Hematology — MCQs
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Which of the following is commonly seen in Polycythemia Vera?
What is the recommended time frame for completing a blood transfusion after initiation?
Response to iron therapy in iron deficiency anemia is denoted by?
Cryoprecipitate is useful in which of the following conditions?
Thalassemia gives protection against ?
Which of the following does not synthesize von Willebrand factor?
Anemia with reticulocytosis is seen in -
Which of the following diseases is NOT associated with Anti-Neutrophil Cytoplasmic Antibodies (ANCA)?
In a patient with suspected vitamin B12 deficiency, which condition would result in an abnormal Schilling test?
Which of the following statements about Sickle Cell Anemia is FALSE?
Hematology Indian Medical PG Practice Questions and MCQs
Question 1091: Which of the following is commonly seen in Polycythemia Vera?
- A. Hyperuricemia
- B. Prone for acute leukemia
- C. Spontaneous severe infection
- D. Thrombosis (Correct Answer)
Explanation: ***Spontaneous severe infection*** - In Polycythemia Vera, there is usually an **increased red blood cell mass** leading to complications like thrombosis, rather than a predisposition to severe infections. - Severe infections are not a typical feature, as the condition usually maintains **functional immunity** despite hyperviscosity. *Thrombosis* - Individuals with Polycythemia Vera have increased blood viscosity that results in a higher risk of **thrombosis**, which is a common complication [1]. - Events like **deep vein thrombosis (DVT)** or **cerebral venous sinus thrombosis** are often observed due to altered hemodynamics. *Hyperuricemia* - Hyperuricemia occurs due to increased cell turnover and breakdown of red cells in Polycythemia Vera, leading to elevated **uric acid levels** [1]. - Patients may experience **gout attacks** as a consequence of this elevated uric acid [1]. *Prone for acute leukemia* - While there is an increased risk of transformation to myeloid neoplasms, the risk for **acute leukemia** is not directly attributed to Polycythemia Vera in most cases. - It is more related to myelofibrosis or secondary conditions developing over time rather than a direct association.
Question 1092: What is the recommended time frame for completing a blood transfusion after initiation?
- A. 1-4 hours (Correct Answer)
- B. 3-6 hours
- C. 4-8 hours
- D. 8-12 hours
Explanation: ***1-4 hours*** - This timeframe is recommended to **minimize the risk of bacterial growth** in the blood product, as bacteria can multiply quickly at room temperature. - Completing the transfusion within 4 hours also reduces the likelihood of **red blood cell degeneration** and loss of efficacy. *3-6 hours* - This period extends beyond the recommended maximum of 4 hours, increasing the risk of **bacterial proliferation** in the blood product. - Prolonged infusion times can also lead to a **decrease in the viability and function** of transfused cells. *4-8 hours* - Transfusing over 4-8 hours significantly elevates the risk of **bacterial contamination** and potential septic reactions. - The extended duration compromises the **quality and safety** of the blood product. *8-12 hours* - This timeframe is unacceptably long for a blood transfusion, posing a **critical risk of severe bacterial growth** and infection. - Blood products should not be administered beyond 4 hours due to the rapid decline in **cell integrity and increased adverse reaction potential**.
Question 1093: Response to iron therapy in iron deficiency anemia is denoted by?
- A. Increase in hemoglobin
- B. Reticulocytosis (Correct Answer)
- C. Restoration of enzymes
- D. Increase in iron binding capacity
Explanation: Reticulocytosis - Reticulocytosis is one of the earliest signs of a positive response to iron therapy in iron deficiency anemia, occurring within 5-10 days. - It signifies that the bone marrow is effectively producing new red blood cells after iron supplementation. Restoration of enzymes - While iron is a crucial component of many enzymes (e.g., catalase, cytochrome oxidase), its restoration takes time and is not the primary immediate indicator of therapeutic response. - Clinical improvement and other hematological parameters precede the full restoration of enzyme function. Increase in hemoglobin - An increase in hemoglobin is a definitive sign of successful treatment, but it occurs later than reticulocytosis, typically visible after several weeks to months of therapy. - Hemoglobin levels rise as the new, iron-sufficient red blood cells fully mature and replace the older, iron-deficient ones. Increase in iron binding capacity - In iron deficiency anemia, total iron-binding capacity (TIBC) is typically increased due to more transferrin being available to bind iron [1]. - Successful iron therapy would lead to a decrease in TIBC as transferrin sites become saturated with iron, not an increase.
Question 1094: Cryoprecipitate is useful in which of the following conditions?
