Leukemias — MCQs
In the evaluation of a newly diagnosed case of acute lymphoid leukemia (ALL), which of the following tests is not routinely included?
A bone marrow aspirate shows blast cells with multiple Auer rods arranged in bundles ('faggot cells'). Which molecular finding would confirm acute promyelocytic leukemia?
Which is the cell of origin of Chronic Lymphocytic Leukaemia / Small Lymphocytic Lymphoma?
Chemotherapeutic Agent of Choice for the treatment of CML?
Auer rods are a characteristic feature of which type of leukemia?
In APML (Acute Promyelocytic Leukemia), all of the following are seen except:
Most common hematological malignancy associated with Rheumatoid Arthritis (RA)?
First line therapy in chronic phase of chronic myeloid leukemia is
Which of the following statements about CNS leukemia is false?
Autoimmune hemolytic anemia is seen in: A) Sickle cell anemia B) Chronic lymphocytic leukemia (CLL) C) Acute myelocytic leukemia (AML) D) Multiple myeloma
Leukemias Indian Medical PG Practice Questions and MCQs
Question 1: In the evaluation of a newly diagnosed case of acute lymphoid leukemia (ALL), which of the following tests is not routinely included?
- A. Plasma viscosity (Correct Answer)
- B. Bone marrow biopsy
- C. Complete metabolic panel
- D. Cell surface phenotyping
Explanation: ### Plasma viscosity - **Plasma viscosity** measurement is not a standard diagnostic or staging test for **acute lymphoid leukemia (ALL)**. [1] - While it can be elevated in conditions with high protein levels or hypergammaglobulinemia, it does not provide specific information relevant to ALL diagnosis or treatment planning. [1] *Bone marrow biopsy* - A **bone marrow biopsy** is crucial for diagnosing ALL, confirming the presence of **lymphoblasts**, and assessing disease burden. [2] - It also helps in identifying cytogenetic and molecular abnormalities. [2] *Cell surface phenotyping* - **Cell surface phenotyping** (immunophenotyping) via **flow cytometry** is essential for classifying the subtype of ALL (e.g., B-ALL, T-ALL) and identifying specific markers. [2] - This information guides treatment protocols and predicts prognosis. [2] *Complete metabolic panel* - A **complete metabolic panel (CMP)** assesses organ function (e.g., kidney, liver), **electrolyte balance**, and levels of substances like **uric acid** and **lactate dehydrogenase (LDH)**. - These measurements are vital for identifying complications, assessing baseline health, and monitoring for **tumor lysis syndrome** which can be seen in ALL.
Question 2: A bone marrow aspirate shows blast cells with multiple Auer rods arranged in bundles ('faggot cells'). Which molecular finding would confirm acute promyelocytic leukemia?
- A. BCR-ABL translocation
- B. PML-RARA translocation (Correct Answer)
- C. AML1-ETO translocation
- D. inv(16) mutation
Explanation: PML-RARA translocation - The presence of Auer rods arranged in bundles forming faggot cells is highly characteristic of acute promyelocytic leukemia (APL) [1]. - APL is genetically defined by the t(15;17) translocation, which creates the PML-RARA fusion gene [1], [2]. BCR-ABL translocation - This translocation, t(9;22), is characteristic of chronic myeloid leukemia (CML) and some cases of acute lymphoblastic leukemia (ALL), not APL [2]. - It does not typically present with the morphologic features of APL, such as faggot cells. AML1-ETO translocation - The t(8;21) translocation results in the AML1-ETO fusion gene and is associated with a specific subtype of acute myeloid leukemia (AML) with maturation, typically M2 [1]. - While Auer rods can be seen, the bundled faggot cells are not characteristic of this subtype [1]. inv(16) mutation - The inv(16)(p13q22) mutation is associated with acute myelomonocytic leukemia (AMML) with eosinophilia (M4Eo) [1]. - This subtype also features a specific morphology with abnormal eosinophils, not the faggot cells seen in APL [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, pp. 620-621. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 605-607.
Question 3: Which is the cell of origin of Chronic Lymphocytic Leukaemia / Small Lymphocytic Lymphoma?
