Hematopathology — MCQs

A 25-year-old asymptomatic female underwent a preoperative coagulation test. Her bleeding time (BT) is 3 minutes, prothrombin time (PT) is 15/14 seconds, activated partial thromboplastin time (aPTT) is 45/35 seconds, platelet count is 2.5 lac/mm3, and factor VIII levels were 60 IU/dL. She most likely has:

Q970Medium

All the following cause extravascular hemolysis except?

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 961: Hemoglobinuria may be seen in all of the following conditions EXCEPT?

A. Mismatched blood transfusion
B. Paroxysmal cold hemoglobinuria
C. Thermal burns
D. Hereditary spherocytosis (Correct Answer)

Explanation: The presence of hemoglobin in urine (hemoglobinuria) is a hallmark of **intravascular hemolysis**, where red blood cells (RBCs) rupture within the blood vessels, releasing free hemoglobin into the plasma [1]. When the haptoglobin-binding capacity is saturated, the excess hemoglobin is filtered by the glomeruli [1]. **Why Hereditary Spherocytosis (HS) is the correct answer:** HS is the classic example of **extravascular hemolysis**. In HS, a defect in the RBC membrane proteins (like ankyrin or spectrin) leads to the formation of spherical, rigid cells [2]. These spherocytes are trapped and destroyed by splenic macrophages in the splenic cords [2]. Since the destruction occurs outside the circulation, free hemoglobin is not released into the plasma, and thus, **hemoglobinuria does not occur.** **Analysis of Incorrect Options:** * **Mismatched Blood Transfusion:** This causes an acute hemolytic transfusion reaction (Type II hypersensitivity). Complement-mediated lysis of donor RBCs occurs directly in the bloodstream, leading to massive intravascular hemolysis and hemoglobinuria. * **Paroxysmal Cold Hemoglobinuria (PCH):** This is caused by the Donath-Landsteiner antibody (IgG). It binds to RBCs at low temperatures and fixes complement, which then causes potent intravascular lysis upon rewarming. * **Thermal Burns:** Severe heat injury can cause direct physical damage to RBC membranes as they pass through heated tissues, leading to immediate intravascular fragmentation and hemoglobinuria. **NEET-PG High-Yield Pearls:** * **Intravascular Hemolysis markers:** ↓ Haptoglobin, ↑ Indirect Bilirubin, Hemoglobinuria, and Hemosiderinuria [1]. * **Extravascular Hemolysis markers:** Splenomegaly, ↑ Indirect Bilirubin, and Spherocytes on peripheral smear (no hemoglobinuria) [1][2]. * **Gold Standard Test for HS:** Osmotic Fragility Test (now increasingly replaced by the Eosin-5-maleimide (EMA) binding test). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 639-640. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603.

Question 962: What is the finding seen in DIC?

A. Increased fibrinogen, increased antithrombin III, increased thrombin-antithrombin III complexes
B. Increased FDP, decreased PT, increased antithrombin III
C. Increased FDP, prolonged PT, increased thrombin-antithrombin complexes
D. Increased FDP, prolonged PT, reduced platelets (Correct Answer)

Explanation: **Explanation:** Disseminated Intravascular Coagulation (DIC) is a **consumptive coagulopathy** characterized by the systemic activation of the coagulation cascade, leading to widespread microthrombi and subsequent depletion of clotting factors and platelets [1]. 1. **Why Option D is Correct:** * **Increased FDP (Fibrin Degradation Products):** As microthrombi form, the fibrinolytic system is activated to break them down, resulting in elevated FDPs and **D-dimers** (the most specific marker) [1]. * **Prolonged PT (Prothrombin Time):** Massive consumption of clotting factors (Factors V, VIII, and Prothrombin) leads to prolongation of PT, aPTT, and Thrombin Time [1]. * **Reduced Platelets:** Platelets are consumed during the formation of extensive systemic microthrombi, leading to thrombocytopenia [1]. 2. **Why Other Options are Incorrect:** * **Option A & B:** In DIC, **Fibrinogen** and **Antithrombin III** levels are **decreased**, not increased, because they are consumed during the uncontrolled clotting process [1]. * **Option C:** While FDP and Thrombin-Antithrombin complexes are increased, this option is less comprehensive than D for a clinical diagnosis. Furthermore, the hallmark of DIC is the "consumption" of cellular elements (platelets), making Option D the classic laboratory profile [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Peripheral Smear:** Look for **Schistocytes** (fragmented RBCs) due to microangiopathic hemolytic anemia (MAHA) [1]. * **Best Screening Test:** Platelet count (usually low) [1]. * **Most Specific Test:** D-dimer (indicates cross-linked fibrin degradation). * **Common Triggers:** Sepsis (Gram-negative), Obstetric complications (Abruptio placentae), and Malignancy (APML - M3 variant). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626.

