Hematopathology Practice Questions

Q: Which of the following is a poor prognostic factor in Acute Myeloid Leukemia (AML)?

Monosomy. ### Explanation In Acute Myeloid Leukemia (AML), cytogenetic and molecular abnormalities are the most significant predictors of clinical outcome and treatment response [1]. **1. Why Monosomy is the Correct Answer:** Monosomies (loss of an entire chromosome), particularly of **chromosomes 5 or 7**, or the presence of a **complex karyotype** (≥3 abnormalities), are classified as **adverse/poor prognostic factors**. These are often associated with therapy-related AML or AML evolving from Myelodysplastic Syndrome (MDS). They typically show poor response to standard induction chemotherapy and high relapse rates. **2. Analysis of Incorrect Options:** * **Deletion of X or Y chromosome:** These are considered **isolated secondary changes** and do not carry an adverse prognosis. In many cases, the loss of a sex chromosome is considered a "neutral" or "favorable" finding compared to complex karyotypes. * **t(8;21):** This translocation involves the *RUNX1-RUNX1T1* genes. It is a hallmark of **favorable prognosis** AML (specifically AML-M2 in the FAB classification) and generally responds well to cytarabine-based therapy [1]. * **Nucleophosmin (NPM1) mutation:** In the absence of *FLT3-ITD* mutations, an *NPM1* mutation is a **favorable prognostic marker** [1]. It is one of the most common genetic alterations in adult AML with a normal karyotype. **Clinical Pearls for NEET-PG:** * **Favorable Prognosis:** t(8;21), inv(16), t(15;17) [APML], and isolated *NPM1* or *CEBPA* mutations [1]. * **Poor Prognosis:** Monosomy 5/7, del(5q), 11q23 (MLL gene) rearrangements, and *FLT3-ITD* mutations [1]. * **APML (t15;17):** While it has a high risk of early mortality due to DIC, it has the **best long-term prognosis** with ATRA and Arsenic Trioxide therapy. **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.

Q: The AB blood group antigen is also known as the ... factor?

Landsteiner. **Explanation:** The correct answer is **Landsteiner**. **1. Why Landsteiner is correct:** The ABO blood group system was discovered by **Karl Landsteiner** in 1900. He identified the A, B, and O antigens on the surface of red blood cells and formulated "Landsteiner’s Law," which states that if an agglutinogen (antigen) is present on the RBCs, the corresponding agglutinin (antibody) must be absent from the serum [1]. Because of his pioneering work in defining the major blood groups, the AB antigens are eponymously referred to as the Landsteiner factor. He was awarded the Nobel Prize in Physiology or Medicine in 1930 for this discovery. **2. Why other options are incorrect:** * **Duffy (Option A):** This is a minor blood group system (Fy antigens). It is clinically significant because the Duffy antigen acts as a receptor for *Plasmodium vivax*; individuals who are Duffy-negative (common in African populations) are resistant to vivax malaria. * **Rhesus (Option C):** Also discovered by Landsteiner (along with Alexander Wiener), the Rh factor (D antigen) is a separate system from ABO [1]. It is the primary cause of Hemolytic Disease of the Newborn (HDN) [1]. * **Lutheran (Option D):** This is another minor blood group system (Lu antigens) located on chromosome 19, primarily involved in cell adhesion. **High-Yield Clinical Pearls for NEET-PG:** * **Universal Donor:** O negative (no A, B, or Rh antigens). * **Universal Recipient:** AB positive (no anti-A, anti-B, or anti-D antibodies). * **Bombay Blood Group:** Lacks the H-antigen (genotype hh). These individuals phenotypically test as 'O' but have potent anti-H antibodies, making them compatible only with other Bombay group donors. * **Inheritance:** ABO blood groups follow **codominance**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628.

Q: Auer rods are characteristic features of which subtype of acute myeloid leukemia (AML)?

