Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1491: A 17-year-old boy presented with a total leukocyte count of 138 × 10^9/L, with 80% blasts on the peripheral smear. Chest X-ray demonstrated a large mediastinal mass. Immunophenotyping of this patient's blasts would most likely demonstrate:

A. Markers associated with myeloid lineage
B. Markers associated with immature T-cell lineage (Correct Answer)
C. Markers associated with B-cell lineage
D. A null phenotype (no surface antigens)

Explanation: ***An immature T cell phenotype (Tdt/CD34/CD7 positive)*** - Given the age of the patient and presentation, the high percentage of blasts along with the mediastinal mass suggests **T-cell acute lymphoblastic leukemia (T-ALL)** [1], which commonly presents with an immature T cell phenotype. - The presence of **Tdt, CD34, and CD7** indicates the immature nature of the T cells, which is characteristic of this condition. *No surface antigens (null phenotype)* - A null phenotype typically indicates a **lack of differentiation**, which is not consistent with the high blast count seen here. - Most leukemias or lymphomas usually express some markers, especially in a case with significant blast population like this one. *Myeloid markers, such as CD13, CD33 and CD15* - These markers are indicative of **myeloid lineage**, which is not relevant in this case as it suggests an **acute myeloid leukemia (AML)**, not T-ALL. - The clinical context and immunophenotyping results would not support myeloid lineage in a patient with such a presentation. *B cell markers, such as CD 19, CD20 and CD22* - These are **characteristic of B-cell lineage** [1], which is not relevant in this scenario, given the presence of a mediastinal mass often associated with T-cell malignancies. - The blast cells in this patient are clearly indicative of a **T-cell disorder**, rather than a B-cell neoplasm. **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. 598-600.

Question 1492: Which of the following is a false statement regarding disseminated intravascular coagulation (DIC)?

A. Decreased PTT (Correct Answer)
B. Decreased fibrinogen
C. Increased PT
D. Thrombocytopenia

Explanation: ***Decreased PTT (FALSE Statement)*** - In DIC, the **partial thromboplastin time (PTT)** is typically **prolonged/increased**, NOT decreased [1] - The widespread activation of the coagulation cascade leads to consumption of clotting factors within the intrinsic and common pathways [1] - This depletion of factors (VIII, IX, XI, XII) causes the blood to take longer to clot [1] - Therefore, "decreased PTT" is the FALSE statement *Thrombocytopenia (True Statement)* - **Thrombocytopenia** (low platelet count) is a hallmark feature of DIC [1], [2] - Platelets are consumed during widespread formation of microthrombi throughout the vasculature [1] - This consumption contributes to both thrombotic and hemorrhagic complications [1] *Decreased fibrinogen (True Statement)* - **Fibrinogen** is a major clotting factor that is consumed during massive thrombus formation in DIC [1] - Its depletion is characteristic of DIC and contributes to hemorrhagic tendencies [1], [2] - Fibrinogen levels typically fall below 100 mg/dL in acute DIC *Increased PT (True Statement)* - The **prothrombin time (PT)** is typically **prolonged/increased** in DIC [1] - Clotting factors from the extrinsic and common pathways (VII, X, V, II, fibrinogen) are consumed [1] - This prolongation indicates deficiency in these factors, leading to impaired clot formation **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 624-626. [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. 151-152.

Question 1493: A 45-year-old female patient presented with painless supraclavicular lymphadenopathy. Biopsy revealed binucleated acidophilic owl eye appearance with floating lymphocytes in empty space, which were CD15 and CD30 positive. What is the most probable diagnosis?

A. Lymphocytic predominant Hodgkin lymphoma
B. Mixed cellularity Hodgkin lymphoma
C. Nodular sclerosis Hodgkin lymphoma (NSHL) (Correct Answer)
D. Lymphocytic depleted Hodgkin lymphoma

Explanation: ***Nodular sclerosis Hodgkin lymphoma*** - Characterized by a **painless supraclavicular lymphadenopathy** and the presence of **binucleated Reed-Sternberg cells** with the "owl eye" appearance. - **CD15** and **CD30 positivity** confirm the diagnosis, common in this subtype of Hodgkin lymphoma [2]. *Lymphocytic predominant Hodgkin lymphoma* - Typically shows **lymphocyte-rich background** and may present with fewer **Reed-Sternberg cells**, which differ from the described findings [3]. - **CD15** and **CD30 positivity** is generally low, contrasting with the strong positivity seen in this case. *Lymphocytic depleted lymphoma* - Characterized by a **lack of lymphocytes** and high numbers of **Reed-Sternberg cells**, not matching the floating lymphocyte description [1]. - **Usually CD15 and CD30** positive but presents with **more aggressive clinical features** than nodular sclerosis. *Mixed cellularity Hodgkin lymphoma* - This form also presents with Reed-Sternberg cells but typically involves a more **heterogeneous population** of inflammatory cells [2,3]. - Presentation of **painless lymphadenopathy** can occur, but the specific histological findings here are more indicative of nodular sclerosis. **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. 559-560. [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. 616-618. [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. 618.

