Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1301: In APML (Acute Promyelocytic Leukemia), all of the following are seen except:

A. Retinoic acid is used in treatment
B. 15/17 translocation may be seen
C. CD 15/34 both seen in same cell (Correct Answer)
D. Associated with Disseminated intravascular coagulation (DIC)

Explanation: ***CD 15/34 both seen in same cell*** - This statement is incorrect because **Acute Promyelocytic Leukemia (APML)** is characterized by **CD34 negativity**, meaning CD34 is typically absent in APML cells. - While **CD15 may be positive** in APML, **CD34 is negative** in the vast majority of cases (unlike other AML subtypes where CD34 is often positive). - Therefore, **CD15 and CD34 are NOT both seen in the same cell** in APML. - The disease involves **immature myeloid cells** at the promyelocyte stage, which are beyond the most primitive stem cell stage (hence the lack of CD34 expression). *Retinoic acid is used in treatment* - **All-trans retinoic acid (ATRA)** is a cornerstone of treatment for APML. - ATRA induces differentiation of the **promyelocytes**, which helps overcome the **differentiation block** caused by the PML-RARA fusion protein. *15/17 translocation may be seen* - The characteristic genetic abnormality in APML is the **t(15;17) translocation** [1]. - This translocation results in the fusion of the **PML (promyelocytic leukemia) gene** on chromosome 15 with the **RARA (retinoic acid receptor alpha) gene** on chromosome 17 [2]. *Associated with Disseminated intravascular coagulation (DIC)* - APML is frequently associated with a high risk of developing **Disseminated Intravascular Coagulation (DIC)** [1]. - The abnormal promyelocytes release **procoagulant substances** that activate the coagulation cascade, leading to severe bleeding and thrombosis. **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. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 605-607.

Question 1302: Radiation is most commonly associated with which of the following cancer?

A. Lymphoma
B. Lung carcinoma
C. Osteosarcoma
D. Leukemia (Correct Answer)

Explanation: ***Leukemia*** - Exposure to **ionizing radiation**, such as from atomic bomb blasts or therapeutic radiation, is a well-established risk factor for developing **leukemia**, particularly acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) [1], [2]. - Radiation causes **DNA damage** in hematopoietic stem cells, leading to chromosomal rearrangements and oncogenic mutations [2]. *Lymphoma* - While certain types of lymphoma, such as Hodgkin lymphoma, can be treated with radiation therapy, and radiation exposure can increase the risk of secondary malignancies, lymphoma is not the most commonly associated cancer type with radiation exposure as a **primary cause** [2]. - Risk factors for lymphoma are more strongly linked to **viral infections** (e.g., EBV, HIV) or **immunodeficiency states** [1], [2]. *Lung carcinoma* - The primary risk factor for **lung carcinoma** is **smoking**, which accounts for approximately 85-90% of cases. - While radiation exposure (e.g., radon gas, therapeutic radiation to the chest) can increase the risk, it is not the most common or strongest association compared to smoking. *Osteosarcoma* - **Osteosarcoma** is a primary malignant bone tumor, and its etiology is often complex, involving genetic predispositions or rapid bone growth phases. - While high doses of **therapeutic radiation** (e.g., for other cancers) can induce secondary osteosarcoma, it is a relatively rare occurrence and not the most common cancer primarily associated with radiation exposure. **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. 220-221. [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. 595-596.

Question 1303: Necrotizing lymphadenitis is seen in

A. Kimura disease
B. Kikuchi-Fujimoto disease (Correct Answer)
C. Hodgkin's lymphoma
D. Castleman disease

Explanation: ***Kikuchi-Fujimoto disease*** - Kikuchi-Fujimoto disease (KFD), also known as **histiocytic necrotizing lymphadenitis**, is characterized by **necrotizing lymphadenitis** without granulocytic infiltration. - It typically presents with **cervical lymphadenopathy**, fever, and leukopenia, often in young women. *Kimura disease* - Kimura disease is characterized by chronic, painless **subcutaneous masses** and **lymphadenopathy**, often in the head and neck. - Histologically, it shows **follicular hyperplasia** and prominent **eosinophilic infiltration**, not necrotizing lymphadenitis. *Castleman disease* - Castleman disease is a group of rare disorders that involve **overgrowth of lymph node cells**, leading to enlarged lymph nodes. - Histologically, it presents with **hyaline vascular** or **plasma cell variants**, but not necrotizing changes. *Hodgkin's lymphoma* - Hodgkin's lymphoma is a type of cancer characterized by the presence of **Reed-Sternberg cells** within a heterogeneous inflammatory infiltrate. - While it affects lymph nodes, its characteristic features are specific giant cells and an inflammatory background, **not necrotizing lymphadenitis** as the primary finding [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. 592-593.

