Hematopathology — MCQs
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Heinz bodies are removed by?
Where are Dutcher bodies typically seen?
Which oncogene is associated with Burkitt's lymphoma?
Which factor is primarily found in cryoprecipitate?
TEL-AML1 fusion is associated with?
In which condition is the 'Swiss cheese pattern' typically observed in pathology?
What is the most important diagnostic feature for beta thalassemia trait?
Which of the following is a quantitative defect in globin synthesis?
Which of the following is a feature not typically associated with Hereditary Spherocytosis?
Which type(s) of hemophilia is/are X-linked?
Hematopathology Indian Medical PG Practice Questions and MCQs
Question 1351: Heinz bodies are removed by?
- A. Macrophages (Correct Answer)
- B. Lymphocytes
- C. Neutrophils
- D. Fibroblasts
Explanation: ***Macrophages*** - Macrophages, particularly those in the **spleen**, are responsible for pitting out Heinz bodies from red blood cells. - This process is part of the **extravascular hemolysis** that occurs when red blood cells containing Heinz bodies are prematurely destroyed. *Lymphocytes* - Lymphocytes are primary cells of the **adaptive immune system**, involved in recognizing and targeting specific pathogens or abnormal cells. - They do not play a role in the removal of intracellular inclusions like Heinz bodies from red blood cells. *Neutrophils* - Neutrophils are a type of **phagocyte** and a crucial component of the **innate immune system**, primarily involved in fighting bacterial and fungal infections. - Their function is mainly in acute inflammation and phagocytosing microbes, not in the removal of inclusions from red blood cells. *Fibroblasts* - Fibroblasts are responsible for producing the **extracellular matrix** and **collagen**, playing a critical role in wound healing and tissue repair. - They are not immune cells and are not involved in the removal of cellular debris or inclusions like Heinz bodies.
Question 1352: Where are Dutcher bodies typically seen?
- A. Brain
- B. Spleen
- C. Bone marrow (Correct Answer)
- D. Liver
Explanation: ***Bone marrow*** - **Dutcher bodies** are **intranuclear inclusions** of immunoglobulin, characteristically seen in **plasma cells** within the bone marrow. - Their presence is a classic morphological feature of **Waldenström macroglobulinemia** and other lymphoproliferative disorders. *Brain* - The brain is not the typical site for finding Dutcher bodies; structures like **Lewy bodies** (Parkinson's disease) or **neurofibrillary tangles** (Alzheimer's disease) are seen here. - Dutcher bodies are specifically associated with plasma cell abnormalities and **B-cell lymphomas**. *Spleen* - While the spleen can be involved in various hematological malignancies, Dutcher bodies are not primarily identified within splenic tissue but rather in the **plasma cells** of the **bone marrow**. - Splenic pathology typically involves changes in spleen size and cellular architecture, not intranuclear inclusions like Dutcher bodies. *Liver* - The liver is not the primary site for the detection of Dutcher bodies. Liver pathology might show infiltration by malignant cells in some systemic diseases, but not these specific inclusions within hepatocytes or other liver cells. - **Councilman bodies** (apoptotic hepatocytes in viral hepatitis) are an example of liver-specific microscopic findings.
Question 1353: Which oncogene is associated with Burkitt's lymphoma?
- A. C-MYC (Correct Answer)
- B. BCL-1 (IgH)
- C. BCL-2 (IgH)
- D. Anaplastic Lymphoma Kinase (ALK)
Explanation: ***C-MYC*** - Burkitt's lymphoma is associated with the translocation involving the **C-MYC gene**, which drives cell proliferation [1]. - This oncogene is typically involved in the **t(8;14)** translocation, linking C-MYC to the immunoglobulin heavy chain locus [1]. *ALK* - The **ALK gene** is primarily associated with anaplastic large cell lymphoma and is not linked to Burkitt's lymphoma. - ALK rearrangements lead to mutations that result in uncontrolled growth in other lymphomas, but not in Burkitt's. *BCL-1, IgH* - **BCL-1** (also known as CCND1) is associated with mantle cell lymphoma and is linked to the **t(11;14)** translocation, not Burkitt's. - It primarily involves cyclin D1 overexpression in the tumor pathogenesis distinct from Burkitt's behavior. *BCL-2, IgH* - The **BCL-2 gene** is commonly associated with follicular lymphoma and contributes to anti-apoptotic functions, unrelated to Burkitt's. - Burkitt's typically shows rapid proliferation and high apoptosis, unlike the mechanisms driven by BCL-2. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325.
Question 1354: Which factor is primarily found in cryoprecipitate?