Question 1494: Prothrombin time is prolonged in all of the following conditions except:

A. Liver disease
B. Disseminated intravascular coagulation
C. Warfarin therapy
D. Von Willebrand's disease (Correct Answer)

Explanation: ***Von Willebrand's disease*** - **Von Willebrand's disease** primarily affects **platelet adhesion** and the **intrinsic coagulation pathway** (by carrying factor VIII), rather than the extrinsic pathway measured by PT [1]. - Patients typically have a **normal prothrombin time (PT)** and activated partial thromboplastin time (aPTT) that may be normal or slightly prolonged. *Liver disease* - The **liver** synthesizes most **coagulation factors**, including those measured by PT (factor VII from the extrinsic pathway and factors II, V, X from the common pathway) [3]. - Severe **liver disease** impairs factor synthesis, leading to **deficiencies** and a prolonged PT [1]. *Disseminated intravascular coagulation* - **DIC** involves widespread activation of the coagulation system, leading to the consumption of **clotting factors**, including those measured by PT [2]. - This **consumption coagulopathy** results in prolonged PT, aPTT, and thrombocytopenia [2]. *Warfarin therapy* - **Warfarin** is a **vitamin K antagonist** that inhibits the synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) [1], [3]. - By inhibiting **factor VII** (extrinsic pathway) and the **common pathway factors**, warfarin prolongs the **prothrombin time (PT)**, which is used to monitor its anticoagulant effect [3]. **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] 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 Blood And Bone Marrow Disease, pp. 582-583.

Question 1495: Loose fibrin accumulated in a tight clot in the coagulation pathway is caused by which factor?

A. Factor X
B. Factor XI
C. Factor XII
D. Factor XIII (Correct Answer)

Explanation: ***Factor XIII*** - **Factor XIII** (fibrin-stabilizing factor) is responsible for **cross-linking fibrin monomers**, converting loose fibrin into a stable, insoluble clot [1]. - This cross-linking process strengthens the clot, preventing premature degradation and ensuring effective hemostasis [2]. *Factor X* - **Factor X** (Stuart-Prower factor) is a key enzyme in the coagulation cascade that, when activated to Factor Xa, forms part of the **prothrombinase complex** that converts **prothrombin to thrombin** [2]. - It does not directly cause the cross-linking of fibrin to form a tight clot. *Factor XI* - **Factor XI** (plasma thromboplastin antecedent) is involved in the intrinsic pathway, activating **Factor IX**. - Its primary role is in propagating the coagulation cascade, not in the final stabilization of the fibrin clot. *Factor XII* - **Factor XII** (Hageman factor) initiates the intrinsic pathway of coagulation and is involved in fibrinolysis and inflammation. - It does not directly influence the stability or cross-linking of the fibrin clot structure. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 130. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583.

Question 1496: Which of the following statements regarding hereditary spherocytosis is false?

A. Anemia
B. It is due to intrinsic defect in RBC membrane skeleton
C. Spherocytes are the characteristic finding on peripheral blood smear
D. Splenomegaly is not a feature of hereditary spherocytosis (Correct Answer)

Explanation: ***Spherocytosis is a pathognomic finding*** - Spherocytosis is not **pathognomic** for hereditary spherocytosis as it can also occur in other conditions like autoimmune hemolytic anemia. - While **spherocytes** are a notable finding in hereditary spherocytosis, they are not exclusive to this disorder. *Anemia* - Anemia is a common result of **hemolysis** in hereditary spherocytosis due to the destruction of spherical red blood cells [1]. - Patients often present with **mild to moderate anemia** [1][2], but this is a characteristic finding, not an exception. *Splenomegaly* - Splenomegaly is frequently observed in hereditary spherocytosis due to **hypertrophy** from increased red blood cell destruction. - This finding is **typical** in cases of hereditary spherocytosis and serves as an important clinical indicator [2]. *It is due to intrinsic defect in RBC membrane skeleton* - Hereditary spherocytosis is primarily caused by an **intrinsic defect in the red blood cell membrane**, particularly affecting proteins like spectrin and ankyrin [1]. - This intrinsic defect leads to the formation of **spherocytes**, which are less deformable and prone to hemolysis [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, pp. 640-642. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598.