Question 963: What are the cytogenetic abnormalities associated with lymphoplasmacytoid lymphoma?

A. t(9;14)(p13;q32) (Correct Answer)
B. t(2;5)(p23;q35)
C. t(11;14)(q13;q32)
D. t(14;18)(q32;q21)

Explanation: **Explanation:** **Lymphoplasmacytoid Lymphoma (LPL)**, often associated with **Waldenström Macroglobulinemia**, is a B-cell neoplasm characterized by the proliferation of small B lymphocytes, plasmacytoid lymphocytes, and plasma cells. [1] **Why Option A is correct:** The characteristic cytogenetic abnormality in LPL is **t(9;14)(p13;q32)**. This translocation involves the **PAX5 gene** on chromosome 9 and the **Immunoglobulin Heavy Chain (IgH) locus** on chromosome 14. This results in the overexpression of PAX5, a transcription factor essential for B-cell proliferation and differentiation, leading to the development of the lymphoma. **Analysis of Incorrect Options:** * **Option B: t(2;5)(p23;q35):** This is the hallmark of **Anaplastic Large Cell Lymphoma (ALCL)**, involving the *ALK* gene on chromosome 2 and the *NPM* gene on chromosome 5. * **Option C: t(11;14)(q13;q32):** This is diagnostic for **Mantle Cell Lymphoma**, leading to the overexpression of **Cyclin D1** (*PRAD1/BCL-1*). * **Option D: t(14;18)(q32;q21):** This is the classic translocation seen in **Follicular Lymphoma**, resulting in the overexpression of the anti-apoptotic protein **BCL-2**. **High-Yield Clinical Pearls for NEET-PG:** * **MYD88 L265P Mutation:** While t(9;14) is a known translocation, the **MYD88 L265P somatic mutation** is found in >90% of LPL cases and is a more frequent diagnostic marker in modern practice. * **Clinical Presentation:** Patients often present with **hyperviscosity syndrome** (due to monoclonal IgM paraprotein), hepatosplenomegaly, and lymphadenopathy. [1] * **Dutcher Bodies:** Look for PAS-positive intranuclear inclusions (Dutcher bodies) in malignant cells, which are highly suggestive of LPL. **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. 609-610.

Question 964: Transformation of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) into diffuse large B-cell lymphoma (DLBCL) is called?

A. Richter syndrome (Correct Answer)
B. Evans syndrome
C. Li Fraumeni syndrome
D. Kostmann syndrome

Explanation: ### Explanation **Correct Option: A. Richter Syndrome** Richter syndrome (or Richter transformation) refers to the sudden progression of **Chronic Lymphocytic Leukemia/Small Lymphocytic Lymphoma (CLL/SLL)** into a more aggressive high-grade non-Hodgkin lymphoma [1], most commonly **Diffuse Large B-cell Lymphoma (DLBCL)** (approx. 90-95%) or rarely Hodgkin Lymphoma. Clinically, it is characterized by a rapid increase in lymph node size, worsening systemic symptoms (B-symptoms), and a poor prognosis. **Incorrect Options:** * **B. Evans Syndrome:** An autoimmune condition defined by the simultaneous or sequential occurrence of Immune Thrombocytopenic Purpura (ITP) and Autoimmune Hemolytic Anemia (AIHA). While it can occur in CLL patients [1], it is not a transformation into a high-grade lymphoma. * **C. Li-Fraumeni Syndrome:** A cancer predisposition syndrome caused by germline mutations in the **TP53** tumor suppressor gene, leading to various early-onset cancers (SBLA syndrome: Sarcoma, Breast, Leukemia, Adrenal). * **D. Kostmann Syndrome:** Also known as Severe Congenital Neutropenia, it is an autosomal recessive disorder characterized by a maturation arrest of neutrophil precursors in the bone marrow. **High-Yield Clinical Pearls for NEET-PG:** * **Incidence:** Occurs in approximately 2–10% of CLL patients. * **Genetic Marker:** Often associated with **NOTCH1** mutations, TP53 disruptions, and CDKN2A deletions. * **Diagnosis:** PET-CT is useful to identify the site of transformation (high SUV uptake), but **Excisional Lymph Node Biopsy** is the gold standard. * **Morphology:** Look for large cells with prominent nucleoli (centroblasts/immunoblasts) replacing the previous small lymphocyte architecture. **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 965: Which CD marker is specific for the myeloid series?

