Hematopathology — MCQs

A 52-year-old man presents with back pain, fatigue, polyuria, and polydipsia. Imaging reveals lytic lesions in the lumbar vertebrae. Laboratory tests show hypoalbuminemia, mild anemia, and thrombocytopenia. Serum electrophoresis indicates a monoclonal immunoglobulin peak, and bone marrow aspiration reveals atypical plasma cells. Urinalysis shows significant proteinuria. What amyloid precursor protein is most likely to be deposited in this patient?

Q1470

A 12-month-old girl of Punjabi parents developed pallor since 3 months of age. One unit of blood transfusion was done at 5 months of age. She now presents with pallor and hepatosplenomegaly. Her hemoglobin level is 3.8 g/dL, MCV is 68, and MCH is 19. A peripheral smear examination showed schistocytes, and bone marrow examination revealed erythroid hyperplasia. What is the diagnosis?

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1461: 'Hairy cell leukemia' is a neoplastic proliferation of which type of cells?

A. Myeloid cells
B. Macrophages
C. B lymphocytes (Correct Answer)
D. T cells

Explanation: ***B lymphocytes*** - **Hairy cell leukemia** is a rare, chronic lymphoproliferative disorder characterized by the clonal proliferation of **mature B lymphocytes** [1]. - These malignant B cells have distinctive cytoplasmic projections, giving them a "hairy" appearance under a microscope [1]. *T cells* - While T-cell leukemias exist (e.g., T-cell prolymphocytic leukemia), **hairy cell leukemia** specifically originates from B lymphocytes, not T cells. - T-cell neoplasms have different clinical presentations and immunophenotypes [2]. *Myeloid cells* - Myeloid cells give rise to conditions like **acute myeloid leukemia** or **chronic myeloid leukemia**. - These are distinct from lymphoid malignancies like **hairy cell leukemia**, which involves lymphocytes. *Macrophages* - Macrophages are phagocytic cells involved in immune responses and do not typically proliferate in a neoplastic manner to cause **leukemia**. - **Hairy cell leukemia** is a lymphoid malignancy, not a disorder of macrophages. **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. 612. [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 1462: Which of the following is a characteristic bone marrow finding in myelofibrosis?

A. Increased reticulin fibrosis (Correct Answer)
B. Absence of fibroblasts
C. Decreased megakaryocytes
D. Hypocellular marrow from onset

Explanation: ***Leucoerythroblastosis*** - A hallmark finding in myelofibrosis is **leucoerythroblastosis**, characterized by the presence of immature white cells and nucleated red blood cells in the bloodstream [1][3]. - This reflects an **extramedullary hematopoiesis** due to the failure of normal marrow function and is commonly seen in myelofibrosis [1][2]. *Tear drop cells* - While **tear drop cells** (dacryocytes) can be associated with myelofibrosis, they are not exclusive findings and can appear in other conditions [1]. - They are indicative of **extramedullary hematopoiesis** but are not definitive for myelofibrosis specifically. *Leucocytopenia* - Myelofibrosis is associated with **neutrophilia** rather than leucocytopenia, which presents as low white blood cell counts. - The condition often leads to an increase in white blood cell counts due to reactive changes rather than a decrease. *All of the above* - This option is incorrect as it suggests that all previously mentioned findings are present in myelofibrosis. - Both **tear drop cells** and **leucocytopenia** are not definitive or accurate findings compared to **leucoerythroblastosis**. **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. 628-629. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 615-616. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 589-590.

Question 1463: A baby's blood group was determined as O negative. Which of the following blood groups can the baby's mother or father not have?

