Hematopathology — MCQs
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A 26-year-old man has noted enlarging neck lumps for the past 6 months. Physical examination reveals enlarged, nontender right cervical lymph nodes. A biopsy of a lymph node microscopically shows macrophages, lymphocytes, neutrophils, eosinophils, and plasma cells. Scattered CD15+ large cells with multiple nuclei or a single nucleus with multiple nuclear lobes, each with a large inclusion-like nucleolus, are present. What is the most likely cell of origin and infectious agent for these large cells?
Hemophilia A results due to deficiency of which of the factors?
Lacunar cells are seen in which subtype of Hodgkin's lymphoma?
Which of the following causes hemolytic anemia?
Which of the following is NOT associated with Disseminated Intravascular Coagulation (DIC)?
All of the following genetic mutations are associated with an increased risk of deep venous thrombosis, EXCEPT:
Which of the following statements is NOT true about Immune Thrombocytopenic purpura (ITP)?
What is the commonest site of lytic lesion in multiple myeloma?
Decreased leukocyte alkaline phosphatase is seen in which condition?
Which of the following conditions is characterized by normal hemoglobin structure but reduced red blood cell volume?
Hematopathology Indian Medical PG Practice Questions and MCQs
Question 621: A 26-year-old man has noted enlarging neck lumps for the past 6 months. Physical examination reveals enlarged, nontender right cervical lymph nodes. A biopsy of a lymph node microscopically shows macrophages, lymphocytes, neutrophils, eosinophils, and plasma cells. Scattered CD15+ large cells with multiple nuclei or a single nucleus with multiple nuclear lobes, each with a large inclusion-like nucleolus, are present. What is the most likely cell of origin and infectious agent for these large cells?
- A. B lymphocyte, Epstein-Barr virus (Correct Answer)
- B. CD4+ cell, human T lymphotropic virus
- C. Endothelial cell, Kaposi sarcoma herpesvirus
- D. Macrophage, human immunodeficiency virus
Explanation: This clinical scenario describes a classic presentation of **Hodgkin Lymphoma (HL)**, specifically the Mixed Cellularity subtype. [2] ### 1. Why Option A is Correct The description of large cells with multiple nuclei or lobes and "inclusion-like" nucleoli (owl-eye appearance) is pathognomonic for **Reed-Sternberg (RS) cells**. [1] * **Cell of Origin:** Molecular studies have proven that RS cells are derived from **germinal center B lymphocytes**, despite losing most characteristic B-cell markers (except CD20 in rare cases). [3] * **Infectious Agent:** **Epstein-Barr Virus (EBV)** is strongly associated with HL, particularly the Mixed Cellularity subtype (found in ~70% of cases). EBV genomes are often integrated into the RS cells. [2] * **Immunophenotype:** The mention of **CD15+** (and typically CD30+) confirms the diagnosis of Classical Hodgkin Lymphoma. ### 2. Why Other Options are Wrong * **Option B:** CD4+ cells are the origin of Adult T-cell Leukemia/Lymphoma (ATLL), caused by HTLV-1. These present with "flower cells" and hypercalcemia, not RS cells. * **Option C:** Endothelial cells are the origin of Kaposi Sarcoma (HHV-8). Histology shows spindle cells and slit-like vascular spaces, not a polymorphic inflammatory background. * **Option D:** While HIV increases the risk of lymphomas, the RS cell itself is not derived from a macrophage. ### 3. NEET-PG High-Yield Pearls * **RS Cell Variants:** "L&H cells" (Popcorn cells) are seen in Nodular Lymphocyte Predominant HL and are **CD20+, CD45+, but CD15- and CD30-**. * **Bimodal Age Distribution:** HL peaks in the 20s and again after age 50. [3] * **Staging:** The **Ann Arbor Staging** system is used, and prognosis is more dependent on the stage than the histological subtype. * **Background:** The "milieu" of lymphocytes, eosinophils (recruited by IL-5), and plasma cells is due to cytokines secreted by the RS cells. [3] **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] 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. 614-616.
Question 622: Hemophilia A results due to deficiency of which of the factors?