A. CD34
B. CD45
C. CD99
D. CD117 (Correct Answer)

Explanation: **CD117 (c-kit)** is a transmembrane tyrosine kinase receptor that is highly expressed on hematopoietic stem cells and committed myeloid progenitors. In the context of hematopathology, it is considered a **specific marker for the myeloid series**, particularly in the diagnosis of **Acute Myeloid Leukemia (AML)**. While it is also found on mast cells and interstitial cells of Cajal, its presence in a blast population strongly indicates myeloid differentiation [1]. **Analysis of Incorrect Options:** * **CD34:** This is a marker of **hematopoietic stem cells (HSCs)** and primitive progenitors. It is not lineage-specific, as it is expressed in both lymphoblasts (ALL) and myeloblasts (AML). * **CD45:** Known as the **Leukocyte Common Antigen (LCA)**, it is expressed on almost all white blood cells. It is a pan-leukocyte marker, not specific to the myeloid series. * **CD99:** This marker is classically associated with **Ewing sarcoma/PNET**. In hematology, it can be expressed in T-cell lymphoblastic lymphoma, but it lacks specificity for myeloid cells. **Clinical Pearls for NEET-PG:** * **MPO (Myeloperoxidase):** The most specific gold-standard marker for myeloid differentiation (detected via cytochemistry or IHC). * **CD13 & CD33:** Other common pan-myeloid markers used in flow cytometry [2]. * **CD117 & GIST:** Beyond AML, CD117 is the diagnostic marker for **Gastrointestinal Stromar Tumors (GIST)**, where it serves as a target for Imatinib therapy. * **Systemic Mastocytosis:** CD117 is also a key marker for identifying neoplastic mast cells [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. 620-625. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 609-611.

Question 966: Absolute monocytosis is seen in which of the following conditions?

A. Brucellosis
B. Kala-azar
C. Tuberculosis
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Absolute monocytosis** is defined as a peripheral blood monocyte count exceeding **800/µL** in adults. Monocytes are the precursors to macrophages and are primarily involved in the body’s response to chronic infections, granulomatous diseases, and certain malignancies [2]. **Why "All of the above" is correct:** The underlying medical concept is that monocytes are recruited in diseases where **cell-mediated immunity** is the primary defense mechanism [3]. 1. **Tuberculosis (C):** This is the classic cause of monocytosis [1]. Monocytes are recruited to the site of infection to differentiate into epithelioid cells and Langhans giant cells to form granulomas [3]. 2. **Brucellosis (A) and Kala-azar (B):** Both are chronic intracellular infections. In Brucellosis, the bacteria reside within the reticuloendothelial system. In Kala-azar (Visceral Leishmaniasis), the parasite *Leishmania donovani* infects the macrophages themselves. Both conditions trigger a compensatory increase in monocyte production to replace and support the phagocytic system [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Monocytosis (STAMPS):** **S**yphilis [3], **T**uberculosis [1], **A**mibiases, **M**onocytic Leukemia (AMML M5), **P**rotozoal infections (Malaria/Kala-azar), and **S**arcoidosis. * **Subacute Bacterial Endocarditis (SBE):** Often presents with monocytosis and is a frequent "distractor" or alternative correct option in exams. * **CMML (Chronic Myelomonocytic Leukemia):** Suspect this if monocytosis is persistent (>3 months) and >1000/µL in an elderly patient. * **Recovery phase:** Monocytosis is often a sign of recovery from acute infections or bone marrow suppression (e.g., post-chemotherapy). **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. 195-196. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 580-581. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360.

Question 967: What is the anticoagulant of choice for the Wintrobe method of ESR determination?

