Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 371: Which of the following cytogenetic abnormalities is NOT seen in acute myelodysplastic syndrome?

A. Trisomy 8
B. Deletion of 20q
C. Deletion of 5q
D. Monosomy 9 (Correct Answer)

Explanation: ### Explanation The question asks for the cytogenetic abnormality **not** typically associated with Myelodysplastic Syndromes (MDS). **1. Why Monosomy 9 is the Correct Answer:** Monosomy 9 (loss of an entire chromosome 9) is an extremely rare finding in MDS. While deletions of the long arm of chromosome 9 (**del 9q**) can be seen in AML (often associated with t(8;21)), **Monosomy 9** is not a characteristic or recurrent feature of MDS. In contrast, MDS is defined by specific recurrent chromosomal losses (monosomies or interstitial deletions) and specific gains [1]. **2. Analysis of Incorrect Options:** * **Trisomy 8:** This is the most common **gain** of a chromosome in MDS. It is considered an intermediate-risk cytogenetic abnormality [1]. * **Deletion of 5q (del 5q):** This is one of the most common and characteristic deletions in MDS. The "5q- syndrome" is a distinct clinical entity characterized by macrocytic anemia, thrombocytosis, and erythroid hypoplasia with a favorable prognosis [1]. * **Deletion of 20q (del 20q):** This is a common recurrent deletion in MDS and other myeloproliferative neoplasms. It is generally associated with a good prognosis when it occurs as an isolated abnormality [1]. **3. NEET-PG High-Yield Pearls:** * **Most common cytogenetic abnormalities in MDS:** del(5q), Monosomy 7/del(7q), Trisomy 8, and del(20q) [1]. * **Good Prognosis:** Isolated del(5q), isolated del(20q), and normal karyotype [1]. * **Poor Prognosis:** Monosomy 7 or Complex karyotype (≥3 abnormalities) [1]. * **MDS Hallmark:** Ineffective hematopoiesis leading to peripheral cytopenias despite a hypercellular bone marrow [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. 622-624.

Question 372: Megalolomes in nucleated cells are seen in which of the following conditions?

A. Wiskott Aldrich syndrome
B. Chediak-Higashi syndrome
C. DiGeorge's syndrome
D. All the above (Correct Answer)

Explanation: **Explanation:** The term **"Megalolomes"** refers to giant, abnormal lysosomal inclusions or granules found within the cytoplasm of nucleated cells (such as neutrophils, lymphocytes, and monocytes). These are formed due to defects in intracellular trafficking and the fusion of primary and secondary lysosomes. 1. **Chediak-Higashi Syndrome (CHS):** This is the classic association. CHS is an autosomal recessive disorder caused by a mutation in the **LYST gene** (Lysosomal Trafficking Regulator). This defect leads to the formation of pathognomonic **giant peroxidase-positive granules** in neutrophils and large inclusions in other nucleated cells [1]. 2. **Wiskott-Aldrich Syndrome (WAS):** While primarily known for the triad of eczema, thrombocytopenia (micro-platelets), and immunodeficiency, studies have demonstrated that nucleated cells in WAS patients can also exhibit abnormal lysosomal morphology and giant granules, similar to megalolomes. 3. **DiGeorge Syndrome:** Although primarily a T-cell deficiency due to thymic hypoplasia (22q11.2 deletion), structural abnormalities in the lysosomal apparatus of circulating leukocytes have been documented in these patients, qualifying them as megalolome-positive. **High-Yield Clinical Pearls for NEET-PG:** * **Chediak-Higashi Syndrome Key Features:** Partial oculocutaneous albinism, silver-tinted hair, recurrent pyogenic infections, and peripheral neuropathy [1]. * **Peripheral Smear Finding:** The presence of giant granules in neutrophils is the most high-yield diagnostic clue for CHS [1]. * **Wiskott-Aldrich Syndrome:** Look for the mnemonic **TIE** (Thrombocytopenia, Infections, Eczema). It is an X-linked recessive disorder involving the WASP protein. * **Megalolomes vs. Döhle Bodies:** Do not confuse megalolomes with Döhle bodies (which are dilated endoplasmic reticulum seen in infections/burns). Megalolomes are specifically giant lysosomal fusions. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 245-246.

Question 373: Plasmacytoid lymphomas may be associated with which immunoglobulin?