- A. Mature B cells
- B. Progenitor T cells
- C. Mature T cells
- D. Naïve B cells (Correct Answer)
Explanation: ***Naïve B cells*** - Chronic Lymphocytic Leukaemia (CLL) and Small Lymphocytic Lymphoma (SLL) originate from **CD5-positive B lymphocytes** arrested in a mature but **naïve differentiation stage** [1]. - These cells express both **B-cell markers (CD19, CD20, CD23)** and a T-cell marker (CD5), which is characteristic of the clone [4]. *Mature B cells* - While CLL/SLL are derived from B cells, they are specifically from **naïve, not fully mature, B cells**. - **Other B-cell lymphomas** like follicular lymphoma or mantle cell lymphoma originate from distinct stages of mature B-cell differentiation [2]. *Progenitor T cells* - **Progenitor T cells** are the cells of origin for **T-cell acute lymphoblastic leukaemia (T-ALL)**, not CLL/SLL [3]. - T-ALL involves immature T lymphocytes and presents with different clinical and immunophenotypic features [3]. *Mature T cells* - **Mature T cells** can give rise to various **peripheral T-cell lymphomas**, like peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS) or cutaneous T-cell lymphoma (Mycosis Fungoides). - These are distinct from CLL/SLL, which is a B-cell neoplasm [4]. **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. 596-598. [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. 610-612. [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. 598-599. [4] 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. 598.
Question 4: Chemotherapeutic Agent of Choice for the treatment of CML?
- A. Imatinib (Correct Answer)
- B. Vincristine
- C. Cyclophosphamide
- D. Methotrexate
Explanation: ***Imatinib*** - **Imatinib** is a **tyrosine kinase inhibitor** specifically targeting the **BCR-ABL fusion protein**, which is the hallmark of CML [1][2]. - It dramatically improved the prognosis of CML patients, making it the **first-line therapy** and agent of choice due to its high efficacy and relatively low toxicity compared to conventional chemotherapy [2]. *Vincristine* - **Vincristine** is a **vinca alkaloid** that inhibits microtubule formation, primarily used in acute leukemias and lymphomas. - It is not the agent of choice for CML due to its different mechanism of action and the availability of more targeted therapies for CML. *Cyclophosphamide* - **Cyclophosphamide** is an **alkylating agent** that causes DNA damage, used in various cancers and autoimmune diseases. - While it can be used in some hematologic malignancies, it is not the preferred or most effective treatment for CML, especially given the success of targeted therapies. *Methotrexate* - **Methotrexate** is an **antimetabolite** that interferes with DNA synthesis, commonly used in acute leukemias, lymphomas, and autoimmune conditions. - It is not considered the chemotherapeutic agent of choice for CML, as its mechanism of action is not specific to the BCR-ABL anomaly characteristic of CML.
Question 5: Auer rods are a characteristic feature of which type of leukemia?
- A. Chronic lymphocytic leukemia (CLL)
- B. Myelodysplastic syndromes (MDS)
- C. Acute myeloid leukemia (AML) (Correct Answer)
- D. Acute lymphoblastic leukemia (ALL)
Explanation: ***Auer rods*** - Auer rods are **needle-shaped cytoplasmic inclusions** found in myeloid leukemias, particularly in acute myeloid leukemia (AML) [1]. - They are indicative of myeloid differentiation and are a classic **diagnostic feature** observed in bone marrow or peripheral blood smears [1]. *Intercytoplasmic granules* - While **intercytoplasmic granules** may appear in various leukemias, they are not specific or characteristic for Auer rods. - These granules do not serve as a **specific diagnostic marker** for any particular type of leukemia. *Eosinophils* - Eosinophils are associated with **allergic reactions** and parasitic infections, majorly presenting with **bilobed nuclei** and prominent granules. - They do not have **Auer rods**, making this option incorrect regarding the context of leukemia. *Leukemic cells* - While leukemic cells represent neoplastic white blood cells, they do not specifically refer to the **presence of Auer rods**. - Different types of leukemic cells have various **morphologies** and features that may not include Auer rods. **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. 620.
Question 6: In APML (Acute Promyelocytic Leukemia), all of the following are seen except:
- A. Retinoic acid is used in treatment
- B. 15/17 translocation may be seen
- C. CD 15/34 both seen in same cell (Correct Answer)
- D. Associated with Disseminated intravascular coagulation (DIC)
Explanation: ***CD 15/34 both seen in same cell*** - This statement is incorrect because **Acute Promyelocytic Leukemia (APML)** is characterized by **CD34 negativity**, meaning CD34 is typically absent in APML cells. - While **CD15 may be positive** in APML, **CD34 is negative** in the vast majority of cases (unlike other AML subtypes where CD34 is often positive). - Therefore, **CD15 and CD34 are NOT both seen in the same cell** in APML. - The disease involves **immature myeloid cells** at the promyelocyte stage, which are beyond the most primitive stem cell stage (hence the lack of CD34 expression). *Retinoic acid is used in treatment* - **All-trans retinoic acid (ATRA)** is a cornerstone of treatment for APML. - ATRA induces differentiation of the **promyelocytes**, which helps overcome the **differentiation block** caused by the PML-RARA fusion protein. *15/17 translocation may be seen* - The characteristic genetic abnormality in APML is the **t(15;17) translocation** [1]. - This translocation results in the fusion of the **PML (promyelocytic leukemia) gene** on chromosome 15 with the **RARA (retinoic acid receptor alpha) gene** on chromosome 17 [2]. *Associated with Disseminated intravascular coagulation (DIC)* - APML is frequently associated with a high risk of developing **Disseminated Intravascular Coagulation (DIC)** [1]. - The abnormal promyelocytes release **procoagulant substances** that activate the coagulation cascade, leading to severe bleeding and thrombosis. **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. 620. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 605-607.
