Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 441: Which of the following is NOT true of Hodgkin's lymphoma?

A. Bimodal age pattern
B. Less common in females
C. Contiguous spread
D. Osteolytic metastasis (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Osteolytic metastasis**. In Hodgkin’s Lymphoma (HL), bone involvement is relatively uncommon compared to other malignancies. When it does occur, it typically presents as **osteoblastic (sclerotic) lesions**, famously known as the **"Ivory Vertebra"** sign on X-ray. Osteolytic lesions are more characteristic of Multiple Myeloma or certain Non-Hodgkin Lymphomas (NHL). **Analysis of other options:** * **A. Bimodal age pattern:** This is a classic feature of HL. The first peak occurs in young adults (15–35 years), and the second peak occurs in the elderly (>50 years) [1]. * **B. Less common in females:** HL shows a distinct male preponderance (M:F ratio approx. 1.5:1), except for the **Nodular Sclerosis** subtype, which is more common in females [3]. * **C. Contiguous spread:** Unlike NHL, which spreads hematogenously and unpredictably, HL typically spreads in an orderly, predictable fashion to **anatomically contiguous** lymph node chains (e.g., from cervical to mediastinal nodes) [1], [2]. **High-Yield NEET-PG Pearls:** * **Reed-Sternberg (RS) Cells:** The hallmark of HL [1]. They are CD15+ and CD30+ (except for the Nodular Lymphocyte Predominant type, which is CD20+ and CD45+). * **Most Common Subtype:** Nodular Sclerosis (also has the best prognosis in many series) [3]. * **Best Prognosis:** Lymphocyte Rich. * **Worst Prognosis:** Lymphocyte Depleted (associated with HIV/EBV). * **EBV Association:** Most strongly linked with the Mixed Cellularity subtype [4]. **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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 557-558. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 558-559. [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. 616-618.

Question 442: Which CD marker is expressed by human stem cells?

A. CD14
B. CD8
C. CD34 (Correct Answer)
D. CD10

Explanation: **Explanation:** **CD34** is the hallmark surface marker for **Hematopoietic Stem Cells (HSCs)** and progenitor cells [1]. It is a transmembrane phosphoglycoprotein that mediates cell adhesion to the bone marrow extracellular matrix. As these stem cells differentiate into mature lineages, the expression of CD34 is lost; therefore, it is used clinically to identify, quantify, and isolate stem cells for peripheral blood stem cell transplantation [2]. **Analysis of Incorrect Options:** * **CD14:** This is a specific marker for the **monocyte/macrophage** lineage. It acts as a co-receptor for bacterial lipopolysaccharide (LPS). * **CD8:** This is a marker for **Cytotoxic T-cells** and a subset of Natural Killer (NK) cells. It interacts with MHC Class I molecules. * **CD10:** Also known as **CALLA** (Common Acute Lymphoblastic Leukemia Antigen), it is expressed on pre-B cells and germinal center B-cells. It is a key diagnostic marker for Childhood B-ALL and Follicular Lymphoma. **High-Yield Clinical Pearls for NEET-PG:** * **Stem Cell Harvest:** In clinical practice, a minimum dose of **$2 \times 10^6$ CD34+ cells/kg** is required for successful engraftment in a transplant recipient. * **Flow Cytometry:** CD34 is essential for diagnosing **Acute Myeloid Leukemia (AML)**, as it helps distinguish blasts from mature cells. * **Other Stem Cell Markers:** While CD34 is the most common, **CD133** is another marker used to identify primitive hematopoietic and neural stem cells. * **Negative Markers:** True HSCs are typically **CD34+** but **Lin-** (lineage negative) and **CD38-**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 588-589. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 584-586.

Question 443: Neoplastic cells in Franklin disease express which of the following markers?

