Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1381: Shelf life of platelets in a blood bank is

A. 5 days (Correct Answer)
B. 7 days
C. 10 days
D. 21 days

Explanation: **5 days** - Platelets stored at **room temperature (20-24°C)** have a limited shelf life due to the risk of bacterial contamination and metabolic changes. - This short storage period ensures the **viability and function** of platelets for transfusion. *7 days* - A 7-day shelf life was initially proposed but was not widely adopted due to concerns about increased **bacterial growth** and the practical challenges of extended storage at room temperature. - The risk of **bacterial sepsis** significantly increases with longer room temperature storage. *10 days* - This duration is beyond the currently accepted shelf life for platelets, leading to an unacceptably high risk of **bacterial contamination** and reduced therapeutic efficacy. - Storing platelets for 10 days would likely result in an increased incidence of **transfusion-associated sepsis**. *21 days* - A shelf life of 21 days is typical for **red blood cells** when stored at 1-6°C with specific anticoagulants, but it is far too long for platelets. - Platelets stored for this duration at room temperature would be significantly **non-viable** and pose a severe risk of bacterial infection.

Question 1382: Which of the following is NOT seen in polycythemia vera?

A. Increased erythropoietin (Correct Answer)
B. Intrinsic abnormality of hematopoietic precursors
C. Erythropoietin independent growth of red cell progenitors
D. Most common cause of primary polycythemia

Explanation: ***Increased erythropoietin*** - In polycythemia vera, patients usually exhibit **low erythropoietin levels** due to feedback inhibition from increased red blood cell mass. - The condition is driven by a **myeloproliferative disorder** [2], not by increased erythropoietin stimulation. *Most common cause of polycythemia* - This option is incorrect because polycythemia vera is specifically a type of **primary polycythemia** [1], rather than the most common cause, which is often **secondary causes** such as hypoxia or abnormal erythropoietin production. - Other causes including chronic lung disease or renal tumors are more prevalent sources of increased red blood cell production. *Intrinsic abnormality of hematopoietic precursors* - While polycythemia vera indeed involves an **abnormality in hematopoietic stem cells** [1], it is not the only mechanism leading to polycythemia; many cases have secondary causes. - Hence, this option misrepresents the specific and more accurate characterization of polycythemia vera. *Erythropoietin independent growth of red cell progenitors* - Polycythemia vera is associated with **erythropoietin-independent** proliferation of hematopoietic cells [2], which is characteristic of the condition due to mutations in **JAK2** [2,3]. - This accurately reflects a significant feature of the disease, aligning closely with the pathophysiology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 663-664. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615. [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. 626-627.

Question 1383: Osmotic fragility test is commonly used for which of the following conditions?

A. Megaloblastic anemia
B. Aplastic anemia
C. Hereditary spherocytosis (Correct Answer)
D. Iron deficiency anemia

Explanation: ***Hereditary spherocytosis*** - The **osmotic fragility test** helps in diagnosing hereditary spherocytosis, where **spherical red blood cells** are more prone to hemolysis in hypotonic solutions [1][2]. - This condition is characterized by **spherocytes** (abnormally shaped RBCs) leading to increased osmotic fragility [1][3]. *Megaloblastic anemia* - Megaloblastic anemia is primarily associated with **deficiencies in B12 or folate**, affecting the size and maturation of red blood cells, not their osmotic fragility. - The diagnosis focuses on **serum vitamin levels** and **bone marrow examination** rather than osmotic fragility. *Iron deficiency anemia* - Iron deficiency anemia features **microcytic** and **hypochromic RBCs**, and its diagnosis relies on **iron studies**, not osmotic fragility tests. - The osmotic fragility test does not reveal significant changes in red blood cells for this condition. *Aplastic anemia* - Aplastic anemia involves **pancytopenia** due to bone marrow failure and does not typically show altered osmotic fragility. - The diagnosis is confirmed through **bone marrow biopsy**, not by assessing osmotic fragility. **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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638.

Question 1384: Which of the following statements is true regarding the Duffy Fy(a-b-) blood group?

A. lacks H- antigen
B. lacks A-antigen
C. All of the options
D. lacks Fy(b) antigen (Correct Answer)

Explanation: ***lacks Fy(b) antigen*** - The **Duffy Fy(a-b-)** phenotype indicates absence of both Fya and Fyb antigens on red blood cells. - Since the phenotype is **Fy(a-b-)**, it definitively lacks the **Fyb antigen** (indicated by the "b-" notation). - This phenotype is common in people of **African descent** and confers natural **resistance to Plasmodium vivax malaria**, as these antigens serve as receptors for the parasite to enter RBCs. *lacks H- antigen* - The **H antigen** belongs to the **H/h blood group system** and is a precursor to A and B antigens in the ABO system. - The absence of H antigen (Bombay phenotype - Oh) is completely **unrelated to the Duffy blood group system**. - Duffy antigens are on the **DARC (Duffy Antigen Receptor for Chemokines)** protein, distinct from the H antigen. *lacks A-antigen* - The **A antigen** is part of the **ABO blood group system** and defines blood types A and AB. - The Duffy blood group system is **genetically and structurally independent** from the ABO system. - Having Fy(a-b-) phenotype does not affect A antigen expression. *All of the options* - This is incorrect because the Duffy Fy(a-b-) phenotype **specifically refers only to the absence of Duffy antigens** (Fya and Fyb). - It has **no relationship** with A, B, or H antigens, which belong to different blood group systems controlled by different genes on different chromosomes.

