Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 471: Hemophilia clinically manifests as a rise in which laboratory parameter?

A. Activated Partial Thromboplastin Time (APTT) (Correct Answer)
B. Prothrombin Time (PT)
C. Clotting Time (CT)
D. Fibrin Degradation Products (FDP)

Explanation: **Explanation:** Hemophilia A (Factor VIII deficiency) and Hemophilia B (Factor IX deficiency) are X-linked recessive disorders characterized by defects in the **intrinsic pathway** of the coagulation cascade. **Why APTT is the correct answer:** The **Activated Partial Thromboplastin Time (APTT)** measures the integrity of the intrinsic and common pathways (Factors XII, XI, IX, VIII, X, V, II, and I) [1]. Since Hemophilia involves a deficiency in Factor VIII or IX, the intrinsic pathway is impaired, leading to a prolonged (elevated) APTT. This is the most sensitive screening test for Hemophilia. **Analysis of Incorrect Options:** * **Prothrombin Time (PT):** This measures the **extrinsic** and common pathways (Factor VII). Since Factor VII levels are normal in Hemophilia, the PT remains normal [1]. * **Clotting Time (CT):** While CT can be prolonged in severe Hemophilia, it is a crude, non-specific, and insensitive test that is no longer used for primary diagnosis or monitoring in modern clinical practice. * **Fibrin Degradation Products (FDP):** These are markers of fibrinolysis (clot breakdown), typically elevated in conditions like DIC or DVT, not in primary coagulation factor deficiencies. **NEET-PG High-Yield Pearls:** * **Mixing Study:** If APTT is prolonged, a mixing study (patient plasma + normal plasma) is done. If the APTT **corrects**, it indicates a factor deficiency (like Hemophilia). If it does not correct, it suggests an inhibitor (like Lupus anticoagulant). * **Bleeding Time (BT):** This measures platelet function. BT is **normal** in Hemophilia but prolonged in von Willebrand Disease (vWD) and platelet disorders. * **Clinical Presentation:** Hemophilia typically presents with **hemarthrosis** (bleeding into joints) and hematomas, rather than superficial petechiae. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 128-130.

Question 472: A young female patient presented with symptoms related to anemia. Peripheral blood smear showed neutrophil hypersegmentation and bone marrow aspirate smear showed giant myelocytes. Which of the following is the likely etiology?

A. Sideroblastic anemia
B. Iron deficiency anemia
C. Thalassemia
D. Folic acid deficiency (Correct Answer)

Explanation: ### Explanation The clinical presentation and morphological findings point towards **Megaloblastic Anemia**, which is most commonly caused by a deficiency of Vitamin B12 or **Folic acid (Option D)** [4], [5]. **Why Folic Acid Deficiency is Correct:** Megaloblastic anemia is characterized by **impaired DNA synthesis** while RNA synthesis remains intact [5]. This leads to **nuclear-cytoplasmic asynchrony**, where the nucleus matures slower than the cytoplasm [1]. * **Peripheral Smear:** The hallmark is **hypersegmented neutrophils** (defined as >5% of neutrophils having 5 or more lobes, or a single neutrophil with 6 or more lobes) [2]. This is often the earliest sign of megaloblastic change. * **Bone Marrow:** The marrow shows "megaloblastic" changes in all cell lines [3]. **Giant myelocytes** and giant metamyelocytes are characteristic findings in the granulocytic series, while erythroid precursors show open, "checkered" chromatin [1], [3]. **Why Other Options are Incorrect:** * **Iron Deficiency Anemia (B) & Thalassemia (C):** These are microcytic hypochromic anemias. They are characterized by a defect in hemoglobin synthesis, not DNA synthesis. Peripheral smears typically show microcytes and target cells, not hypersegmented neutrophils. * **Sideroblastic Anemia (A):** This involves a defect in heme synthesis leading to iron-laden mitochondria surrounding the nucleus (Ring Sideroblasts). It does not typically present with giant myelocytes or hypersegmented neutrophils. **High-Yield Clinical Pearls for NEET-PG:** * **Earliest sign of Megaloblastic Anemia:** Hypersegmented neutrophils in the peripheral blood [2]. * **Earliest sign of recovery after treatment:** Increase in Reticulocyte count (usually within 3–5 days). * **Pancytopenia:** Severe megaloblastic anemia can present with low RBCs, WBCs, and platelets due to ineffective hematopoiesis. * **Neurological symptoms:** If the question mentioned subacute combined degeneration (SCD) of the spinal cord, Vitamin B12 deficiency would be the specific answer, as folate deficiency does not cause neurological deficits [4]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 593-594. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 654. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 654-655. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 594-595. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 656-657.

