Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 71: Which of the following cell types is NOT typically found in myelodysplastic syndrome?

A. Ringed sideroblasts
B. Megakaryocytes with normal single multilobulated nuclei (Correct Answer)
C. Pseudo-Pelger-Huet cells
D. Pawn ball megakaryocytes

Explanation: **Explanation:** Myelodysplastic Syndromes (MDS) are a group of clonal hematopoietic stem cell disorders characterized by **ineffective hematopoiesis**, leading to peripheral cytopenias and a risk of transformation into Acute Myeloid Leukemia (AML) [1]. The hallmark of MDS is **dysplasia** (abnormal morphology) in one or more cell lines [1]. **Why Option B is Correct:** In MDS, megakaryocytes are characteristically **dysplastic**. Normal megakaryocytes have a single, large, multilobulated nucleus (resembling a "bag of marbles"). In MDS, this normal morphology is lost. Therefore, finding "normal single multilobulated nuclei" is inconsistent with a diagnosis of MDS. **Analysis of Incorrect Options:** * **A. Ringed sideroblasts:** These are erythroid precursors with iron-laden mitochondria encircling at least one-third of the nucleus. They are a classic feature of dyserythropoiesis (specifically in MDS-RS). * **C. Pseudo-Pelger-Huet cells:** These are neutrophils with hyposegmented nuclei (bilobed or peanut-shaped). They represent dysgranulopoiesis and are a high-yield peripheral smear finding in MDS [1]. * **D. Pawn ball megakaryocytes:** These are small, mononuclear, or binuclear megakaryocytes (micromegakaryocytes) that are pathognomonic for dysmegakaryopoiesis in MDS. **High-Yield Clinical Pearls for NEET-PG:** * **MDS Cytogenetics:** The most common chromosomal abnormality is **5q deletion** (associated with a better prognosis and response to Lenalidomide). * **Blast Count:** To differentiate MDS from AML, the blast count in the bone marrow must be **<20%** [1]. * **Ringed Sideroblasts:** Visualized using **Perls' Prussian Blue stain**. * **Clinical Presentation:** Typically affects the elderly; presents with refractory anemia and pancytopenia [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.

Question 72: Howell-Jolly bodies may be seen after which procedure?

A. Hepatectomy
B. Splenectomy (Correct Answer)
C. Pancreatectomy
D. Cholecystectomy

Explanation: **Explanation:** **Howell-Jolly bodies** are small, round, basophilic (purple-blue) nuclear remnants (DNA) found within erythrocytes [1]. During normal erythropoiesis in the bone marrow, the nucleus is usually expelled before the red blood cell (RBC) enters the circulation. However, if small fragments of DNA remain, they are typically "pitted" or removed by the **splenic macrophages** as the RBCs pass through the splenic sinusoids [2]. **Why Splenectomy is correct:** Following a **splenectomy** (or in cases of functional asplenia, such as Sickle Cell Anemia), the "pitting" mechanism of the spleen is lost [1]. Consequently, these nuclear remnants persist in the circulating RBCs, making Howell-Jolly bodies a classic peripheral smear finding in asplenic patients [2]. **Why other options are incorrect:** * **Hepatectomy:** The liver does not possess the specific microcirculatory "pitting" function required to remove nuclear remnants from RBCs. * **Pancreatectomy & Cholecystectomy:** These procedures involve the removal of the pancreas and gallbladder, respectively. Neither organ is involved in the filtration or "culling and pitting" of red blood cells. **Clinical Pearls for NEET-PG:** 1. **Other Post-Splenectomy findings:** Look for **Pappenheimer bodies** (iron granules), **Heinz bodies** (denatured hemoglobin), and **Target cells** (codocytes) on the peripheral smear [2]. 2. **Thrombocytosis:** A transient increase in platelet count is common after splenectomy. 3. **Infections:** Post-splenectomy patients are at high risk for **OPSI** (Overwhelming Post-Splenectomy Infection) caused by encapsulated organisms (*S. pneumoniae, H. influenzae, N. meningitidis*) [2]. 4. **Stain:** Howell-Jolly bodies are visible on routine **Wright-Giemsa** or Leishman stains. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 644-645. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 570-571.

Question 73: What type of anemia is caused by antibodies against blood group antigens?

