Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1081: Which of the following is NOT a characteristic feature of Chronic Lymphocytic Leukemia (CLL)?

A. Presence of small lymphocytes in peripheral smear
B. Hepatosplenomegaly
C. Onset typically in individuals over 50 years of age, with a slight predilection for males (Correct Answer)
D. Expression of ZAP-70 is a marker

Explanation: ### Explanation The question asks for the feature that is **NOT** characteristic of Chronic Lymphocytic Leukemia (CLL). While Option C describes the typical demographic (older males), it is marked as the "correct" answer in this specific context likely due to a nuance in the phrasing or a comparison of clinical significance. However, in standard medical literature, all four options are technically associated with CLL. Let’s analyze the features: **1. Why Option C is the designated answer:** In many high-stakes exams like NEET-PG, if all options seem correct, the "incorrect" one is often the one that is a **generalization** rather than a **diagnostic hallmark**. While CLL is indeed a disease of the elderly (median age ~70) with a male predilection (2:1), this is a demographic trend rather than a pathognomonic feature [1]. **2. Analysis of Incorrect Options:** * **Option A (Small Lymphocytes):** This is a **hallmark** of CLL. The peripheral smear typically shows an absolute lymphocytosis of small, mature-appearing lymphocytes with "block-like" chromatin and scant cytoplasm [1]. * **Option B (Hepatosplenomegaly):** This is a common clinical finding. As the disease progresses (Rai Stage III/IV), leukemic infiltration leads to enlargement of the liver and spleen, alongside generalized lymphadenopathy [1]. * **Option D (ZAP-70):** This is a crucial **prognostic marker**. Expression of ZAP-70 (and CD38) correlates with unmutated *IGHV* genes, indicating a more aggressive clinical course and poorer prognosis. **High-Yield Clinical Pearls for NEET-PG:** * **Smudge Cells:** Characteristically seen in CLL due to the fragility of the neoplastic lymphocytes [1]. * **Immunophenotype:** CLL cells are unique because they co-express **CD5** (a T-cell marker) and B-cell markers (**CD19, CD20, CD23**) [1]. * **Richter Transformation:** The progression of CLL into Diffuse Large B-cell Lymphoma (DLBCL), seen in ~5-10% of cases. * **Hypogammaglobulinemia:** Most common complication leading to recurrent bacterial infections. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 602.

Question 1082: A patient presents with a platelet count of 700 x 10^9/L with abnormalities in size, shape, and granularity of platelets. The WBC count is 12 x 10^9/L, hemoglobin is 11 g/dL, and the Philadelphia chromosome is absent. What is the most likely diagnosis?

A. Polycythemia vera
B. Essential thrombocythemia (Correct Answer)
C. Chronic myeloid leukemia
D. Leukemoid reaction

Explanation: ### Explanation The correct diagnosis is **Essential Thrombocythemia (ET)**. **1. Why Essential Thrombocythemia is correct:** ET is a Myeloproliferative Neoplasm (MPN) characterized by a sustained increase in platelet count (>450 x 10⁹/L). The patient presents with significant thrombocytosis (700 x 10⁹/L) and morphological abnormalities (size, shape, and granularity), which are hallmark features of megakaryocytic hyperplasia in the bone marrow [1]. The absence of the **Philadelphia chromosome (BCR-ABL1)** is crucial, as it excludes Chronic Myeloid Leukemia (CML) and points toward the "triple-negative" MPN group (ET, PV, or PMF). **2. Why other options are incorrect:** * **Polycythemia Vera (PV):** While PV can present with elevated platelets, its defining feature is a significantly increased red cell mass (high Hemoglobin/Hematocrit) [3]. This patient has a hemoglobin of 11 g/dL (mildly low/normal), making PV unlikely. * **Chronic Myeloid Leukemia (CML):** CML typically presents with massive leukocytosis and a left shift in the myeloid series [3]. Most importantly, CML is defined by the presence of the **Philadelphia chromosome [t(9;22)]**, which is absent here. * **Leukemoid Reaction:** This is a reactive increase in WBC count (usually >50 x 10⁹/L) due to infection or inflammation. It does not cause primary thrombocytosis or platelet morphological abnormalities. **3. High-Yield Clinical Pearls for NEET-PG:** * **Genetic Markers:** Approximately 50-60% of ET cases carry the **JAK2 V617F** mutation [2]. Other mutations include **CALR** (Calreticulin) and **MPL** [1]. * **Bone Marrow Findings:** Look for "staghorn" or "giant" megakaryocytes in clusters [1]. * **Clinical Complication:** Paradoxically, patients can present with both **thrombosis** (due to high counts) and **bleeding** (due to acquired von Willebrand syndrome). * **Diagnosis of Exclusion:** Always rule out reactive thrombocytosis (due to iron deficiency, splenectomy, or inflammation) before diagnosing ET [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. 627-628. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 626-627.

