Hematopathology — MCQs

A 7-month-old child presents with failure to thrive and a hemoglobin level of 4.4 g/dL. Peripheral smear examination reveals very small red blood cells with marked pallor. Laboratory tests show very low levels of hemoglobin A, with elevated fractions of hemoglobin A2 and hemoglobin F. Which of the following underlying mechanisms is most likely responsible for these findings?

Q300Easy

Which of the following characterizes Chronic Lymphocytic Leukemia (CLL)?

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 291: Patients with Classic Von Willebrand's disease have what laboratory findings?

A. Decreased bleeding time, prolonged activated partial thromboplastin time (APTT)
B. Prolonged bleeding time, decreased activated partial thromboplastin time (APTT)
C. Decreased bleeding time, decreased activated partial thromboplastin time (APTT)
D. Prolonged bleeding time, prolonged activated partial thromboplastin time (APTT) (Correct Answer)

Explanation: **Explanation:** Von Willebrand Disease (vWD) is the most common inherited bleeding disorder. To understand the laboratory findings, one must understand the dual role of **Von Willebrand Factor (vWF)**: 1. **Platelet Adhesion:** vWF acts as a bridge between platelet glycoprotein Ib (GpIb) receptors and the subendothelial collagen [1]. A deficiency leads to defective primary hemostasis, which manifests as a **prolonged Bleeding Time (BT)**. 2. **Stabilization of Factor VIII:** vWF acts as a carrier protein for Factor VIII, protecting it from rapid degradation in the circulation [1]. A deficiency in vWF leads to a secondary decrease in Factor VIII levels, which impairs the intrinsic pathway of coagulation, resulting in a **prolonged Activated Partial Thromboplastin Time (aPTT)**. **Analysis of Options:** * **Option D (Correct):** Reflects both the defect in platelet plug formation (↑BT) and the secondary deficiency of Factor VIII (↑aPTT). * **Options A, B, and C:** Are incorrect because they suggest either a decreased (shortened) bleeding time or a decreased aPTT. In vWD, bleeding time is never decreased; it is either prolonged or occasionally normal in mild cases. Similarly, aPTT is either prolonged or normal, never decreased. **NEET-PG High-Yield Pearls:** * **Screening Test of Choice:** Ristocetin Cofactor Assay (measures vWF-induced platelet agglutination). * **Platelet Count:** Usually **normal** in vWD (except in Type 2B, where mild thrombocytopenia may occur). * **Prothrombin Time (PT):** Always **normal**, as the extrinsic pathway is unaffected. * **Clinical Presentation:** Mucocutaneous bleeding (epistaxis, menorrhagia, gingival bleeding). * **Treatment:** Desmopressin (DDAVP) is used in Type 1 to release stored vWF from Weibel-Palade bodies. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-670.

Question 292: In a patient with acute leukemia, the immunophenotype pattern shows CD 19+ve, CD 10+ve, CD33+ve, and CD13+ve. What is the most likely diagnosis?

A. Biphenotypic leukemia (Correct Answer)
B. Acute Lymphoblastic Leukemia (ALL)
C. Acute Myeloid Leukemia - M2 (AML-M2)
D. Acute Myeloid Leukemia - M0 (AML-M0)

Explanation: **Explanation:** The correct answer is **Biphenotypic Leukemia**, now classified under **Mixed Phenotype Acute Leukemia (MPAL)** according to the WHO classification [1]. **1. Why it is correct:** Biphenotypic leukemia is characterized by the expression of markers from two different lineages on a single population of blasts. In this case: * **CD19 and CD10** are definitive markers for **B-lymphoid** lineage. * **CD33 and CD13** are definitive markers for **Myeloid** lineage. The simultaneous presence of both B-cell and myeloid markers satisfies the criteria for MPAL, as the blasts do not belong to a single restricted lineage. **2. Why the other options are incorrect:** * **B. Acute Lymphoblastic Leukemia (ALL):** While CD19 and CD10 are classic for B-ALL, the strong expression of myeloid markers (CD13, CD33) excludes a diagnosis of pure ALL [1]. * **C & D. AML (M2 and M0):** Although CD13 and CD33 are hallmarks of AML, the presence of B-cell specific markers like CD19 and CD10 is not typical for pure myeloid leukemia [1]. While "lineage infidelity" (weak expression of lymphoid markers) can occur in AML, the combination provided here strongly points toward a mixed phenotype. **High-Yield Clinical Pearls for NEET-PG:** * **MPAL Criteria:** Diagnosis relies on the **EGIL scoring system** or the **WHO criteria**, which require specific "strong" markers (e.g., MPO for myeloid; CD19/CD22/CD79a for B-lymphoid; cytoplasmic CD3 for T-lymphoid). * **Cytogenetics:** MPAL is frequently associated with **t(9;22)** (Philadelphia chromosome) or **MLL gene rearrangements** (11q23) [1]. * **Prognosis:** Generally carries a **poorer prognosis** compared to standard AML or ALL and often requires intensive "hybrid" chemotherapy protocols. **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. 596-600.