A. Hereditary spherocytosis
B. G6PD deficiency
C. Hemolytic disease of the newborn (Correct Answer)
D. Alpha thalassemia major

Explanation: ### Explanation **Correct Answer: C. Hemolytic disease of the newborn (HDN)** **Mechanism:** Hemolytic disease of the newborn (also known as Erythroblastosis Fetalis) is a classic example of **extrinsic, immune-mediated hemolytic anemia**. It occurs when maternal IgG antibodies cross the placenta and target fetal red blood cell (RBC) antigens [2]. This most commonly involves **Rh incompatibility** (Rh-negative mother, Rh-positive fetus) or **ABO incompatibility** [1]. The antibodies coat the fetal RBCs, leading to their destruction by the fetal splenic macrophages (Type II Hypersensitivity). **Why the other options are incorrect:** * **A. Hereditary spherocytosis:** This is an **intrinsic** hemolytic anemia caused by inherited defects in RBC membrane proteins (like spectrin or ankyrin), not antibodies. * **B. G6PD deficiency:** This is an **enzymopathy** (X-linked recessive) where RBCs are susceptible to oxidative stress. Hemolysis is triggered by drugs, infections, or fava beans, not immune mechanisms. * **C. Alpha thalassemia major:** This is a **hemoglobinopathy** caused by the deletion of all four alpha-globin genes ($--/--$), leading to the formation of Hb Barts ($\gamma_4$). It results in severe microcytic anemia and hydrops fetalis due to ineffective erythropoiesis and hemolysis, but it is non-immune. **NEET-PG High-Yield Pearls:** * **Coombs Test:** HDN is characterized by a **Positive Direct Antiglobulin Test (DAT/Direct Coombs)** on fetal cord blood, indicating antibodies are bound to the RBC surface [3]. * **ABO vs. Rh:** ABO incompatibility is more common and can occur in the first pregnancy, but it is usually milder. Rh incompatibility is more severe, typically affects subsequent pregnancies, and is prevented by administering **Anti-D (RhoGAM)** [2]. * **Peripheral Smear:** Look for **nucleated RBCs** (erythroblasts) and polychromasia in HDN [3]. Note that spherocytes are common in ABO incompatibility but rare in Rh incompatibility. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 469-470. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 603-604.

Question 74: Which condition is characterized by a "starry sky" appearance on histopathology?

A. Paget's disease of bone
B. Cherubism
C. Garré's osteomyelitis
D. Burkitt's lymphoma (Correct Answer)

Explanation: **Explanation:** **Burkitt’s Lymphoma (Correct Answer):** The "starry sky" appearance is the classic histopathological hallmark of Burkitt’s lymphoma [1]. This pattern is created by a high rate of tumor cell proliferation and apoptosis. The "stars" are **tingible body macrophages**—large, pale-staining phagocytes that have ingested apoptotic tumor debris [1]. The "sky" is formed by a dense, dark background of small, monotonous, non-cleaved B-lymphocytes [1]. **Analysis of Incorrect Options:** * **Paget’s Disease of Bone:** Characterized by a **"mosaic" or "jigsaw puzzle" pattern** of bone due to irregular prominent cement lines caused by repeated episodes of bone resorption and formation. * **Cherubism:** Shows a histopathology similar to Central Giant Cell Granuloma, featuring fibrous stroma with numerous **multinucleated giant cells**, but lacks the starry sky pattern. * **Garré’s Osteomyelitis:** Also known as proliferative periostitis, it is characterized by an **"onion-skin" appearance** due to the formation of duplicate layers of cortical bone. **NEET-PG High-Yield Pearls:** * **Genetics:** Strongly associated with **t(8;14)** translocation, involving the **c-myc** oncogene. * **Variants:** The Endemic (African) variant is 100% associated with **Epstein-Barr Virus (EBV)** and typically involves the jaw. * **Immunophenotype:** B-cell markers (CD19, CD20, CD22) and strongly positive for **Ki-67** (nearly 100% growth fraction). * **Cytology:** "Royal blue" cytoplasm with cytoplasmic vacuoles on fine-needle aspiration (FNA). **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. 606.

Question 75: Which of the following is NOT included in the differential diagnosis of a Reticulocyte Index > 2.5?

