Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1071: A biopsy of a nasopharyngeal mass in a 30-year-old man shows a plasma cell proliferation. Serum electrophoresis reveals a monoclonal IgG spike. Bone marrow examination does not show plasma cell proliferation, and skeletal x-rays are negative for lesions. What is the most likely diagnosis?

A. Heavy chain disease
B. Monoclonal gammopathy of undetermined significance
C. Multiple myeloma
D. Plasmacytoma (Correct Answer)

Explanation: **Explanation:** The clinical presentation describes an **Extramedullary Plasmacytoma (EMP)**. This is a localized proliferation of neoplastic plasma cells occurring outside the bone marrow, most commonly in the upper respiratory tract (nasopharynx, tonsils, or paranasal sinuses) [1], [2]. **Why Plasmacytoma is correct:** The diagnosis is confirmed by the presence of a localized plasma cell mass (nasopharyngeal biopsy) in the absence of systemic features of Multiple Myeloma. Key diagnostic criteria met here include: 1. **Tissue biopsy** showing plasma cell infiltration [2]. 2. **Normal bone marrow** (no systemic involvement) [1]. 3. **Negative skeletal survey** (no lytic lesions) [1]. 4. While a monoclonal (M) protein spike can be present in serum (as seen here), it is usually at a lower concentration than in Multiple Myeloma [1]. **Why other options are incorrect:** * **Multiple Myeloma (MM):** Requires evidence of systemic involvement, often remembered by the **CRAB** mnemonic (Calcium elevation, Renal insufficiency, Anemia, and Bone lesions) [3]. The negative bone marrow and X-rays rule this out [4]. * **Monoclonal Gammopathy of Undetermined Significance (MGUS):** This is an asymptomatic condition characterized by an M-spike (<3g/dL) and <10% marrow plasma cells, but it **does not** present with a localized tumor mass (plasmacytoma). * **Heavy Chain Disease:** A rare B-cell lymphoproliferative disorder characterized by the production of truncated heavy chains without light chains [1]. It typically presents with lymphadenopathy or abdominal involvement (Alpha-chain disease), not a localized nasopharyngeal plasma cell mass. **High-Yield Pearls for NEET-PG:** * **Most common site for EMP:** Upper respiratory tract (80% of cases). * **Progression:** EMP has a better prognosis than solitary plasmacytoma of the bone; only about 15% progress to Multiple Myeloma. * **Treatment of choice:** Localized radiotherapy (plasmacytomas are highly radiosensitive). * **Rule of thumb:** If you see a "plasma cell mass" + "normal marrow" + "no lytic lesions" = **Plasmacytoma**. **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 Respiratory Tract Disease, pp. 314-315. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 617-618.

Question 1072: Which of the following is a differentiating feature between Hodgkin's lymphoma and non-Hodgkin's lymphoma?

A. Presence of B symptoms (fever, night sweats, weight loss)
B. Generalized lymphadenopathy
C. Predominance in the elderly
D. Presence of Reed-Sternberg cells (Correct Answer)

Explanation: **Explanation:** The fundamental histological distinction between Hodgkin’s Lymphoma (HL) and Non-Hodgkin’s Lymphoma (NHL) lies in the cellular composition of the tumor. [1] **1. Why the Correct Answer is Right:** **Reed-Sternberg (RS) cells** are the hallmark of Hodgkin’s Lymphoma. These are large, multinucleated B-cells (classically described as having "owl-eye" nuclei) that reside in a rich background of non-neoplastic inflammatory cells. [1], [3] In HL, the malignant cells constitute only 1–5% of the total tumor mass, whereas the reactive background makes up greater than 90%. [1] In contrast, NHL is characterized by a diffuse or follicular proliferation of malignant lymphocytes that make up the bulk of the tumor mass, without the presence of classic RS cells. **2. Why the Other Options are Wrong:** * **A. Presence of B symptoms:** While B symptoms (fever, drenching night sweats, weight loss) are classic for HL, they also occur frequently in aggressive subtypes of NHL. [2] Therefore, they are not a definitive differentiating feature. * **B. Generalized lymphadenopathy:** This is more characteristic of **NHL**, which often involves multiple peripheral nodes and non-contiguous spread. HL typically presents with localized, contiguous spread (e.g., starting in a single cervical node group). [1] * **C. Predominance in the elderly:** NHL incidence increases steadily with age. HL, however, shows a **bimodal age distribution** (peaks in the 20s and again after 50), making this a poor differentiating factor for the elderly population. [1], [4] **High-Yield Clinical Pearls for NEET-PG:** * **Spread:** HL spreads in a predictable, **contiguous** fashion; NHL is often **disseminated** at diagnosis and involves extranodal sites (GIT, Waldeyer’s ring, Bone Marrow) more frequently. [1] * **RS Cell Markers:** Classic RS cells are typically **CD15+ and CD30+**, but **CD45 negative**. * **Alcohol-induced pain:** Pain in the lymph nodes after alcohol consumption is a rare but highly specific clinical sign for Hodgkin’s Lymphoma. **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, pp. 616-618. [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. 616. [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. 618.