Question 1083: What are the diagnostic criteria for Chronic Myeloid Leukemia (CML)?

A. Auer rods
B. Basophilia
C. Leukocyte Alkaline Phosphatase (LAP) score
D. Philadelphia chromosome (t(9;22)) (Correct Answer)

Explanation: **Explanation:** **1. Why the Correct Answer is Right:** Chronic Myeloid Leukemia (CML) is a myeloproliferative neoplasm characterized by the presence of the **Philadelphia chromosome (Ph)**, which is a reciprocal translocation between chromosomes 9 and 22, **t(9;22)(q34;q11)** [1], [2]. This translocation results in the fusion of the *BCR* and *ABL1* genes, creating a chimeric **BCR-ABL1 protein** with constitutive tyrosine kinase activity [1]. This molecular hallmark is the "gold standard" for diagnosis and is essential for initiating targeted therapy with Tyrosine Kinase Inhibitors (TKIs) like Imatinib. **2. Why the Other Options are Incorrect:** * **Auer Rods:** These are pathognomonic for **Acute Myeloid Leukemia (AML)**, specifically the M1, M2, M3, and M4 subtypes. They are never seen in the chronic phase of CML. * **Basophilia:** While an increase in basophils is a characteristic feature of CML (and rising levels often signal progression to the accelerated phase), it is a supportive finding rather than a definitive diagnostic criterion. * **LAP Score:** In CML, the **Leukocyte Alkaline Phosphatase (LAP) score is characteristically low/decreased**. While this helps differentiate CML from a Leukemoid reaction (where LAP is high), it is a biochemical marker, not a definitive genetic diagnostic criterion. **3. High-Yield Clinical Pearls for NEET-PG:** * **Peripheral Smear:** Shows a "myelocyte bulge" (predominance of myelocytes and metamyelocytes) and a "whole spectrum of myeloid cells." * **Triad of CML:** Splenomegaly (often massive), Leukocytosis, and the Philadelphia chromosome. * **Blast Crisis:** CML can transform into AML (70%) or ALL (30%). * **Monitoring:** Quantitative PCR for *BCR-ABL1* transcripts is used to monitor Minimal Residual Disease (MRD). **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. 624. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 605-607.

Question 1084: Giant platelets are seen in all the following conditions except:

A. Bernard-Soulier syndrome
B. Glanzmann thrombasthenia (Correct Answer)
C. May-Hegglin anomaly
D. Gray platelet syndrome

Explanation: **Explanation:** The presence of **giant platelets** (platelets larger than a normal red blood cell) is a hallmark of specific inherited and acquired disorders of platelet production or structure. **Why Glanzmann Thrombasthenia (GT) is the correct answer:** In Glanzmann Thrombasthenia, there is a qualitative defect due to a deficiency or dysfunction of **GP IIb/IIIa**, the receptor responsible for platelet aggregation via fibrinogen binding [1]. Crucially, the **size and number of platelets are normal** in GT. The peripheral smear shows isolated platelets with a failure to form clumps, but they do not exhibit the "giant" morphology seen in macrothrombocytopenias. **Analysis of Incorrect Options:** * **Bernard-Soulier Syndrome (BSS):** Characterized by a deficiency of **GP Ib-IX-V** (the von Willebrand factor receptor) [1]. It is the classic "giant platelet" disorder. The defect in the membrane skeleton leads to the production of abnormally large platelets. * **May-Hegglin Anomaly:** An autosomal dominant disorder caused by **MYH9 gene** mutations. It presents with a triad of giant platelets, thrombocytopenia, and characteristic **Döhle-like inclusion bodies** in neutrophils. * **Gray Platelet Syndrome:** A rare alpha-granule deficiency. Platelets appear large and "gray" or pale on Wright-Giemsa stain due to the absence of electron-dense alpha granules. **High-Yield Clinical Pearls for NEET-PG:** * **BSS vs. GT:** BSS has giant platelets and fails to aggregate with Ristocetin. GT has normal-sized platelets and fails to aggregate with ADP, Epinephrine, and Collagen (but aggregates normally with Ristocetin) [1]. * **MYH9 Disorders:** Include May-Hegglin, Sebastian, Fechtner, and Epstein syndromes; all feature macrothrombocytopenia. * **Rule of Thumb:** If the question mentions "Giant Platelets + Neutrophil inclusions," think May-Hegglin. If it mentions "Giant Platelets + Bleeding + No Ristocetin aggregation," think Bernard-Soulier. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 666-669.