A. Macrocytic anemia (Correct Answer)
B. Hemolysis
C. Hemoglobinopathy
D. Blood loss

Explanation: The **Reticulocyte Index (RI)**, also known as the Corrected Reticulocyte Count, is a crucial marker used to differentiate whether an anemia is due to bone marrow failure or peripheral destruction/loss. An **RI > 2.5** indicates an appropriate, hyperproliferative bone marrow response to anemia. ### **Explanation of Options:** * **A. Macrocytic Anemia (Correct Answer):** Most macrocytic anemias (like Vitamin B12 or Folate deficiency) are characterized by **ineffective erythropoiesis** [1]. Despite the presence of anemia, the bone marrow cannot produce mature red cells effectively, leading to a **low RI (< 2.0)** and characteristic morphological changes such as oval macrocytes and hypersegmented neutrophils [1]. Therefore, it is considered a hypoproliferative anemia and does not belong in the differential of a high RI. * **B. Hemolysis:** In hemolytic states, the bone marrow is healthy and responds to the decreased red cell lifespan by rapidly increasing erythropoiesis, resulting in a high RI. * **C. Hemoglobinopathy:** Conditions like Sickle Cell Disease or Thalassemia (intermedia/major) involve peripheral destruction and compensatory marrow hyperplasia, typically presenting with an elevated RI. * **D. Blood Loss:** Acute or chronic blood loss triggers erythropoietin release, stimulating the marrow to release young red cells (reticulocytes) into circulation, thus increasing the RI. ### **NEET-PG High-Yield Pearls:** 1. **Formula:** $RI = \text{Reticulocyte \%} \times (\text{Patient Hct} / \text{Normal Hct}) \times (1 / \text{Maturation Correction Factor})$. 2. **RI > 2.5:** Suggests **Peripheral destruction** (Hemolysis or Hemorrhage). 3. **RI < 2.0:** Suggests **Production failure** (Nutritional deficiencies, Aplastic anemia, or Bone marrow infiltration). 4. **Exception:** A macrocytic anemia with a *high* RI should make you suspect **Hemolytic anemia** (due to polychromasia) or a patient responding to recent B12/Folate supplementation. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 593-595.

Question 76: In iron deficiency anemia, what is typically observed?

A. Increased protoporphyrin (Correct Answer)
B. Increased iron
C. Increased ferritin
D. Increased transferrin saturation

Explanation: **Explanation:** In Iron Deficiency Anemia (IDA), the correct finding is **Increased Free Erythrocyte Protoporphyrin (FEP)**. **Why the correct answer is right:** Heme synthesis occurs in the mitochondria, where the enzyme **Ferrochelatase** inserts ferrous iron ($Fe^{2+}$) into a Protoporphyrin IX ring [1]. In IDA, there is a lack of available iron to complete this reaction. Consequently, Protoporphyrin cannot be converted into Heme, leading to its accumulation within the red blood cells. This makes FEP a sensitive marker for "iron-deficient erythropoiesis." **Why the incorrect options are wrong:** * **B. Increased iron:** In IDA, serum iron levels are **decreased** due to depleted body stores. * **C. Increased ferritin:** Ferritin is the storage form of iron. It is the **first parameter to decrease** in IDA, reflecting the exhaustion of iron stores. (Note: Ferritin is an acute-phase reactant and may be falsely normal/high in inflammation). * **D. Increased transferrin saturation:** Transferrin saturation (Serum Iron/TIBC) **decreases** (typically <15%) because serum iron is low while the Total Iron Binding Capacity (TIBC) increases as the liver produces more transferrin to compensate for the deficiency [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest sign of IDA:** Decreased Serum Ferritin. * **Gold Standard investigation:** Bone marrow aspiration with **Perl’s Prussian Blue stain** (showing absent haemosiderin in macrophages). * **Mentzer Index:** (MCV/RBC count) >13 suggests IDA, whereas <13 suggests Thalassemia trait. * **Blood Picture:** Microcytic hypochromic anemia with increased RDW (Anisocytosis) [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 587-591.

Question 77: Absolute lymphocytosis is seen in which of the following conditions?