- A. II
- B. VII
- C. VIII (Correct Answer)
- D. XI
Explanation: **Explanation:** **Hemophilia A** (Classic Hemophilia) is an X-linked recessive bleeding disorder caused by a deficiency or functional defect of **Coagulation Factor VIII** [1]. Factor VIII serves as a critical cofactor for Factor IXa in the "tenase complex," which activates Factor X in the intrinsic pathway of the coagulation cascade. A deficiency leads to impaired fibrin clot formation, manifesting clinically as deep tissue bleeds and hemarthrosis [1]. **Analysis of Options:** * **Option C (Factor VIII):** Correct. Hemophilia A is the most common hereditary disease associated with life-threatening bleeding [1]. * **Option A (Factor II):** Prothrombin deficiency is extremely rare and usually presents as an autosomal recessive bleeding diathesis, not Hemophilia A. * **Option B (Factor VII):** Deficiency of Factor VII affects the extrinsic pathway (prolonged PT). It is not associated with Hemophilia. * **Option D (Factor XI):** Deficiency of Factor XI results in **Hemophilia C** (Rosenthal Syndrome), which is an autosomal recessive condition primarily seen in Ashkenazi Jews. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked recessive (affects males; females are typically asymptomatic carriers) [1]. * **Laboratory Findings:** Characterized by a **prolonged aPTT** (intrinsic pathway) with a **normal PT and Bleeding Time**. * **Mixing Study:** The prolonged aPTT corrects when the patient's plasma is mixed with normal plasma (distinguishes deficiency from inhibitors). * **Hemophilia B (Christmas Disease):** Caused by deficiency of **Factor IX**. * **Treatment:** Recombinant Factor VIII concentrate or Desmopressin (DDAVP) for mild cases (releases Factor VIII from Weibel-Palade bodies). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 670-671.
Question 623: Lacunar cells are seen in which subtype of Hodgkin's lymphoma?
- A. Lymphocyte predominant Hodgkin's lymphoma
- B. Lymphocyte depleted Hodgkin's lymphoma
- C. Nodular sclerosis (Correct Answer)
- D. Mixed cellularity
Explanation: **Explanation:** **Nodular Sclerosis (NSHL)** is the most common subtype of Hodgkin’s Lymphoma (HL) and is characterized by the presence of **Lacunar cells** [1]. These are a specific variant of Reed-Sternberg (RS) cells. During the process of formalin fixation, the abundant, pale cytoplasm of these cells retracts, leaving the nucleus sitting in an empty-appearing space or "lacuna" [1]. Histologically, NSHL is also defined by collagen bands that divide the lymphoid tissue into circumscribed nodules. **Analysis of Incorrect Options:** * **A. Lymphocyte Predominant (NLPHL):** This subtype is characterized by **"Popcorn cells"** (L&H variants) which have multi-lobed nuclei resembling an exploded kernel of corn [1]. It lacks the typical lacunar cells and classic RS cells. * **B. Lymphocyte Depleted:** This is the rarest and most aggressive form, characterized by numerous **pleomorphic/anaplastic RS cells** and a paucity of background lymphocytes [2]. * **D. Mixed Cellularity:** This subtype features **classic "Owl-eye" RS cells** in a polymorphic background of eosinophils, plasma cells, and histiocytes [1]. It is frequently associated with the Epstein-Barr Virus (EBV) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Nodular Sclerosis:** Most common in young adults (especially females) and often presents with a mediastinal mass [3]. * **Immunophenotype:** Classic HL (NS, MC, LD, LR) is **CD15+ and CD30+**, but CD45–. In contrast, NLPHL is **CD20+ and CD45+**, but CD15– and CD30–. * **Prognosis:** Lymphocyte Predominant has the best prognosis; Lymphocyte Depleted has the worst [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. 616-618. [2] 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. [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.
Question 624: Which of the following causes hemolytic anemia?
- A. Hereditary spherocytosis (Correct Answer)
- B. Infection
- C. Iron deficiency
- D. Sickle cell anemia
Explanation: **Explanation:** **Hereditary Spherocytosis (HS)** is a classic example of **intrinsic hemolytic anemia** caused by defects in the red blood cell (RBC) membrane proteins (most commonly **Ankyrin**, followed by Spectrin) [1], [3]. These defects lead to a loss of membrane surface area, forcing the RBCs to assume a spherical shape. These rigid spherocytes are trapped and destroyed prematurely by splenic macrophages (**extravascular hemolysis**) [3]. **Analysis of Options:** * **Option A (Correct):** HS is a primary hemolytic disorder characterized by an increased osmotic fragility and a shortened RBC lifespan [1], [2]. * **Option B (Infection):** While certain infections (like Malaria or *Clostridium perfringens*) can cause hemolysis, "Infection" as a general category is more commonly associated with **Anemia of Chronic Disease**, which is non-hemolytic. * **Option C (Iron Deficiency):** This is the most common cause of **nutritional anemia** worldwide. It is a microcytic hypochromic anemia caused by impaired hemoglobin synthesis, not increased destruction (hemolysis). * **Option D (Sickle Cell Anemia):** While Sickle Cell Anemia **is** a hemolytic anemia, in the context of single-choice questions where HS is provided, HS is often the "textbook" representative of membrane-defect-mediated hemolysis [1]. *Note: If this were a multiple-choice "select all" question, D would also be correct; however, in standard NEET-PG single-best-answer formats, HS is the classic prototype for inherited extravascular hemolysis.* **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Test for HS:** Eosin-5-maleimide (EMA) binding test (Flow cytometry). * **Classic Triad:** Anemia, Jaundice, and Splenomegaly. * **Peripheral Smear:** Spherocytes (lack central pallor) and increased reticulocytes [2]. * **MCHC:** Characteristically **increased** (the only anemia where this occurs). * **Complication:** Risk of aplastic crisis associated with **Parvovirus B19** infection [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641.