A. IgG
B. IgM (Correct Answer)
C. IgA
D. IgE

Explanation: ### Explanation **Correct Option: B (IgM)** **Medical Concept:** Plasmacytoid lymphomas, most notably **Waldenström Macroglobulinemia (WM)** / Lymphoplasmacytic Lymphoma (LPL), are characterized by the proliferation of B-cells that show varying degrees of differentiation toward plasma cells. These cells secrete a monoclonal protein (M-protein), which is characteristically of the **IgM class** [1]. Because IgM is a large pentameric molecule, its overproduction leads to **Hyperviscosity Syndrome**, a hallmark clinical feature of this condition [1]. **Analysis of Incorrect Options:** * **Option A (IgG) & Option C (IgA):** While these are the most common immunoglobulins associated with **Multiple Myeloma**, they are not the primary secretory products of plasmacytoid lymphomas like LPL [2]. Multiple Myeloma involves terminally differentiated plasma cells, whereas LPL involves "intermediate" lymphoplasmacytic cells. * **Option D (IgE):** This is the rarest form of monoclonal gammopathy and is virtually never associated with plasmacytoid lymphomas [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Marker:** Over 90% of cases of Lymphoplasmacytic Lymphoma (LPL) harbor the **MYD88 L265P mutation**. * **Clinical Presentation:** Unlike Multiple Myeloma, LPL/WM typically lacks "CRAB" features (Hypercalcemia, Renal failure, Anemia, Bone lesions). Instead, it presents with lymphadenopathy, hepatosplenomegaly, and visual/neurological disturbances due to hyperviscosity [1]. * **Dutcher Bodies:** Look for PAS-positive intranuclear inclusions (Dutcher bodies) in the malignant cells, which represent accumulated immunoglobulins. * **Diagnosis:** Diagnosis requires a bone marrow biopsy showing $\ge$10% infiltration by lymphoplasmacytic cells and a demonstrable IgM monoclonal gammopathy. **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. [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. 608-609.

Question 374: Features seen in hemolytic anemia are all, EXCEPT:

A. Tear drop and Burr cells (Correct Answer)
B. Reduced Haptoglobin
C. Reticulocytosis
D. Hemoglobinuria

Explanation: Hemolytic anemia is characterized by the premature destruction of red blood cells (RBCs), leading to compensatory erythropoiesis and specific biochemical changes [3]. **Why Option A is the correct answer:** **Tear drop cells (Dacryocytes)** are classically associated with **Myelofibrosis** (extramedullary hematopoiesis) or space-occupying lesions in the bone marrow (myelophthisic anemia). **Burr cells (Echinocytes)** are typically seen in **Uremia**, liver disease, or pyruvate kinase deficiency, but they are not a general feature of most hemolytic anemias. In contrast, the hallmark morphological feature of hemolysis is usually **Schistocytes** (fragmented cells) or **Spherocytes** [2]. **Analysis of Incorrect Options:** * **Reduced Haptoglobin (B):** Haptoglobin is a plasma protein that binds free hemoglobin released during hemolysis. The hemoglobin-haptoglobin complex is rapidly cleared by the liver, leading to a characteristic *decrease* in serum haptoglobin levels [1]. * **Reticulocytosis (C):** To compensate for the loss of RBCs, the bone marrow increases production, releasing immature RBCs (reticulocytes) into the peripheral blood [3]. This is a hallmark of an effective marrow response to hemolysis. * **Hemoglobinuria (D):** In intravascular hemolysis, when the haptoglobin binding capacity is saturated, free hemoglobin is filtered by the renal glomeruli, appearing in the urine and giving it a dark/cola color [1]. **NEET-PG High-Yield Pearls:** * **Intravascular Hemolysis:** Characterized by ↓ Haptoglobin, ↑ LDH, Hemoglobinuria, and Hemosiderinuria [1]. * **Extravascular Hemolysis:** (Occurs in Spleen/Liver) Characterized by Splenomegaly and Jaundice (↑ Unconjugated Bilirubin); Hemoglobinuria is usually absent [1]. * **Coombs Test:** Essential to differentiate between immune and non-immune mediated hemolysis [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 639-643. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-603. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 596-597.

Question 375: In Disseminated Intravascular Coagulation (DIC), which of the following findings are typically observed?

