Hematopathology — MCQs

A 54-year-old male presents with massive splenomegaly, early fatigue, malaise, low-grade fever, gout, increased susceptibility to infections, anemia, a total leukocyte count of 125,000/mm³, and thrombocytopenia with easy bruising. Which chromosomal translocation is most commonly associated with this diagnosis?

Q209Medium

How do haemopoietic stem cells differ from committed progenitor cells in bone marrow?

Q210Easy

Destruction of Heinz bodies in the spleen is performed by which cells?

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 201: Decreased osmotic fragility is not seen in which of the following conditions?

A. Thalassemia
B. Hereditary spherocytosis (Correct Answer)
C. Sickle cell anemia
D. Iron deficiency

Explanation: ### Explanation **Core Concept: Osmotic Fragility (OF)** Osmotic fragility measures the resistance of red blood cells (RBCs) to hemolysis when exposed to varying concentrations of hypotonic saline. It is primarily determined by the **surface area-to-volume (SA:V) ratio**. **1. Why Hereditary Spherocytosis (HS) is the Correct Answer:** In HS, defects in membrane proteins (like Spectrin or Ankyrin) lead to the loss of membrane fragments, resulting in **Spherocytes** [3]. These cells have a **decreased SA:V ratio**. Because they are already maximally spherical, they cannot expand further when water enters in a hypotonic solution [3]. Consequently, they rupture easily at higher saline concentrations [1]. Therefore, HS is characterized by **Increased Osmotic Fragility**, not decreased. **2. Why the Other Options are Incorrect:** * **Thalassemia & Iron Deficiency Anemia (IDA):** These are microcytic hypochromic anemias [2]. The cells are "flat" or thin (Leptocytes) with an **increased SA:V ratio**. They can accommodate more water before stretching the membrane to the breaking point, leading to **Decreased Osmotic Fragility**. * **Sickle Cell Anemia:** Similar to Thalassemia, the presence of target cells and dehydrated cells increases the SA:V ratio, resulting in **Decreased Osmotic Fragility**. **3. NEET-PG High-Yield Pearls:** * **Increased OF:** Seen in Hereditary Spherocytosis and Autoimmune Hemolytic Anemia (AIHA). * **Decreased OF:** Seen in Thalassemia, IDA, Sickle Cell Anemia, and Liver Disease (due to target cells). * **Confirmatory Test for HS:** The **Eosin-5-maleimide (EMA) binding test** (Flow cytometry) is now the gold standard, replacing the traditional Osmotic Fragility test. * **Incubation:** The sensitivity of the OF test increases after incubating the blood at 37°C for 24 hours. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 590-591. [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 202: What condition is characterized by an M spike on serum electrophoresis?

A. Lymphoblastic leukemia
B. Waldenstrom's macroglobulinaemia (Correct Answer)
C. Alpha-chain disease
D. AIDS

Explanation: **Explanation:** The presence of an **M spike** (Monoclonal spike) on serum protein electrophoresis (SPEP) indicates the proliferation of a single clone of plasma cells or B-lymphocytes that produces a large amount of a specific monoclonal immunoglobulin [1]. **Why Waldenstrom's Macroglobulinaemia (WM) is correct:** WM is a lymphoplasmacytic lymphoma characterized by the infiltration of the bone marrow by neoplastic cells that secrete **monoclonal IgM** [2]. Because IgM is a large pentameric molecule, it creates a prominent M spike in the gamma-globulin region [3]. This condition is clinically distinguished by hyperviscosity syndrome, hepatosplenomegaly, and the absence of lytic bone lesions (unlike Multiple Myeloma) [1]. **Analysis of Incorrect Options:** * **A. Lymphoblastic leukemia:** This is a neoplasm of immature lymphoblasts. While it involves B or T cells, these immature cells do not typically secrete organized monoclonal proteins; hence, no M spike is seen. * **C. Alpha-chain disease:** This is a type of Heavy Chain Disease (Immunoproliferative Small Intestinal Disease). It involves the production of incomplete alpha heavy chains without light chains [1]. On SPEP, it usually presents as a broad, indistinct band in the alpha-2 or beta region rather than a sharp M spike. * **D. AIDS:** HIV infection typically causes a **polyclonal gammopathy** (a broad-based increase in the gamma region) due to chronic immune stimulation, rather than a monoclonal spike. **High-Yield Pearls for NEET-PG:** * **Differential for M Spike:** Multiple Myeloma (IgG > IgA), MGUS (most common cause), Waldenstrom’s (IgM), and Plasmacytoma [1]. * **Bence-Jones Proteins:** These are monoclonal light chains found in the urine, common in Multiple Myeloma but less frequent in WM [3]. * **Dutcher Bodies:** Periodic Acid-Schiff (PAS) positive intranuclear inclusions of immunoglobulins, highly characteristic of WM. **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. 606-607. [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. 609-610. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617.

