Hematology — MCQs
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Most common hematological malignancy associated with Rheumatoid Arthritis (RA)?
What are the key characteristics of Evans syndrome?
Cryoprecipitate is useful in which of the following conditions?
Thalassemia gives protection against ?
Which of the following does not synthesize von Willebrand factor?
Response to iron therapy in iron deficiency anemia is denoted by?
Anemia with reticulocytosis is seen in -
All the following are true about multiple myeloma except for which of the following?
Which of the following statements about Sickle Cell Anemia is FALSE?
In a severely anaemic pregnant patient presenting with cardiac failure, what is the most appropriate choice of transfusion?
Hematology Indian Medical PG Practice Questions and MCQs
Question 1091: Most common hematological malignancy associated with Rheumatoid Arthritis (RA)?
- A. Diffuse large B cell lymphoma
- B. Chronic lymphocytic leukemia
- C. T-cell prolymphocytic leukemia
- D. Large granular lymphocytic leukemia (LGLL) (Correct Answer)
Explanation: ***Large granular lymphocytic leukemia (LGLL)*** - **LGLL** is the most common hematological malignancy strongly associated with **rheumatoid arthritis (RA)**, often presenting with features such as **neutropenia** and splenomegaly. - Approximately 80% of patients with LGLL have a **T-cell phenotype**, and a significant subset experiences **autoimmune diseases**, with RA being the most frequent. *Diffuse large B cell lymphoma* - While patients with **RA** have an increased risk of **lymphoma**, **diffuse large B-cell lymphoma (DLBCL)** is a more aggressive type but not the most common hematologic malignancy directly associated with the disease itself in terms of prevalence [3]. - Inflammatory conditions like **RA** can contribute to chronic immune stimulation, increasing the risk of certain lymphomas, but LGLL holds a more direct and prevalent association [1]. *Chronic lymphocytic leukemia* - **Chronic lymphocytic leukemia (CLL)** is a lymphoproliferative disorder of **B lymphocytes**, but it does not have a particularly strong or common association with **RA** compared to LGLL [2]. - The elevated risk of hematological malignancies in RA patients typically points more towards lymphoproliferative disorders driven by specific immune dysregulations characteristic of RA. *T-cell prolymphocytic leukemia* - **T-cell prolymphocytic leukemia (T-PLL)** is a rare and aggressive **T-cell leukemia** that generally presents with a high white blood cell count and splenomegaly, but it is not commonly linked with **RA**. - Its clinical presentation and biology are distinct from the more indolent leukemias like LGLL that are often seen in conjunction with autoimmune conditions.
Question 1092: What are the key characteristics of Evans syndrome?
- A. Autoimmune hemolytic anemia and immune thrombocytopenia (Correct Answer)
- B. Low lymphocyte and red blood cell counts
- C. High platelet and lymphocyte counts
- D. A reduction in all blood cell types
Explanation: ***Autoimmune hemolytic anemia and immune thrombocytopenia*** - **Evans syndrome** is defined by the simultaneous or sequential occurrence of **autoimmune hemolytic anemia (AIHA)** and **immune thrombocytopenia (ITP)** [1], [2]. - Both conditions involve the immune system mistakenly attacking and destroying **red blood cells** and **platelets**, respectively [1], [2]. *Low lymphocyte and red blood cell counts* - While **red blood cell counts** are low in Evans syndrome due to AIHA, **lymphocyte counts** are not a defining characteristic; they can vary. - This option does not fully capture the dual autoimmune destruction of red blood cells and platelets specific to Evans syndrome. *High platelet and lymphocyte counts* - **Platelet counts** are **low** in Evans syndrome due to ITP, not high. - **Lymphocyte counts** are not characteristically high; a high count might suggest other conditions like leukemias or lymphomas. *A reduction in all blood cell types* - A reduction in all (red blood cells, white blood cells, and platelets) is known as **pancytopenia**, which is not the defining feature of Evans syndrome. - Evans syndrome specifically involves the destruction of **red blood cells** and **platelets**, but not necessarily all white blood cell types.
Question 1093: 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 1094: 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 1095: 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 1096: 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 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: All the following are true about multiple myeloma except for which of the following?
- A. Hypercalcemia
- B. Presence of Bence-Jones proteins in urine
- C. Osteolytic bone disease
- D. Chromosomal translocation t(8;14), commonly seen in Burkitt's lymphoma (Correct Answer)
Explanation: ***t(8-14) translocation*** - The **t(8;14) translocation** is not typically associated with multiple myeloma; rather, it is commonly seen in **Burkitt lymphoma** [2]. - Multiple myeloma is primarily linked with chromosomal abnormalities such as **deletions** and **translocations involving different chromosomes**. *Osteolytic bone disease* - A hallmark feature of multiple myeloma, **osteolytic lesions** result from increased osteoclastic activity and are often seen in the skull, spine, and ribs [1]. - Patients frequently present with **bone pain** due to these lesions, which are characteristic of the disease [1]. *Light chain proliferation* - In multiple myeloma, a significant feature is the overproduction of **monoclonal light chains** [1]. - This leads to **light chain disease** or **renal impairment**, further supporting the diagnosis [1]. *Bence-Jones proteins in urine* - The presence of **Bence-Jones proteins**, which are free light chains, is a classic finding in multiple myeloma [1]. - They are often detected in the **urine** and can be used to monitor disease progression or response to treatment [1].
Question 1099: 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].
Question 1100: In a severely anaemic pregnant patient presenting with cardiac failure, what is the most appropriate choice of transfusion?
- A. Platelets
- B. Packed cells (Correct Answer)
- C. Whole blood
- D. Exchange transfusion
Explanation: ***Packed cells*** - **Packed red blood cells (PRBCs)** increase **oxygen-carrying capacity** with minimal volume expansion, which is crucial in patients with cardiac compromise [1]. - Slow infusion of PRBCs, often with a **diuretic**, can improve anaemia and cardiac function while preventing **fluid overload**. *Platelets* - **Platelets** are primarily transfused for **thrombocytopenia** or **platelet dysfunction** to prevent or treat bleeding. - They do not address the low haemoglobin and oxygen-carrying deficit directly contributing to cardiac failure in an anaemic patient. *Whole blood* - **Whole blood** contains plasma, which can significantly increase circulatory volume and worsen **cardiac failure** in patients already struggling with fluid balance. - While it does provide red cells, the added volume makes it a less safe option compared to packed cells in this scenario. *Exchange transfusion* - An **exchange transfusion** involves removing a patient's blood and replacing it with donor blood, typically used for severe conditions like **sickle cell crisis** or **severe hyperbilirubinemia** [2]. - This procedure is complex and carries higher risks, and is not the first-line treatment for anaemia-induced cardiac failure in pregnancy.
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
Practice Questions
Thalassemias
Practice Questions
Platelet Disorders
Practice Questions
Coagulation Disorders
Practice Questions
Thrombotic Disorders
Practice Questions
Leukemias
Practice Questions
Lymphomas
Practice Questions
Multiple Myeloma and Plasma Cell Disorders
Practice Questions
Myeloproliferative Neoplasms
Practice Questions
Transfusion Medicine
Practice Questions
Hematopoietic Stem Cell Transplantation
Practice Questions
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