Question 293: Appearance of characteristic “burr cells”, “helmet cells” and “triangle cells” in peripheral blood smears is indicative of:

A. Polychromasia
B. Anisocytosis
C. Poikilocytosis
D. Schistocytosis (Correct Answer)

Explanation: The presence of fragmented red blood cells, such as **burr cells (echinocytes)**, **helmet cells**, and **triangle cells**, is the hallmark of **Schistocytosis**. 1. **Why Schistocytosis is correct:** Schistocytes are fragmented parts of red blood cells formed when the RBC membrane is mechanically severed. This typically occurs in **Microangiopathic Hemolytic Anemia (MAHA)**, such as TTP, HUS, or DIC, where fibrin strands in small vessels "slice" the RBCs as they pass through. They are also seen in mechanical heart valve-induced hemolysis. 2. **Why other options are incorrect:** * **Polychromasia:** Refers to the presence of young, bluish-grey RBCs (reticulocytes) on a peripheral smear, indicating active erythropoiesis in the bone marrow. * **Anisocytosis:** Refers to a variation in the **size** of RBCs (measured by RDW). It is a non-specific finding seen in most anemias (e.g., Iron Deficiency Anemia). * **Poikilocytosis:** This is a general umbrella term for any variation in the **shape** of RBCs. While schistocytes are a type of poikilocyte, "Schistocytosis" is the specific and most accurate clinical term for the fragments described in the question. **NEET-PG High-Yield Pearls:** * **Burr cells (Echinocytes):** Characterized by small, uniform blunt projections. Commonly seen in **Uremia** and chronic kidney disease. * **Acanthocytes (Spur cells):** Irregular, sharp projections. Seen in **Abetalipoproteinemia** and Liver disease. * **Bite cells (Degmacytes):** Result from splenic macrophages pitting out Heinz bodies. Diagnostic of **G6PD Deficiency** [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. 642-643.

Question 294: Which of the following is a Vitamin K dependent clotting factor?

A. Factor VII (Correct Answer)
B. Factor I
C. Factor XI
D. Factor XII

Explanation: **Explanation:** Vitamin K is an essential cofactor for the post-translational modification of specific clotting factors [1]. It facilitates the **gamma-carboxylation of glutamic acid residues** [2], a process necessary for these factors to bind calcium and adhere to phospholipid surfaces during the coagulation cascade. **Why Factor VII is correct:** The Vitamin K-dependent factors include **Factors II (Prothrombin), VII, IX, and X**, as well as the anticoagulant proteins **Protein C and Protein S** [1]. Factor VII has the shortest half-life (approx. 6 hours) among these, making it the first factor to decline in Vitamin K deficiency or at the start of Warfarin therapy. This is why the Prothrombin Time (PT/INR) is the first lab value to prolong in these conditions. **Analysis of Incorrect Options:** * **Factor I (Fibrinogen):** This is a soluble plasma glycoprotein synthesized in the liver, but its production does not require Vitamin K. * **Factor XI (Plasma Thromboplastin Antecedent):** Part of the intrinsic pathway; its synthesis is independent of Vitamin K. * **Factor XII (Hageman Factor):** The factor that initiates the intrinsic pathway upon contact with negative surfaces; it is not Vitamin K-dependent. **High-Yield Clinical Pearls for NEET-PG:** * **Warfarin Mechanism:** Inhibits **Vitamin K Epoxide Reductase (VKOR)**, preventing the recycling of Vitamin K [1]. * **Mnemonic:** Remember **"1972"** (Factors 10, 9, 7, and 2) to recall the Vitamin K-dependent factors. * **Newborns:** They are Vitamin K deficient due to a sterile gut and poor placental transfer; hence, a prophylactic Vitamin K injection is given at birth to prevent **Hemorrhagic Disease of the Newborn** [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 624-625. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 622-623.