- A. Factor II
- B. Factor V
- C. Factor VIII (Correct Answer)
- D. Factor IX
Explanation: ***Factor VIII*** - Cryoprecipitate is enriched with **Factor VIII**, essential for blood coagulation and hemophilia treatment [1]. - It also contains **fibrinogen**, **Factor XIII**, and von Willebrand factor, crucial for stable clot formation [1]. *Factor II* - Factor II, also known as **prothrombin**, is mainly found in **plasma**, not concentrated in cryoprecipitate. - It is not specifically extracted through cryoprecipitation, which focuses on fibrinogen and other factors. *Factor V* - Factor V is generally present in **plasma**, but not in significant amounts in cryoprecipitate. - It plays a role in the coagulation cascade but is not a primary component of cryoprecipitate. *Factor IX* - Factor IX is mainly associated with the **intrinsic pathway** of coagulation and is part of plasma, not concentrated in cryoprecipitate. - While it is vital for hemophilia B, it does not form part of the cryoprecipitate's key components. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 669-670.
Question 1355: TEL-AML1 fusion is associated with?
- A. CLL
- B. CML
- C. AML
- D. ALL (Correct Answer)
Explanation: ***ALL*** - The **TEL-AML1 fusion gene** (also known as ETV6-RUNX1) is a common chromosomal abnormality found in approximately 25% of cases of **B-cell precursor acute lymphoblastic leukemia (ALL)**, particularly in children. - This fusion creates an abnormal protein that interferes with normal blood cell development, leading to the uncontrolled proliferation of immature lymphocytes characteristic of ALL. *CLL* - **Chronic lymphocytic leukemia (CLL)** is a cancer of mature lymphocytes, specifically B cells, and is not associated with the TEL-AML1 fusion. - Typical genetic abnormalities in CLL include deletions or mutations in chromosomes 13q, 17p, 11q, and trisomy 12. *CML* - **Chronic myeloid leukemia (CML)** is characterized by the presence of the **Philadelphia chromosome (BCR-ABL1 fusion gene)**, which results from a translocation between chromosomes 9 and 22. - CML is a myeloproliferative neoplasm affecting myeloid stem cells, distinct from the lymphoid origin of ALL. *AML* - **Acute myeloid leukemia (AML)** involves the myeloid lineage and is associated with various chromosomal translocations and mutations, but **TEL-AML1 fusion is not characteristic of AML**. - Common genetic alterations in AML include t(8;21), inv(16), t(15;17) (PML-RARA), and mutations in FLT3, NPM1, or CEBPA.
Question 1356: In which condition is the 'Swiss cheese pattern' typically observed in pathology?
- A. Endometrial hyperplasia (Correct Answer)
- B. Disseminated intravascular coagulation (DIC)
- C. Acute myocardial infarction
- D. Chronic gastritis
Explanation: ***Metropathica hemorrhagica*** - Characterized by a **Swiss cheese pattern** due to multiple cystic changes in the endometrium [1], often associated with chronic endometrial irritation. - The pattern arises from **irregular endometrial proliferation** and is indicative of disturbances in menstrual function. *Mucinous cystadenoma* - Typically presents as a **smooth, multilocular cyst** with mucin production, but does not exhibit a Swiss cheese morphology. - Often associated with **abdominal masses** rather than the specific endometrial patterns seen in metropathica hemorrhagica. *Dermoid* - Consists of **teratoma-like tissues** and may show cystic areas, but lacks the Swiss cheese appearance associated with endometrial pathology. - Commonly found in **ovarian masses**, characterized by a variety of tissue types instead of the specific cystic changes related to metropathica hemorrhagica. *Serous cystadenoma* - Features a **serous fluid-filled cyst**, often uniform in appearance, without the Swiss cheese pattern. - Primarily occurs in the ovaries and is noted for its **smooth surface** rather than the cystic irregularities typical of metropathica hemorrhagica. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Female Genital Tract Disease, pp. 473-475.
Question 1357: What is the most important diagnostic feature for beta thalassemia trait?