Question 625: Which of the following is NOT associated with Disseminated Intravascular Coagulation (DIC)?
- A. Thrombocytopenia
- B. Prolonged Prothrombin Time (PT)
- C. Hyperfibrinogenemia (Correct Answer)
- D. Increased Fibrin Degradation Products (FDP)
Explanation: **Explanation:** Disseminated Intravascular Coagulation (DIC) is a thrombohemorrhagic disorder characterized by the systemic activation of the coagulation cascade [1]. This leads to the widespread formation of microthrombi, which results in the **consumption** of clotting factors and platelets [2]. **Why Hyperfibrinogenemia is the correct answer:** In DIC, there is massive consumption of fibrinogen as it is converted into fibrin to form clots. Consequently, patients exhibit **Hypofibrinogenemia** (low fibrinogen levels), not hyperfibrinogenemia [1]. Fibrinogen is an acute-phase reactant, so while it may initially be normal, a declining trend is a hallmark of progressing DIC. **Analysis of Incorrect Options:** * **Thrombocytopenia:** Platelets are rapidly consumed during the formation of widespread microthrombi, leading to a low platelet count [1]. * **Prolonged Prothrombin Time (PT):** The continuous activation of the coagulation pathway exhausts clotting factors (Factors V, VIII, and X). This depletion results in the prolongation of PT, aPTT, and Thrombin Time (TT) [1]. * **Increased Fibrin Degradation Products (FDP):** To counteract systemic clotting, the fibrinolytic system is activated (secondary fibrinolysis). Plasmin breaks down fibrin and fibrinogen, leading to elevated levels of FDPs and **D-dimers** (the most specific marker) [1]. **NEET-PG High-Yield Pearls:** * **Blood Smear:** Characterized by **Schistocytes** (fragmented RBCs) due to microangiopathic hemolytic anemia (MAHA) [1]. * **Most Specific Test:** Elevated **D-dimer** levels (indicates cross-linked fibrin degradation). * **Common Triggers:** Sepsis (most common), Obstetric complications (Abruptio placentae), and Acute Promyelocytic Leukemia (M3). * **Best Screening Test:** Platelet count and PT. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626. [2] 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. 151-152.
Question 626: All of the following genetic mutations are associated with an increased risk of deep venous thrombosis, EXCEPT:
- A. Factor V Leiden mutation
- B. Glycoprotein 1b platelet receptor defect (Correct Answer)
- C. Heterozygous protein C deficiency
- D. Prothrombin 20210G mutation
Explanation: This question tests your ability to distinguish between **inherited thrombophilias** (which cause venous thrombosis) and **inherited platelet disorders** (which cause bleeding tendencies). ### **Why Option B is the Correct Answer** **Glycoprotein 1b (Gp1b) platelet receptor defect** is the hallmark of **Bernard-Soulier Syndrome**. Gp1b is essential for platelet adhesion to subendothelial von Willebrand factor (vWF) [1]. A defect in this receptor leads to a **bleeding disorder**, not thrombosis [3]. Patients typically present with macrothrombocytopenia, prolonged bleeding time, and a failure of platelets to aggregate with Ristocetin. ### **Analysis of Incorrect Options (Thrombophilic States)** * **Option A: Factor V Leiden mutation:** The most common cause of inherited thrombophilia [2]. A point mutation (Arg506Gln) makes Factor V resistant to cleavage by Activated Protein C (APC resistance), leading to a hypercoagulable state [2]. * **Option C: Heterozygous Protein C deficiency:** Protein C is a natural anticoagulant that inactivates Factors Va and VIIIa [4]. Deficiency leads to unchecked thrombin generation and an increased risk of DVT and Warfarin-induced skin necrosis. * **Option D: Prothrombin 20210G mutation:** A single nucleotide polymorphism in the 3' untranslated region of the prothrombin gene leads to elevated plasma prothrombin levels, significantly increasing the risk of venous thromboembolism [2]. ### **NEET-PG High-Yield Pearls** * **Virchow’s Triad:** Endothelial injury, stasis, and hypercoagulability [5]. * **Most common inherited risk factor for DVT:** Factor V Leiden [2]. * **Second most common inherited risk factor:** Prothrombin G20210A mutation [2]. * **Bernard-Soulier Syndrome vs. Glanzmann Thrombasthenia:** BSS is a defect in **Gp1b** (Adhesion defect; giant platelets); Glanzmann is a defect in **GpIIb/IIIa** (Aggregation defect; normal platelet size) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 133-134. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 669-670. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 132-133.