Question 1085: All of the following can cause aplastic anemia except?

A. Fanconi's anemia
B. Wiskott-Aldrich syndrome (Correct Answer)
C. Dyskeratosis congenital
D. Reticular dysgenesis

Explanation: **Explanation:** Aplastic anemia is characterized by pancytopenia resulting from bone marrow failure. The correct answer is **Wiskott-Aldrich syndrome (WAS)** because it is primarily an immunodeficiency disorder, not a cause of aplastic anemia. **1. Why Wiskott-Aldrich Syndrome is the correct answer:** WAS is an X-linked recessive disorder caused by mutations in the *WASP* gene [2]. It is characterized by the triad of **thrombocytopenia** (with micro-platelets), **eczema**, and **recurrent infections** (due to combined B and T cell deficiency) [2]. While it involves low platelets, it does not cause global bone marrow failure or aplastic anemia. **2. Why the other options are incorrect (Causes of Aplastic Anemia):** * **Fanconi’s Anemia:** The most common inherited cause of aplastic anemia [1]. It is an autosomal recessive DNA repair defect associated with physical anomalies (thumb/radius defects, short stature) and a high risk of AML. * **Dyskeratosis Congenita:** A telomere maintenance disorder (telomeropathy) presenting with the triad of abnormal skin pigmentation, nail dystrophy, and oral leukoplakia. Bone marrow failure develops in 80% of cases. * **Reticular Dysgenesis:** The most severe form of Combined Immunodeficiency (SCID). It is characterized by a lack of granulocytes and lymphoid cells due to a failure in hematopoietic stem cell differentiation, leading to neonatal bone marrow failure. **Clinical Pearls for NEET-PG:** * **Most common cause of Aplastic Anemia:** Idiopathic (Immune-mediated T-cell destruction of stem cells) [1]. * **Drug-induced:** Chloramphenicol (most common drug), Gold salts, and Phenylbutazone [1]. * **Viral-induced:** Hepatitis (Non-A, Non-B, Non-C, Non-G) is the most common viral cause [1]. Parvovirus B19 causes **Pure Red Cell Aplasia**, not total aplastic anemia (except in underlying hemolytic states) [1]. * **Gold Standard Diagnosis:** Bone marrow biopsy showing "dry tap" and replacement of marrow with fat cells (hypocellularity). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 595-596. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 250-251.

Question 1086: Which of the following conditions exhibits X-linked recessive inheritance?

A. G6PD deficiency (Correct Answer)
B. Sickle cell anaemia
C. Thalassemia
D. Hereditary spherocytosis

Explanation: **Explanation:** **1. Correct Option: G6PD Deficiency** Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is an **X-linked recessive** enzymopathy. The G6PD gene is located on the long arm of the X chromosome (Xq28). Because of this inheritance pattern, the condition primarily affects males, while females are typically asymptomatic carriers [1]. However, females can manifest the disease due to **unfavorable lyonization** (random X-inactivation). The deficiency leads to inadequate NADPH production, making RBCs susceptible to oxidative stress, resulting in hemolysis and the formation of **Heinz bodies** and **Bite cells**. **2. Incorrect Options:** * **Sickle Cell Anaemia:** This is an **Autosomal Recessive** disorder caused by a point mutation (Glu → Val) in the β-globin chain. * **Thalassemia:** Both Alpha and Beta thalassemias are **Autosomal Recessive** conditions involving quantitative defects in globin chain synthesis. * **Hereditary Spherocytosis:** This is most commonly inherited in an **Autosomal Dominant** pattern (approx. 75% of cases), involving defects in RBC membrane proteins like Ankyrin or Spectrin. **3. NEET-PG High-Yield Pearls:** * **Common Triggers:** Fava beans, infections, and drugs (Primaquine, Sulphonamides, Nitrofurantoin). * **Morphology:** Heinz bodies (denatured hemoglobin) are visualized with **Supravital stains** (Crystal violet/Methylene blue). Bite cells (Degmacytes) are formed in the splenic sinusoids. * **Protection:** G6PD deficiency provides a selective advantage against *Plasmodium falciparum* malaria. * **Timing of Test:** Do not perform the G6PD enzyme assay during an acute hemolytic episode, as young reticulocytes have normal enzyme levels, leading to a **false-negative** result. Wait 6–8 weeks. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 151.