Question 203: What percentage of Chronic Myeloid Leukemia (CML) cases are positive for the Philadelphia chromosome?

A. 30-40%
B. 50-60%
C. 70-80%
D. 90-95% (Correct Answer)

Explanation: **Explanation:** **1. Why Option D is Correct:** The Philadelphia chromosome (Ph) is the cytogenetic hallmark of Chronic Myeloid Leukemia (CML) [2]. It results from a reciprocal translocation between chromosomes 9 and 22, denoted as **t(9;22)(q34;q11)** [1],[3]. This translocation fuses the *ABL1* gene on chromosome 9 with the *BCR* gene on chromosome 22, creating the *BCR-ABL1* fusion oncogene [3]. This gene encodes a constitutively active tyrosine kinase that drives uncontrolled myeloid proliferation [1]. In clinical practice, approximately **90-95%** of patients with a clinical diagnosis of CML demonstrate this classic translocation via routine karyotyping. **2. Why Other Options are Incorrect:** * **Options A, B, and C:** These percentages are too low. While other leukemias may harbor the Philadelphia chromosome (e.g., 25-30% of adult B-ALL and 3-5% of pediatric B-ALL), its presence in CML is nearly universal [1]. The remaining 5-10% of CML cases that appear "Ph-negative" on standard karyotyping usually harbor "cryptic" translocations that can only be detected by more sensitive methods like FISH (Fluorescence In Situ Hybridization) or RT-PCR. **3. NEET-PG High-Yield Pearls:** * **The "Ph-negative" CML:** If a patient has the CML phenotype but is negative for *BCR-ABL1* even by PCR, the diagnosis is usually shifted to atypical CML (aCML) or another Myelodysplastic/Myeloproliferative neoplasm. * **Protein Product:** The most common fusion protein in CML is **p210**. * **Treatment:** The discovery of this translocation led to the development of **Imatinib** (a Tyrosine Kinase Inhibitor), which is the first-line targeted therapy. * **LAP Score:** CML characteristically shows a **decreased** Leukocyte Alkaline Phosphatase (LAP) score, helping differentiate it from a Leukemoid reaction. **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. 624. [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. 225-226. [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. 624-625.

Question 204: Which of the following statements is true regarding Chronic Myeloid Leukemia (CML)?

A. The size of splenomegaly indicates prognosis.
B. Phagocytic activity of white blood cells is reduced.
C. Sudan black stain is specific for myeloblasts.
D. Myeloblasts, granuloblasts, and lymphoblasts are Philadelphia chromosome positive. (Correct Answer)

Explanation: **Explanation:** **1. Why Option D is Correct:** Chronic Myeloid Leukemia (CML) is a **myeloproliferative neoplasm** originating from a **pluripotent hematopoietic stem cell**. The hallmark of CML is the Philadelphia chromosome [t(9;22)], which results in the *BCR-ABL1* fusion gene [1]. Because the mutation occurs at the level of the multipotent stem cell, the Philadelphia chromosome is present in all lineages derived from it, including **myeloid, erythroid, megakaryocytic, and even B-lymphoid cells**. This explains why CML can transform into either an Acute Myeloid Leukemia (AML) or an Acute Lymphoblastic Leukemia (ALL) during a blast crisis [2]. **2. Why Other Options are Incorrect:** * **Option A:** While massive splenomegaly is a classic feature of CML [2], the **degree of splenomegaly does not correlate directly with prognosis**. Prognosis is better determined by the percentage of blasts, basophilia, and cytogenetic evolution (e.g., Sokal or Hasford scores). * **Option B:** In CML, the white blood cells (granulocytes) are morphologically normal and their **phagocytic activity is generally preserved**, unlike in acute leukemias where functional defects are common. * **Option C:** Sudan Black B (SBB) stains lipids in the granules of **myeloid cells** (neutrophils and precursors). While it helps differentiate AML from ALL, it is **not specific for myeloblasts**; it also stains promyelocytes, myelocytes, and mature neutrophils. **Clinical Pearls for NEET-PG:** * **LAP Score:** Low or zero Leukocyte Alkaline Phosphatase (LAP) score is a high-yield diagnostic marker for CML (differentiates it from a Leukemoid reaction). * **Peripheral Smear:** Characterized by a "myelocyte bulge" and absolute basophilia [2]. * **Treatment:** Imatinib (Tyrosine Kinase Inhibitor) is the first-line therapy [2]. * **Blast Crisis:** Defined as ≥20% blasts in blood or bone marrow. 70% are myeloid, 30% are lymphoid. **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. 624-626. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612.

