells, rather than the presence of constitutional symptoms. [1] ### **Explanation of the Correct Answer** **D. Associated symptoms:** In the context of lymphoma, "associated symptoms" usually refers to **B-symptoms** (fever, night sweats, and weight loss). While B-symptoms are critical for **staging** (e.g., Stage IIB vs. IIA) and help guide treatment intensity, they are generally considered less powerful independent predictors of long-term prognosis compared to tumor burden and anatomical spread. In many modern prognostic indices, such as the International Prognostic Index (IPI) for Non-Hodgkin Lymphoma, B-symptoms are not included as a primary prognostic variable. ### **Explanation of Incorrect Options** * **A. Number of lymph node sites:** This is a key component of the IPI score. Involvement of multiple nodal or extranodal sites indicates a higher tumor burden and a poorer prognosis. * **B. Tumour size:** "Bulky disease" (typically defined as a mass >10 cm) is a well-established poor prognostic factor, as large masses are often more resistant to chemotherapy and radiation. * **C. Tumour stage:** The Ann Arbor Staging system (Stages I-IV) is the gold standard for determining the extent of spread. Higher stages (III and IV) signify disseminated disease and carry a worse prognosis than localized stages (I and II). [2] ### **High-Yield Clinical Pearls for NEET-PG** * **IPI Score (International Prognostic Index):** Remember the mnemonic **APLES** (Age >60, Performance status, LDH levels, Extranodal sites >1, Stage III/IV). Note that B-symptoms are **not** part of this score. * **Ann Arbor Staging:** Stage I (single node), Stage II (two+ nodes on same side of diaphragm), Stage III (both sides of diaphragm), Stage IV (disseminated/extranodal). * **Most Important Factor:** For most lymphomas, the **histological subtype** (grade) is the single most important determinant of survival and treatment approach. [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. 618. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 357-358.

Question 50: HbH disease is characterized by which of the following genetic defects?

A. Deletion of three alpha-globin genes (Correct Answer)
B. Deletion of three alpha-globin genes and one beta-globin gene
C. Deletion of two alpha-globin and two beta-globin genes
D. Deletion of four alpha-globin genes

Explanation: Alpha-thalassemia is a genetic disorder characterized by the reduced or absent synthesis of alpha-globin chains. Since humans have four alpha-globin genes (two on each chromosome 16), the clinical severity depends on the number of genes deleted. **1. Why Option A is correct:** **HbH disease** occurs when **three out of four alpha-globin genes are deleted** (- - / - α) [2]. This results in a severe shortage of alpha chains. In adults, the excess beta-globin chains (which have no alpha chains to bind to) form tetramers called **HbH (β4)**. These tetramers are unstable, lead to moderate to severe hemolytic anemia, and appear as "golf ball" inclusions on supra-vital staining [1]. **2. Why the other options are incorrect:** * **Option B & C:** Alpha-thalassemia specifically involves the alpha-globin gene cluster. Combined deletions of alpha and beta genes are not the standard definition of HbH disease and would present as complex thalassemic syndromes. * **Option D:** The deletion of all **four alpha-globin genes** (- - / - -) results in **Hb Barts (γ4)**. This condition is known as **Hydrops Fetalis**, which is incompatible with extrauterine life as the hemoglobin has an extremely high affinity for oxygen and fails to deliver it to tissues. **NEET-PG High-Yield Pearls:** * **Silent Carrier:** 1 gene deletion (- α / α α); asymptomatic. * **Alpha-Thal Trait:** 2 gene deletions; can be *cis* (- - / α α, common in Asians) or *trans* (- α / - α, common in Africans). * **Diagnosis:** HbH inclusions are best visualized using **Brilliant Cresyl Blue** stain (supra-vital) [1]. * **Electrophoresis:** HbH migrates faster than HbA (it is a "fast" hemoglobin) [1]. * **Hb Barts:** Seen in neonates with alpha-thalassemia; it consists of four gamma chains (γ4). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 600-601. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 649-650.

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Hemolytic Anemias

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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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