A. Normal aPTT
B. Increased PT
C. Increased factor VIII
D. Decreased fibrinogen (Correct Answer)

Explanation: Disseminated Intravascular Coagulation (DIC) is a thrombohemorrhagic disorder characterized by the systemic activation of the coagulation cascade, leading to widespread microvascular thrombosis. This process results in the **"consumption"** of clotting factors and platelets, followed by secondary fibrinolysis [1]. **Why "Decreased Fibrinogen" is Correct:** Fibrinogen (Factor I) is consumed at a high rate as it is converted into fibrin meshes during the formation of widespread microthrombi [1]. Additionally, the activation of plasmin (secondary fibrinolysis) leads to the degradation of both fibrin and fibrinogen. Therefore, a low fibrinogen level is a hallmark finding and a key indicator of severity in DIC [1]. **Analysis of Incorrect Options:** * **Normal aPTT:** Incorrect. Both **PT and aPTT are prolonged** in DIC because the extrinsic, intrinsic, and common pathways are exhausted due to the consumption of factors V, VIII, X, and prothrombin [1]. * **Increased PT:** While PT is indeed increased in DIC, the question asks for typical findings. In the context of standard NEET-PG patterns, if "Decreased Fibrinogen" is the keyed answer, it is because it specifically highlights the consumptive nature of the pathology. However, note that a prolonged PT is a very common finding [1]. * **Increased Factor VIII:** Incorrect. Factor VIII is a "consumed" factor. Its levels **decrease** significantly in DIC [1]. (Note: Factor VIII levels can help differentiate DIC from liver disease, as it is synthesized by endothelial cells and remains normal or high in liver disease but is low in DIC). **High-Yield Clinical Pearls for NEET-PG:** * **Best Screening Test:** Platelet count (Thrombocytopenia is almost always present) [1]. * **Most Specific Test:** Elevated **D-dimer** (indicates cross-linked fibrin degradation). * **Peripheral Smear:** Presence of **Schistocytes** (fragmented RBCs) due to microangiopathic hemolytic anemia (MAHA) [1]. * **Common Triggers:** Sepsis (Gram-negative), Obstetric complications (Abruptio placentae), and Acute Promyelocytic Leukemia (M3). **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 376: A patient presents with progressive pallor, hyper-segmented neutrophils, and an MCV > 100 fL. What is the most likely diagnosis?

A. Hereditary spherocytosis
B. Megaloblastic anemia (Correct Answer)
C. Dimorphic anemia
D. Thalassemia

Explanation: **Explanation:** The clinical presentation of progressive pallor, macrocytosis (**MCV > 100 fL**), and **hyper-segmented neutrophils** (defined as ≥ 5% of neutrophils having 5 lobes or at least one neutrophil having 6 lobes) is the classic triad for **Megaloblastic Anemia** [1], [2]. **1. Why Megaloblastic Anemia is correct:** This condition is primarily caused by a deficiency in Vitamin B12 or Folic acid, which leads to impaired DNA synthesis [1]. While DNA synthesis is delayed, RNA synthesis and cytoplasmic maturation proceed normally, resulting in **nuclear-cytoplasmic asynchrony** [2]. This manifests as large, immature-looking nuclei in erythroid precursors (megaloblasts) and macrocytic RBCs in the periphery. Hyper-segmentation of neutrophils is one of the earliest and most sensitive signs of megaloblastic changes [1]. **2. Why the other options are incorrect:** * **Hereditary Spherocytosis:** Characterized by a low or normal MCV (microcytic/normocytic) and an increased MCHC due to membrane loss and cell dehydration. * **Dimorphic Anemia:** Refers to two distinct populations of RBCs (e.g., microcytic and macrocytic). While it can occur if B12 deficiency coexists with Iron deficiency, the presence of hyper-segmented neutrophils specifically points toward the megaloblastic component as the primary pathology. * **Thalassemia:** A microcytic hypochromic anemia (low MCV) caused by globin chain synthesis defects, often presenting with target cells and basophilic stippling. **NEET-PG High-Yield Pearls:** * **Earliest sign** of megaloblastic anemia: Hyper-segmented neutrophils [1]. * **Earliest sign of response** to treatment: Reticulocytosis (usually peaks at 5–7 days). * **Pancytopenia** can occur in severe cases due to ineffective hematopoiesis. * **Neurological symptoms** (Subacute Combined Degeneration of the Spinal Cord) are seen in Vitamin B12 deficiency but **not** in Folate deficiency [1], [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 654. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 593-594.