Question 627: Which of the following statements is NOT true about Immune Thrombocytopenic purpura (ITP)?
- A. Autoimmune mediated
- B. Massive splenomegaly
- C. Increased megakaryocytes in bone marrow (Correct Answer)
- D. Intravenous immunoglobulin is given
Explanation: ### Explanation In Immune Thrombocytopenic Purpura (ITP), the primary pathology is the **autoimmune destruction of platelets**, usually by IgG antibodies against platelet membrane glycoproteins [3]. **Why Option C is the Correct Answer (The "NOT True" statement):** Actually, Option C is a **true** statement regarding ITP, but it is marked as the "correct" choice in the context of this question's structure. In ITP, the bone marrow shows a **compensatory increase in megakaryocytes** to make up for the peripheral destruction of platelets [1, 2]. Therefore, if the question asks for what is **NOT** true, the answer should be **Option B**. **Analysis of Options:** * **A. Autoimmune mediated:** This is **True**. It is a Type II hypersensitivity reaction where anti-platelet antibodies lead to splenic sequestration and phagocytosis of platelets [3]. * **B. Massive splenomegaly:** This is **NOT True**. In ITP, the spleen is usually **normal in size** or only minimally enlarged [2]. The presence of massive splenomegaly should lead a clinician to suspect other diagnoses like Leukemia, Lymphoma, or Myelofibrosis [4]. * **C. Increased megakaryocytes:** This is **True**. The marrow responds to peripheral low platelet counts by increasing the number and size of megakaryocytes [1, 2]. * **D. IVIG is given:** This is **True**. IVIG is a standard treatment used to "block" the Fc receptors on splenic macrophages, preventing them from destroying antibody-coated platelets [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis of Exclusion:** ITP is diagnosed only after ruling out other causes of thrombocytopenia [1]. * **Peripheral Smear:** Shows "Giant Platelets" (megathrombocytes), reflecting accelerated thrombopoiesis [1]. * **Treatment:** First-line is usually Corticosteroids. Splenectomy is considered for refractory cases [1]. * **Key Distinction:** Unlike TTP (Thrombotic Thrombocytopenic Purpura), ITP does **not** feature schistocytes or microangiopathic hemolytic anemia (MAHA). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 666-667. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 620-621. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 665-666. [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, pp. 631-632.
Question 628: What is the commonest site of lytic lesion in multiple myeloma?
- A. Vertebral column (Correct Answer)
- B. Femur
- C. Clavicle
- D. Pelvis
Explanation: **Explanation:** Multiple myeloma is a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells [1]. These cells produce osteoclast-activating factors (such as RANKL and IL-6), leading to the characteristic "punched-out" lytic lesions [2]. **Why the Vertebral Column is Correct:** The distribution of lytic lesions in multiple myeloma follows the distribution of **red (hematopoietic) bone marrow** in adults [1]. The **vertebral column** is the most frequently involved site (approximately 66% of cases), followed by the ribs, skull, pelvis, femur, clavicle, and scapula [1]. The high concentration of axial bone marrow makes the spine the primary target for plasma cell infiltration and subsequent bone destruction [2]. **Analysis of Incorrect Options:** * **Femur:** While the proximal femur is a common site for pathological fractures in myeloma, it is involved less frequently than the axial skeleton (spine and ribs) [1]. * **Clavicle:** The clavicle is involved in advanced stages but is significantly less common than the vertebrae or skull [1]. * **Pelvis:** The pelvis is a major site of red marrow and is frequently involved, but statistically, it ranks below the vertebral column in frequency of initial lytic lesions [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Order of Frequency:** Vertebrae > Ribs > Skull > Pelvis > Femur [1]. * **Radiology:** Classic "punched-out" lesions are most iconic in the **skull** (Raindrop skull), but the **spine** remains the most common site overall [2]. * **Bone Scan Paradox:** Multiple myeloma lesions are usually **cold on a Technetium-99m bone scan** because there is minimal osteoblastic activity; X-rays or MRI are preferred. * **CRAB Criteria:** Calcium (elevated), Renal insufficiency, Anemia, and Bone lesions [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-618. [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. 606-608.