A. CD5
B. CD10
C. CD55
D. CD79a (Correct Answer)

Explanation: ### Explanation **Franklin Disease**, also known as **Gamma Heavy Chain Disease ($\gamma$-HCD)**, is a rare B-cell lymphoproliferative disorder characterized by the production of truncated monoclonal gamma heavy chains that lack associated light chains. **Why CD79a is correct:** The neoplastic cells in Franklin Disease are typically a mixture of lymphocytes, plasma cells, and plasmacytoid lymphocytes (lymphoplasmacytic infiltrate). Since these are cells of **B-cell lineage**, they consistently express pan-B-cell markers. **CD79a** is a highly reliable pan-B-cell marker expressed throughout B-cell differentiation, from the pre-B stage to plasma cells. Other markers often positive in this condition include CD19, CD20, and CD138. **Analysis of Incorrect Options:** * **CD5:** This is a T-cell marker also expressed in specific B-cell malignancies like Chronic Lymphocytic Leukemia (CLL) and Mantle Cell Lymphoma. It is typically **negative** in Franklin Disease. * **CD10:** Known as CALLA, this is a marker for germinal center B-cells (e.g., Follicular Lymphoma, Burkitt Lymphoma). It is usually **negative** in heavy chain diseases. * **CD55:** This is a complement regulatory protein (Decay-Accelerating Factor). While present on many cells, its clinical significance is primarily linked to **Paroxysmal Nocturnal Hemoglobinuria (PNH)**, where it is deficient. It is not a diagnostic marker for Franklin Disease. **High-Yield Clinical Pearls for NEET-PG:** * **Definition:** Franklin disease is the $\gamma$-heavy chain subtype of Heavy Chain Diseases (HCD). * **Clinical Presentation:** Often presents with lymphadenopathy, splenomegaly, and involvement of **Waldeyer’s ring** (leading to palatal edema). * **Diagnosis:** Serum protein electrophoresis shows a broad band (not always a sharp M-spike) in the beta or gamma region; diagnosis is confirmed by **immunofixation** showing gamma heavy chains without light chains. * **Key Association:** Unlike Multiple Myeloma, **Bence-Jones proteinuria is absent** because no light chains are produced.

Question 444: Paroxysmal nocturnal hemoglobinuria is due to what type of defect?

A. Acquired red cell defect (Correct Answer)
B. Congenital red cell defect
C. Autoimmune defect
D. Lead poisoning

Explanation: **Explanation:** **Paroxysmal Nocturnal Hemoglobinuria (PNH)** is a unique hematological disorder characterized by an **acquired intracorpuscular defect** [2]. 1. **Why Option A is correct:** PNH is caused by an acquired somatic mutation in the **PIGA (Phosphatidylinositol Glycan class A) gene** within a hematopoietic stem cell [2]. This mutation leads to a deficiency of **GPI (Glycosylphosphatidylinositol) anchors**, which are necessary to attach protective proteins like **CD55 (DAF)** and **CD59 (MIRL)** to the red cell membrane. Without these proteins, RBCs become hypersensitive to complement-mediated lysis, leading to intravascular hemolysis [1]. 2. **Why other options are incorrect:** * **Option B:** Although it is a red cell defect, PNH is **not inherited** (congenital); it is acquired during an individual's lifetime [2]. * **Option C:** PNH is not autoimmune; hemolysis is caused by an innate complement system defect, not by autoantibodies (Coombs test is negative). * **Option D:** Lead poisoning causes acquired sideroblastic anemia and inhibits enzymes like ALA dehydratase, but it does not involve GPI-anchor defects. **High-Yield Clinical Pearls for NEET-PG:** * **Triad:** Hemolytic anemia, Pancytopenia, and Venous thrombosis (often in unusual sites like the Budd-Chiari syndrome) [1]. * **Gold Standard Diagnosis:** **Flow Cytometry** (shows absence of CD55 and CD59) [1]. * **Ham’s Test & Sucrose Lysis Test:** Historical tests (now largely replaced by flow cytometry). * **Treatment:** **Eculizumab** (a monoclonal antibody against Complement C5). * **Association:** PNH often arises in the setting of **Aplastic Anemia**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-651. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 601-602.

Question 445: In alloimmune thrombocytopenia, against which Human Platelet Antigen (HPA) is the antibody typically found?