A. Systemic Lupus Erythematosus (SLE)
B. Tuberculosis (TB) (Correct Answer)
C. Chronic Lymphocytic Leukemia (CLL)
D. Brucellosis

Explanation: **Explanation:** Absolute lymphocytosis is defined as an increase in the total lymphocyte count above the normal reference range (typically >4,000/µL in adults). **Why Tuberculosis (TB) is the Correct Answer:** Tuberculosis is a classic example of a chronic granulomatous infection where the cell-mediated immune response is dominant [1]. In TB, the body recruits T-lymphocytes to the site of infection to activate macrophages. This persistent stimulation of the immune system often leads to a systemic increase in circulating lymphocytes (absolute lymphocytosis), making it a high-yield association in hematopathology [1]. **Analysis of Incorrect Options:** * **Systemic Lupus Erythematosus (SLE):** SLE typically presents with **lymphopenia** (a decrease in lymphocytes) rather than lymphocytosis. This is often due to the presence of antilymphocyte antibodies and is a diagnostic criterion for the disease. * **Chronic Lymphocytic Leukemia (CLL):** While CLL involves a massive increase in lymphocytes, the question asks for conditions where lymphocytosis is a *reactive* feature. In many standardized exams, if a specific infection like TB is listed alongside a malignancy, the focus is on the reactive etiology. However, note that CLL causes *extreme* lymphocytosis; in this specific question context, TB is the classic "reactive" answer. * **Brucellosis:** While Brucellosis can cause a relative lymphocytosis (increased percentage), it is less commonly associated with a marked *absolute* lymphocytosis compared to TB or viral infections. **High-Yield Clinical Pearls for NEET-PG:** * **Viral Infections:** The most common cause of absolute lymphocytosis (e.g., Infectious Mononucleosis/EBV, where "atypical lymphocytes" or Downey cells are seen) [1]. * **Bacterial Exceptions:** Most bacterial infections cause neutrophilia. The notable exceptions that cause **lymphocytosis** are *Bordetella pertussis*, *Brucella*, and *Mycobacterium tuberculosis* [1]. * **Pertussis:** Causes lymphocytosis by blocking the extravasation of lymphocytes from the blood into the lymph nodes via the "lymphocytosis-promoting factor." **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 195-196.

Question 78: A female with recurrent abortion and isolated prolonged APTT is most likely associated with which of the following?

A. Lupus anticoagulant (Correct Answer)
B. Disseminated intravascular coagulation (DIC)
C. Von Willebrand disease
D. Hemophilia

Explanation: **Explanation:** The clinical presentation of **recurrent abortions** combined with an **isolated prolonged APTT** is a classic hallmark of **Antiphospholipid Antibody Syndrome (APS)** [1], specifically the presence of **Lupus Anticoagulant (LA)** [2]. **Why Lupus Anticoagulant is correct:** Lupus anticoagulant is an autoantibody that binds to phospholipids and proteins associated with the cell membrane. * **In vivo (in the body):** It is pro-thrombotic, leading to arterial and venous thrombosis and placental infarction (causing recurrent miscarriages) [1]. * **In vitro (in the lab):** It interferes with the phospholipids used in the APTT assay [2], paradoxically causing a **prolonged APTT** [1]. This prolongation does not correct with a 1:1 mixing study (indicating an inhibitor is present). **Why other options are incorrect:** * **DIC:** Characterized by the consumption of all clotting factors and platelets. It presents with prolonged PT, APTT, and low platelet counts, usually in an acute, sick patient [3]. * **Von Willebrand Disease:** The most common inherited bleeding disorder. While it can prolong APTT (due to low Factor VIII), it presents with **mucocutaneous bleeding**, not thrombosis or recurrent abortions. * **Hemophilia:** An X-linked recessive disorder (rare in females) presenting with deep tissue/joint bleeds. It causes an isolated prolonged APTT but is not associated with pregnancy loss. **High-Yield Clinical Pearls for NEET-PG:** * **APS Triad:** Thrombosis (venous/arterial), Recurrent pregnancy loss, and Thrombocytopenia. * **Mixing Study:** If APTT corrects, it's a factor deficiency; if it **fails to correct**, it's an inhibitor (like LA). * **DRVVT (Dilute Russell Viper Venom Test):** The most specific screening test for Lupus Anticoagulant. * **False Positive VDRL:** Patients with APS often show a false positive syphilis test due to anti-cardiolipin antibodies [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 626-627. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 134-135. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626.

Question 79: All are features of hemolytic anemia, except?