- A. Increased HbF
- B. Decreased MCH
- C. Decreased MCV
- D. Increased HbA2 (Correct Answer)
Explanation: ***Raised HbA2*** - In beta thalassemia trait, the most significant diagnostic feature is an **increased level of HbA2** (>3.5%), which helps differentiate it from other types of anemias [1]. - This is due to a compensatory mechanism as the body attempts to produce more **alpha globin chains** in response to decreased beta globin production. *Reduced MCV* - While **reduced mean corpuscular volume (MCV)** can indicate microcytic anemia, it is not specific enough for beta thalassemia trait as it can appear in other conditions. - MCV can vary in individuals, making it less reliable as a **diagnostic feature** compared to HbA2 levels. *Raised HbF* - An increase in **hemoglobin F (HbF)** is more characteristic of beta thalassemia major rather than the trait; levels in the trait do not typically rise significantly. - This feature can also be elevated in other conditions, thus not serving as a definitive marker for the trait. *Reduced MCH* - A **decreased mean corpuscular hemoglobin (MCH)** is indicative of microcytic anemia but lacks specificity for beta thalassemia trait alone. - Similar to MCV, it can occur in various types of anemia and does not pinpoint the diagnosis effectively. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 649-650.
Question 1358: Which of the following is a quantitative defect in globin synthesis?
- A. Thalassemia (Correct Answer)
- B. Sickle cell hemoglobinopathy
- C. G6PD deficiency
- D. Diamond-Blackfan syndrome
Explanation: ***Thalassemia*** - **Thalassemia** is characterized by a **quantitative defect** in globin chain synthesis, leading to reduced hemoglobin production [1][2][5]. - It results in **microcytic anemia** due to ineffective erythropoiesis and imbalanced globin chain production [2]. *Diamond-Blackfan syndrome* - This condition is a type of **macrocytic anemia** due to failure of red blood cell production, rather than a globin synthesis defect. - It generally presents with **normocytic or macrocytic** anemia and is associated with **erythroblastopenia**. *Sickle cell hemoglobinopathy* - Sickle cell disease involves a **qualitative defect** in hemoglobin (Hb S) rather than a quantitative one [3][4][5]. - Symptoms include pain episodes, **vaso-occlusive crises**, and organ damage due to sickling of red blood cells [3][4]. *G6PD deficiency* - G6PD deficiency is an **enzyme deficiency** leading to hemolytic anemia under oxidative stress, not a defect in globin synthesis [4][5]. - Characterized by **episodic hemolytic anemia**, it primarily affects red blood cell stability rather than hemoglobin production [4]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 587-588. [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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 652-654. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638.
Question 1359: Which of the following is a feature not typically associated with Hereditary Spherocytosis?
- A. Gall stones
- B. Direct Coombs Positive (Correct Answer)
- C. Splenomegaly
- D. Increased Osmotic Fragility
Explanation: ***Direct Coomb's Positive*** - In Hereditary Spherocytosis, the **Coomb's test** is typically **negative**, indicating that hemolysis is not due to autoimmune factors. - Presence of **spherocytes** on the blood smear and increased fragility are hallmark findings, not antibodies against red cells [1]. *Splenomegaly* - **Splenomegaly** is common in Hereditary Spherocytosis as the spleen actively removes abnormal spherocytes from circulation [1]. - It can lead to **hypersplenism**, with resultant anemia and thrombocytopenia. *Increased Osmotic Fragility* - Increased osmotic fragility is a key feature of Hereditary Spherocytosis, as red blood cells are less able to withstand hypotonic solutions [1]. - This results from a defect in the red cell membrane, causing spherocyte shape and fragility. *Gall stones* - Patients may develop **gallstones** due to increased bilirubin from the breakdown of spherocytes, leading to **bilirubin stones** [1]. - Gallstones are a common complication due to chronic hemolysis. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598.
Question 1360: Which type(s) of hemophilia is/are X-linked?
- A. Hemophilia A
- B. Hemophilia B
- C. Hemophilia C
- D. Both A & B (Correct Answer)
Explanation: ***Both A & B*** - Both **Hemophilia A** and **Hemophilia B** are **X-linked recessive** disorders [1][2] caused by deficiency of specific clotting factors (Factor VIII for A and Factor IX for B). - They are inherited through **carrier females**, affecting predominantly males, showcasing their X-linked transmission [1]. *Hemophilia A* - It is indeed an **X-linked recessive** disorder [2] but does not encompass all types of hemophilia. - It results from a deficiency in **Factor VIII** [2], leading to bleeding disorders, yet is just one form of hemophilia. *Hemophilia C* - This form is **autosomal recessive** and not linked to the X chromosome, primarily affecting both genders equally. - It involves a deficiency of **Factor XI**, distinguishing it from the X-linked nature of A and B. *Hemophilia B* - Like Hemophilia A, it is X-linked but by itself does not account for all hemophilias. - It results from a deficiency in **Factor IX**, yet the question about X-linkage applies to both A and B together. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 151. [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.
Practice by Chapter
Anemias: Classification and Approach
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Hemolytic Anemias
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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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