Hematopathology Practice Questions

Q: The immunoglobulin most commonly involved in Multiple Myeloma is:

IgG. ***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.

Q: Which of the following conditions does not provide protection against malaria?

PNH. ***PNH*** - **Paroxysmal Nocturnal Hemoglobinuria (PNH)** does not provide protection against malaria; it is a disorder of the blood that leads to red blood cell destruction, but malaria specifically targets red blood cells. - PNH is associated with increased risk of venous thrombosis and hemolytic anemia, rather than any protective mechanism against malaria. *Sickle cell anemia* - The sickle cell trait provides a **protective advantage** against malaria by offering some resistance due to the abnormal shape of the cells [1]. - Individuals with the trait have a lower risk of severe malaria, particularly caused by *Plasmodium falciparum* [1]. *Duffy blood group* - People with the **Duffy negative phenotype** are resistant to certain strains of malaria, as the Duffy antigen serves as a receptor for *Plasmodium vivax*. - Therefore, those lacking the Duffy antigen are less susceptible to infections by this malaria strain. *Thalassemia* - Thalassemia provides a protective effect against malaria by producing **abnormal hemoglobin**, which malaria parasites cannot easily thrive in [2]. - This leads to an altered red blood cell environment that is less favorable for *Plasmodium* infection [1].

Q: In which condition is Hemoglobin F typically elevated?

Beta-thalassemia. ***Beta-thalassemia*** - In **beta-thalassemia**, there is reduced or absent synthesis of beta-globin chains, leading to an excess of alpha-globin chains. - To compensate, the body markedly increases production of fetal hemoglobin (**HbF**, α2γ2), which can constitute **50-90% of total hemoglobin** in beta-thalassemia major. - This compensatory mechanism helps alleviate the severity of anemia and ineffective erythropoiesis, making elevated HbF a **defining laboratory feature** of beta-thalassemia. *Hereditary spherocytosis* - This condition is characterized by defects in **erythrocyte membrane proteins** (spectrin, ankyrin, band 3), leading to fragile, spherical red blood cells. - While it causes **hemolytic anemia**, it does not involve elevated HbF levels; the defect is structural, not related to globin chain synthesis. *Congenital red cell aplasia* - This condition (e.g., **Diamond-Blackfan anemia**) involves a primary defect in early **erythroid progenitor cells**, leading to severe anemia. - While some patients may have elevated HbF, it is not a consistent or defining feature; the main problem is the lack of adequate red blood cell production, not a compensatory shift in globin synthesis. *Sickle cell disease* - In **sickle cell disease**, there is an abnormal beta-globin chain leading to the production of **hemoglobin S (HbS)**. - While HbF is indeed elevated in most patients (typically **2-15%**, compared to <1% in normal adults), the elevation is **less marked and consistent** compared to beta-thalassemia. - The primary defect is the presence of HbS, and while HbF elevation provides some clinical benefit (it inhibits HbS polymerization), beta-thalassemia remains the condition most characteristically associated with high HbF levels.

Q: Which of the following is not typically screened for in blood donations?

Epstein-Barr Virus (EBV). ***Epstein-Barr Virus (EBV)*** ✓ - EBV is **NOT routinely screened** for in blood donations in India and most countries - While EBV is a common virus (>90% adults are seropositive), it is **not considered a major transfusion-transmitted infection** - The virus is primarily transmitted through saliva; transfusion-associated EBV transmission is **extremely rare and usually not clinically significant** in immunocompetent recipients - Risk-benefit analysis does not support routine screening due to **high prevalence, low clinical impact, and cost considerations** - EBV screening may only be considered for specific recipients (e.g., severely immunocompromised patients) *HIV* - **Routinely screened** in all blood donations worldwide - Screening includes HIV-1 and HIV-2 antibodies and/or HIV antigen/RNA testing - Transfusion-transmitted HIV causes AIDS with severe consequences - Mandatory screening under the Drugs and Cosmetics Act in India *HBV* - **Routinely screened** in all blood donations - Screening includes HBsAg (Hepatitis B surface antigen) testing, and often anti-HBc or HBV DNA - Can cause acute and chronic hepatitis, cirrhosis, and hepatocellular carcinoma - Mandatory screening in India and globally *HCV* - **Routinely screened** in all blood donations - Screening includes anti-HCV antibodies and/or HCV RNA (nucleic acid testing) - Major cause of chronic hepatitis, cirrhosis, and liver cancer - Mandatory screening under blood safety regulations

Q: PNH patients have deficient surface proteins that normally protect red blood cells from activated complements. Which two surface proteins are deficient in these patients?