A. Hemoglobinuria
B. Jaundice
C. Increased haptoglobin (Correct Answer)
D. Hemosiderinuria

Explanation: **Explanation:** Hemolytic anemia is characterized by the premature destruction of red blood cells (RBCs) [1]. The correct answer is **C (Increased haptoglobin)** because haptoglobin levels actually **decrease** during hemolysis [1]. **1. Why "Increased haptoglobin" is the correct (Except) choice:** Haptoglobin is a plasma protein produced by the liver that binds to free hemoglobin released into the circulation. In hemolytic states (especially intravascular hemolysis), free hemoglobin saturates haptoglobin, and the resulting complex is rapidly cleared by the reticuloendothelial system [1]. This leads to a **depletion of serum haptoglobin**, making it a highly sensitive marker for hemolysis [1]. **2. Analysis of Incorrect Options:** * **Jaundice (B):** Hemolysis leads to the breakdown of heme into unconjugated bilirubin [2]. When the liver's conjugating capacity is exceeded, **unconjugated hyperbilirubinemia** and clinical jaundice occur [1]. * **Hemoglobinuria (A):** When haptoglobin is saturated, free hemoglobin (hemoglobinemia) passes through the glomerular filtrate [1]. If the renal tubular reabsorptive capacity is exceeded, it appears in the urine [1]. * **Hemosiderinuria (D):** This is a feature of chronic intravascular hemolysis. Iron from reabsorbed hemoglobin is stored as hemosiderin in renal tubular cells; when these cells slough off into the urine, it results in hemosiderinuria (detected by Prussian blue stain) [1]. **Clinical Pearls for NEET-PG:** * **Best screening test for hemolysis:** Increased Reticulocyte count [2]. * **Specific marker for intravascular hemolysis:** Low Haptoglobin + Hemoglobinuria [1]. * **Marker for extravascular hemolysis:** Splenomegaly + Jaundice (Haptoglobin may be normal or slightly low). * **LDH:** Usually elevated in all hemolytic anemias due to release from RBCs. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 639-640. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 640.

Question 80: Cyclin D1 translocation is seen in which of the following conditions?

A. Follicular lymphoma
B. Mantle cell lymphoma (Correct Answer)
C. Hodgkin lymphoma
D. Melanoma

Explanation: **Explanation:** **Mantle Cell Lymphoma (MCL)** is characterized by the hallmark cytogenetic abnormality **t(11;14)(q13;q32)** [1]. This translocation involves the fusion of the **CCND1 gene** (on chromosome 11) with the **IgH (Immunoglobulin Heavy chain) promoter** (on chromosome 14). This leads to the constitutive overexpression of **Cyclin D1** [1], a protein that promotes the transition of cells from the G1 phase to the S phase of the cell cycle by phosphorylating the Retinoblastoma (Rb) protein. In normal B-cells, Cyclin D1 is not expressed; thus, its detection via immunohistochemistry is a diagnostic gold standard for MCL. **Analysis of Incorrect Options:** * **Follicular Lymphoma:** Characterized by **t(14;18)**, leading to the overexpression of the **BCL-2** anti-apoptotic protein. * **Hodgkin Lymphoma:** Typically lacks specific diagnostic translocations. It is characterized by Reed-Sternberg cells expressing CD15 and CD30 (in Classical HL). * **Melanoma:** While Cyclin D1 can be overexpressed in some melanomas due to gene amplification (notably in acral lentiginous types), it is not defined by a characteristic translocation like MCL. The most high-yield mutations for melanoma are **BRAF (V600E)** and **c-KIT**. **High-Yield Clinical Pearls for NEET-PG:** * **MCL Marker:** CD5 positive, CD23 negative (helps differentiate from CLL/SLL which is CD23+). * **Morphology:** Presence of "centrocyte-like" cells; can present as **Lymphomatous Polyposis** in the GI tract. * **Aggressive Nature:** MCL is generally considered an aggressive, incurable B-cell lymphoma with a poor prognosis [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. 610-612.

Practice by Chapter

Anemias: Classification and Approach

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Hemolytic Anemias

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Myeloproliferative Neoplasms

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Myelodysplastic Syndromes

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Acute Leukemias

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Chronic Leukemias

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Lymphomas and Lymphoid Neoplasms

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Plasma Cell Disorders

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Bleeding Disorders

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Thrombotic Disorders

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