Question 473: Hemophilia is associated with which chromosome?

A. X chromosome (Correct Answer)
B. Y chromosome
C. Chromosome 3
D. Chromosome 16

Explanation: **Explanation:** **1. Why the Correct Answer is Right:** Hemophilia A (Factor VIII deficiency) and Hemophilia B (Factor IX deficiency, also known as Christmas disease) are both inherited in an **X-linked recessive** pattern [1], [4]. The genes responsible for encoding coagulation Factors VIII and IX are located on the long arm of the **X chromosome** (Xq28 and Xq27, respectively) [2]. Because males have only one X chromosome (XY), a single defective gene results in the clinical manifestation of the disease. Females (XX) are typically asymptomatic carriers unless they experience extreme lyonization (X-inactivation) [2] or have Turner syndrome [3]. **2. Why Incorrect Options are Wrong:** * **Option B (Y chromosome):** Very few genetic disorders are Y-linked (holandric inheritance), and they typically involve male fertility (e.g., SRY gene defects), not coagulation factors [1]. * **Option C (Chromosome 3):** While many proteins are coded here, it is not associated with primary or secondary hemostasis disorders like Hemophilia. * **Option D (Chromosome 16):** This chromosome is high-yield for **Alpha-thalassemia** (HBA1 and HBA2 genes), but not for Hemophilia. **3. NEET-PG Clinical Pearls:** * **Inheritance Pattern:** X-linked recessive (Males are affected; Females are carriers) [4]. * **Coagulation Profile:** Characterized by a **prolonged aPTT** (intrinsic pathway) with a **normal PT and normal Bleeding Time**. * **Clinical Hallmark:** Hemarthrosis (bleeding into joints, most commonly the knee) and muscle hematomas. * **Hemophilia C:** A rare variant (Factor XI deficiency) that follows an **autosomal recessive** pattern and is more common in Ashkenazi Jews. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 151. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 670-671. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 173-174. [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. 53-54.

Question 474: Which of the following causes of anemia is associated with a hypoplastic marrow?

A. Fanconi's Anemia (Correct Answer)
B. Paroxysmal Nocturnal Hemoglobinuria (PNH)
C. Hypersplenism
D. Myelofibrosis

Explanation: **Explanation:** **Fanconi’s Anemia (Correct Answer):** Fanconi’s Anemia is the most common inherited cause of **Aplastic Anemia** [1]. It is an autosomal recessive disorder characterized by a defect in DNA repair (specifically, the FANC protein complex). This leads to progressive bone marrow failure, resulting in a **hypoplastic marrow** where hematopoietic stem cells are replaced by fat cells [2]. Clinical hallmarks include pancytopenia, short stature, thumb anomalies, and café-au-lait spots. **Analysis of Incorrect Options:** * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** While PNH can coexist with aplastic anemia, it is primarily an acquired clonal stem cell disorder leading to intravascular hemolysis. The marrow is typically normocellular or hypercellular (compensatory) unless it has evolved into a bone marrow failure syndrome [1]. * **Hypersplenism:** This causes peripheral destruction or sequestration of blood cells. The bone marrow in hypersplenism is characteristically **hyperplastic** as it attempts to compensate for the low peripheral counts. * **Myelofibrosis:** This is a myeloproliferative neoplasm characterized by a "dry tap" on aspiration. However, the marrow is not hypoplastic; it is replaced by **fibrosis (collagen/reticulin)** and often shows an initial hypercellular phase with atypical megakaryocytes. **NEET-PG High-Yield Pearls:** * **Gold Standard Diagnosis for Fanconi’s:** Chromosomal breakage study (using Mitomycin C or Diepoxybutane). * **Marrow Appearance:** In hypoplastic/aplastic anemia, the biopsy shows "dry" marrow with >70% fat space [2]. * **Pancytopenia with Hyperplastic Marrow:** Think of Megaloblastic anemia, Aleukemic leukemia, or Hypersplenism. * **Pancytopenia with Hypoplastic Marrow:** Think of Aplastic anemia (Idiopathic or Fanconi’s) and certain drug toxicities. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 595-596. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 662-663.