Question 295: In microangiopathic hemolytic anemia, what type of red blood cells are typically seen?

A. Fragmented RBCs
B. Schistocytes (Correct Answer)
C. Spherocytes
D. Anisocytes

Explanation: **Explanation:** **Microangiopathic Hemolytic Anemia (MAHA)** is characterized by the mechanical destruction of red blood cells (intravascular hemolysis) as they pass through small vessels partially occluded by microthrombi (fibrin or platelet plugs) [1]. **Why Schistocytes are correct:** As RBCs attempt to squeeze through these narrowed, fibrin-rich vascular channels, they are physically "sliced" or sheared by the fibrin strands. This mechanical trauma results in fragmented, irregularly shaped RBC remnants [1] known as **Schistocytes** (also called helmet cells or triangle cells). Their presence on a peripheral blood smear is the hallmark of MAHA. **Analysis of Incorrect Options:** * **Fragmented RBCs (Option A):** While schistocytes are technically fragmented RBCs, "Schistocyte" is the specific morphological term used in hematopathology. In NEET-PG, always choose the most specific medical term provided. * **Spherocytes (Option C):** These are small, round RBCs lacking central pallor, typically seen in **Hereditary Spherocytosis** or **Autoimmune Hemolytic Anemia (AIHA)**, where splenic macrophages "bite" off portions of the cell membrane. * **Anisocytes (Option D):** This term refers to a variation in RBC **size** (measured by RDW). While seen in many anemias (like Iron Deficiency), it is not the diagnostic feature of MAHA. **Clinical Pearls for NEET-PG:** * **Classic Triad of MAHA:** Anemia, Schistocytes on smear, and elevated LDH/low haptoglobin. * **Key Conditions:** MAHA is seen in **TTP** (ADAMTS13 deficiency), **HUS** (Shiga toxin), **DIC**, and Malignant Hypertension [1]. * **Coombs Test:** MAHA is characteristically **Coombs Negative** (distinguishing it from AIHA). **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. 540-541.

Question 296: What bone marrow finding is characteristic of myelofibrosis?

A. Leucoerythroblastosis
B. Tear drop cells
C. Leucocytopenia
D. All of the above (Correct Answer)

Explanation: **Explanation:** Primary Myelofibrosis (PMF) is a chronic myeloproliferative neoplasm characterized by the clonal proliferation of megakaryocytes which release cytokines (like TGF-β), leading to reactive **bone marrow fibrosis** (collagen deposition) [2]. **Why "All of the above" is correct:** The pathophysiology of myelofibrosis explains all the listed findings: * **Leucoerythroblastosis:** As the marrow becomes fibrotic ("dry tap" on aspiration), hematopoiesis shifts to extramedullary sites like the spleen and liver [1]. These organs lack the "blood-bone marrow barrier," allowing immature white cells (myelocytes) and nucleated red cells to escape into the peripheral blood [1]. * **Tear drop cells (Dacrocytes):** As red blood cells attempt to squeeze through the narrow, fibrotic slits of the marrow or the distorted splenic sinuses, they undergo mechanical stretching, resulting in their characteristic "tear drop" shape [1]. * **Leucocytopenia:** While early stages may show leukocytosis, the progressive replacement of marrow space by dense fibrous tissue (spent phase) eventually leads to **pancytopenia** (anemia, leucocytopenia, and thrombocytopenia) [2]. **High-Yield Clinical Pearls for NEET-PG:** * **JAK2 V617F Mutation:** Present in approximately 50-60% of cases [3]. Other mutations include **CALR** and **MPL**. * **Splenomegaly:** PMF often presents with "Massive Splenomegaly" due to compensatory extramedullary hematopoiesis [1]. * **Silver Stain:** Reticulin fibers are best demonstrated using silver impregnation stains. * **Dry Tap:** A hallmark finding during bone marrow aspiration; diagnosis requires a **trephine biopsy** [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, pp. 628-629. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 615-616. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615.

Question 297: A patient with cirrhosis of the liver has the following coagulation parameters: Platelet count 2,00,000/µL, Prothrombin time 25s (control 12s), Activated partial thromboplastin time 60s (control 35s), Thrombin time 15s (control 15s). What is expected in this patient?

