Hematopathology — MCQs
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Intracorpuscular hemolytic anemia is seen in ?
Which of the following myeloid leukemias is not classified as a myeloproliferative neoplasm?
In which condition are Pseudo-Pelger-Huët cells typically seen?
Donath-Landsteiner antibody is seen in?
Which of the following statements is false regarding hereditary spherocytosis?
What is the typical bone marrow finding in myelofibrosis?
What is the major fibril protein associated with Primary Amyloidosis?
Which is not a feature of paroxysmal nocturnal hemoglobinuria?
Which of the following is a characteristic feature of Hereditary Spherocytosis?
The immunoglobulin most commonly involved in Multiple Myeloma is:
Hematopathology Indian Medical PG Practice Questions and MCQs
Question 1391: Intracorpuscular hemolytic anemia is seen in ?
- A. Thalassemia (Correct Answer)
- B. Infection
- C. Thrombotic thrombocytopenic purpura (TTP)
- D. Autoimmune hemolytic anemia
Explanation: ***Thalassemia*** - Thalassemia is characterized by **intracorpuscular hemolysis** due to defective hemoglobin synthesis, leading to premature destruction of red blood cells [1][2]. - It manifests as **microcytic anemia** with associated **extramedullary erythropoiesis** in severe cases [1]. *Autoimmune hemolytic anemia* - This condition leads to **extravascular hemolysis**, primarily affecting red blood cells in the spleen, not within the plasma [2]. - It is often associated with **positive direct Coombs test**, indicating reactants on the RBC surface. *TIP* - TIP (Thrombotic Microangiopathy) primarily involves **microangiopathic hemolytic anemia** and is not classified as intracorpuscular [2]. - The hemolysis in TIP occurs due to **microthrombi**, causing damage to red blood cells as they pass through narrowed vessels. *Infection* - Infections can lead to **hemolysis**, but this is typically **extravascular** due to splenic clearance or due to other mechanisms like **malaria** [2]. - The hemolytic mechanism is not intracorpuscular, as seen in conditions like thalassemia. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 601-602. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 596-597.
Question 1392: Which of the following myeloid leukemias is not classified as a myeloproliferative neoplasm?
- A. Acute myeloid leukemia (Correct Answer)
- B. Chronic myeloid leukemia
- C. Chronic lymphocytic leukemia
- D. Acute lymphoblastic leukemia
Explanation: ***Acute myeloid leukemia*** - Acute myeloid leukemia is classified as a **malignant hematological disorder**, not a myeloproliferative disease, which includes chronic diseases with increased blood cell production. - It is characterized by the **rapid accumulation of immature blood cells**, leading to acute symptoms rather than a gradual proliferation. *Polycythemia vera* - Polycythemia vera is a myeloproliferative neoplasm resulting in an **increase in red blood cells**, causing symptoms like increased blood viscosity [1][2]. - It is associated with a mutation in the **JAK2 gene**, which leads to overproduction of erythrocytes [1][2]. *Chronic myeloid leukemia* - Chronic myeloid leukemia is a myeloproliferative disorder characterized by the proliferation of myeloid cells and often involves the **Philadelphia chromosome** [2][3]. - It shows a gradual increase in cell number and is typically diagnosed based on the presence of **elevated white blood cell counts**. *Essential thrombocytosis* - Essential thrombocytosis is a myeloproliferative neoplasm characterized by an **elevated platelet count**, increasing the risk of thrombotic events [1][2]. - Like other myeloproliferative disorders, it is associated with mutations in **JAK2** or other myeloid-related genes [1][2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615. [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, p. 624. [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, pp. 624-625.
Question 1393: In which condition are Pseudo-Pelger-Huët cells typically seen?
- A. Hairy cell leukemia
- B. Multiple myeloma
- C. Hodgkin's lymphoma
- D. Myelodysplastic syndrome (Correct Answer)
Explanation: ***Mylodysplastic syndrome*** - Pseudo-Pelger-Huet cells are characteristic and often observed in myelodysplastic syndromes, indicating an ineffective hematopoiesis [1]. - These cells appear as **hyposegmented neutrophils** and are associated with dysplastic changes in the bone marrow [1]. *Hairy cell leukemia* - Typically presents with **hairy cells** in peripheral blood and often involves splenomegaly; pseudo-Pelger-Huet cells are not usual in this condition. - Associated with **PANCYTOPENIA** and reticulin fibrosis, differing from myelodysplastic syndrome. *Hodgkin's lymphoma* - Characterized by the presence of **Reed-Sternberg cells** and typically involves lymphadenopathy. - Peripheral blood findings generally do not include pseudo-Pelger-Huet cells; the focus is on lymphatic tissue. *Multiple myeloma* - Commonly presents with **plasma cells** and related symptoms like bone pain and renal failure, not associated with pseudo-Pelger-Huet cells. - It primarily causes an increase in monoclonal proteins rather than dysplastic changes seen in myelodysplastic syndrome. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.