CD 45 and CD 55. ***CD 55 and CD 59*** - **CD 55 (decay accelerating factor)** and **CD 59 (protectin)** are crucial for inhibiting the complement system, protecting red blood cells from lysis in PNH. - Deficiencies in these proteins lead to increased **susceptibility** of red cells to **complement-mediated hemolysis**. *CD58 and CD 59* - **CD 58** is involved in T-cell interaction but does not solely protect red cells from complement. - While **CD 59** is a correct answer, the absence of **CD 55** makes this option incorrect for PNH. *CD 45 and CD 59* - **CD 45** is primarily a **leukocyte common antigen**, not involved in protecting red cells from complement activation. - This orrectly mentions **CD 59**, but lacks **CD 55**, making it unsuitable as an answer. *CD 51 and CD 59* - **CD 51** is associated with integrin functions and does not play a role in protecting red blood cells from complements. - Although **CD 59** is relevant, the deficiency in **CD 55** highlights the incompleteness of this option.

Q: What is the chromosomal translocation associated with Acute Myeloid Leukemia M3?

t(15;17). ***T (15,17)*** [1][2][3] - This translocation pertains to **Acute Promyelocytic Leukemia (APL)**, associated with the fusion gene **PML-RARA** [1][3]. - APL is characterized by **promyelocytes** with heavy granulation and a clinical presentation that includes coagulopathy [2][3]. *T (8, 21)* - This translocation is associated with **AML M2**, involving the **RUNX1-RUNX1T1** fusion gene [3]. - It does not correlate with the classic features of AML M3, which is specifically characterized by T (15,17). *T (9,11)* - Primarily seen in **AML M5**, this translocation is not related to the pathophysiology of AML M3. - The fusion commonly observed here is **MLL-AFF1**, which affects different types of leukemias, not APL. *T (18,21)* - This translocation does not have a significant association with any specific type of acute myeloid leukemia. - Unlike T (15,17), it is not linked to the classic features or unique clinical presentation seen in AML M3. **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. 620-621. [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. 621-622. [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, p. 620.

Q: Which of the following conditions is the classic example of acute intravascular hemolysis triggered by oxidative stress?

Acute G6PD deficiency. ***b and c*** - Intravascular hemolysis is commonly associated with both **Acute G6PD deficiency** and **Hereditary spherocytosis**, leading to destruction of red blood cells in the bloodstream [1]. - These conditions are characterized by **high levels of hemoglobinuria** and **low haptoglobin**, indicative of intravascular hemolysis. *Sickle cell ds* - Sickle cell disease primarily causes **extravascular hemolysis** due to splenic sequestration rather than **intravascular** destruction [3]. - The clinical features include **vaso-occlusive crises** and splenic infarction rather than hemolysis within the blood vessels. *Acute G6PD* - While acute G6PD deficiency can lead to hemolysis, it is typically **triggered by oxidative stress** rather than occurring continuously [2]. - The hemolysis in G6PD deficiency occurs more in an **extravascular** manner unless acute stress occurs, which can result in **acute intravascular hemolysis, marked by anemia, hemoglobinemia, and hemoglobinuria** [4]. *Hereditary spherocytosis* - This condition primarily causes **extravascular hemolysis** through the spleen, where abnormal spherocytes are destroyed [1]. - Although it leads to anemia, the hallmark of hereditary spherocytosis is the **spleen's role** in hemocyte destruction rather than intravascular hemolysis.

Q: Which of the following is not typically seen in Disseminated Intravascular Coagulation (DIC)?

Normal aPTT. ***Normal APTT*** - In Disseminated Intravascular Coagulation (**DIC**), **APTT** is typically **prolonged** due to consumption of clotting factors [1]. - The presence of normal APTT indicates that coagulation pathways are not significantly affected, which is contrary to what is seen in DIC. *Fibrinogen decreased* - **Decreased fibrinogen levels** are common in DIC, reflecting its consumption during the coagulation process [1]. - This depletion is linked to the increased clotting and is a hallmark of DIC, making this statement false in the context of the question. *Thrombocytopenia* - **Thrombocytopenia** occurs in DIC as platelets are consumed during the formation of microclots [1]. - A significant drop in platelet count is a key feature of DIC, therefore this statement does not align with the "except" clause. *PT elevation* - Prothrombin Time (**PT**) is usually **elevated** in DIC due to the consumption of clotting factors [1]. - This reflects the ongoing activation of the coagulation cascade, supporting the exclusion in the question context. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626.

Q: Which condition is commonly associated with Disseminated Intravascular Coagulation (D.I.C.)?