- A. Hemophilia A
- B. Thrombosthenia
- C. Warfarin reversal
- D. Afibrinogenemia (Correct Answer)
Explanation: ***Afibrinogenemia*** - Cryoprecipitate is rich in **fibrinogen**, factor VIII, factor XIII, von Willebrand factor, and fibronectin. It is the only blood product with a substantial concentration of fibrinogen. - **Afibrinogenemia** (or hypofibrinogenemia) is a condition characterized by low or absent levels of fibrinogen, a critical clotting factor that cryoprecipitate replaces effectively. *Hemophilia A* - Hemophilia A is a deficiency of **Factor VIII**. While cryoprecipitate contains factor VIII, **recombinant Factor VIII concentrates** are the preferred treatment due to better safety (reduced risk of viral transmission) and more precise dosing [1]. - Cryoprecipitate was historically used for Hemophilia A before the availability of safer, more specific factor concentrates [2]. *Thrombosthenia* - Thrombasthenia is a platelet function disorder characterized by defective **glycoprotein IIb/IIIa receptors** on platelets, leading to impaired platelet aggregation. - Cryoprecipitate does not contain platelets or factors that directly correct platelet function, making **platelet transfusions** the treatment of choice for severe bleeding in thrombasthenia. *Warfarin reversal* - Warfarin reversal is primarily achieved using **Vitamin K**, which restores levels of functional clotting factors II, VII, IX, and X. - For rapid reversal in emergencies, **prothrombin complex concentrate (PCC)** is preferred because it contains high concentrations of these vitamin K-dependent factors, addressing the primary deficiency caused by warfarin [1].
Question 1095: Thalassemia gives protection against ?
- A. Protection against filaria
- B. Protection against kala-azar
- C. Protection against leptospirosis
- D. Protection against malaria (Correct Answer)
Explanation: Protection against malaria - Individuals with thalassemia, particularly thalassemia trait, have some degree of protection against severe forms of malaria, specifically Plasmodium falciparum [1]. - The altered red blood cell structure and reduced hemoglobin content in thalassemia make the red blood cells less hospitable for the parasites, hindering their replication and survival [1]. Protection against filaria - Filaria is caused by parasitic worms (nematodes) transmitted by mosquitoes, leading to lymphatic filariasis (elephantiasis) or onchocerciasis (river blindness). - Thalassemia's primary impact is on red blood cell health and oxygen transport, offering no known protective effect against nematode infections or their associated pathology. Protection against kala-azar - Kala-azar (visceral leishmaniasis) is caused by Leishmania parasites transmitted by sandflies, primarily affecting the reticuloendothelial system (spleen, liver, bone marrow). - There is no established scientific evidence indicating that thalassemia provides protection against Leishmania infections or their clinical manifestations. Protection against leptospirosis - Leptospirosis is a bacterial infection caused by Leptospira bacteria, typically acquired through contact with contaminated water or animal urine. - Thalassemia is a genetic blood disorder; its physiological effects are unrelated to the mechanisms of infection or immunity against bacterial pathogens like Leptospira.
Question 1096: Which of the following does not synthesize von Willebrand factor?
- A. Endothelial cells
- B. Hepatocytes (Correct Answer)
- C. Megakaryocytes
- D. None of the options
Explanation: ***Hepatocytes*** - Von Willebrand factor (vWF) is primarily synthesized by **endothelial cells** and **megakaryocytes** [1], not hepatocytes. - Hepatocytes are responsible for synthesizing other proteins like **clotting factors**, but not vWF. *Megakaryoctyes* - Megakaryocytes play a crucial role in the synthesis of **platelet-derived factors**, including von Willebrand factor (vWF) [1]. - They release vWF into the bloodstream, facilitating platelet adhesion, especially in vascular injury sites. *None* - The option implies all listed cell types synthesize vWF, which is incorrect, as **only endothelial cells and megakaryocytes** produce it [1]. - Suggests a misunderstanding of the synthesis of coagulation-related factors, as hepatocytes do not produce vWF. *Endothelial cells* - Endothelial cells are the primary source of **von Willebrand factor** [1], releasing it to assist in platelet aggregation and clotting. - They are essential for the body's response to vascular injury, facilitating hemostasis. **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 1097: Anemia with reticulocytosis is seen in -
- A. Hemolysis (Correct Answer)
- B. Iron deficiency anemia
- C. Vitamin B12 deficiency
- D. Aplastic anemia
Explanation: ***Hemolysis*** - Reticulocytosis indicates a compensatory response to anemia, often occurring in hemolytic processes where the **bone marrow increases red blood cell production** in response to red blood cell destruction. - Conditions like **sickle cell disease** or **autoimmune hemolytic anemia** lead to hemolysis, further confirming increased reticulocyte count. *Iron deficiency anemia* - Typically presents with a **low reticulocyte count** as the bone marrow does not have sufficient iron to produce new red blood cells. - This condition is characterized by **microcytic, hypochromic** red blood cells due to inadequate iron stores. *Vitamin B12 deficiency* - Often results in a **macrocytic anemia** with a variable reticulocyte count; however, reticulocytosis is generally not seen initially. - This deficiency affects DNA synthesis, leading to ineffective erythropoiesis and the presence of **megaloblastic changes**. *Aplastic anemia* - Characterized by a **decrease in all types of blood cells** (pancytopenia) and typically has a **low reticulocyte count** due to bone marrow failure. - There is insufficient production of red blood cells, hence **reticulocytosis is not observed**.