Question 1073: Burkitt's lymphoma is associated with which of the following genetic abnormalities?

A. t(9:22)
B. del.5q
C. t(8:14) (Correct Answer)
D. t(17:15)

Explanation: **Explanation:** **Burkitt’s Lymphoma** is a highly aggressive B-cell non-Hodgkin lymphoma characterized by the translocation **t(8;14)** [1]. This genetic abnormality involves the transposition of the **c-MYC proto-oncogene** from chromosome 8 to the **Immunoglobulin Heavy chain (IgH)** locus on chromosome 14 [1]. Because the IgH promoter is constitutively active in B-cells, this results in the overexpression of the MYC protein, a potent transcription factor that drives rapid cellular proliferation and oncogenesis [1]. **Analysis of Incorrect Options:** * **t(9;22):** Known as the **Philadelphia chromosome**, this is the hallmark of **Chronic Myeloid Leukemia (CML)** and some cases of ALL [2]. It creates the *BCR-ABL1* fusion gene with tyrosine kinase activity [2]. * **del.5q:** This deletion is characteristic of **Myelodysplastic Syndromes (MDS)**, specifically the "5q-minus syndrome," often presenting with macrocytic anemia and thrombocytosis. * **t(15;17):** This is the diagnostic marker for **Acute Promyelocytic Leukemia (APL - AML M3)**, involving the *PML-RARA* fusion gene, which responds to All-trans retinoic acid (ATRA) [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Classically shows a **"Starry sky appearance"** on histology (tingible body macrophages acting as "stars" against a background of dark neoplastic B-cells). * **Variants:** Endemic (African; associated with **EBV** and jaw involvement), Sporadic (abdominal involvement), and Immunodeficiency-associated. * **Immunophenotype:** CD19+, CD20+, CD10+, and **BCL-6+**. Crucially, it is **BCL-2 negative**. * **Proliferation Index:** The Ki-67 index is typically near **100%**, reflecting its rapid doubling time. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 605-607.

Question 1074: Thrombocytosis is seen in which of the following conditions?

A. Osteopetrosis
B. Disseminated intravascular coagulation
C. Haemolytic anaemia (Correct Answer)
D. Thiazide therapy

Explanation: **Explanation:** **Correct Answer: C. Haemolytic anaemia** Thrombocytosis (a platelet count >450,000/µL) in hemolytic anemia is a form of **reactive (secondary) thrombocytosis**. When red blood cells are destroyed, the bone marrow undergoes compensatory hyperplasia [3]. Since erythroid and megakaryocytic lineages share a common myeloid progenitor (CFU-GEMM), the intense drive to produce new RBCs often leads to a "cross-stimulation" or "bystander effect," resulting in increased platelet production. Additionally, iron deficiency (often associated with chronic hemolysis/hemoglobinuria) is a potent stimulator of thrombopoiesis. **Analysis of Incorrect Options:** * **A. Osteopetrosis:** This condition involves defective osteoclast function leading to abnormally dense bones that obliterate the marrow cavity (myelophthisis). This typically results in **pancytopenia** (including thrombocytopenia) and extramedullary hematopoiesis. * **B. Disseminated Intravascular Coagulation (DIC):** DIC is characterized by widespread activation of the coagulation cascade, leading to the "consumption" of platelets and clotting factors. Therefore, **thrombocytopenia** is a hallmark finding. * **D. Thiazide therapy:** Thiazide diuretics are a well-known cause of drug-induced **thrombocytopenia** due to direct bone marrow suppression of megakaryocytes. **High-Yield Clinical Pearls for NEET-PG:** * **Reactive Thrombocytosis:** Common causes include acute hemorrhage, iron deficiency anemia, chronic inflammation (IL-6 mediated), and post-splenectomy states. * **Spurious Thrombocytosis:** Can occur in severe hemolysis when RBC fragments (schistocytes) are small enough to be miscounted as platelets by automated analyzers [2]. * **Essential Thrombocythemia (ET):** A primary myeloproliferative neoplasm (often JAK2 or CALR positive) where platelet counts often exceed 1 million/µL, unlike reactive causes [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 596-597. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 640.