A. HPA 1a (Correct Answer)
B. HPA 1b
C. HPA 2a
D. HPA 2b

Explanation: **Fetal and Neonatal Alloimmune Thrombocytopenia (FNAIT)** is the platelet equivalent of Hemolytic Disease of the Newborn (Rh incompatibility). It occurs when a mother lacks a specific platelet antigen that the fetus has inherited from the father. The mother develops IgG antibodies against these fetal antigens, which cross the placenta and cause fetal platelet destruction. **Why HPA-1a is the correct answer:** The most common and clinically significant target in Caucasians (accounting for approximately **80-90% of cases**) is the **HPA-1a** antigen (also known as $Zw^a$ or $Pl^{A1}$). This antigen is located on **Glycoprotein IIIa** (part of the GPIIb/IIIa complex). Typically, an HPA-1a negative mother (genotype 1b/1b) becomes sensitized to the HPA-1a antigen on fetal platelets. **Analysis of Incorrect Options:** * **HPA-1b:** This is the allelic variant of HPA-1a. While antibodies against 1b can occur, they are significantly rarer than 1a. * **HPA-2a and 2b:** These antigens are located on **Glycoprotein Ib**. While they can occasionally be involved in alloimmunization, they are far less frequent causes of FNAIT compared to the HPA-1 system. (Note: In certain Asian populations, HPA-4 antibodies are more prevalent than in Western populations, but HPA-1a remains the classic "textbook" answer for exams). **High-Yield Clinical Pearls for NEET-PG:** * **Target:** HPA-1a is located on **GPIIIa**. * **Difference from Rh Disease:** Unlike Rh incompatibility, FNAIT can occur during the **first pregnancy** (in ~50% of cases). * **Clinical Presentation:** Severe thrombocytopenia and a high risk of **intracranial hemorrhage (ICH)** in the fetus or neonate [1]. * **Treatment:** IVIG (Intravenous Immunoglobulin) administered to the mother during pregnancy or transfusion of HPA-matched (HPA-1a negative) platelets to the neonate. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 665-667.

Question 446: What is the most common cause of myelophthisic anemia?

A. Multiple myeloma
B. Non-Hodgkin lymphoma (NHL)
C. Leukemia
D. Multiple metastatic secondaries (Correct Answer)

Explanation: **Explanation:** **Myelophthisic anemia** (or myelophthisis) refers to bone marrow failure resulting from the infiltration and replacement of normal hematopoietic tissue by non-hematopoietic cells or abnormal tissue. **Why Option D is Correct:** The most common cause of myelophthisic anemia is **metastatic solid tumors** (secondaries). Carcinomas originating from the **breast, lung, prostate, and stomach** are the most frequent culprits. These malignant cells physically crowd out the marrow and induce fibrosis, disrupting the marrow-blood barrier [1]. This leads to the classic **leukoerythroblastic blood picture**, characterized by the presence of immature red cells (nucleated RBCs) and immature white cells (metamyelocytes/myelocytes) in the peripheral smear [1][2], along with **teardrop-shaped RBCs (dacrocytes)** [2]. **Analysis of Incorrect Options:** * **A, B, and C (Multiple Myeloma, NHL, and Leukemia):** While these hematological malignancies involve the bone marrow and can cause anemia through marrow replacement, they are statistically less common causes of a true "myelophthisic" clinical presentation compared to the high incidence of metastatic solid tumors. In these conditions, anemia is often multifactorial (e.g., cytokine-mediated or due to direct marrow involvement), whereas "myelophthisis" specifically emphasizes the "wasting away" of marrow by space-occupying lesions. **NEET-PG High-Yield Pearls:** * **Classic Peripheral Smear:** Leukoerythroblastic picture + Dacrocytes (Teardrop cells) [2]. * **Most Common Primary Source:** Breast cancer is frequently cited as the most common primary tumor leading to myelophthisis. * **Non-Neoplastic Causes:** Granulomatous diseases (e.g., Sarcoidosis, Tuberculosis) and Myelofibrosis can also cause a myelophthisic pattern [1][3]. * **Diagnostic Gold Standard:** Bone marrow biopsy (often shows a "dry tap" on aspiration due to underlying fibrosis). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 589-590. [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. 628-629. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 615-616.

Question 447: Non-specific esterase is present in which of the following conditions?