Question 629: Decreased leukocyte alkaline phosphatase is seen in which condition?
- A. Chronic myeloid leukemia (CML) (Correct Answer)
- B. Acute myeloid leukemia (AML)
- C. Polycythemia vera
- D. Myelofibrosis
Explanation: **Explanation:** The **Leukocyte Alkaline Phosphatase (LAP) score** (also known as the Neutrophil Alkaline Phosphatase or NAP score) is a measure of the enzyme activity within the secondary granules of mature neutrophils. **Why CML is the Correct Answer:** In **Chronic Myeloid Leukemia (CML)**, there is a malignant proliferation of myeloid cells [1]. These cells, despite appearing mature, are functionally defective and lack the LAP enzyme. Therefore, a **low LAP score** is a hallmark diagnostic feature of CML (specifically in the chronic phase). This is crucial for differentiating CML from a "Leukemoid Reaction" (an exaggerated response to infection), where the LAP score is characteristically elevated. **Analysis of Incorrect Options:** * **Polycythemia Vera (PV) & Myelofibrosis:** These are other Myeloproliferative Neoplasms (MPNs) [2]. Unlike CML, the LAP score in these conditions is typically **increased** or normal. * **Acute Myeloid Leukemia (AML):** While LAP is generally low in AML, it is not the classic diagnostic marker used for this condition. The LAP score is specifically used to differentiate mature neutrophilic proliferations. **High-Yield Clinical Pearls for NEET-PG:** * **Low LAP Score:** CML, Paroxysmal Nocturnal Hemoglobinuria (PNH), Hypophosphatasia, and sometimes Aplastic Anemia. * **High LAP Score:** Leukemoid reaction, Pregnancy (3rd trimester), Polycythemia Vera, and Myelofibrosis. * **CML Exception:** The LAP score may **increase** in CML during a "Blast Crisis" or if there is a concurrent infection. * **Normal Range:** Typically 40–100 (based on staining intensity in 100 neutrophils). **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. 624-625. [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. 628-629.
Question 630: Which of the following conditions is characterized by normal hemoglobin structure but reduced red blood cell volume?
- A. Chronic blood loss
- B. Sickle cell anemia
- C. Hemolytic anemia
- D. Thalassemia (Correct Answer)
Explanation: **Explanation:** The correct answer is **Thalassemia**. This condition is defined as a **quantitative defect** in hemoglobin synthesis [2]. In Thalassemia, the amino acid sequence of the globin chains is entirely normal (normal structure), but there is a reduced rate of synthesis of one or more globin chains ($\alpha$ or $\beta$) [2], [4]. This leads to a deficiency of hemoglobin per cell, resulting in **microcytic hypochromic anemia** (reduced Mean Corpuscular Volume or MCV) [1], [3]. **Analysis of Incorrect Options:** * **Sickle Cell Anemia:** This is a **qualitative defect** [2]. The structure of hemoglobin is abnormal due to a point mutation (valine replacing glutamic acid at the 6th position of the $\beta$-globin chain), leading to HbS formation. * **Chronic Blood Loss:** While this eventually leads to Iron Deficiency Anemia (which is microcytic), the primary issue is a lack of iron for heme synthesis, not a primary genetic defect in globin production [1]. * **Hemolytic Anemia:** Most acute hemolytic anemias (like G6PD deficiency or Hereditary Spherocytosis) are **normocytic**, meaning the RBC volume (MCV) remains within the normal range (80-100 fL). **High-Yield Clinical Pearls for NEET-PG:** * **Thalassemia vs. Iron Deficiency Anemia (IDA):** Use the **Mentzer Index** (MCV/RBC count). A ratio **<13** suggests Thalassemia trait, while **>13** suggests IDA. * **Peripheral Smear:** Look for **Target cells** (codocytes) and basophilic stippling in Thalassemia. * **Gold Standard Diagnosis:** Hemoglobin Electrophoresis (HbA2 is increased >3.5% in $\beta$-Thalassemia minor) [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 590-591. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 587-588. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 649-650. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 646-647.
Practice by Chapter
Anemias: Classification and Approach
Practice Questions
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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