AML M3. **Explanation:** **Auer rods** are needle-like, azurophilic cytoplasmic inclusions formed by the fusion of primary granules (lysosomes) containing peroxidase. Their presence is a pathognomonic hallmark of **Acute Myeloid Leukemia (AML)**, specifically indicating a myeloid lineage [1]. **Why AML M3 is the correct answer:** While Auer rods can be seen in several AML subtypes (M1, M2, M3, and M4), they are most characteristic and numerous in **AML M3 (Acute Promyelocytic Leukemia)**. In M3, cells often contain bundles of Auer rods known as **"faggot cells"** [1]. These rods are rich in tissue factor; when the cells are lysed (either naturally or by chemotherapy), they release these contents, triggering **Disseminated Intravascular Coagulation (DIC)**, a critical clinical emergency associated with M3 [1]. **Analysis of Incorrect Options:** * **AML M0 (Undifferentiated):** These are primitive blasts that lack morphological and cytochemical evidence of differentiation; therefore, Auer rods are absent. * **AML M5 (Monocytic):** This subtype typically shows monocytic differentiation (monoblasts/promonocytes) [1]. Auer rods are rarely seen in pure monocytic lineages. * **AML M7 (Megakaryoblastic):** This subtype involves platelet precursors. Auer rods are never found in M7 as they are specific to the granulocytic lineage. **High-Yield NEET-PG Pearls:** * **Genetics of M3:** Associated with **t(15;17)**, involving the *PML-RARA* fusion gene [1]. * **Treatment:** Managed with **ATRA** (All-trans retonic acid) and Arsenic Trioxide, which force the maturation of promyelocytes. * **Staining:** Auer rods are strongly **Myeloperoxidase (MPO) positive**. * **Clinical Warning:** Always screen for DIC in a patient with suspected AML M3 [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. 620-622.

Question 1

Oxidative injury of the red blood cells leading to hemolysis is associated with which of the following clinical conditions?

Accepted Answer

G6PD deficiency

Answer

Hereditary spherocytosis

Answer

Sickle cell anemia

Answer

Hemophilia

Question 2

Which of the following is a poor prognostic factor in Acute Myeloid Leukemia (AML)?

Accepted Answer

Monosomy

Answer

Deletion of X or Y chromosome

Answer

t (8; 21) translocation

Answer

Nucleophosphin mutation

Question 3

The AB blood group antigen is also known as the ... factor?

Accepted Answer

Landsteiner

Answer

Duffy

Answer

Rhesus

Answer

Lutheran

Question 4

Spontaneous bleeding usually occurs when the platelet count falls below which value?

Accepted Answer

20,000/uL

Answer

50,000/uL

Answer

100,000/uL

Answer

120,000/uL

Question 5

Which of the following is not a B cell neoplasm?

Accepted Answer

Mycosis fungoides

Answer

Hairy cell leukemia

Answer

Mantle cell lymphoma

Answer

Burkitt's lymphoma

Question 6

Auer rods are characteristic features of which subtype of acute myeloid leukemia (AML)?

Accepted Answer

AML M3

Answer

AML M0

Answer

AML M5

Answer

AML M7

Question 7

Which anticoagulant is the preferred choice for use in a blood bank?

Accepted Answer

Acid citrate dextrose solution

Answer

Calcium oxalate

Answer

Heparin solution

Answer

Sodium fluoride

Question 8

In coagulation failure, what is the serum level of fibrinogen?

Accepted Answer

Less than 100 mg/dL

Answer

Less than 150 mg/dL

Answer

Less than 200 mg/dL

Answer

Less than 250 mg/dL

Question 9

Which of the following statements is NOT true regarding Bernard-Soulier syndrome?

Accepted Answer

Ristocetin-induced platelet aggregation is normal.

Answer

Platelet aggregation with collagen and ADP is normal.

Answer

Platelets are large.

Answer

There is thrombocytopenia.

Question 10

Which of the following is true regarding Hemophilia A?

Accepted Answer

Serum levels of factor VIII are decreased

Answer

Deficiency of factor IX

Answer

PT increased

Answer

FVIII decreased

Hematopathology — MCQs

Hematopathology — MCQs

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