A. Citrate
B. Heparin (Correct Answer)
C. Oxalate
D. EDTA

Explanation: **Explanation:** The **Wintrobe method** is a traditional technique used to determine the Erythrocyte Sedimentation Rate (ESR) and Packed Cell Volume (PCV). The anticoagulant of choice for this method is **Heparin** (specifically ammonium heparin or balanced heparin), as it does not alter the size or shape of the red blood cells, ensuring accurate sedimentation and volume measurement. **Analysis of Options:** * **Heparin (Correct):** It acts by activating antithrombin III. It is preferred in the Wintrobe method because it prevents hemolysis and does not cause shrinkage or swelling of erythrocytes, which is critical for the simultaneous measurement of PCV. * **Citrate (Incorrect):** Sodium citrate (3.8%) is the anticoagulant of choice for the **Westergren method** (the gold standard for ESR). It is used in a 1:4 ratio. Using it in the Wintrobe method would dilute the sample significantly, leading to inaccurate results. * **Oxalate (Incorrect):** While "Double Oxalate" (Wintrobe’s mixture) was historically used, it is less preferred today because potassium oxalate can cause RBC shrinkage, potentially affecting the ESR and PCV readings. * **EDTA (Incorrect):** While EDTA is the standard for routine hematology (CBC), it is not the traditional choice for the Wintrobe method as it can lead to cell shrinkage over time, falsely increasing the ESR. **High-Yield Clinical Pearls for NEET-PG:** * **Wintrobe Tube:** 110 mm long, 3 mm bore. It measures both ESR (0–100 mm) and PCV (0–100%). * **Westergren Tube:** 300 mm long, 2.5 mm bore. It is more sensitive for ESR because of the greater column height. * **Ratio:** Westergren uses 4 parts blood to 1 part citrate; Wintrobe uses undiluted heparinized blood. * **Fact:** ESR is a non-specific marker of inflammation, primarily driven by **Fibrinogen** (the most potent pro-sedimentation factor).

Question 968: In anemia due to lead poisoning, what will the bone marrow characteristically show?

A. Dwarf megakaryocyte
B. Ring sideroblasts
C. Pelger-Huet anomaly
D. Basophilic stippling (Correct Answer)

Explanation: **Explanation:** **Correct Answer: D. Basophilic stippling** Lead poisoning (Plumbism) interferes with the activity of the enzyme **5'-nucleotidase**, which is responsible for the degradation of ribosomal RNA. This inhibition leads to the persistence of ribosomal RNA aggregates within the cytoplasm of erythrocytes, appearing as fine, blue granules known as **basophilic stippling**. While this is classically seen in the peripheral smear, it is a characteristic finding in the erythroid precursors of the bone marrow in lead-affected erythropoiesis. **Analysis of Incorrect Options:** * **A. Dwarf megakaryocyte (Micromegakaryocyte):** These are characteristic of **Myelodysplastic Syndromes (MDS)** and certain types of Myeloid Leukemias. They are not associated with lead toxicity. * **B. Ring sideroblasts:** While lead poisoning inhibits ferrochelatase (leading to iron accumulation in mitochondria), **Ring sideroblasts** are the hallmark of **Sideroblastic Anemia**. In the context of NEET-PG, if both are options, Basophilic Stippling is the more "characteristic" morphological finding for lead, whereas Ring Sideroblasts are more specific to MDS (RARS) or hereditary sideroblastic anemia. * **C. Pelger-Huet anomaly:** This refers to hyposegmented neutrophils (pince-nez appearance). It is seen in **MDS (Pseudo-Pelger Huet)** or as a benign autosomal dominant condition. **Clinical Pearls for NEET-PG:** * **Enzymes inhibited by Lead:** δ-aminolevulinic acid dehydratase (ALA-D) and Ferrochelatase. * **Clinical Signs:** Burtonian lines (lead lines on gums), wrist drop/foot drop (peripheral neuropathy), and colic [1]. * **Radiology:** "Lead lines" at the metaphysis of long bones in children [1]. * **Treatment:** Chelation therapy with Succimer (oral), Ca-EDTA, or British Anti-Lewisite (BAL). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 418-419.

Question 969: A 25-year-old asymptomatic female underwent a preoperative coagulation test. Her bleeding time (BT) is 3 minutes, prothrombin time (PT) is 15/14 seconds, activated partial thromboplastin time (aPTT) is 45/35 seconds, platelet count is 2.5 lac/mm3, and factor VIII levels were 60 IU/dL. She most likely has:

A. Factor IX deficiency
B. Von-Willebrands disease type III
C. Factor VIII inhibitors (Correct Answer)
D. Lupus anticoagulant