Question 475: Lacunar cells are characteristic of which of the following conditions?

A. Nodular sclerosing type of Hodgkin’s disease (Correct Answer)
B. Pleomorphic adenoma
C. Hurler’s syndrome
D. None of the above

Explanation: **Explanation:** **Lacunar cells** are a specific morphological variant of Reed-Sternberg (RS) cells. They are characterized by a small, shrunken nucleus situated within a large, clear space (the "lacuna") [1]. This appearance is an artifact of formalin fixation, where the abundant pale cytoplasm of the cell retracts from the surrounding tissue [1]. 1. **Why Option A is correct:** Lacunar cells are the hallmark diagnostic feature of the **Nodular Sclerosis** subtype of Hodgkin’s Lymphoma (NSHL) [1]. NSHL is the most common subtype of Hodgkin’s disease and is further characterized by the presence of broad collagen bands (fibrosis) dividing the lymphoid tissue into nodules [2]. 2. **Why other options are incorrect:** * **Option B (Pleomorphic adenoma):** This is a benign mixed tumor of the salivary glands. While it features a diverse histology (myxoid, chondroid, and epithelial components), it does not contain lacunar RS cells. * **Option C (Hurler’s syndrome):** This is a lysosomal storage disorder (Mucopolysaccharidosis Type I). Histologically, it is associated with "Gargoyle cells" (vacuolated cells due to accumulation of dermatan and heparan sulfate), not lacunar cells. **High-Yield Clinical Pearls for NEET-PG:** * **RS Cell Variants:** * **Lacunar cells:** Nodular Sclerosis HL [1]. * **Popcorn cells (L&H cells):** Nodular Lymphocyte Predominant HL (CD20 positive) [1]. * **Mummified cells:** Mixed Cellularity HL. * **NSHL Profile:** Most common in young females; typically involves mediastinal lymph nodes; excellent prognosis [3]. * **Immunophenotype:** Classic RS cells (including lacunar cells) are typically **CD15+ and CD30+**, but CD45 negative. **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. 614-616. [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 476: What is the cause of fragmented RBCs in peripheral blood?

A. Microangiopathic hemolytic anemia
B. Disseminated intravascular coagulation (DIC)
C. Option 1, 2, and 4 (Correct Answer)
D. Malignant hypertension

Explanation: **Explanation:** Fragmented red blood cells, also known as **Schistocytes** (or helmet cells), are the hallmark of **Microangiopathic Hemolytic Anemia (MAHA)** [1], [2]. The underlying mechanism is the mechanical shearing of RBCs as they pass through small blood vessels partially obstructed by fibrin strands or platelet thrombi [3]. **Why the correct answer is right:** The correct answer (Option C) encompasses Microangiopathic Hemolytic Anemia, DIC, and Malignant Hypertension. 1. **MAHA:** This is a broad category including conditions like TTP (Thrombotic Thrombocytopenic Purpura) and HUS (Hemolytic Uremic Syndrome), where microthrombi shred passing RBCs [2]. 2. **DIC:** Widespread activation of the coagulation cascade leads to fibrin mesh formation in the microvasculature, causing significant fragmentation [3]. 3. **Malignant Hypertension:** Extreme blood pressure causes endothelial injury and fibrinoid necrosis of arterioles, leading to the same mechanical shearing effect. **Analysis of Options:** * **Option A, B, and D:** While each of these individually causes schistocytes, they are all part of the same pathophysiological spectrum. Therefore, the combined option is the most accurate. **NEET-PG High-Yield Pearls:** * **Schistocytes** are often described as "helmet cells," "triangle cells," or "fragmented cells." * **Common Causes (The "Big 5"):** TTP, HUS, DIC, Malignant Hypertension, and Pre-eclampsia/HELLP syndrome [2]. * **Prosthetic Heart Valves:** Can also cause fragmentation due to "Waring Blender Syndrome" (macroangiopathic hemolysis). * **Lab Finding:** In these conditions, you will see increased LDH, decreased haptoglobin, and a negative Direct Coombs Test (as the hemolysis is mechanical, not immune-mediated). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 540-541. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 667-668. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626.

