Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1471: Pappenheimer bodies are composed of:

A. Copper
B. Iron (Correct Answer)
C. Lead
D. Zinc

Explanation: ***Iron*** - **Pappenheimer bodies** are composed of **iron granules** that have not been incorporated into hemoglobin. - They appear as small, irregular, basophilic inclusions within red blood cells on a **Wright-Giemsa stain**. *Copper* - **Copper** is an essential trace element but does not form these specific erythrocyte inclusions. - Its presence in excess can lead to conditions like **Wilson's disease**, affecting organs like the liver and brain. *Lead* - **Lead poisoning** can cause various red blood cell abnormalities, notably **basophilic stippling**, which represents aggregated ribosomes and not iron. - It interferes with heme synthesis, leading to **anemia**. *Zinc* - **Zinc** is a critical component of many enzymes, but it does not form the characteristic inclusions known as Pappenheimer bodies. - **Zinc deficiency** can impact immune function and growth, while excess can interfere with copper absorption.

Question 1472: Which of the following red cell disorders is characterized by the presence of macrocytes in the peripheral smear?

A. Hereditary spherocytosis
B. Iron deficiency anemia
C. Sickle cell anemia
D. Megaloblastic anemia (Correct Answer)

Explanation: ***Megaloblastic anemia*** - The presence of **macropolycytes** (larger than normal red blood cells) is a hallmark of megaloblastic anemia, commonly due to vitamin B12 or folate deficiency [1]. - This condition leads to **impaired DNA synthesis**, resulting in ineffective erythropoiesis and abnormal cell morphology [1]. *Hereditary spherocytosis* - Characterized by the presence of **spherocytes** which are small, round, and lack central pallor, not macropolycytes. - It is associated with **hemolytic anemia** but does not show the abnormal cell size seen in megaloblastic anemia. *Iron deficiency anemia* - Typically shows **microcytic, hypochromic red blood cells**, not enlarged cells like macropolycytes. - This disorder results from insufficient iron, leading to inadequate hemoglobin synthesis rather than abnormal cell size. *Sickle cell anemia* - Characterized by **sickle-shaped cells** due to hemoglobin S polymerization; it does not feature macropolycytes. - The primary issue is the **deformation of red blood cells**, leading to vaso-occlusive crises rather than increased cell size. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 593-594.

Question 1473: The marker for B-lymphocyte is

A. CD19 (Correct Answer)
B. CD34
C. CD4
D. CD68

Explanation: ***CD19*** - **CD19** is a specific surface marker expressed on **B-lymphocytes**, crucial for their development and activation [1]. - It is used in diagnosing and monitoring B-cell neoplasms, making it a reliable **biomarker** for these cells [1]. *CD34* - **CD34** is a marker associated with **hematopoietic stem and progenitor cells**, not specifically limited to B-lymphocytes. - It is primarily found on **hematopoietic stem cells** and endothelial cells, indicating its roles in various cell types. *CD68* - **CD68** is predominantly a marker for **macrophages** and is not specific to B-lymphocytes. - It is involved in the identification of **activated macrophages** during inflammation and immune responses. *CD4* - **CD4** is primarily associated with **T-helper cells**, playing a critical role in the immune response and is not a marker for B-lymphocytes [1]. - Its presence indicates helper T-cell function rather than B-cell identification. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 598.

Question 1474: The coagulation profile in a 13-year-old girl with menorrhagia having von Willebrand's disease is

A. Isolated prolonged PTT with a normal PT (Correct Answer)
B. Isolated prolonged PT with a normal PTT
C. Prolongation of both PT and PTT
D. Prolongation of thrombin time

Explanation: ***Isolated prolonged PTT with a normal PT*** - von Willebrand Factor (vWF) is a carrier protein for **Factor VIII**, protecting it from degradation. - Since factor VIII is part of the **intrinsic coagulation pathway**, its deficiency or malfunction (as seen in von Willebrand's disease) leads to a **prolonged PTT** without affecting the extrinsic pathway (PT). *Isolated prolonged PT with a normal PTT* - This pattern suggests a defect in the **extrinsic coagulation pathway**, which is not primarily affected in von Willebrand's disease. - Conditions like **Factor VII deficiency** or certain stages of liver disease would cause an isolated prolonged PT. *Prolongation of both PT and PTT* - This indicates a defect in the **common coagulation pathway** or severe deficiencies affecting both intrinsic and extrinsic pathways. - Examples include deficiencies of **Factor X, V, II (prothrombin)**, or fibrinogen, or severe liver failure. *Prolongation of thrombin time* - A prolonged **thrombin time** points to an issue with **fibrinogen** concentration or function, or the presence of thrombin inhibitors like heparin. - This is not a primary finding in von Willebrand's disease, which primarily impacts platelet adhesion and factor VIII.