Question 1087: Purpura fulminans is seen in which of the following conditions?

A. Severe DIC (Correct Answer)
B. Leukocytoclastic vasculitis
C. Viral hemorrhagic fever
D. Tularemia

Explanation: **Explanation:** **Purpura Fulminans (PF)** is a life-threatening hematological emergency characterized by rapid skin necrosis, disseminated intravascular coagulation (DIC), and multi-organ failure. **Why Option A is Correct:** The underlying pathophysiology of PF involves a massive derangement of the coagulation cascade, specifically a **deficiency in the Protein C or Protein S anticoagulant pathways**. This leads to uncontrolled thrombin generation and widespread microvascular thrombosis. This process is the hallmark of **Severe DIC** [2]. It is most commonly seen in: 1. **Infectious PF:** Classically associated with *Neisseria meningitidis* (Meningococcemia) [1]. 2. **Neonatal PF:** Due to homozygous Protein C/S deficiency. 3. **Idiopathic PF:** Following viral infections (depletion of Protein S). **Why Other Options are Incorrect:** * **B. Leukocytoclastic vasculitis:** This presents as "palpable purpura" due to immune complex deposition in small vessels, but it does not typically cause the massive, confluent gangrenous necrosis and systemic DIC seen in PF. * **C. Viral hemorrhagic fever:** While these can cause petechiae and bleeding due to thrombocytopenia, they do not typically present with the specific thrombotic-necrotic pattern of PF. * **D. Tularemia:** This is a zoonotic infection presenting with skin ulcers and lymphadenopathy (ulceroglandular form), not primary purpura fulminans. **NEET-PG High-Yield Pearls:** * **Waterhouse-Friderichsen Syndrome:** Adrenal hemorrhage associated with Meningococcemia and PF [1]. * **Histopathology:** PF shows fibrin thrombi in small vessels without significant inflammatory cell infiltration (unlike vasculitis) [1]. * **Treatment:** Immediate administration of Protein C concentrate or Fresh Frozen Plasma (FFP) is critical in protein-deficient states. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 672-673. [2] 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. 63-64.

Question 1088: What is true about nodular lymphocytic predominant Hodgkin's lymphoma?

A. Consists predominantly of classical Reed-Sternberg cells
B. CD15 and CD30 positive
C. Composed of T lymphocytes
D. Has a good prognosis (Correct Answer)

Explanation: **Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLPHL)** is a distinct clinical and biological entity that differs significantly from Classical Hodgkin Lymphoma (CHL) [1]. ### **Explanation of the Correct Answer** **Option D is correct.** NLPHL is characterized by an indolent clinical course and an excellent long-term prognosis [1]. Most patients present with localized (Stage I or II) peripheral lymphadenopathy, typically involving cervical, axillary, or inguinal nodes [1]. It has a high cure rate, although it is prone to late relapses and carries a small risk (approx. 3-5%) of transformation into Diffuse Large B-Cell Lymphoma (DLBCL) [1]. ### **Why Other Options are Incorrect** * **Option A:** Instead of classical Reed-Sternberg (RS) cells, NLPHL features **"Popcorn cells"** (L&H cells—Lymphocytic and Histiocytic variants) [1]. These cells have multi-lobed, delicate nuclei resembling popped corn [1]. * **Option B:** Unlike CHL, Popcorn cells are **CD15 negative and CD30 negative**. They represent a B-cell lineage and are characteristically **CD20 positive** and **BCL6 positive**. * **Option C:** While the background contains many reactive T cells, the neoplastic cells (Popcorn cells) are of **B-lymphocyte origin** [1]. ### **High-Yield Clinical Pearls for NEET-PG** * **Immunophenotype:** CD20+, CD45+, CD75+, BCL6+, EMA (often positive); CD15-, CD30-. * **Gender/Age:** More common in males, typically in the 30–50 age group [1]. * **Microscopic Pattern:** Shows a nodular growth pattern of small B-lymphocytes, follicular dendritic cell meshworks, and scattered L&H cells [1]. * **Treatment:** Because it is CD20+, **Rituximab** is an effective targeted therapy, unlike in Classical Hodgkin 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. 614-618.

Question 1089: Glucose added to stored blood is beneficial for which of the following reasons?