A. D-dimer will be normal (Correct Answer)
B. Fibrinogen will be <100 mg/dL
C. Antithrombin III will be high
D. Protein C will be elevated

Explanation: **Explanation:** In chronic liver disease (cirrhosis), the liver's synthetic function is impaired, leading to a decrease in almost all coagulation factors (except Factor VIII and von Willebrand Factor) [1]. This results in a prolonged **Prothrombin Time (PT)** and **Activated Partial Thromboplastin Time (aPTT)** [2]. **1. Why Option A is Correct:** The **Thrombin Time (TT)** in this patient is normal (15s), which indicates that fibrinogen levels are quantitatively and qualitatively sufficient to form a clot. **D-dimer** is a degradation product of cross-linked fibrin. In stable cirrhosis, while there is decreased synthesis of factors, there is no massive systemic activation of the coagulation-fibrinolysis cycle (unlike in DIC). Therefore, D-dimer levels remain normal. Unlike DIC, factor VIII is typically not consumed in liver disease [2]. **2. Why Incorrect Options are Wrong:** * **Option B:** A normal Thrombin Time (15s) effectively rules out significant hypofibrinogenemia (<100 mg/dL). Fibrinogen is an acute-phase reactant and often remains in the normal range until end-stage liver failure. * **Option C & D:** The liver synthesizes natural anticoagulants like **Antithrombin III, Protein C, and Protein S** [1]. In cirrhosis, the levels of these proteins **decrease** alongside procoagulant factors [3]. They would be low, not high or elevated. **Clinical Pearls for NEET-PG:** * **PT** is the most sensitive marker for liver synthetic function due to the short half-life of Factor VII [1]. * **Factor VIII** is NOT synthesized by hepatocytes (it is made in sinusoidal endothelial cells); thus, it is often normal or elevated in liver disease [2]. * **DIC vs. Liver Disease:** Both show prolonged PT/aPTT and low platelets, but **elevated D-dimer** and **low Factor VIII** specifically point toward DIC [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 396-398.

Question 298: Direct Coombs test positive is seen in all of the following conditions EXCEPT?

A. ABO incompatibility
B. Hemolytic disease of the newborn
C. Aplastic anemia (Correct Answer)
D. Autoimmune hemolysis

Explanation: **Explanation:** The **Direct Coombs Test (Direct Antiglobulin Test - DAT)** is used to detect antibodies (IgG) or complement (C3) that are already bound to the surface of red blood cells (RBCs) *in vivo*. A positive result indicates immune-mediated hemolysis. **Why Aplastic Anemia is the correct answer:** Aplastic anemia is a **hypoproliferative bone marrow failure** syndrome characterized by pancytopenia and a hypocellular marrow [3]. It is not an immune-mediated hemolytic process; rather, it involves a lack of production of all blood cell lines [3]. Therefore, there are no antibodies coating the RBCs, making the Direct Coombs test **negative**. **Analysis of other options:** * **ABO Incompatibility:** This involves a reaction where maternal antibodies (anti-A or anti-B) bind to the fetal RBCs. While the DAT can sometimes be weakly positive or even negative in ABO incompatibility compared to Rh incompatibility, it is classically considered a cause of a positive Direct Coombs test [1]. * **Hemolytic Disease of the Newborn (HDN):** Most commonly due to Rh isoimmunization (Rh-negative mother, Rh-positive fetus). Maternal IgG crosses the placenta and coats fetal RBCs, leading to a **strongly positive** Direct Coombs test in the newborn [2]. * **Autoimmune Hemolysis (AIHA):** This is the prototype for a positive DAT. In Warm AIHA (IgG) and Cold Agglutinin Disease (C3), the test detects the immune proteins coating the patient's own erythrocytes [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Direct Coombs:** Detects antibodies **on** the RBC surface (used for AIHA, HDN, Transfusion reactions). * **Indirect Coombs:** Detects antibodies **in** the serum (used for cross-matching and prenatal screening). * **Drug-induced AIHA:** Common culprits like **Methyldopa** or Penicillin can cause a positive Direct Coombs test [4]. * **Aplastic Anemia Hallmark:** Low reticulocyte count (distinguishes it from hemolytic anemias where reticulocytes are high) [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-604. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 662-663. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 651-652.

Question 299: A 7-month-old child presents with failure to thrive and a hemoglobin level of 4.4 g/dL. Peripheral smear examination reveals very small red blood cells with marked pallor. Laboratory tests show very low levels of hemoglobin A, with elevated fractions of hemoglobin A2 and hemoglobin F. Which of the following underlying mechanisms is most likely responsible for these findings?