A. Megakaryocytic leukemia
B. Lymphocytic leukemia
C. Erythroleukemia
D. Acute Myeloid Leukemia (AML) (Correct Answer)

Explanation: **Explanation:** The correct answer is **Acute Myeloid Leukemia (AML)**, specifically the monocytic subtypes (AML-M4 and M5) [1]. **1. Why the Correct Answer is Right:** Non-specific esterase (NSE), such as alpha-naphthyl acetate esterase, is a cytochemical stain used to identify cells of **monocytic lineage** [1]. In the FAB classification of AML, **AML-M4 (Acute Myelomonocytic Leukemia)** and **AML-M5 (Acute Monocytic Leukemia)** show strong positivity for NSE [1]. The enzyme helps differentiate these monocytic blasts from myeloblasts (which are typically NSE negative but Myeloperoxidase positive). A key diagnostic feature is that NSE activity in monocytes is **inhibited by Sodium Fluoride (NaF)**. **2. Why Incorrect Options are Wrong:** * **Megakaryocytic leukemia (AML-M7):** These cells are typically negative for NSE but may show positivity for Acid Phosphatase or specific markers like Platelet Peroxidase (PPO) and CD41/CD61. * **Lymphocytic leukemia (ALL):** Lymphoblasts are characteristically NSE negative. They are typically identified by Periodic Acid-Schiff (PAS) positivity in a "block-like" pattern and TdT expression. * **Erythroleukemia (AML-M6):** Erythroblasts are generally NSE negative but show strong, globular PAS positivity. **3. High-Yield Clinical Pearls for NEET-PG:** * **MPO (Myeloperoxidase):** Most sensitive stain for myeloid differentiation (Positive in M1, M2, M3, M4). * **Sudan Black B (SBB):** Stains phospholipids; mimics MPO but can be used on older smears. * **NSE (Non-specific Esterase):** Marker for **Monocytes** (M4, M5) [1]. * **Specific Esterase (Chloroacetate Esterase):** Marker for **Granulocytes** (Neutrophils). * **PAS (Periodic Acid-Schiff):** Positive in ALL (block-like) and AML-M6 (diffuse/globular). **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 448: Fibrin degradation products help in the detection of which condition?

A. Hemophilia
B. Disseminated Intravascular Coagulation (DIC) (Correct Answer)
C. Thrombocytopenic purpura
D. Thrombasthenia

Explanation: ### Explanation **Correct Answer: B. Disseminated Intravascular Coagulation (DIC)** **Mechanism:** Disseminated Intravascular Coagulation (DIC) is characterized by systemic activation of the coagulation cascade, leading to widespread microthrombi formation. This massive consumption of clotting factors is followed by **secondary fibrinolysis**. Plasmin cleaves both fibrinogen and cross-linked fibrin, resulting in the release of **Fibrin Degradation Products (FDPs)** and **D-dimers** into the circulation [1]. Therefore, elevated FDPs are a hallmark laboratory finding used to diagnose DIC [2]. **Why other options are incorrect:** * **Hemophilia (A):** This is a qualitative or quantitative deficiency of clotting factors (Factor VIII or IX). It affects the intrinsic pathway of coagulation, not the fibrinolytic system. * **Thrombocytopenic Purpura (C):** Conditions like ITP or TTP involve low platelet counts or microangiopathic hemolysis [2]. While TTP involves thrombi, the primary diagnostic markers are schistocytes and ADAMTS13 levels, not FDPs. * **Thrombasthenia (D):** Glanzmann Thrombasthenia is a qualitative platelet disorder (deficiency of GpIIb/IIIa). It affects platelet aggregation, not the formation or breakdown of fibrin. **High-Yield Clinical Pearls for NEET-PG:** * **D-Dimer vs. FDP:** While FDPs indicate the breakdown of both fibrinogen and fibrin, **D-dimers** are specific for the breakdown of *cross-linked* fibrin, making them a more specific marker for active clot lysis [3]. * **DIC Lab Profile:** Look for prolonged PT/aPTT, decreased fibrinogen, thrombocytopenia, and the presence of **Schistocytes** (fragmented RBCs) on peripheral smear [2]. * **Common Triggers:** Sepsis (most common), Obstetric complications (Abruptio placentae), and Malignancy (APML - M3 subtype). **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. 151-152. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 130-132.

Question 449: Flame cells are seen in which condition?