A. To prevent hemolysis (Correct Answer)
B. To provide nutrition for one week
C. To increase blood acidosis
D. To prevent hyperkalemia

Explanation: **Explanation:** The correct answer is **A. To prevent hemolysis.** Stored red blood cells (RBCs) are living metabolic units that require energy to maintain their structural integrity. RBCs rely exclusively on **anaerobic glycolysis** (the Embden-Meyerhof pathway) to generate ATP. This ATP is essential for fueling the **Na+/K+ ATPase pumps** located in the cell membrane [1]. These pumps maintain the osmotic balance by keeping sodium out and potassium inside the cell. When glucose levels are depleted, ATP production fails, causing the pumps to stop. This leads to an influx of water into the cell, causing the RBC to swell (spherocytosis) and eventually rupture (**hemolysis**). Therefore, glucose is added to preservative solutions (like CPD or CPDA-1) to provide a continuous substrate for ATP generation, thereby preventing hemolysis and extending the shelf life of the blood. [1] **Analysis of Incorrect Options:** * **B. To provide nutrition for one week:** This is incorrect because glucose is intended to sustain the blood for much longer. Modern preservatives like CPDA-1 allow blood to be stored for up to **35 days**, and SAGM (Saline-Adenine-Glucose-Mannitol) extends this to **42 days**. * **C. To increase blood acidosis:** This is a side effect, not a benefit. As RBCs metabolize glucose, they produce **lactic acid**, which actually decreases the pH (increases acidosis) of the stored blood. * **D. To prevent hyperkalemia:** Glucose does not prevent hyperkalemia; in fact, during storage, potassium slowly leaks out of the RBCs into the plasma, leading to **increased** extracellular potassium levels. **High-Yield Facts for NEET-PG:** * **CPDA-1:** Contains Citrate (anticoagulant), Phosphate (buffer), Dextrose (energy), and Adenine (helps resynthesize ATP). * **Storage Temperature:** Blood is stored at **2–6°C** to slow down glycolysis and bacterial growth. * **Storage Lesion:** Refers to the biochemical and morphological changes in stored blood, including decreased pH, decreased 2,3-DPG (shifting the oxygen dissociation curve to the left), and increased plasma potassium. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 56-57.

Question 1090: In Non-Hodgkin's lymphoma, early involvement of the bone marrow is typical of which variety?

A. Diffuse
B. Nodular (Correct Answer)
C. Lymphocytic well differentiated
D. Lymphocytic poorly differentiated

Explanation: **Explanation:** In Non-Hodgkin’s Lymphoma (NHL), the pattern of involvement and the cell type significantly influence the timing of bone marrow (BM) dissemination. **Why Nodular (Follicular) is correct:** The **Nodular (Follicular) pattern** of NHL is characterized by a high frequency of early, systemic spread. Even when the disease appears clinically localized to a single lymph node group, the bone marrow is involved in approximately **60–85% of cases** at the time of diagnosis [1], [2]. This is a hallmark of low-grade, indolent B-cell lymphomas (like Follicular Lymphoma), which tend to circulate through the vascular and lymphatic systems more readily than aggressive types. **Analysis of Incorrect Options:** * **Diffuse (A):** Diffuse lymphomas (e.g., Diffuse Large B-Cell Lymphoma) are more aggressive and often present with localized bulky disease. Bone marrow involvement occurs later in the disease course and in a smaller percentage of patients (approx. 15–20%) compared to the nodular variety. * **Lymphocytic well-differentiated (C):** While this often involves the marrow (as seen in SLL/CLL), the question specifically asks for the "variety" (pattern) most typically associated with early involvement. The nodular architecture is the classic teaching point for early BM dissemination in NHL. * **Lymphocytic poorly differentiated (D):** This is an older terminology for intermediate-grade lymphomas. While they can involve the marrow, they do not do so as consistently or as early as the nodular/follicular types. **High-Yield Pearls for NEET-PG:** * **Pattern of BM involvement:** In Follicular Lymphoma, the marrow involvement is characteristically **paratrabecular** (lymphoid aggregates adjacent to the bone trabeculae). * **Cleaved Cells:** Nodular lymphomas often consist of "buttock cells" (centrocytes with indented/cleaved nuclei) [1]. * **Cytogenetics:** Follicular lymphoma is strongly associated with **t(14;18)** and overexpression of the **BCL-2** anti-apoptotic protein [1], [2]. * **Rule of Thumb:** Low-grade lymphomas (Nodular) = Early BM involvement; High-grade lymphomas (Diffuse) = Late BM involvement. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 561-562. [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. 602-604.

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Hemolytic Anemias

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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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