Acute promyelocytic leukemia. ***Acute promyelocytic leukemia*** - **Disseminated Intravascular Coagulation (D.I.C.)** is commonly associated with acute promyelocytic leukemia due to the release of **tissue factor** from promyelocytes [1]. - Patients typically present with **severe bleeding** and coagulopathy [1], driven by the rapid proliferation of these abnormal cells. *Acute myelomonocytic leukemia* - While this type of leukemia presents with myelomonocytic features, it is less frequently associated with **D.I.C.** compared to acute promyelocytic leukemia. - This condition is often characterized by **monocytic infiltration** but does not typically cause the severe coagulopathy associated with D.I.C. *Autoimmune hemolytic anemia* - This condition causes **hemolysis** due to antibodies but is mainly associated with **anemia**, not a coagulation disorder like D.I.C. - **D.I.C.** involves widespread **consumption coagulopathy** [1], which is not a feature of autoimmune hemolytic anemia. *CMC* - CMC refers to **Chronic Myeloid Leukemia**, which does not commonly lead to **D.I.C.** and presents primarily with splenomegaly and **chronic symptoms**. - The coagulation profile in CMC tends to be stable, with no link to the acute coagulopathy seen in D.I.C.

Q: In which type of Hodgkin's Lymphoma are lacunar cells typically observed?

Nodular Sclerosis type. ***Nodular Sclerosis Type*** - **Lacunar cells** are characteristically seen in **Nodular Sclerosis Hodgkin lymphoma**, which is the most common subtype [1][3]. - These cells are large **Reed-Sternberg cells** with a distinctive morphology, typically found in **fibrous areas** of the lymph node [1]. *Mixed cellularity type* - This subtype is associated with a diverse cell population but does not primarily feature **lacunar cells** [2][4]. - It predominantly contains **Reed-Sternberg cells** without the specific morphology seen in nodular sclerosis [2]. *Lymphocyte predominant* - Lymphocyte predominant type mainly consists of **lymphocytes** with few Reed-Sternberg cells, and lacks **lacunar cells** [5]. - The histology is significantly different, exhibiting a more lymphocytic composition and not the classic lucent spaces [5]. *All of the above* - This option is incorrect as neither **Mixed cellularity** nor **Lymphocyte predominant** types contain **lacunar cells** [2][4][5]. - Lacunar cells are a distinctive feature solely of the **Nodular Sclerosis type** in Hodgkin lymphoma [1]. **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. 616. [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. 616-618. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 558-559. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 559-560. [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. 618.

Question 1

The immunoglobulin most commonly involved in Multiple Myeloma is:

Accepted Answer

IgG

Answer

IgM

Answer

IgA

Answer

IgD

Question 2

Which of the following conditions does not provide protection against malaria?

Accepted Answer

PNH

Answer

Sickle cell anemia

Answer

Thalassemia

Answer

Duffy blood group

Question 3

In which condition is Hemoglobin F typically elevated?

Accepted Answer

Beta-thalassemia

Answer

Congenital red cell aplasia

Answer

Hereditary spherocytosis

Answer

Sickle cell disease

Question 4

Which of the following is not typically screened for in blood donations?

Accepted Answer

Epstein-Barr Virus (EBV)

Answer

HIV

Answer

HBV

Answer

HCV

Question 5

PNH patients have deficient surface proteins that normally protect red blood cells from activated complements. Which two surface proteins are deficient in these patients?

Accepted Answer

CD 45 and CD 55

Answer

CD 55 and CD 58

Answer

CD 55 and CD 59

Answer

CD 51 and CD 55

Question 6

What is the chromosomal translocation associated with Acute Myeloid Leukemia M3?

Accepted Answer

t(15;17)

Answer

t(18;21)

Answer

t(9;11)

Answer

t(8;21)

Question 7

Which of the following conditions is the classic example of acute intravascular hemolysis triggered by oxidative stress?

Accepted Answer

Acute G6PD deficiency

Answer

Hereditary spherocytosis

Answer

Sickle cell disease

Answer

None of the options

Question 8

Which of the following is not typically seen in Disseminated Intravascular Coagulation (DIC)?

Accepted Answer

Normal aPTT

Answer

Thrombocytopenia

Answer

PT elevation

Answer

Fibrinogen decreased

Question 9

Which condition is commonly associated with Disseminated Intravascular Coagulation (D.I.C.)?

Accepted Answer

Acute promyelocytic leukemia

Answer

Acute myelomonocytic leukemia

Answer

Chronic myeloid leukemia

Answer

Autoimmune hemolytic anemia

Question 10

In which type of Hodgkin's Lymphoma are lacunar cells typically observed?

Accepted Answer

Nodular Sclerosis type

Answer

Mixed cellularity type

Answer

Lymphocyte predominant type

Answer

All of the options

Hematopathology — MCQs

Hematopathology — MCQs

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