A. A Positive
B. B Positive
C. AB Negative (Correct Answer)
D. O positive

Explanation: ***AB Negative*** - A parent with **AB blood type** cannot have an O blood type child because an individual with AB blood type only has A and B alleles to pass on (i.e., *IAIB* genotype). - For a child to have **O blood type**, they must inherit the *i* allele from both parents (*ii* genotype), which is impossible if one parent is AB. *A Positive* - A parent with **A positive blood type** can have an O negative child if their genotype is *IAi* for A/B/O and *Rr* for Rh factor. - The child would inherit the *i* allele from this parent and the *r* allele for Rh, along with the same from the other parent. *B Positive* - Similar to A positive, a parent with **B positive blood type** can have an O negative child if their genotype is *IBi* and *Rr*. - The child would inherit the *i* allele from this parent and the *r* allele for Rh, along with the same from the other parent. *O positive* - A parent with **O positive blood type** can certainly have an O negative child; their genotype would be *ii* for A/B/O and *Rr* for Rh factor. - The child would inherit the *i* allele from this parent and the *r* allele for Rh.

Question 1464: Auer rods are a characteristic feature of which type of leukemia?

A. Chronic lymphocytic leukemia (CLL)
B. Myelodysplastic syndromes (MDS)
C. Acute myeloid leukemia (AML) (Correct Answer)
D. Acute lymphoblastic leukemia (ALL)

Explanation: ***Auer rods*** - Auer rods are **needle-shaped cytoplasmic inclusions** found in myeloid leukemias, particularly in acute myeloid leukemia (AML) [1]. - They are indicative of myeloid differentiation and are a classic **diagnostic feature** observed in bone marrow or peripheral blood smears [1]. *Intercytoplasmic granules* - While **intercytoplasmic granules** may appear in various leukemias, they are not specific or characteristic for Auer rods. - These granules do not serve as a **specific diagnostic marker** for any particular type of leukemia. *Eosinophils* - Eosinophils are associated with **allergic reactions** and parasitic infections, majorly presenting with **bilobed nuclei** and prominent granules. - They do not have **Auer rods**, making this option incorrect regarding the context of leukemia. *Leukemic cells* - While leukemic cells represent neoplastic white blood cells, they do not specifically refer to the **presence of Auer rods**. - Different types of leukemic cells have various **morphologies** and features that may not include Auer rods. **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 1465: Neoplasm associated with Waldenström's macroglobulinemia is also known as:

A. Smoldering myeloma
B. Primary CNS lymphoma
C. Lymphoplasmacytic lymphoma (Correct Answer)
D. MGUS (Monoclonal gammopathy of undetermined significance)

Explanation: ***Lymphoplasmacytic lymphoma*** - **Waldenström's macroglobulinemia** is a type of **lymphoplasmacytic lymphoma (LPL)** that produces large amounts of **monoclonal IgM** protein [1]. - LPL is a **B-cell non-Hodgkin lymphoma** characterized by the presence of **lymphocytes, plasma cells, and plasmacytoid lymphocytes** in the bone marrow [1]. *Smoldering myeloma* - **Smoldering multiple myeloma (SMM)** is an **asymptomatic precursor** to multiple myeloma, characterized by high levels of **monoclonal protein (IgG or IgA)** and clonal plasma cells, but without end-organ damage. - It is distinct from Waldenström's macroglobulinemia, which involves **IgM paraprotein** and lymphoplasmacytic infiltration [1]. *Primary CNS lymphoma* - **Primary CNS lymphoma** is a rare and aggressive **non-Hodgkin lymphoma** that originates in the brain, spinal cord, or eyes, and is not typically associated with systemic **IgM paraproteinemia**. - Its clinical presentation involves **neurological symptoms** specific to CNS involvement, rather than symptoms of hyperviscosity or IgM-related coagulopathy. *MGUS (Monoclonal gammopathy of undetermined significance)* - **Monoclonal gammopathy of undetermined significance (MGUS)** is an asymptomatic condition with a **monoclonal protein (M-protein)** in the blood but no evidence of malignancy or end-organ damage. - While it can involve any immunoglobulin type, **IgM MGUS** is a precursor to Waldenström's macroglobulinemia, not the neoplasm itself. **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.

Question 1466: What is the primary basis for the Working Formulation in the classification of non-Hodgkin's lymphoma?