Question 1075: Which of the following is a pan B lymphocyte marker?

A. CD 19 (Correct Answer)
B. CD 5
C. CD 10
D. CD 38

Explanation: **Explanation:** **1. Why CD19 is the Correct Answer:** CD19 is considered the most reliable **pan-B cell marker** because it is expressed throughout B-cell development, from the earliest pro-B cell stage until just before terminal differentiation into plasma cells [1]. It is a transmembrane glycoprotein that acts as a co-receptor for B-cell receptor (BCR) signaling. In clinical practice, CD19 (along with CD20) is used in flow cytometry to identify the B-cell lineage in leukemias and lymphomas [1]. **2. Analysis of Incorrect Options:** * **CD5:** This is primarily a **T-cell marker**. However, it is aberrantly expressed on B-cells in specific malignancies like **Chronic Lymphocytic Leukemia (CLL)** and **Mantle Cell Lymphoma (MCL)** [1]. * **CD10:** Also known as **CALLA** (Common Acute Lymphoblastic Leukemia Antigen). It is a marker for pre-B cells and germinal center B-cells [1]. It is not "pan-B" because it is lost as the B-cell matures. * **CD38:** This is a marker for **plasma cells** and activated lymphocytes. It is not specific to the entire B-cell lineage and is often used as a prognostic marker in CLL. **3. High-Yield Clinical Pearls for NEET-PG:** * **Pan-B Markers:** CD19, CD20, CD22, and PAX-5 (PAX-5 is the most specific B-cell lineage marker) [1]. * **Pan-T Markers:** CD2, CD3, CD5, CD7 [1]. * **Plasma Cell Markers:** CD138 (most specific), CD38. * **CD20 Note:** While CD20 is a pan-B marker, it is **not** expressed on pro-B cells or plasma cells; CD19 appears earlier in ontogeny [1]. * **Rituximab:** A monoclonal antibody used in treatment that targets **CD20**. **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. 598.

Question 1076: What happens to hepcidin levels in Anemia of chronic disease?

A. Increases (Correct Answer)
B. Decreases
C. Remains normal
D. Any of the above

Explanation: **Explanation:** **1. Why the Correct Answer is Right:** In Anemia of Chronic Disease (ACD), the primary driver is chronic inflammation. [1] Inflammatory cytokines, most notably **Interleukin-6 (IL-6)**, stimulate the liver to increase the synthesis of **Hepcidin**, an acute-phase reactant. [1] Hepcidin acts as the "master regulator" of iron homeostasis. It binds to and triggers the degradation of **ferroportin**, the only known iron exporter on the surface of enterocytes and macrophages. [1] This leads to: * **Reduced intestinal iron absorption.** [1] * **Sequestration of iron** within the Reticuloendothelial System (macrophages). [1] Consequently, while total body iron stores are normal or high, the iron is "locked away" and unavailable for erythropoiesis, leading to anemia. **2. Why Incorrect Options are Wrong:** * **B (Decreases):** Hepcidin levels decrease in **Iron Deficiency Anemia (IDA)** and conditions with ineffective erythropoiesis (like Thalassemia) to maximize iron absorption. [1] In ACD, the inflammatory stimulus overrides the body's need for iron. * **C (Remains Normal):** A normal hepcidin level would not explain the characteristic finding of low serum iron despite high ferritin levels seen in ACD. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Diagnostic Triad of ACD:** Low serum iron, Low TIBC (Total Iron Binding Capacity), and **High/Normal Ferritin**. * **Hepcidin vs. Ferroportin:** Remember that Hepcidin is the "brake" on iron flow; more Hepcidin = less iron in the blood. [1] * **Morphology:** ACD is typically **normocytic normochromic**, but can become microcytic hypochromic in long-standing cases. * **Key Cytokine:** IL-6 is the specific inducer of Hepcidin in inflammatory states. [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. 658-662.