Question 1497: A 9-year-old boy with elevation in both prothrombin time (PT) and activated partial thromboplastin time (APTT) is diagnosed with what?

A. Defect in common pathway (Correct Answer)
B. Platelet function defect
C. Defect in the extrinsic pathway
D. Defect in the intrinsic pathway

Explanation: ***Defect in common pathway*** - Elevation in both **prothrombin time (PT)** and **activated partial thromboplastin time (APTT)** indicates a problem in the **common pathway**, affecting factors I, II, V, X [1]. - This defect can result from conditions such as **vitamin K deficiency** or **liver dysfunction**, which impact multiple coagulation factors. *Platelet function defect* - Typically presents with **prolonged bleeding times** but does not affect PT or APTT, which remain normal. - Symptoms often include **petechiae** or **easy bruising**, rather than the coagulation profile observed here. *Defect in extrinsic pathway* - Primarily affects **PT** only, not APTT, as this pathway involves factors VII and tissue factor [1]. - Conditions like **vitamin K deficiency** can cause prolonged PT, but APTT would not be elevated simultaneously in isolation. *Defect in intrinsic pathway* - Affects **APTT** primarily, causing a prolonged APTT while PT remains normal [1]. - Common conditions include **Hemophilia A or B**, but the simultaneous elevation of both PT and APTT rules this out. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 128-130.

Question 1498: Which of the following statements about reticulocytes is correct?

A. Larger than RBC
B. Contain nucleus
C. Increased in hemolytic anemia (Correct Answer)
D. Staining is done by Romanowsky stains

Explanation: ***↑in hemolytic anemia*** - Reticulocyte count is typically **increased** in hemolytic anemia as the bone marrow responds to **acute blood loss** or increased hemolysis by producing more red blood cells [1]. - This reflects the body's mechanism to replace **lost RBCs**, making reticulocyte counts a useful marker in diagnosing anemia types. *Contain nucleus* - Reticulocytes do not contain a **nucleus**; they are immature red blood cells that have **already extruded** their nucleus. - Their main function is to mature into erythrocytes, which are **anucleate** cells. *Staining is done by Romanowsky stain* - Reticulocytes are typically stained using **methylene blue** or **brilliant cresyl blue**, not Romanowsky stain, which is used for **WBC and smears**. - These specific stains highlight the **reticulated cytoplasm**, indicating RNA presence, crucial for identifying reticulocytes. *Smaller than RBC* - Reticulocytes are generally **larger** than mature red blood cells (RBCs) due to their **cellular contents**, which are not fully extruded yet. - Their size is an important factor in distinguishing them from mature RBCs during evaluation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 638-639.

Question 1499: Which of the following is a characteristic finding in hereditary spherocytosis?

A. Increased Reticulocyte Count
B. Increased Osmotic Fragility (Correct Answer)
C. Splenomegaly
D. Negative Direct Coombs Test

Explanation: ***Increased Osmotic Fragility*** - **Hereditary spherocytosis** is characterized by defective red blood cell membrane proteins (spectrin, ankyrin, band 3, protein 4.2), leading to fragile, sphere-shaped red blood cells with reduced surface area-to-volume ratio [2]. - The **osmotic fragility test** measures the red blood cell's resistance to osmotic lysis in hypotonic solutions; in hereditary spherocytosis, the abnormally shaped spherocytes lyse more readily, showing **increased osmotic fragility** [1]. - This is the **diagnostic hallmark** and most characteristic laboratory finding of hereditary spherocytosis [1]. *Negative Direct Coombs Test* - The **Direct Coombs test (DCT)** detects antibodies or complement bound to red blood cell surfaces, which is characteristic of **autoimmune hemolytic anemias**. - Hereditary spherocytosis is a **hereditary intrinsic red blood cell membrane defect**, not an autoimmune process, so the DCT is **negative**. - While true, a negative test result helps differentiate HS from autoimmune hemolytic anemia but is not the primary diagnostic characteristic. *Increased Reticulocyte Count* - An **increased reticulocyte count** (reticulocytosis) is a common finding in various forms of hemolytic anemia, including hereditary spherocytosis, reflecting compensatory bone marrow response to accelerated red blood cell destruction [1]. - This is a **non-specific marker of hemolysis**, not pathognomonic for hereditary spherocytosis. *Splenomegaly* - **Splenomegaly** is a common clinical feature in hereditary spherocytosis due to the spleen's role in trapping and prematurely destroying the abnormal spherocytes through extravascular hemolysis [1], [2]. - This is a **clinical consequence** of the disease rather than the diagnostic laboratory hallmark related to the red blood cell's inherent membrane defect. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641.

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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