Question 1098: Which of the following diseases is NOT associated with Anti-Neutrophil Cytoplasmic Antibodies (ANCA)?
- A. Wegener's granulomatosis
- B. Henoch schonlein purpura (Correct Answer)
- C. Microscopic PAN
- D. Churg Strauss syndrome
Explanation: ***Henoch schonlein purpura*** - **Henoch-Schönlein purpura (HSP)** is not associated with **ANCA**; it primarily involves IgA deposition [1]. - Commonly presents with **purpura**, **abdominal pain**, and **glomerulonephritis**, differentiating it from ANCA-associated vasculitides [1]. *Wegener's granulomatosis* - **Wegener's granulomatosis**, now known as **Granulomatosis with polyangiitis**, is strongly associated with **c-ANCA** and anti-PR3 antibodies. - It typically presents with **respiratory** and **renal symptoms** due to vasculitis [2]. *Microscopic PAN* - **Microscopic polyangiitis (PAN)** is associated with **p-ANCA** and myeloperoxidase (MPO) antibodies. - It leads to **glomerulonephritis** and **pulmonary hemorrhage**, indicating its vasculitic nature. *Churg Strauss syndrome* - **Churg-Strauss syndrome**, or **Eosinophilic Granulomatosis with Polyangiitis**, is associated with **p-ANCA** and perinuclear staining [1]. - Often presents with **asthma**, **eosinophilia**, and systemic vasculitis affecting multiple organs [1].
Question 1099: In a patient with suspected vitamin B12 deficiency, which condition would result in an abnormal Schilling test?
- A. Amylase deficiency
- B. Pancreatic endocrine insufficiency
- C. Lipase deficiency
- D. Intrinsic factor deficiency (Correct Answer)
Explanation: ***Intrinsic factor deficiency*** - The Schilling test assesses the absorption of **vitamin B12**. **Intrinsic factor** is crucial for B12 absorption in the ileum. - Deficiency of intrinsic factor, as seen in **pernicious anemia**, directly impairs B12 absorption, leading to an abnormal Schilling test result [1]. *Amylase deficiency* - **Amylase** is an enzyme involved in the digestion of carbohydrates, not vitamin B12 absorption [2]. - Its deficiency would primarily cause carbohydrate malabsorption symptoms, not an abnormal Schilling test. *Pancreatic endocrine insufficiency* - **Pancreatic endocrine function** relates to hormone production (e.g., insulin, glucagon), while exocrine function involves digestive enzymes. - Impairment of endocrine function does not directly affect vitamin B12 absorption or the Schilling test. *Lipase deficiency* - **Lipase** is an enzyme essential for the digestion of fats [2]. - Its deficiency would lead to fat malabsorption (steatorrhea) but would not affect vitamin B12 absorption or the Schilling test results.
Question 1100: Which of the following statements about Sickle Cell Anemia is FALSE?
- A. There is a positive correlation between HBS and polymerization of HBS (Correct Answer)
- B. Recurrent infections is the most common cause of death
- C. Patients require frequent blood transfusions
- D. Patients usually present before the age of 6 months
Explanation: ***There is a positive correlation between HBS and polymerization of HBS*** - This statement is false because the polymerization of **hemoglobin S (HbS)** is reduced as HbS levels decrease and is increased as HbS levels increase. Therefore, there is a **direct correlation**, not a positive one, where higher levels of HbS lead to more polymerization and sickling. - The disease is caused by the **polymerization of deoxyhemoglobin S**, which distorts red blood cells into a sickle shape, leading to vaso-occlusion and hemolysis [1]. *Recurrent infections is the most common cause of death* - **Recurrent infections** are indeed a leading cause of morbidity and mortality in sickle cell anemia patients, particularly in children due to **functional asplenia**. [1] - **Splenic dysfunction** impairs the ability to clear encapsulated bacteria, increasing the risk of severe infections like **pneumonia** and **meningitis**. *Patients require frequent blood transfusions* - **Frequent blood transfusions** are a common treatment strategy for sickle cell anemia to manage complications such as severe anemia, acute chest syndrome, and stroke prevention [1]. - **Chronic transfusion therapy** helps to suppress abnormal sickle cell production and dilute existing sickle cells, thereby reducing vaso-occlusive crises. *Patients usually present before the age of 6 months* - Patients with sickle cell anemia typically become symptomatic after 6 months of age, when **fetal hemoglobin (HbF)** levels decline. - **HbF protects** against sickling, so symptoms like **dactylitis** and **splenic sequestration** usually manifest once HbF is replaced by HbS [1].
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
Practice Questions
Thalassemias
Practice Questions
Platelet Disorders
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Coagulation Disorders
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Thrombotic Disorders
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Leukemias
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Lymphomas
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Multiple Myeloma and Plasma Cell Disorders
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Myeloproliferative Neoplasms
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Transfusion Medicine
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Hematopoietic Stem Cell Transplantation
Practice Questions
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