Question 1475: The characteristic chromosomal translocation in acute promyelocytic leukemia is:

A. t(21;17)
B. t(9;22)
C. t(8;21)
D. t(15;17) (Correct Answer)

Explanation: ***+ (15;17)*** - The **translocation t(15;17)** is a hallmark of **acute promyelocytic leukemia (APL)**, leading to the formation of the **PML**-**RARA** fusion gene [1,2]. - This genetic anomaly is associated with **clinical features** such as **promyelocyte predominance** and can lead to coagulopathy [1]. *+ (22;9)* - This translocation is not associated with APL; instead, it is indicative of **chronic myelogenous leukemia (CML)**. - In CML, the **Philadelphia chromosome (BCR-ABL)** fusion is the primary genetic abnormality, leading to different clinical presentations. *+ (21;17)* - This specific translocation does not typically occur in APL; it is generally found in other types of **hematological malignancies**. - APL is specifically linked with the **t(15;17)** translocation, which distinctly separates its genetic features [1]. *+ (9;22)* - The **9;22** translocation is primarily found in **CML** and results in the **BCR-ABL** fusion gene, not APL. - APL is characterized by its unique translocation involving chromosomes 15 and 17, emphasizing the importance of genetic identification for accurate diagnosis [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. 620-622. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 326.

Question 1476: Multiple myeloma is characterized by which of the following?

A. Monoclonal gammopathy (Correct Answer)
B. Bence Jones proteins
C. Presence of light chains
D. Hypergammaglobulinemia

Explanation: ***Monoclonal gammopathy*** - **Multiple myeloma** is defined by the proliferation of a **single clone of plasma cells** that produce a characteristic **monoclonal immunoglobulin** (M-protein) detected in serum or urine [1]. - This **monoclonal expansion** leads to the accumulation of abnormal, identical **immunoglobulins** or their fragments [2]. *Presence of light chains* - While the presence of **monoclonal free light chains** (either kappa or lambda) is typical in myeloma, this option describes only a component and not the overarching characteristic that defines the disease [2]. - Not all light chain presence indicates myeloma; a **monoclonal proliferation** of these light chains is what is significant. *Bence Jones proteins* - **Bence Jones proteins** are **monoclonal light chains** excreted in the urine, a common finding in multiple myeloma [2]. - However, like the presence of light chains, this is a **consequence** or **manifestation** of the underlying monoclonal gammopathy, not the defining characteristic itself. *Hypergammaglobulinemia* - This term refers to an **elevated total level of immunoglobulins** in the blood, which can be **polyclonal** (diverse antibodies) or **monoclonal** in nature. - In multiple myeloma, the elevation is specifically due to a **monoclonal immunoglobulin**, making "monoclonal gammopathy" a more precise and defining term [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. 606-609. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617.

Question 1477: Earliest manifestation of megaloblastic anemia is

A. Macrocytosis
B. Hypersegmented neutrophils (Correct Answer)
C. Basophilic stippling
D. Cabot ring

Explanation: ***Hypersegmented neutrophils*** - The earliest manifestation of megaloblastic anemia includes the presence of **hypersegmented neutrophils**, which have more than five lobes in their nuclei [1][2]. - This finding is indicative of impaired DNA synthesis often associated with **vitamin B12** or **folate deficiency**. *Basophilic stippling* - **Basophilic stippling** is more commonly linked to lead poisoning and certain alcohol-related disorders rather than megaloblastic anemia. - It reflects RNA aggregate remnants in red blood cells, which is not a primary feature of this type of anemia. *Cabot ring* - **Cabot rings** are seen in conditions like **pernicious anemia** but are not the **earliest manifestation**; they are infrequently encountered. - This abnormality is related to nuclear remnant material and lacks direct correlation to megaloblastic changes. *Macrocytosis* - **Macrocytosis** refers to the increased size of red blood cells and can be found in megaloblastic anemia but is not the **initial manifestation**. - It may develop later as the anemia progresses, whereas hypersegmented neutrophils appear much earlier. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 593-594. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 654.

Question 1478: In the context of myelodysplastic syndromes (MDS) and acute myelogenous leukemia (AML), which of the following cytogenetic abnormalities is associated with the worst prognosis?