Question 1304: Necrotizing lymphadenopathy is characteristically seen in:

A. Kikuchi disease (Correct Answer)
B. Non-Hodgkin's lymphoma
C. Castleman's disease
D. Kimura disease

Explanation: ***Kikuchi disease*** - Also known as **histiocytic necrotizing lymphadenitis**, it is characterized by **tender cervical lymphadenopathy** with histological evidence of **necrotizing lymphadenitis** with an influx of **histiocytes and immunoblasts**. - The disease is **self-limiting**, typically resolving in 1-4 months, though it can recur and is more common in **young women of Asian descent**. - Histology shows **paracortical necrosis** with abundant karyorrhectic debris and absence of neutrophils. *Non-Hodgkin's lymphoma* - This is a diverse group of **malignancies** originating from lymphocytes, primarily presenting as **lymphadenopathy** that is typically **painless** and can be widespread. - While some aggressive NHL subtypes may show areas of necrosis, the defining characteristic is **clonal proliferation of malignant lymphocytes** rather than the necrotizing histiocytic features of Kikuchi disease. *Castleman's disease* - This is a rare disorder characterized by the **overgrowth of lymphoid tissue**, presenting with **large, often solitary lymph nodes** (unicentric form) or generalized lymphadenopathy (multicentric form). - It is histologically distinguished by **hypervascularity** and **abnormal germinal centers** (onion-skinning pattern), not by necrotizing lymphadenopathy. *Kimura disease* - A **rare chronic inflammatory disorder** presenting with **subcutaneous nodules** and **lymphadenopathy**, commonly in the head and neck region [1]. - Histologically, it is characterized by **lymphoid hyperplasia with prominent eosinophilic infiltration** and increased vascularity, but **not necrosis** of lymph nodes [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. 592-593.

Question 1305: Fetomaternal transfusion of fetal RBCs in mother can be detected by: UPSC 08; TN 08; AIIMS 10

A. Electrophoresis
B. Indirect Coomb's test
C. Direct Coomb's test
D. Betke-Kleihauer test (Correct Answer)

Explanation: ***Betke-Kleihauer test*** - The **Kleihauer-Betke test** (or acid elution test) detects fetal hemoglobin (HbF) in maternal blood. Fetal red blood cells, which contain HbF, are more resistant to acid elution and retain their hemoglobin, appearing stained, while adult red blood cells containing HbA lose their hemoglobin and appear as 'ghost' cells. - This visual differentiation allows for the quantification of **fetomaternal hemorrhage**, which is crucial for determining the appropriate dose of anti-D immunoglobulin in Rh-negative mothers [1]. - This is the **gold standard test** for detecting and quantifying fetomaternal transfusion. *Electrophoresis* - **Hemoglobin electrophoresis** is used to identify and quantify different types of hemoglobin (e.g., HbA, HbS, HbC, HbF) in a blood sample. While it can detect HbF, it is not the primary or most practical method for routinely quantifying the small percentage of fetal cells in maternal circulation in the context of fetomaternal hemorrhage. - It is typically used for diagnosing **hemoglobinopathies** and thalassemias, not for accurately determining the extent of fetomaternal transfusion. *Indirect Coombs test* - The **Indirect Coombs Test** (ICT) detects *antibodies circulating in the serum* that are capable of binding to red blood cells [1]. It is commonly used for **antibody screening** in prenatal care and for cross-matching blood transfusions. - While it can screen for maternal antibodies against fetal red blood cell antigens, it does not directly quantify the volume of fetal blood that has entered the maternal circulation. *Direct Coombs test* - The **Direct Coombs Test** (DCT) detects antibodies *attached directly to the surface of red blood cells*, typically indicating autoimmune hemolytic anemia or a hemolytic transfusion reaction. - It is used to detect antibodies on the infant's red blood cells in cases of **hemolytic disease of the newborn**, but not to quantify fetal cells in the mother's circulation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 469-470.