Question 1394: Donath-Landsteiner antibody is seen in?
- A. PNH
- B. Waldenstrom's macroglobulinemia
- C. Malaria
- D. Paroxysmal cold hemoglobinuria (Correct Answer)
Explanation: ***Paroxysmal cold hemoglobinuria*** - **Donath-Landsteiner antibody** is a **biphasic IgG autoantibody** that binds to red blood cells in the cold and causes **hemolysis** upon warming, characteristic of paroxysmal cold hemoglobinuria. - This antibody has **anti-P specificity**, meaning it targets the P antigen on red blood cells, leading to complement activation and cell lysis. *PNH* - **Paroxysmal nocturnal hemoglobinuria** (PNH) is characterized by a deficiency in **GPI-anchored proteins** on red blood cells, notably **CD55** and **CD59**, making them susceptible to complement-mediated lysis. - It is not associated with the Donath-Landsteiner antibody; rather, it is identified by **flow cytometry** showing absence of CD55/CD59. *Waldenstrom's macroglobulinemia* - This is a **B-cell lymphoma** characterized by the overproduction of **monoclonal IgM antibodies**, leading to hyperviscosity syndrome and other symptoms. - It does not involve Donath-Landsteiner antibodies or cold-induced hemolysis in the same manner as paroxysmal cold hemoglobinuria. *Malaria* - **Malaria** is caused by **Plasmodium parasites** that infect and destroy red blood cells, leading to hemolytic anemia and fever. - While it causes **hemolysis**, it is not mediated by the Donath-Landsteiner antibody; the destruction is primarily due to parasitic replication and immune responses against infected cells.
Question 1395: Which of the following statements is false regarding hereditary spherocytosis?
- A. Defect in ankyrin
- B. Reticulocytosis
- C. Decreased MCHC (Correct Answer)
- D. Normal to increased MCV
Explanation: ***Decreased MCHC*** - Hereditary spherocytosis typically presents with an **increased MCHC** due to the spherocytes being more concentrated. - MCHC is a measure of the hemoglobin concentration in red blood cells, and in spherocytosis, this value is often elevated rather than decreased. *Defect in ankyrin* - This is a true statement; hereditary spherocytosis is associated with a defect in **ankyrin**, a protein that helps maintain the cell's membrane structure [2]. - Mutations in ankyrin lead to instability of the red blood cell membrane, resulting in spherocyte formation [2]. *Decreased MCV* - In hereditary spherocytosis, MCV is often **normal or slightly increased**, as it reflects the volume of red blood cells, which can be misinterpreted due to the presence of spherocytes. - Spherocytes are smaller cells, which can mistakenly suggest a falsely decreased MCV if not properly interpreted [1]. *Reticulocytosis* - This condition typically presents with **reticulocytosis** as a response to hemolysis, indicating the bone marrow is producing more red blood cells to compensate [1]. - The presence of reticulocytosis is a common finding in hereditary spherocytosis due to increased destruction of spherocytes. **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.
Question 1396: What is the typical bone marrow finding in myelofibrosis?
- A. Megaloblastic cells
- B. Microcytic cells
- C. Thrombocytosis
- D. Dry tap (hypocellular) (Correct Answer)
Explanation: ***Dry tap (hypocellular)*** - In myelofibrosis, the bone marrow is often **hypocellular** due to fibrosis [1][2], leading to a **dry tap** during aspiration. - The presence of **reticulin** and collagen deposition replaces normal hematopoietic cells [2], resulting in ineffective hematopoiesis. *Thrombocytosis* - Myelofibrosis typically leads to **thrombocytopenia**, not thrombocytosis, due to ineffective megakaryopoiesis and splenic sequestration. - Though elevated platelets can occur, they are generally a **secondary response** to the disease and not a hallmark finding. *Megaloblastic cells* - Megaloblastic changes are associated with **vitamin B12** or **folate deficiencies**, which do not occur in myelofibrosis. - In myelofibrosis, the predominant issue is **marrow fibrosis** [1][2], which does not lead to megaloblastosis. *Microcytic cells* - Microcytic cells are commonly linked to **iron deficiency anemia**, not myelofibrosis. - Myelofibrosis typically results in **variable red cell morphology** [1], but microcytic anemia is not a primary characteristic. **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.
Question 1397: What is the major fibril protein associated with Primary Amyloidosis?