A. Morphology of cells (Correct Answer)
B. Cell surface markers
C. Survival characteristic of cells
D. Cellular genetics

Explanation: ***Morphology of cells*** - The **Working Formulation** primarily classified non-Hodgkin's lymphomas based on the **histological appearance** of the malignant cells, such as cell size, nuclear features, and growth patterns. - This classification aimed to group lymphomas with similar prognoses, broadly categorizing them into low, intermediate, and high-grade based on their **cytological features**. *Cell surface markers* - While cell surface markers (immunophenotyping) are crucial in modern lymphoma classification (e.g., WHO classification), they were not the **primary basis** for the Working Formulation. - Immunophenotyping identifies the lineage and differentiation stage of lymphoid cells (e.g., B-cell, T-cell) but became widely integrated into lymphoma classification later. *Survival characteristic of cells* - The Working Formulation did indirectly consider survival by grouping lymphomas with similar prognoses, but **survival characteristics** themselves were not the primary *basis* for classifying each specific lymphoma type. - Prognosis was an outcome derived from the morphological classification, not the initial classifying factor. *Cellular genetics* - **Cellular genetics**, including chromosomal translocations and gene mutations, are fundamental to current World Health Organization (WHO) classifications of lymphoma. - However, comprehensive genetic analysis was not readily available or the primary method for classifying lymphomas when the Working Formulation was developed.

Question 1467: Which of the following conditions is least likely to be associated with a high reticulocyte count?

A. Acute bleed
B. Hemolytic anemia
C. Nutritional deficiency anemia under treatment
D. Megaloblastic anemia (due to vitamin B12 or folate deficiency) (Correct Answer)

Explanation: ***Megaloblastic anemia*** [1] - Associated with ineffective erythropoiesis, leading to a **low reticulocyte count** rather than a high one. - Often results from deficiencies in **Vitamin B12** or **folate** [1], which impair proper red blood cell production. *Response to treatment in nutrition deficiency anemia* - Typically shows a **high reticulocyte count** as the bone marrow responds to **corrected deficiency**. - Indicates the body's effort to produce more red blood cells to address anemia. *Hemolytic anemia* [2,3] - Characterized by increased destruction of red blood cells [2,3], leading to a **high reticulocyte count** as the marrow compensates. - Commonly presents with **jaundice** and elevated **bilirubin levels** due to increased breakdown of RBCs. *Acute bleed* [2] - Results in increased reticulocyte production as the body compensates for blood loss [2], leading to a **high reticulocyte count**. - Often accompanied by features like **hypotension** and **tachycardia** due to acute blood loss. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 593-595. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 652-654.

Question 1468: In which of the following conditions are Gamma-Gandy bodies typically not seen?

A. Chronic myeloid leukemia (Correct Answer)
B. Cirrhosis with portal hypertension
C. Hemosiderosis
D. Sickle Cell anemia

Explanation: ***Chronic myeloid leukemia*** - **Gamma-Gandy bodies** are fibrotic nodules in the spleen with **hemosiderin** and **calcium deposits**, typically resulting from **chronic passive congestion** or **repeated hemorrhages**. - **CML** causes massive **splenomegaly** due to **infiltration by leukemic cells** and extramedullary hematopoiesis, not the chronic vascular congestion or infarction pattern that produces Gamma-Gandy bodies. - While CML involves increased splenic iron turnover, it does NOT typically form the organized fibrotic nodules characteristic of Gamma-Gandy bodies. *Cirrhosis with portal hypertension* - **Portal hypertension** leads to **chronic passive congestion** of the spleen and splenomegaly. - This chronic congestion with elevated venous pressure and repeated microhemorrhages creates the ideal environment for **Gamma-Gandy body formation**. - This is one of the **classic associations** with Gamma-Gandy bodies. *Hemosiderosis* - While hemosiderosis involves **diffuse hemosiderin deposition** in tissues including the spleen, it represents generalized iron overload without the specific pathologic features of Gamma-Gandy bodies. - The organized **fibrotic nodules with calcium** that characterize Gamma-Gandy bodies are not a primary feature of hemosiderosis. - However, some sources consider hemosiderosis can be associated with these lesions in the context of chronic congestion. *Sickle Cell anemia* - **Repeated splenic infarctions** from vaso-occlusive crises lead to chronic injury, fibrosis, and hemosiderin deposition. - This creates the pathologic substrate for **Gamma-Gandy body formation**. - These bodies reflect chronic splenic damage in sickle cell disease, especially before autosplenectomy occurs.