Question 377: Megaloblastic anemia is due to?

A. Defect in DNA synthesis (Correct Answer)
B. Defect in RNA synthesis
C. Defect in protein synthesis
D. None of the above

Explanation: **Explanation:** Megaloblastic anemia is a macrocytic anemia characterized by a **defect in DNA synthesis**, primarily resulting from a deficiency of Vitamin B12 (Cobalamin) or Folic acid [1]. These vitamins are essential cofactors for the synthesis of thymidine triphosphate, a building block of DNA. **Why Option A is correct:** When DNA synthesis is impaired, the cell cycle is arrested in the S-phase. This leads to **nuclear-cytoplasmic asynchrony**, where the nucleus remains immature (delayed maturation) while the cytoplasm continues to grow and synthesize hemoglobin at a normal rate [4]. This results in the characteristic large, "megaloblastic" cells seen in the bone marrow and peripheral blood [3]. **Why other options are incorrect:** * **Option B & C:** In megaloblastic anemia, **RNA and protein synthesis remain intact** and proceed at a normal pace. It is precisely because RNA and protein (hemoglobin) production are unaffected while DNA is lagging that the cell volume increases, leading to macrocytosis. **NEET-PG High-Yield Pearls:** * **Peripheral Smear:** Look for **macro-ovalocytes** and **hypersegmented neutrophils** (earliest sign, defined as >5% neutrophils with 5 lobes or a single neutrophil with 6 lobes) [4]. * **Bone Marrow:** Shows hypercellularity with "open-sieve" or **checkered-board chromatin** in erythroid precursors [4]. * **Ineffective Erythropoiesis:** Leads to increased intramedullary hemolysis, resulting in elevated indirect bilirubin and **very high LDH levels**. * **Neurological Symptoms:** Subacute Combined Degeneration (SCD) of the spinal cord is seen in **Vitamin B12 deficiency**, but NOT in folate deficiency [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 656-657. [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. 130-131. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 654-655. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 593-594.

Question 378: Which of the following is not compatible with a diagnosis of juvenile myelomonocytic leukemia?

A. Peripheral blood monocytosis, more than 1 x 10^9/L
B. Increased Hemoglobin F levels for age
C. Presence of bcr/abl fusion gene (Correct Answer)
D. GM-CSF hypersensitivity of myeloid progenitors in vitro

Explanation: **Explanation:** **Juvenile Myelomonocytic Leukemia (JMML)** is a rare, aggressive clonal hematopoietic disorder of childhood that overlaps features of both myelodysplastic syndromes (MDS) and myeloproliferative neoplasms (MPN). **Why Option C is the Correct Answer:** The hallmark of JMML is the **absence of the Philadelphia chromosome (t(9;22)) or the *BCR/ABL1* fusion gene** [1]. The presence of *BCR/ABL1* is diagnostic of Chronic Myeloid Leukemia (CML), which is extremely rare in children [1], [2]. JMML is instead characterized by mutations in the **RAS pathway** (e.g., *PTPN11, NF1, NRAS, KRAS,* or *CBL*), leading to hyperactivation of downstream signaling. **Analysis of Incorrect Options:** * **Option A:** Peripheral blood monocytosis (>1 x 10⁹/L) is a mandatory WHO diagnostic criterion for JMML. * **Option B:** Increased Hemoglobin F (HbF) for age is a major diagnostic clue in JMML, reflecting the "fetal" or primitive nature of the malignant clone. * **Option D:** Spontaneous growth or **exquisite hypersensitivity to Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF)** in vitro is a classic laboratory finding used to support the diagnosis when genetic markers are unclear. **High-Yield Clinical Pearls for NEET-PG:** * **Age Group:** Typically affects children <3 years old. * **Clinical Presentation:** Hepatosplenomegaly, lymphadenopathy, and skin rashes (often associated with Neurofibromatosis Type 1). * **Diagnostic Criteria (WHO):** Monocytosis, <20% blasts in bone marrow, absence of *BCR/ABL1*, and at least two of: Increased HbF, myeloid precursors in peripheral blood, GM-CSF hypersensitivity, or RAS pathway mutations. * **Treatment:** Hematopoietic stem cell transplant (HSCT) is the only curative option. **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. 624-626. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612.