Question 1306: Which of the following stains is used for reticulocyte staining?

A. Indigo carmine
B. Brilliant cresyl blue (Correct Answer)
C. Sudan black
D. Methyl violet

Explanation: **Correct Answer: Brilliant cresyl blue** - **Brilliant cresyl blue** is a **supravital stain** commonly used to visualize **reticulocytes** [1] - It precipitates the **ribosomal RNA** and other organelles present in reticulocytes, making them visible as a **reticular network** within the cell - This is one of the two most common stains used for reticulocyte counting (along with New methylene blue) *Incorrect: Indigo carmine* - **Indigo carmine** is a vital dye used for diagnostic procedures in **gastroenterology and urology** (e.g., to detect mucosal lesions or assess kidney function) - Used in endoscopic procedures as a **chromoscopic agent** to enhance visualization, but not for reticulocyte staining *Incorrect: Sudan black* - **Sudan black B** is a stain primarily used for detecting **lipids** and **lipofuscin** in various cells and tissues - Often utilized in **hematology** to differentiate myeloid cells from lymphoid cells based on their granule content, but not for reticulocytes *Incorrect: Methyl violet* - **Methyl violet** is a basic dye used as a **histological stain** and for staining **Gram-positive bacteria** in bacteriology - While it can stain cellular components, it is not specifically used for the identification or enumeration of reticulocytes **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 578-579.

Question 1307: ALL L3 morphology is a malignancy arising from which cell lineage –

A. Mature B cell (Correct Answer)
B. Mixed B cell & T cell
C. Immature T cell
D. Precursor B cell

Explanation: ***Mature B cell*** - ALL L3, also known as **Burkitt-type ALL**, arises from a **mature B-cell lineage**. [1] - This is characterized by specific immunophenotypic markers (e.g., strong expression of **surface immunoglobulin** and **CD20**) and frequent chromosomal translocations involving the **MYC oncogene**, typically t(8;14). [1] *Mixed B cell & T cell* - This refers to **mixed phenotype acute leukemia (MPAL)**, which exhibits features of both B-cell and T-cell lineages. - MPAL is distinct from ALL L3, which is definitively B-cell in origin based on morphology and immunophenotype. *Immature T cell* - Malignancies arising from immature T cells are classified as **T-cell ALL**, which have a different morphology (L1 or L2) and distinct immunophenotype (e.g., expression of **cytoplasmic CD3**, CD1a, CD2, CD5, CD7). [1] - T-cell ALL is characterized by **T-cell receptor gene rearrangements** and typically presents with a mediastinal mass, unlike ALL L3. [1] *Precursor B cell* - Most cases of ALL (ALL L1 and L2) arise from **precursor B cells**, also known as B-lymphoblastic leukemia. [2] - These are characterized by lack of surface immunoglobulin expression and generally express **CD10, CD19, CD22**, and **TdT**, contrasting with the mature B-cell immunophenotype of ALL L3. [2] **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. 606. [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. 596-598.

Question 1308: Packed red cells are commonly stored in which preservative solution?