Question 1077: Acute myeloid leukemia (AML) is characterized by which of the following findings?

A. Philadelphia chromosome
B. Auer rods (Correct Answer)
C. Hemolytic anemia
D. Dohle bodies

Explanation: **Explanation:** **Acute Myeloid Leukemia (AML)** is a clonal proliferation of myeloid precursors (blasts) in the bone marrow. The presence of **Auer rods** is a pathognomonic hallmark of AML [1]. These are needle-like, azurophilic cytoplasmic inclusions formed by the crystallization of fused primary granules (lysosomes) containing **myeloperoxidase (MPO)** [2]. They are most commonly seen in the M1, M2, M3 (APML), and M4 subtypes of the FAB classification. **Analysis of Incorrect Options:** * **A. Philadelphia chromosome [t(9;22)]:** This is the hallmark of **Chronic Myeloid Leukemia (CML)**, involving the *BCR-ABL1* fusion gene. While it can occur in some cases of B-ALL or AML (as a poor prognostic marker), it is not a defining characteristic of AML. * **C. Hemolytic anemia:** While AML patients present with anemia due to bone marrow infiltration (myelophthisis), it is typically **normocytic normochromic** and non-hemolytic. * **D. Dohle bodies:** These are light blue, peripheral cytoplasmic inclusions (remnants of rough endoplasmic reticulum) found in **neutrophils** during states of inflammation, infection, or burns (toxic changes), rather than in leukemic blasts. **High-Yield Clinical Pearls for NEET-PG:** * **M3 Subtype (APML):** Characterized by "faggot cells" (bundles of Auer rods) and a high risk of **DIC** due to the release of procoagulants [1]. * **Diagnosis:** According to WHO criteria, AML requires **≥20% blasts** in the peripheral blood or bone marrow. * **Cytochemistry:** AML blasts are typically **MPO positive** and Sudan Black B positive, helping differentiate them from ALL. **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. 620. [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. 621-622.

Question 1078: Osmotic fragility is:

A. Negative in iron deficiency anemia (Correct Answer)
B. Negative in autoimmune hemolytic anemia
C. Based on the principle of lysis in serial dilutions of hypertonic saline
D. Best if performed in a citrated blood sample

Explanation: ### Explanation **1. Why Option A is Correct:** Osmotic Fragility (OF) measures the resistance of red blood cells (RBCs) to hemolysis when exposed to varying concentrations of hypotonic saline. In **Iron Deficiency Anemia (IDA)**, RBCs are microcytic and hypochromic with a high surface-area-to-volume ratio (flatter cells) [1]. These cells can absorb more fluid before the membrane stretches to the point of rupture. Therefore, OF is **decreased** (often referred to as "negative" or "reduced fragility") in IDA, Thalassemia, and Sickle Cell Anemia. **2. Why the Other Options are Incorrect:** * **Option B:** In **Autoimmune Hemolytic Anemia (AIHA)**, antibodies coat the RBCs, leading to partial membrane loss by splenic macrophages [1]. This transforms cells into **spherocytes**. Spherocytes have a low surface-area-to-volume ratio and rupture easily; thus, OF is **increased** (positive), not negative [1]. * **Option C:** The test is based on the principle of lysis in serial dilutions of **hypotonic** saline (0.9% down to 0.0%), not hypertonic. Normal RBCs begin to lyse at 0.45% and complete lysis at 0.3% NaCl. * **Option D:** The test is best performed using **heparinized** whole blood. Citrate or oxalate anticoagulants are avoided because they add additional salts to the medium, which can alter the tonicity and interfere with the results. **3. NEET-PG High-Yield Pearls:** * **Hereditary Spherocytosis (HS):** The classic condition where OF is significantly **increased** [1]. * **Incubated OF Test:** If the initial OF test is normal but HS is strongly suspected, incubating blood at 37°C for 24 hours increases the sensitivity of the test. * **Confirmatory Test for HS:** While OF is traditional, the **EMA Binding test** (Flow cytometry) is now the gold standard due to higher sensitivity and specificity. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 590-603.

Question 1079: Eosin-5-maleimide flow cytometry is used for the diagnosis of which condition?