Question 205: What are the typical Antithrombin III levels in disseminated intravascular coagulation?

A. Decreased (Correct Answer)
B. Increased
C. Unchanged
D. Variable

Explanation: In **Disseminated Intravascular Coagulation (DIC)**, there is systemic, uncontrolled activation of the coagulation cascade [1], [3]. This leads to the widespread formation of microthrombi throughout the microvasculature [3]. **Antithrombin III (AT-III)** is a potent natural anticoagulant that inhibits thrombin (Factor IIa) and other activated clotting factors (IXa, Xa, XIa, and XIIa). During the massive procoagulant state of DIC, AT-III is rapidly consumed as it attempts to neutralize the excessive production of thrombin. Furthermore, DIC often involves endothelial damage and capillary leak, leading to further loss of AT-III. Therefore, **decreased levels** of AT-III are a hallmark finding and serve as a sensitive indicator of the severity of the consumption coagulopathy [1]. **Analysis of Incorrect Options:** * **B. Increased:** AT-III levels never increase in acute DIC because the rate of consumption far exceeds the rate of hepatic synthesis. * **C. Unchanged:** DIC is characterized by the "consumption" of clotting factors and inhibitors; stable levels would suggest the absence of an active systemic thrombotic process [1]. * **D. Variable:** While some parameters in early DIC can be tricky, AT-III is consistently low in established DIC due to its role as the primary inhibitor of the overactive thrombin. **High-Yield Clinical Pearls for NEET-PG:** * **The "Consumption" Profile:** DIC is characterized by decreased Platelets, decreased Fibrinogen, and decreased AT-III [1]. * **Diagnostic Markers:** Elevated **D-dimer** and **FDPs** (Fibrin Degradation Products) are the most specific indicators of fibrinolysis following clot formation in DIC [1], [2]. * **Peripheral Smear:** Look for **Schistocytes** (fragmented RBCs), indicating microangiopathic hemolytic anemia (MAHA) [1]. * **Clinical Correlation:** AT-III deficiency in DIC is associated with resistance to heparin therapy, as heparin requires AT-III as a cofactor to exert its anticoagulant effect. **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. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 671-673.

Question 206: During blood transfusion, clotting of transfused blood is associated with which of the following?

A. ABO incompatibility
B. Minor blood group incompatibility
C. Rh incompatibility
D. Transfusion through Ringer's lactate (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Transfusion through Ringer's lactate.** **Why it is correct:** Blood for transfusion is typically collected in bags containing **CPDA (Citrate-Phosphate-Dextrose-Adenine)**. Citrate acts as an anticoagulant by chelating (binding) calcium ions, which are essential cofactors (Factor IV) in the coagulation cascade. **Ringer’s Lactate (RL)** contains ionized calcium. When blood is mixed with RL in the same infusion line, the calcium in the RL overcomes the chelating capacity of the citrate in the blood bag. This leads to the activation of the clotting cascade, resulting in the formation of **clots within the IV tubing**, which can lead to embolism or line obstruction. **Why the other options are incorrect:** * **A, B, and C (ABO, Minor, and Rh Incompatibility):** These are forms of immune-mediated transfusion reactions [1], [2]. They involve antigen-antibody interactions leading to **hemolysis** (destruction of red cells), not the clotting of the transfused blood itself [2]. While severe ABO incompatibility can trigger Disseminated Intravascular Coagulation (DIC) within the patient’s body [3], it does not cause the transfused blood to clot in the delivery system. **Clinical Pearls for NEET-PG:** * **Compatible Fluids:** Only **0.9% Normal Saline (Isotonic Saline)** is recommended for use with blood components. * **Avoid Dextrose:** 5% Dextrose (D5W) should never be used as it causes red cell aggregation and hemolysis due to its hypotonic nature once glucose is metabolized. * **Calcium Rule:** Never add calcium-containing solutions (like RL or parenteral nutrition) to blood products. * **Filter:** Blood must always be administered through a standard **170–200 micron filter** to remove any pre-existing microaggregates. **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. Red Blood Cell and Bleeding Disorders, pp. 673-674. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 672-673.