- A. Immunoglobulin Light Chain (Correct Answer)
- B. Amyloid Associated protein (AA)
- C. Procalcitonin (PCT)
- D. Transthyretin (TTR)
Explanation: ***AL*** - In Primary Amyloidosis, **AL amyloid** is derived from immunoglobulin light chains produced by **plasma cell dyscrasias** [1]. - This type of amyloidosis is commonly associated with conditions like **multiple myeloma** or monoclonal gammopathy [1]. *Transthyretin* - This protein is associated with **Familial Amyloid Polyneuropathy** and **Senile Systemic Amyloidosis**, not Primary Amyloidosis. - Transthyretin amyloidosis (ATTR) results from **mutations** or **aging**, contributing to different clinical presentations than AL. *AA* - AA amyloidosis is secondary and occurs due to **chronic inflammatory** conditions, such as rheumatoid arthritis or chronic infections. - It is not the main fibril protein in **Primary Amyloidosis**, which is specifically linked to **light chains**. *Procalcitonin* - Procalcitonin is a **biomarker** used primarily for diagnosing bacterial infections, particularly sepsis, and is not involved in amyloidogenesis. - It does not relate to amyloidosis and is not a component of amyloid fibrils. **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.
Question 1398: Which is not a feature of paroxysmal nocturnal hemoglobinuria?
- A. Thrombocytopenia
- B. Hemolysis
- C. Increased LAP score (Correct Answer)
- D. Thrombosis
Explanation: ***Increased LAP score*** - In paroxysmal nocturnal hemoglobinuria, the **LAP score** is typically **low** due to ineffective hematopoiesis and not elevated. - The presence of a low LAP score is inconsistent with the features of this condition, making it the correct choice. *Thrombosis* - Paroxysmal nocturnal hemoglobinuria is **associated with a high risk of thrombosis**, particularly in the **venous system** [2]. - This is due to **increased platelet activation** and excessive thrombin generation resulting from hemolysis. *Hemolysis* - **Hemolysis** is a hallmark feature of paroxysmal nocturnal hemoglobinuria, where there is **destruction of red blood cells** [2,3]. - Patients often present with signs of hemolytic anemia including **elevated bilirubin** and **low haptoglobin** levels. *Thrombocytopenia* - **Thrombocytopenia** is a common finding in paroxysmal nocturnal hemoglobinuria due to **expanded consumption** of platelets during episodes of hemolysis. - This can lead to an **increased risk of bleeding** in affected patients. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 601-602. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-651.
Question 1399: Which of the following is a characteristic feature of Hereditary Spherocytosis?
- A. Splenomegaly
- B. Increased Osmotic Fragility (Correct Answer)
- C. Gallstones
- D. Direct Coombs Test Negative
Explanation: ***Direct Coomb's Positive*** - In hereditary spherocytosis, the **Coomb's test is typically negative**, indicating that the hemolysis is non-immune. - The condition is primarily due to defects in **red blood cell membrane proteins** [2], not autoimmune mechanisms. *Increased Osmotic Fragility* - A hallmark of hereditary spherocytosis; these red blood cells are more **sensitive to osmotic changes** due to their spherical shape [2]. - This fragility is used in clinical tests to help diagnose the condition [1]. *Gall stones* - Patients with hereditary spherocytosis may develop **pigment gallstones** due to chronic hemolysis and excess bilirubin [1]. - This is a common complication resulting from increased breakdown of red blood cells. *Splenomegaly* - Often presents in hereditary spherocytosis as the spleen works harder to clear **damaged red blood cells** [2]. - Splenomegaly is a common clinical feature due to the increased workload on the spleen. **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.
Question 1400: The immunoglobulin most commonly involved in Multiple Myeloma is:
- A. IgG (Correct Answer)
- B. IgM
- C. IgA
- D. IgD
Explanation: ***IgG*** - In Multiple Myeloma, the most commonly involved immunoglobulin is **IgG**, which is often produced in excess by malignant plasma cells [1][2]. - The presence of **monoclonal IgG** in serum is a key indicator of this malignancy, evident in diagnostic tests like serum protein electrophoresis. *IgM* - While **elevated IgM** levels can occur in other conditions like Waldenström's macroglobulinemia, it is not typically associated with Multiple Myeloma [2]. - IgM is produced by a different type of plasma cell and does not reflect the classic presentation of Multiple Myeloma. *IgA* - Although **IgA** can be involved in some cases of Multiple Myeloma, it is much less common than IgG [1][2]. - Patients with predominately **IgA Multiple Myeloma** are relatively rare compared to those with IgG. *IgD* - **IgD** myeloma is a very rare type of Multiple Myeloma, accounting for less than 2% of cases [1][2]. - It is not typically associated with the classic symptoms and conditions that characterize the more common IgG or IgA forms. **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. 608-609. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617.
Practice by Chapter
Anemias: Classification and Approach
Practice Questions
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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