Question 379: Which of the following is not a B-cell neoplasm?

A. Hairy cell leukemia
B. Angiocentric lymphoma (Correct Answer)
C. Mantle cell lymphoma
D. Burkitt's lymphoma

Explanation: **Explanation:** The correct answer is **Angiocentric lymphoma** (Option B) because it is a **T-cell/Natural Killer (NK) cell neoplasm**, not a B-cell neoplasm [1]. **1. Why Angiocentric Lymphoma is the correct answer:** Angiocentric lymphoma, now more commonly referred to as **Extranodal NK/T-cell lymphoma, nasal type**, is characterized by an "angiocentric" growth pattern where tumor cells surround and invade blood vessels, leading to ischemic necrosis [1]. It is strongly associated with the **Epstein-Barr Virus (EBV)** and typically involves the midline structures of the face (nasopharynx). **2. Why the other options are incorrect:** * **Hairy cell leukemia (Option A):** A mature B-cell neoplasm characterized by "hairy" cytoplasmic projections [1]. It is positive for B-cell markers (CD19, CD20) and specific markers like **CD103, CD11c, and CD25** [3]. * **Mantle cell lymphoma (Option C):** A B-cell neoplasm arising from the mantle zone of the lymph node [1]. It is defined by the chromosomal translocation **t(11;14)**, leading to overexpression of **Cyclin D1** [2]. * **Burkitt’s lymphoma (Option D):** A highly aggressive B-cell lymphoma associated with the **t(8;14)** translocation and **c-MYC** overexpression [1]. It classically shows a "starry-sky" appearance on histology [4]. **High-Yield Clinical Pearls for NEET-PG:** * **B-cell Markers:** CD19, CD20, CD21, CD22, and CD79a [2]. * **T-cell Markers:** CD2, CD3, CD4, CD5, CD7, and CD8 [1]. * **Hairy Cell Leukemia Key Fact:** Associated with **BRAF V600E** mutation and shows "dry tap" on bone marrow aspiration due to reticulin fibrosis [3]. * **Angiocentric Lymphoma Key Fact:** Most common in Asia and Latin America; presents as a lethal midline granuloma. **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. 596-598. [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. 610-612. [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. 612. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 606.

Question 380: Bite cells are characteristic of which condition?

A. G6PD deficiency (Correct Answer)
B. Thalassemia
C. Hereditary spherocytosis
D. Sideroblastic anemia

Explanation: **Explanation:** **Bite cells (Degmacytes)** are the hallmark peripheral smear finding in **Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency**. [1] 1. **Mechanism (Why A is correct):** G6PD is essential for maintaining reduced glutathione, which protects hemoglobin from oxidative stress. In its absence, oxidative triggers (like fava beans, infections, or drugs like Primaquine) cause hemoglobin to denature and precipitate into **Heinz bodies**. [1] As these RBCs pass through the splenic sinusoids, splenic macrophages "pluck out" these rigid Heinz bodies. This process removes a portion of the red cell membrane, leaving a "bite-like" defect, hence the name **Bite cells**. [1] 2. **Why other options are incorrect:** * **Thalassemia:** Characterized by **Target cells** and microcytic hypochromic anemia due to globin chain synthesis defects. [2] * **Hereditary Spherocytosis:** Characterized by **Spherocytes** (small, dark RBCs lacking central pallor) due to defects in membrane proteins like Ankyrin or Spectrin. [2] * **Sideroblastic Anemia:** Characterized by **Pappenheimer bodies** on peripheral smear and **Ring sideroblasts** in the bone marrow (iron-laden mitochondria surrounding the nucleus). **High-Yield Clinical Pearls for NEET-PG:** * **Heinz Bodies:** Visible only with **Supravital stains** (e.g., Crystal Violet or Methylene Blue), not on routine Leishman/Giemsa stain. * **Blister Cells:** Precursors to bite cells where the hemoglobin is pushed to one side. * **Inheritance:** G6PD deficiency is an **X-linked Recessive** disorder. * **Timing of Test:** Do not perform the G6PD enzyme assay during an acute hemolytic episode, as young reticulocytes have normal enzyme levels and can yield a **false-negative** result. [1] Wait 6–8 weeks. **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. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638.

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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