A. Glucose-6-phosphate dehydrogenase deficiency
B. Hereditary spherocytosis (Correct Answer)
C. Sickle cell anemia
D. Alpha thalassemia

Explanation: ### Explanation **Hereditary Spherocytosis (HS)** is the correct answer. The **Eosin-5-maleimide (EMA) binding test** is currently the gold standard screening test for HS, replacing the older osmotic fragility test [1] due to its higher sensitivity (93–99%) and specificity. **Mechanism:** EMA is a fluorescent dye that binds covalently to the **Band 3 protein** (and to a lesser extent, Rh-related proteins and CD47) on the red blood cell membrane [2]. In Hereditary Spherocytosis, there is a deficiency of membrane proteins (Ankyrin, Spectrin, or Band 3). Consequently, there is reduced binding of the EMA dye. This reduction in fluorescence is quantified using **flow cytometry**; a decrease in mean fluorescence intensity (MFI) confirms the diagnosis. **Why other options are incorrect:** * **G6PD Deficiency:** Diagnosis is primarily made via the G6PD enzyme assay (Beutler fluorescent spot test) or by observing Heinz bodies with supravital stains [3]. * **Sickle Cell Anemia:** Diagnosis relies on **Hb Electrophoresis** or HPLC to identify HbS, and solubility tests (Sodium metabisulfite) for screening. * **Alpha Thalassemia:** Diagnosis is confirmed via HPLC (showing HbH or Hb Bart’s) and definitive genetic testing (DNA analysis for gene deletions). **High-Yield Clinical Pearls for NEET-PG:** * **Most common molecular defect in HS:** Ankyrin deficiency (most common overall), though Band 3 mutations are also frequent [2]. * **Peripheral Smear:** Shows microspherocytes (hyperchromic cells lacking central pallor) [1]. * **Lab Findings:** Increased **MCHC** (>36 g/dL) and increased RDW. * **Confirmatory Test:** While EMA is the best screening tool, SDS-PAGE (gel electrophoresis) remains the research standard for identifying specific protein deficiencies. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 642-643.

Question 1080: Auer rods are typically not seen in which subtype of Acute Myeloid Leukemia?

A. Acute promyelocytic leukemia (APL) (Correct Answer)
B. Acute myeloid leukemia subtype M2
C. Acute myeloid leukemia subtype M3
D. Acute myeloid leukemia subtype M1

Explanation: **Explanation:** Auer rods are needle-like, azurophilic cytoplasmic inclusions formed by the fusion of primary granules (containing myeloperoxidase) [1]. They are pathognomonic for neoplastic myeloid differentiation and are most commonly associated with **Acute Myeloid Leukemia (AML)**. **Why the correct answer is right:** There appears to be a discrepancy in the provided options. **Acute Promyelocytic Leukemia (APL)**, which is the FAB M3 subtype, is actually the condition where Auer rods are **most abundant** and frequently found in clusters (Faggot cells) [1][2]. However, in the context of standard NEET-PG questions, Auer rods are typically **NOT seen** in: 1. **AML-M0** (Undifferentiated AML) 2. **AML-M6** (Erythroleukemia) 3. **AML-M7** (Megakaryoblastic leukemia) 4. **ALL** (Acute Lymphoblastic Leukemia) – *This is the most common "distractor" in exams.* [3] *Note: If the question intended to ask where they are absent, M0, M6, or M7 would be the correct choices. If the options provided are fixed, there may be a typographical error in the question stem or options, as M3 (APL) is the classic association for Auer rods.* **Analysis of Options:** * **AML-M1 (Minimal maturation):** Auer rods are present but infrequent. * **AML-M2 (With maturation):** Auer rods are frequently seen; often associated with t(8;21) [1]. * **AML-M3 (APL):** Characterized by numerous Auer rods and "Faggot cells" [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Faggot Cells:** Cells containing bundles of Auer rods, characteristic of AML-M3 [1]. * **Composition:** Auer rods are composed of crystallized **Myeloperoxidase (MPO)**. * **Mnemonic for Absence:** Auer rods are absent in the "extremes" of the FAB classification (**M0** and **M6/M7**) and always absent in **ALL** [3]. * **DIC Risk:** The release of granules from Auer rods in M3 can trigger Disseminated Intravascular Coagulation [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, p. 620. [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. 621-622. [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. 599-600.

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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