Question 207: Chediak Higashi syndrome is characterized by which of the following defect of platelets?

A. Platelet formation
B. Platelet adhesion
C. Platelet aggregation
D. Platelet granule release (Correct Answer)

Explanation: **Explanation:** **Chediak-Higashi Syndrome (CHS)** is an autosomal recessive disorder caused by a mutation in the **LYST gene** (Lysosomal Trafficking Regulator). This defect leads to impaired microtubule-dependent intracellular transport and the formation of **giant lysosomal granules** in various cells, including leukocytes and platelets [1]. 1. **Why Option D is Correct:** In CHS, there is a specific deficiency of **dense granules (delta-granules)** in platelets. These granules normally store ADP, ATP, calcium, and serotonin, which are essential for the "release reaction" that recruits more platelets to the site of injury. Because these granules are either absent or fail to release their contents properly, patients exhibit a **storage pool deficiency**, leading to a defect in **platelet granule release** and a subsequent bleeding tendency [1]. 2. **Why Other Options are Incorrect:** * **A. Platelet formation:** Platelet production (thrombopoiesis) in the bone marrow is generally normal, though the platelets produced are functionally defective. * **B. Platelet adhesion:** This is typically a defect of GP Ib-IX-V (Bernard-Soulier Syndrome) or Von Willebrand Factor (vWF) [2]. * **C. Platelet aggregation:** Primary aggregation is usually normal; however, secondary aggregation is impaired due to the lack of ADP release. Primary aggregation defects are characteristic of Glanzmann Thrombasthenia (GP IIb/IIIa defect) [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Partial oculocutaneous albinism, recurrent pyogenic infections (Staph/Strep), and peripheral neuropathy [1]. * **Hematology:** Look for **giant azurophilic granules** in neutrophils on a peripheral smear [1]. * **Accelerated Phase:** A life-threatening hemophagocytic lymphohistiocytosis (HLH)-like syndrome often triggered by EBV. * **Diagnosis:** Genetic testing for *LYST* gene or visualization of giant granules. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 245-246. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669.

Question 208: A 54-year-old male presents with massive splenomegaly, early fatigue, malaise, low-grade fever, gout, increased susceptibility to infections, anemia, a total leukocyte count of 125,000/mm³, and thrombocytopenia with easy bruising. Which chromosomal translocation is most commonly associated with this diagnosis?

A. t(9;22) (Correct Answer)
B. t(11;17)
C. del(5q)
D. None of the above

Explanation: ### Explanation The clinical presentation of **massive splenomegaly**, hypermetabolic symptoms (fever, fatigue), and a markedly elevated total leukocyte count (125,000/mm³) strongly suggests **Chronic Myeloid Leukemia (CML)** [2]. The presence of gout is due to hyperuricemia from high cell turnover, while thrombocytopenia and anemia indicate a transition toward the accelerated phase or blast crisis [3]. **1. Why Option A is Correct:** The hallmark of CML is the **Philadelphia chromosome**, resulting from the reciprocal translocation **t(9;22)(q34;q11)** [4]. This fuses the *ABL1* gene on chromosome 9 with the *BCR* gene on chromosome 22, creating the **BCR-ABL1 fusion protein**. This protein is a constitutively active tyrosine kinase that drives uncontrolled proliferation of the myeloid lineage [1]. **2. Why the Other Options are Incorrect:** * **Option B: t(11;17):** This is associated with a variant of **Acute Promyelocytic Leukemia (APL)** involving the *ZBTB16-RARA* fusion. Unlike the classic t(15;17), this variant is notably resistant to All-Trans Retinoic Acid (ATRA) therapy. * **Option C: del(5q):** This is the cytogenetic marker for **5q-minus syndrome**, a specific subtype of Myelodysplastic Syndrome (MDS) typically seen in elderly females, characterized by macrocytic anemia and thrombocytosis (not massive splenomegaly). **Clinical Pearls for NEET-PG:** * **LAP Score:** Leukocyte Alkaline Phosphatase (LAP) score is characteristically **decreased** in CML, helping differentiate it from a Leukemoid Reaction (where LAP is increased). * **Peripheral Smear:** Shows a "whole spectrum" of myeloid cells (myelocytes, metamyelocytes, etc.) with a characteristic **"Basophilic-Eosinophilic pit."** * **Treatment:** The first-line management is **Imatinib**, a tyrosine kinase inhibitor (TKI) that specifically targets the BCR-ABL1 protein [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. 624. [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. 625-626. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612. [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. 624-625.