Question 477: Which of the following is NOT true about Multiple Myeloma?

A. It involves clonal proliferation of plasma cells.
B. It is more common in individuals over 50 years of age.
C. Amyloidosis can be a complication.
D. Protein casts in the urine are composed of complete immunoglobulin chains. (Correct Answer)

Explanation: ### Explanation **Why Option D is the correct answer (The False Statement):** In Multiple Myeloma, the neoplastic plasma cells often produce an excess of **monoclonal free light chains** (kappa or lambda), rather than complete immunoglobulin molecules [3], [4]. These small light chains are filtered by the glomerulus and reach the renal tubules. Here, they precipitate with **Tamm-Horsfall protein** to form dense, waxy, eosinophilic intratubular casts [1]. These are known as **Bence-Jones proteins**. Therefore, the protein casts are composed of light chains, not complete immunoglobulin chains [1]. **Analysis of Incorrect Options (True Statements):** * **Option A:** Multiple Myeloma is defined as a **monoclonal (clonal) proliferation** of malignant plasma cells in the bone marrow, typically exceeding 10% of the marrow cellularity [3], [5]. * **Option B:** It is primarily a disease of the elderly. The median age at diagnosis is approximately **65–70 years**, making it very rare in individuals under 40 [3]. * **Option C:** In about 5–10% of cases, the excess free light chains deposit in tissues as insoluble fibrils (AL type amyloid), leading to **Systemic AL Amyloidosis** [1]. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** **C**alcium (Hypercalcemia), **R**enal insufficiency, **A**nemia, **B**one lesions (Lytic "punched-out" lesions) [1]. * **M-Spike:** Found on Serum Protein Electrophoresis (SPEP), usually IgG (most common) or IgA [4]. * **Peripheral Smear:** Characterized by **Rouleaux formation** due to increased serum proteins decreasing the zeta potential between RBCs [2]. * **Myeloma Kidney:** Also known as Cast Nephropathy; it is the most common cause of renal failure in these patients [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 618-619. [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. 607-608. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617. [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. 608-609. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 617-618.

Question 478: The lymphocytic and histiocytic variant of Reed-Sternberg cell is seen in which of the following conditions?

A. Follicular center lymphoma
B. Lymphocyte depleted Hodgkin's disease
C. Nodular sclerosis Hodgkin's disease
D. Lymphocyte predominant Hodgkin's disease (Correct Answer)

Explanation: ### Explanation **1. Why the Correct Answer is Right:** The **Lymphocytic and Histiocytic (L&H) variant** of the Reed-Sternberg (RS) cell is the hallmark of **Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLPHL)** [1]. These cells are often referred to as **"Popcorn cells"** because their nuclei are multi-lobed and resemble an exploded kernel of corn [1]. Unlike classic RS cells, L&H cells are **CD20+ and CD45+**, but negative for CD15 and CD30. This is a high-yield distinction for NEET-PG, as NLPHL is now considered a distinct biological entity from Classic Hodgkin Lymphoma (CHL). **2. Why the Incorrect Options are Wrong:** * **Follicular Center Lymphoma (A):** This is a Non-Hodgkin Lymphoma (NHL) characterized by centrocytes and centroblasts. It does not feature RS cells or their variants. * **Lymphocyte Depleted Hodgkin’s Disease (B):** This variant of CHL is characterized by numerous **pleomorphic (anaplastic) RS cells** and a paucity of background lymphocytes. It has the worst prognosis among CHL subtypes. * **Nodular Sclerosis Hodgkin’s Disease (C):** This variant is characterized by **Lacunar cells** (RS cells where the cytoplasm retracts during formalin fixation, leaving the cell in a "lacuna" or empty space) and collagen bands dividing the lymph node into nodules [1]. **3. Clinical Pearls for NEET-PG:** * **Classic RS Cell:** Described as having an **"Owl’s eye"** appearance (bilobed nucleus with prominent eosinophilic nucleoli) [1]. * **Immunophenotype (Classic HL):** CD15+, CD30+, CD45–. * **Immunophenotype (NLPHL/Popcorn cells):** CD20+, CD45+, CD15–, CD30–. * **Prognosis:** NLPHL generally has an excellent prognosis and often presents as localized peripheral lymphadenopathy (e.g., cervical or axillary) in young males [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.