A. inv(16)
B. Normal cytogenetics
C. Monosomy 7 (Correct Answer)
D. t(8;21) translocation

Explanation: ***Monosomy 7*** - Monosomy 7 is associated with **poor prognosis** in conditions like **acute myeloid leukemia (AML)**, often leading to a higher risk of treatment failure. - It implies more aggressive disease and often correlates with **poor response to therapy**. *8/21 translocation* - Generally indicates a more favorable prognosis [1], commonly seen in **Acute Lymphoblastic Leukemia (ALL)**. - Associated with **treatment responsiveness** and a higher chance of remission compared to other cytogenetic abnormalities. *Normal cytogenetics* - In many leukemias, **normal cytogenetics** suggest a relatively **better prognosis** [1] and a more favorable response to treatment. - It is often an indicator of **favorable disease characteristics** and lower risk of relapse. *Inversion 16* - Typically associated with **acute myeloid leukemia (AML)** and indicates a **better prognosis** [1] due to a favorable response to therapy. - Patients with this cytogenetic change generally exhibit **good overall outcomes** compared to other abnormalities. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 620.

Question 1479: What is the most characteristic morphological finding in G6PD deficiency?

A. Bite cells (Correct Answer)
B. Intravascular hemolysis
C. Splenomegaly
D. Hemoglobinuria

Explanation: ***Bite cells*** - **Bite cells** (or **degmacytes**) are red blood cells from which a portion of the cytoplasm has been "bitten off" by macrophages in the spleen [1]. - This occurs due to the removal of **Heinz bodies**, which are precipitated, denatured hemoglobin molecules formed as a result of oxidative stress in G6PD deficient red blood cells [1]. *Intravascular hemolysis* - While **intravascular hemolysis** certainly occurs in G6PD deficiency, causing symptoms like hemoglobinuria and jaundice, it is a clinical consequence and not a direct morphological finding observed on a peripheral blood smear [1]. - The primary defect in G6PD deficiency leads to oxidative damage to red blood cells, which subsequently undergo hemolysis. *Splenomegaly* - **Splenomegaly** can be present in G6PD deficiency due to the increased workload of the spleen in removing damaged red blood cells and Heinz bodies [1]. - However, it is an organ enlargement, a clinical sign, and not a cellular morphological finding characteristic of the red blood cells themselves. *Hemoglobinuria* - **Hemoglobinuria** is the presence of free hemoglobin in the urine, resulting from significant **intravascular hemolysis** [1]. - It is a clinical symptom of acute hemolytic episodes in G6PD deficiency rather than a characteristic morphological feature of the red blood cells themselves. **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 1480: Specific stain for myeloblasts is

A. Sudan black B
B. Periodic acid-Schiff (PAS)
C. Leukocyte alkaline phosphatase (LAP)
D. Myeloperoxidase (Correct Answer)

Explanation: ***Myeloperoxidase*** - **Myeloperoxidase (MPO)** is an enzyme found in the primary granules of myeloblasts and other myeloid cells, making it a specific marker. - A positive MPO stain helps differentiate **acute myeloid leukemia (AML)** from **acute lymphoblastic leukemia (ALL)**. *Sudan black B* - **Sudan black B (SBB)** stains lipids within granules of myeloid and monocytoid cells, including myeloblasts. - While it is positive in myeloblasts, it is **less specific** than MPO as it can also stain monocytes, and its staining mechanism is different from enzyme activity. *Periodic acid-Schiff (PAS)* - **PAS stain** detects glycogen and other carbohydrates, typically showing a granular pattern in ALL and often negative or weakly positive in AML. - It is **not specific for myeloblasts** and is more characteristic of erythroblasts and lymphoblasts. *Leukocyte alkaline phosphatase (LAP)* - **LAP score** is used to distinguish between chronic myeloid leukemia (CML), which typically has a low LAP score, and other myeloproliferative disorders or leukemoid reactions, which have high scores. - It is **not used for the identification of myeloblasts** or for distinguishing AML from ALL.

Practice by Chapter

Anemias: Classification and Approach

Practice Questions

Hemolytic Anemias

Practice Questions

Myeloproliferative Neoplasms

Practice Questions

Myelodysplastic Syndromes

Practice Questions

Acute Leukemias

Practice Questions

Chronic Leukemias

Practice Questions

Lymphomas and Lymphoid Neoplasms

Practice Questions

Plasma Cell Disorders

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Bleeding Disorders

Practice Questions

Thrombotic Disorders

Practice Questions

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