Question 1385: Sezary cells show which type of nucleus?

A. Cerebriform (Correct Answer)
B. Pleomorphic
C. Round
D. Eosinophilic

Explanation: ***Cerebriform*** - **Sezary cells** are characterized by their distinctive **cerebriform nuclei**, giving them an irregular, convoluted appearance [1,2]. - This finding is a hallmark of **cutaneous T-cell lymphoma** and emphasizes their potential malignancy [1,2]. *Round* - Round nuclei do not reflect the typical morphology of **Sezary cells**, which are noted for their **irregular shape**. - Other lymphocytes may exhibit round nuclei, but this does not specifically indicate a **Sezary cell** presence. *Pleomorphic* - While some malignant cells might show **pleomorphic nuclei**, Sezary cells uniquely showcase **cerebriform nuclei** rather than varying shapes [1,2]. - Pleomorphic is not a defining characteristic of **Sezary cells**, making this description inaccurate. *Eosinophillic* - Eosinophilic refers to cells that stain positively for **eosin**, typically associated with **eosinophils**, which is not relevant to **Sezary cells**. - Sezary cells are more about their **nuclear morphology** and less about eosinophilic staining characteristics. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 564-565. [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. 613-614.

Question 1386: The most common translocation seen in patients with Multiple Myeloma is:

A. t(14;16)
B. t(4;14)
C. t(11;14) (Correct Answer)
D. t(14;20)

Explanation: ***t(11;14)*** - This translocation is the **most common cytogenetic abnormality** found in patients with multiple myeloma, occurring in approximately 15-20% of cases. - It results in the juxtaposition of the **IgH gene on chromosome 14** with the **cyclin D1 gene on chromosome 11**, leading to overexpression of cyclin D1. *t(4;14)* - This translocation, occurring in about 5-10% of patients, is associated with a **poor prognosis** in multiple myeloma. - It involves the IgH gene on chromosome 14 and the **FGFR3 and MMSET genes on chromosome 4**, leading to their upregulation. *t(14;16)* - This translocation is also associated with a **poor prognosis** and is less common than t(11;14) or t(4;14), found in about 2-5% of cases. - It involves the **IgH gene on chromosome 14** and the **c-MAF gene on chromosome 16**, leading to overexpression of c-MAF. *t(14;20)* - This translocation is **rarely observed** in multiple myeloma patients, typically occurring in less than 1% of cases. - It involves the **IgH gene on chromosome 14** and the **MAFB gene on chromosome 20**, which can also contribute to disease progression.

Question 1387: What is the Thomsen Friedenreich phenomenon?

A. Agglutination of red blood cells by all blood group sera
B. Agglutination of red blood cells by anti-T antibodies
C. Association with certain malignancies
D. Exposure of cryptic T-antigen on red blood cells (Correct Answer)

Explanation: ***Exposure of cryptic T-antigen on red blood cells*** - The Thomsen Friedenreich phenomenon, also known as **T-activation**, occurs when bacterial enzymes (neuraminidase) remove N-acetylneuraminic acid (sialic acid) residues from red cell surface glycoproteins, **unmasking the cryptic T-antigen** (Thomsen-Friedenreich antigen). - This unmasking leads to the red blood cells becoming agglutinable by naturally occurring **anti-T antibodies** present in almost all adult human sera, resulting in polyagglutination. - The T-antigen is not newly synthesized but is **pre-existing and cryptic**, hidden beneath sialic acid residues until exposed by bacterial neuraminidase activity. *Agglutination of red blood cells by anti-T antibodies* - While agglutination by anti-T antibodies is a *consequence* of the Thomsen Friedenreich phenomenon, it is not the phenomenon itself. The phenomenon describes the underlying cellular change - the **exposure of the cryptic T-antigen**. - This polyagglutination occurs because anti-T antibodies are naturally present in nearly all adult human sera. *Agglutination of red blood cells by all blood group sera* - The Thomsen Friedenreich phenomenon specifically involves agglutination by **anti-T antibodies**, which are naturally occurring and widely present, but it does not mean agglutination by *all* blood group sera (e.g., anti-A, anti-B, anti-D won't cause agglutination based on T-activation alone). - The T-antigen is distinct from the **ABO blood group antigens** and other blood group systems. *Association with certain malignancies* - While T-antigen (Tn antigen) can be expressed on certain **malignant cells** (tumor-associated antigen) and is relevant in cancer immunology, this is a separate clinical context from the Thomsen Friedenreich phenomenon in **blood banking** and transfusion medicine. - The Thomsen Friedenreich phenomenon primarily refers to the **acquired exposure** of cryptic T-antigen on red blood cells due to bacterial neuraminidase action, typically seen in infections or bacterial contamination.

Question 1388: 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 1389: 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 1390: 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.

Practice by Chapter

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Plasma Cell Disorders

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Bleeding Disorders

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Thrombotic Disorders

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