A. Multiple myeloma (Correct Answer)
B. Malignant melanoma
C. Nodular colloid goiter
D. Hashimoto thyroiditis

Explanation: **Explanation:** **Flame cells** are a characteristic morphological variant of plasma cells found in the bone marrow of patients with **Multiple Myeloma**, particularly those associated with **IgA** paraproteinemia. 1. **Why Multiple Myeloma is correct:** Flame cells are plasma cells that exhibit a striking, fiery red-to-pink cytoplasm. This appearance is due to the extensive accumulation of glycoprotein (specifically IgA) within the cisternae of the endoplasmic reticulum [3]. The "flaming" effect is most prominent at the periphery of the cell. While not pathognomonic, their presence is a classic high-yield association with IgA Myeloma [2]. 2. **Why other options are incorrect:** * **Malignant melanoma:** Characterized by atypical melanocytes containing melanin pigment (brown-black) and prominent "cherry-red" nucleoli, but not flame cells. * **Nodular colloid goiter:** Features enlarged follicles filled with eosinophilic colloid and flattened follicular epithelium; it lacks plasma cell abnormalities. * **Hashimoto thyroiditis:** While this condition features an infiltrate of plasma cells and lymphocytes, the hallmark cells are **Hürthle cells** (Askanazy cells)—large epithelial cells with granular, eosinophilic cytoplasm due to abundant mitochondria. **High-Yield Clinical Pearls for NEET-PG:** * **Mott Cells / Grape Cells:** Plasma cells with multiple rounded, proteinaceous cytoplasmic inclusions (Russell bodies). * **Russell Bodies:** Cytoplasmic inclusions of immunoglobulins. * **Dutcher Bodies:** Periodic Acid-Schiff (PAS) positive intranuclear inclusions of immunoglobulins (commonly seen in Waldenström Macroglobulinemia) [1]. * **CRAB Criteria for Myeloma:** **C**alcium elevation, **R**enal insufficiency, **A**nemia, and **B**one 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, pp. 606-607. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 618-619.

Question 450: A 55-year-old man newly diagnosed with leukemia undergoes genetic studies that reveal a t(9;22) translocation (the Philadelphia chromosome). Which of the following would a complete blood count most likely show?

A. Increased lymphocyte count
B. Increased neutrophil count (Correct Answer)
C. Numerous lymphoblasts
D. Numerous myeloblasts

Explanation: **Explanation:** The presence of the **t(9;22) translocation**, known as the **Philadelphia chromosome (Ph+)**, is the hallmark of **Chronic Myeloid Leukemia (CML)** [1]. This translocation results in the *BCR-ABL1* fusion gene, which encodes a constitutively active tyrosine kinase [4]. This leads to the uncontrolled proliferation of the myeloid lineage, specifically the mature and maturing granulocytes. 1. **Why Option B is Correct:** In the chronic phase of CML (the most common presentation), the hallmark is a massive leukocytosis with a "left shift." This is characterized by an **increased neutrophil count** along with a full spectrum of myeloid cells (myelocytes, metamyelocytes, and band forms). A characteristic finding is the "myelocyte bulge" [3] and a significant increase in **basophils** and **eosinophils**. Platelets are also usually increased, sometimes markedly [2]. 2. **Why Options C and D are Incorrect:** Numerous blasts (>20%) are indicative of **Acute Leukemia** (ALL or AML). While t(9;22) can be seen in B-ALL (Option C) or CML in blast crisis (Option D), the most common and classic association for a "newly diagnosed" patient with this translocation is the chronic phase of CML, where blasts are typically <5-10%. 3. **Why Option A is Incorrect:** CML involves the myeloid line, not the lymphoid line. An increased lymphocyte count is characteristic of Chronic Lymphocytic Leukemia (CLL). **High-Yield Clinical Pearls for NEET-PG:** * **Leukocyte Alkaline Phosphatase (LAP) Score:** Characteristically **decreased** in CML (helps differentiate it from a Leukemoid Reaction, where LAP is high). * **Cytogenetics:** t(9;22) involves the *ABL* gene on chromosome 9 and the *BCR* gene on chromosome 22. * **Treatment:** Imatinib (a Tyrosine Kinase Inhibitor) is the first-line therapy [3]. * **Classic Sign:** Splenomegaly is the most common physical finding in CML [2], [3]. **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. 225-226. [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. 625-626. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612. [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, p. 624.

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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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