A. Amino acid substitution on the beta-globin chain
B. Antibody against fetal red blood cells
C. Defect in cytoskeletal proteins
D. Insufficient production of beta-globin (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Insufficient production of beta-globin** The clinical presentation is classic for **Beta-Thalassemia Major**. At 7 months of age, the physiological switch from fetal hemoglobin (HbF) to adult hemoglobin (HbA) is nearly complete [1]. In Beta-Thalassemia, a genetic mutation leads to **insufficient production of $\beta$-globin chains** [2]. * **Mechanism:** Reduced $\beta$-globin leads to a deficiency of HbA ($\alpha_2\beta_2$). To compensate, the body continues to produce $\gamma$ and $\delta$ chains, resulting in **elevated HbF ($\alpha_2\gamma_2$) and HbA2 ($\alpha_2\delta_2$)** [1]. * **Morphology:** The excess unpaired $\alpha$-chains precipitate, causing intramedullary hemolysis (ineffective erythropoiesis) and severe **microcytic hypochromic anemia** (marked pallor and small RBCs) [1]. --- ### Why the other options are incorrect: * **A. Amino acid substitution on the beta-globin chain:** This describes **Sickle Cell Anemia** (Glutamic acid replaced by Valine at the 6th position). While it involves the $\beta$-chain, it typically presents with sickle cells and target cells, not a primary deficiency of HbA production. * **B. Antibody against fetal red blood cells:** This refers to **Hemolytic Disease of the Newborn (HDN)**. This causes macrocytic or normocytic anemia with spherocytes and a positive Coombs test, not microcytic anemia with elevated HbA2. * **C. Defect in cytoskeletal proteins:** This is the hallmark of **Hereditary Spherocytosis** (e.g., Spectrin or Ankyrin deficiency). It presents with spherocytes on peripheral smear and an increased MCHC, rather than microcytosis with Hb electrophoresis changes. --- ### NEET-PG High-Yield Pearls: * **Diagnosis:** Hb Electrophoresis is the gold standard. In $\beta$-Thal Major, HbA is nearly absent, HbF is significantly raised (up to 90%), and HbA2 is variable/elevated [1]. * **X-ray finding:** "Crew-cut" appearance of the skull due to compensatory extramedullary hematopoiesis [3]. * **Peripheral Smear:** Microcytic hypochromic RBCs, Target cells, and nucleated RBCs (normoblasts). * **Mentzer Index:** (MCV/RBC count) < 13 suggests Thalassemia; > 13 suggests Iron Deficiency Anemia. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 648. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 646-647. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 648-649.

Question 300: Which of the following characterizes Chronic Lymphocytic Leukemia (CLL)?

A. Presence of small lymphocytes in peripheral smear
B. Commonly seen in individuals over 50 years of age
C. Hepatosplenomegaly
D. All of the above (Correct Answer)

Explanation: **Explanation:** Chronic Lymphocytic Leukemia (CLL) is a monoclonal proliferation of mature-appearing B-lymphocytes and is the most common leukemia in the Western world [1]. * **Option A:** The hallmark of CLL is the accumulation of **small, mature-looking lymphocytes** with clumped "soccer-ball" chromatin. Due to their fragility, these cells often rupture during smear preparation, forming characteristic **Smudge cells** (Basket cells) [1]. * **Option B:** CLL is predominantly a disease of the **elderly**, with a median age at diagnosis of around 70 years [2]. It is rarely seen in individuals under 40, making "over 50 years" a highly characteristic demographic [2]. * **Option C:** As a systemic lymphoproliferative disorder, malignant cells infiltrate the reticuloendothelial system. This leads to painless generalized lymphadenopathy and **hepatosplenomegaly** in a significant number of patients. Since all three clinical and morphological features are classic presentations of the disease, **Option D** is the correct answer. **High-Yield NEET-PG Pearls:** * **Immunophenotype:** CLL cells characteristically express **CD5** (a T-cell marker), **CD19, CD20, and CD23** [1]. * **Richter Transformation:** In 5-10% of cases, CLL can transform into a high-grade **Diffuse Large B-cell Lymphoma (DLBCL)**, signaled by sudden clinical worsening. * **Diagnosis:** A persistent absolute lymphocyte count of **>5,000/µL** is required for diagnosis. * **Prognosis:** ZAP-70 expression and unmutated IgVH genes indicate a poorer prognosis. **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. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 612-613.

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Thrombotic Disorders

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