Question 209: How do haemopoietic stem cells differ from committed progenitor cells in bone marrow?

A. Presence of elaborate growth factors
B. Ability to alter receptor to protein binding
C. Capacity to provide permanent structure
D. Ability to provide long-term reconstitution of bone marrow (Correct Answer)

Explanation: ### Explanation The fundamental difference between **Hematopoietic Stem Cells (HSCs)** and **Committed Progenitor Cells** lies in two key properties: **Self-renewal** and **Potency**. [1] **Why Option D is Correct:** HSCs are defined by their ability to provide **long-term reconstitution** of the bone marrow. [4] This is because HSCs are "pluripotent" and possess the unique capacity for asymmetrical division (self-renewal), ensuring the stem cell pool is never exhausted. [5] In contrast, committed progenitor cells (like CFU-E or CFU-GM) have lost the ability for self-renewal; they are "transit-amplifying cells" that can only differentiate into specific lineages and eventually die out. [1] Therefore, only HSCs can permanently restore hematopoiesis after bone marrow ablation (e.g., in transplants). [2] **Analysis of Incorrect Options:** * **Option A:** Both HSCs and progenitor cells require and respond to growth factors (like SCF, TPO, and EPO) for survival and differentiation. [2] * **Option B:** Receptor-protein binding (ligand interaction) is a universal cellular mechanism for signaling and is not a distinguishing feature of stemness. * **Option C:** The "permanent structure" or scaffold of the bone marrow is provided by the **stromal cells** (mesenchymal stem cells, adipocytes, osteoblasts), not the hematopoietic cells themselves. **High-Yield Clinical Pearls for NEET-PG:** * **Surface Marker:** HSCs are characteristically **CD34+** and **Lin-** (lineage negative). * **Niche:** HSCs reside in the "Osteoblastic niche" (quiescent state) and "Vascular niche" (active state) of the bone marrow. * **Transplantation:** In clinical practice, the success of a Bone Marrow Transplant (BMT) depends entirely on the dose of CD34+ HSCs infused, as these are the only cells capable of long-term engraftment. [3] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 588-589. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 112-113. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 585-586. [4] 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. 104-105. [5] 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. 84-85.

Question 210: Destruction of Heinz bodies in the spleen is performed by which cells?

A. Macrophages (Correct Answer)
B. Lymphocytes
C. Neutrophils
D. Fibroblasts

Explanation: **Explanation:** The correct answer is **Macrophages**. [1] **Underlying Concept:** Heinz bodies are inclusions of denatured hemoglobin that form within red blood cells (RBCs), most commonly seen in **G6PD deficiency** following oxidative stress. As these RBCs pass through the splenic sinusoids, they must navigate narrow slits to re-enter circulation. The **splenic macrophages** (part of the reticuloendothelial system) identify these rigid Heinz bodies and "pluck" them out of the RBC membrane. [1] This process, known as **"pitting,"** results in the formation of **Bite cells (Degmacytes)**. [1] If the macrophage removes a significant portion of the membrane, the cell may become a smaller, rounder **Spherocyte**, which is eventually sequestered and destroyed. **Why other options are incorrect:** * **Lymphocytes:** These are cells of the adaptive immune system (T-cells and B-cells) involved in antigen recognition and antibody production; they do not have phagocytic or "pitting" functions. * **Neutrophils:** While phagocytic, neutrophils are primarily involved in acute bacterial inflammation and are not resident cells responsible for the filtration of RBCs in the splenic pulp. * **Fibroblasts:** These cells are responsible for synthesizing the extracellular matrix and collagen; they provide structural integrity to the spleen but do not participate in cell destruction. **High-Yield Clinical Pearls for NEET-PG:** * **Stain for Heinz Bodies:** They are not visible on routine Leishman or peripheral smears; they require **Supravital stains** (e.g., Crystal Violet or Methylene Blue). * **Bite Cells vs. Blister Cells:** "Bite cells" are the hallmark of splenic macrophage activity on Heinz bodies. * **G6PD Deficiency:** This is an X-linked recessive disorder. [1] Common triggers for oxidative stress include Fava beans, infections, and drugs (e.g., Primaquine, Sulphonamides). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 642-643.

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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