Question 7: 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 8: First line therapy in chronic phase of chronic myeloid leukemia is
- A. Thalidomide
- B. Rituximab
- C. Imatinib (Correct Answer)
- D. Chlorambucil
Explanation: ***Imatinib*** - **Imatinib** is a **tyrosine kinase inhibitor (TKI)** that specifically targets the **BCR-ABL fusion protein**, which is the hallmark of **chronic myeloid leukemia (CML)** [1][2]. - It is highly effective in inducing **hematologic and cytogenetic remissions** in the chronic phase of CML and has significantly improved prognosis [2]. *Thalidomide* - **Thalidomide** is an immunomodulatory drug primarily used in **multiple myeloma** and as a teratogen. - It does not target the **BCR-ABL fusion protein** and is not indicated for CML. *Rituximab* - **Rituximab** is a **monoclonal antibody** that targets the **CD20 antigen** found on B-lymphocytes. - It is used in the treatment of **B-cell non-Hodgkin lymphoma** and **chronic lymphocytic leukemia**, not CML. *Chlorambucil* - **Chlorambucil** is an **alkylating agent**, a type of chemotherapy drug. - While historically used in some hematologic malignancies, it has been largely superseded by targeted therapies like TKIs in CML due to its non-specific action and greater toxicity [2].
Question 9: Which of the following statements about CNS leukemia is false?
- A. Intrathecal methotrexate is given
- B. Seen with acute myeloid leukemia
- C. CNS irradiation is given
- D. Single blast in CSF is sufficient for diagnosis (Correct Answer)
Explanation: ***Seen with acute myeloid leukemia*** - CNS involvement is typically not a common feature of **acute myeloid leukemia (AML)**; it's more associated with acute lymphoblastic leukemia (ALL) [1]. - While leukemia can affect the CNS, **AML is not predominantly known** for this complication compared to ALL . *Single blast in CSF is sufficient for diagnosis* - A **single blast** in the cerebrospinal fluid (CSF) does **not establish a definitive diagnosis** of CNS leukemia; multiple blasts are typically required. - Diagnosis involves considering clinical symptoms, laboratory findings, and often requires **a combination of findings** to confirm CNS involvement. *Intrathecal methotrexate is given* - **Intrathecal methotrexate** is used for treatment of CNS leukemia; however, this statement is true and does not meet the 'except' criteria. - It is a common practice to deliver chemotherapy directly to the CNS to combat leukemia effectively. *CNS irradiation is given* - CNS irradiation can be used as a treatment modality in certain instances of leukemia; thus, this statement is also true. - It is part of the therapeutic strategies for managing CNS involvement but is not universally applied for all cases.
Question 10: Autoimmune hemolytic anemia is seen in: A) Sickle cell anemia B) Chronic lymphocytic leukemia (CLL) C) Acute myelocytic leukemia (AML) D) Multiple myeloma
- A. Acute myelocytic leukemia (AML)
- B. Multiple myeloma
- C. Sickle cell anemia
- D. Chronic lymphocytic leukemia (CLL) (Correct Answer)
Explanation: ***Chronic lymphocytic leukemia (CLL)*** - **CLL** is strongly associated with **autoimmune hemolytic anemia** due to immune system dysregulation that leads to production of **autoantibodies** against red blood cells [1]. - The malignant B-lymphocytes in CLL cause **immunologic dysfunction**, making AIHA one of the most common autoimmune complications of this disease [1]. *Sickle cell anemia* - **Sickle cell anemia** causes hemolysis through **intrinsic red blood cell defects** due to abnormal hemoglobin S structure, not autoimmune mechanisms. - The hemolysis is **mechanical** and occurs when sickled cells become rigid and fragile, rather than being mediated by autoantibodies. *Acute myelocytic leukemia (AML)* - **AML** is a rapidly progressing cancer of the myeloid blood cell line, primarily affecting early progenitor cells. - Autoimmune hemolytic anemia is **rarely associated** with AML; the primary hematologic issue is **pancytopenia** due to bone marrow suppression. *Multiple myeloma* - **Multiple myeloma** is a plasma cell dyscrasia characterized by proliferation of malignant plasma cells and production of **monoclonal proteins** [2]. - While other hematologic abnormalities can occur, **AIHA is not a common complication** of multiple myeloma [2].
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