Explanation: ### Explanation **1. Analysis of the Correct Answer (Factor VIII Inhibitors):** The patient presents with an **isolated prolongation of aPTT** (45/35 seconds), while the PT, BT, and platelet count are within normal limits. This indicates a defect in the **intrinsic pathway** (Factors VIII, IX, XI, or XII). The key to this question lies in the **Factor VIII level (60 IU/dL)**, which is within the normal range (50–150 IU/dL). In Hemophilia A (deficiency) or VWD, the Factor VIII levels would be significantly low [2]. The presence of **Factor VIII inhibitors** (acquired antibodies) can interfere with the *in vitro* aPTT assay, causing a prolongation despite a seemingly normal quantitative level of the factor, or it may represent a low-titer inhibitor in an asymptomatic patient [1]. In clinical practice, a **Mixing Study** would be the next step; failure to correct the aPTT suggests an inhibitor. **2. Why the Other Options are Incorrect:** * **Factor IX deficiency (Hemophilia B):** While this causes an isolated prolonged aPTT, it would not explain why the question specifies a normal Factor VIII level. * **Von-Willebrand Disease (VWD) Type III:** This is the most severe form of VWD. It presents with a **prolonged BT** (due to lack of VWF) and a **very low Factor VIII level** (usually <10%), as VWF is required to stabilize Factor VIII. * **Lupus Anticoagulant (LA):** While LA prolongs aPTT and is an inhibitor, it is typically associated with a history of thrombosis or pregnancy loss, not an incidental preoperative finding in an asymptomatic patient without further specific testing (like DRVVT) [3]. However, in the context of standardized exams, if Factor VIII levels are normal but aPTT is high, specific factor inhibitors are the preferred answer. **3. Clinical Pearls for NEET-PG:** * **Isolated ↑ PT:** Factor VII deficiency (Extrinsic pathway). * **Isolated ↑ aPTT:** Factors VIII, IX, XI, XII, or Heparin. * **↑ PT and ↑ aPTT:** Common pathway (Factors X, V, II, I) or Vitamin K deficiency. * **Mixing Study:** If aPTT corrects with normal plasma = Factor deficiency; if it does **not** correct = Inhibitor (e.g., Factor VIII inhibitor or Lupus Anticoagulant). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 624-625. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 670-671. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 664-665.

Question 970: All the following cause extravascular hemolysis except?

A. Hereditary spherocytosis
B. Thalassemia
C. Autoimmune hemolytic anemia
D. Blood transfusion reaction (Correct Answer)

Explanation: **Explanation:** The distinction between intravascular and extravascular hemolysis is a high-yield concept in hematopathology. Hemolysis is classified based on where the red blood cell (RBC) destruction occurs. **Why "Blood Transfusion Reaction" is the correct answer:** Acute Hemolytic Transfusion Reactions (AHTR), typically due to ABO incompatibility, are the classic example of **intravascular hemolysis**. In this scenario, pre-formed IgM antibodies bind to donor RBCs, activating the complement cascade up to the Membrane Attack Complex (MAC). This leads to immediate RBC lysis within the circulation, causing hemoglobinemia and hemoglobinuria. [1] **Analysis of Incorrect Options (Extravascular Hemolysis):** Extravascular hemolysis occurs when RBCs are sequestered and destroyed by macrophages in the splenic sinusoids or liver. * **Hereditary Spherocytosis:** A membrane defect (e.g., ankyrin/spectrin deficiency) makes RBCs spherical and rigid. These cells cannot deform to pass through splenic cords and are trapped and destroyed by splenic macrophages. [3] * **Thalassemia:** Globin chain imbalance leads to the precipitation of unpaired chains (Heinz bodies), which damage the RBC membrane. These damaged cells are cleared by the spleen. [4] * **Autoimmune Hemolytic Anemia (AIHA):** Specifically the **Warm-type (IgG)**. IgG-coated RBCs are partially "nibbled" by splenic macrophages, turning them into spherocytes before eventual destruction in the spleen. [2] **Clinical Pearls for NEET-PG:** * **Extravascular Hemolysis:** Characterized by **Splenomegaly** and Jaundice. Haptoglobin may be normal or slightly low. * **Intravascular Hemolysis:** Characterized by **Hemoglobinuria**, Hemosiderinuria, and severely **low Haptoglobin**. [1] * **Exception:** Delayed hemolytic transfusion reactions (Rh incompatibility) are typically extravascular, but "Blood transfusion reaction" in a general MCQ context refers to the acute, life-threatening ABO-mediated intravascular event. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-652. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 601-602.

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