Question 1469: A 52-year-old man presents with back pain, fatigue, polyuria, and polydipsia. Imaging reveals lytic lesions in the lumbar vertebrae. Laboratory tests show hypoalbuminemia, mild anemia, and thrombocytopenia. Serum electrophoresis indicates a monoclonal immunoglobulin peak, and bone marrow aspiration reveals atypical plasma cells. Urinalysis shows significant proteinuria. What amyloid precursor protein is most likely to be deposited in this patient?

A. Amylin protein
B. Apolipoprotein serum amyloid A
C. Fibrinogen protein
D. Immunoglobulin light chain protein (Correct Answer)

Explanation: ***Immunoglobulin light chain*** - The presence of **monoclonal immunoglobulin peak** in serum indicates abnormal proliferation of plasma cells, leading to production of **light chains** which can deposit in tissues as amyloid [1][2]. - This is characteristic of **multiple myeloma** [3][4], which can lead to resultant amyloidosis due to excess light chain production [1]. *Apo serum amyloid A* - This amyloid precursor is primarily associated with **chronic inflammatory states**, not with the underlying **monoclonal gammopathy** observed in this scenario [1]. - It does not correlate with the **light chain deposition** associated with plasma cell disorders like myeloma. *Fibrinogen* - Fibrinogen amyloid is typically seen in **chronic inflammatory disorders** or infections, not primarily in cases of **plasma cell dyscrasias** [4]. - There are no indications of **consistently elevated fibrinogen** levels in this patient's profile that would suggest its deposition as amyloid. *Amylin* - Amylin amyloid is produced in the context of **type 2 diabetes mellitus** and is associated with islet cell amyloidosis, not commonly linked with **multiple myeloma** or its renal manifestations [5]. - This patient's conditions do not suggest hyperglycemia or diabetes, which would lead to amylin deposition. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 266-267. [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. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617. [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, pp. 606-607. [5] 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. 608.

Question 1470: A 12-month-old girl of Punjabi parents developed pallor since 3 months of age. One unit of blood transfusion was done at 5 months of age. She now presents with pallor and hepatosplenomegaly. Her hemoglobin level is 3.8 g/dL, MCV is 68, and MCH is 19. A peripheral smear examination showed schistocytes, and bone marrow examination revealed erythroid hyperplasia. What is the diagnosis?

A. Alpha-thalassemia
B. Sickle cell disease
C. Glucose-6-phosphate dehydrogenase deficiency
D. Beta-thalassemia (major) (Correct Answer)

Explanation: ***Beta-thalassemia (major)*** - The combination of **severe microcytic hypochromic anemia** (Hb 3.8 g/dL, MCV 68, MCH 19), early onset of pallor, **hepatosplenomegaly**, and **erythroid hyperplasia** with a need for transfusions is highly characteristic of **beta-thalassemia major** [1]. - The presence of **schistocytes** on peripheral smear indicates significant ineffective erythropoiesis and hemolysis, which is common in severe thalassemias due to the precipitation of unstable globin chains [1]. *Sickle cell disease* - This condition is characterized by **sickle-shaped red blood cells** and recurrent painful vaso-occlusive crises, which are not mentioned in the presentation, and the peripheral smear showed schistocytes, not sickled cells [1]. - While it can cause anemia, the **MCV is typically normal to high**, unlike the microcytosis seen here. *Alpha-thalassemia* - Severe forms like **Hb Barts hydrops fetalis** usually present *in utero* or at birth with massive edema and profound anemia, and are often fatal [1]. - Less severe forms might cause microcytic anemia, but **hepatosplenomegaly and severe transfusion dependence from 3 months of age** are more typical of beta-thalassemia major [1]. *Glucose-6-phosphate dehydrogenase deficiency* - This condition typically presents with **acute hemolytic anemia** triggered by certain drugs, infections, or fava beans, rather than chronic severe anemia and hepatosplenomegaly from early infancy. - Peripheral smear would show **bite cells** and **Heinz bodies** during a hemolytic episode, not schistocytes as the primary finding. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 644-650.

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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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