A. CPDA-1 solution (Correct Answer)
B. AS-1 (Adsol) solution
C. SAG-M solution
D. AS-3 (Nutricel) solution

Explanation: ***Correct: CPDA-1 solution*** - **CPDA-1** (Citrate-Phosphate-Dextrose-Adenine) is the standard anticoagulant and preservative solution taught in Indian medical curricula - Allows storage of packed red cells for **35 days** at 1-6°C - Contains citrate (anticoagulant), phosphate (buffer), dextrose (RBC energy), and adenine (ATP synthesis) - Most commonly referenced in NEET-PG examinations as the standard storage solution *AS-1 (Adsol) solution* - Additive solution used primarily in the United States for extended PRBC storage (42 days) - Added to red cells after plasma removal to maintain viability - While effective, it is not the primary solution taught in standard Indian medical education *SAG-M solution* - **SAG-M** (Saline-Adenine-Glucose-Mannitol) is an additive solution used primarily in Europe - Extends packed red cell storage to **42 days** - Functionally similar to other additive solutions but less commonly referenced in Indian medical curriculum *AS-3 (Nutricel) solution* - Another additive solution for red blood cell storage used in the US - Designed to extend shelf life to 42 days - Like AS-1, it is not the standard preservative solution taught in Indian medical education **Note:** Modern blood banking increasingly uses additive solutions (AS-1, AS-3, SAG-M) for extended storage, but CPDA-1 remains the fundamental preservative solution taught in medical education.

Question 1309: Glycoprotein IIb-IIIa complex is deficient in

A. Gray platelet syndrome
B. Glanzmann disease (Correct Answer)
C. von Willebrand disease
D. Bernard-Soulier syndrome

Explanation: ***Glanzmann disease*** - This condition is characterized by a deficiency or qualitative defect of the **glycoprotein IIb-IIIa (GPIIb-IIIa) complex** on the platelet surface [1]. - The GPIIb-IIIa complex is crucial for **platelet aggregation** as it acts as a receptor for **fibrinogen**, connecting platelets [1], [2]. *Bernard-Soulier syndrome* - This syndrome involves a deficiency of the **glycoprotein Ib-IX-V complex**, which is responsible for **platelet adhesion** to **von Willebrand factor (vWF)** on the subendothelium [1], [2]. - Patients present with **large platelets** and impaired platelet adhesion. *Gray platelet syndrome* - This is a rare bleeding disorder characterized by a deficiency of **alpha-granules** in platelets [4]. - Platelets in this condition appear 'gray' on a blood smear due to the lack of alpha-granules that contain growth factors and adhesion proteins [4]. *von Willebrand disease* - This is primarily a deficiency or dysfunction of **von Willebrand factor (vWF)**, which is essential for **platelet adhesion** and stability of **factor VIII** [3]. - It does not directly involve a deficiency of the GPIIb-IIIa complex itself. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 128. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 669-670. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 581-582.

Question 1310: Which among the following statements is wrong?

A. M components are detected in chronic myeloid leukemia. (Correct Answer)
B. In 20% of myelomas, only light chains are produced.
C. Light chains are synthesized in slight excess normally in plasma cells.
D. Qualitative assessment of M component can be done by electrophoresis.

Explanation: ***M components are detected in chronic myeloid leukemia.*** - This statement is **incorrect**. M-components (monoclonal proteins) are characteristic of **plasma cell dyscrasias** such as multiple myeloma, MGUS, and Waldenström macroglobulinemia [1]. - **Chronic myeloid leukemia (CML)** is a myeloproliferative neoplasm involving the granulocytic cell line, not plasma cells. CML does not produce M-components unless there is a **coincidental and unrelated plasma cell disorder**. - M-components arise from clonal proliferation of plasma cells producing a single type of immunoglobulin, which is not a feature of CML pathophysiology [2]. *Qualitative assessment of M component can be done by electrophoresis.* - This statement is correct. **Serum protein electrophoresis (SPEP)** is the primary tool for qualitative detection of M-components. - It provides qualitative information by demonstrating the presence of a monoclonal spike and its migration pattern in the gamma, beta, or alpha regions. - While SPEP also provides quantitative data (size/concentration), **immunofixation electrophoresis (IFE)** is subsequently used for specific typing of the heavy chain (IgG, IgA, IgM) and light chain (kappa or lambda). *In 20% of myelomas, only light chains are produced.* - This statement is correct. Approximately **15-20% of multiple myeloma cases** produce only monoclonal light chains without intact heavy chains [1]. - These are called **light chain myelomas**, and the light chains (Bence Jones proteins) are detected in urine and serum [2]. *Light chains are synthesized in slight excess normally in plasma cells.* - This statement is correct. Normal plasma cells produce a **slight excess of light chains** compared to heavy chains to ensure proper immunoglobulin assembly. - The excess free light chains are normally cleared by the kidneys, maintaining a balanced serum free light chain ratio (kappa/lambda ratio of 0.26-1.65). **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.

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