Question 479: Periodic acid-Schiff (PAS) stain shows block positivity in which of the following cells?

A. Myeloblasts
B. Lymphoblasts (Correct Answer)
C. Monoblasts
D. Megakaryoblasts

Explanation: **Explanation:** The **Periodic acid-Schiff (PAS)** stain is a cytochemical stain used to detect glycogen and mucopolysaccharides. In hematopathology, it is a crucial tool for differentiating various types of acute leukemias. **1. Why Lymphoblasts are correct:** In **Acute Lymphoblastic Leukemia (ALL)**, lymphoblasts typically exhibit a characteristic **"block-like" or "chunky" positivity** (coarse granules) against a clear cytoplasmic background. This occurs because lymphoblasts contain large aggregates of glycogen. This pattern is highly suggestive of the L1 or L2 subtypes of ALL [1]. **2. Analysis of Incorrect Options:** * **Myeloblasts (Option A):** These cells are typically **PAS negative** or show only faint, diffuse cytoplasmic tinging. They are better identified using Myeloperoxidase (MPO) or Sudan Black B (SBB) stains. * **Monoblasts (Option B):** These cells usually show a **diffuse, fine granular positivity** scattered throughout the cytoplasm, rather than distinct blocks. They are best identified using Non-specific Esterase (NSE) stains. * **Megakaryoblasts (Option D):** While megakaryoblasts can be PAS positive, the staining is usually **diffuse or peripheral (fringe-like)** rather than the classic coarse blocks seen in lymphoblasts. **Clinical Pearls for NEET-PG:** * **MPO/SBB:** Positive in AML (Myeloid); Negative in ALL. * **PAS Block Positivity:** Classic for **ALL** and **Erythroleukemia (AML-M6)** (where it appears in the proerythroblasts). * **NSE (Non-specific Esterase):** Positive in Monocytic lineages (**AML-M4 and M5**); inhibited by Sodium Fluoride. * **Acid Phosphatase:** Shows focal "polar" positivity in **T-cell ALL** [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. 599-600.

Question 480: In hemolytic anemia, what changes occur in the skull bones?

A. Outer table thickening
B. Diploic space narrowing
C. Diploic space widening (Correct Answer)
D. None of the above

Explanation: In chronic hemolytic anemias (such as Thalassemia major and Sickle Cell Anemia), the fundamental process is **Compensatory Erythroid Hyperplasia** [1]. To compensate for the shortened lifespan of red blood cells, the bone marrow undergoes massive expansion to increase erythropoiesis [1]. ### Why the correct answer is right: * **Diploic Space Widening:** The skull is a major site of hematopoiesis in children. As the bone marrow expands, it pushes against the inner and outer tables of the skull, leading to a significant **widening of the diploic space** (the spongy bone layer between the tables). * **Radiological Correlation:** This expansion causes the characteristic **"Crew-cut" or "Hair-on-end" appearance** on X-ray, as new bone trabeculae are laid down perpendicular to the skull tables [1]. ### Why the incorrect options are wrong: * **Outer Table Thickening:** In reality, the expanding marrow causes **thinning of the outer table** due to pressure atrophy [1]. The inner table is usually spared. * **Diploic Space Narrowing:** This occurs in conditions of osteosclerosis or aging, not in hemolytic anemia where marrow hypercellularity demands more space. ### NEET-PG High-Yield Pearls: 1. **Thalassemia Major:** Shows the most classic "Hair-on-end" appearance due to ineffective erythropoiesis and extreme marrow expansion [1]. 2. **Chipmunk Facies:** Marrow expansion also occurs in the maxillary bones, leading to prominent cheekbones and malocclusion of teeth [1]. 3. **Extramedullary Hematopoiesis:** When the marrow cannot keep up, the liver and spleen take over, leading to hepatosplenomegaly [1]. 4. **Paranasal Sinuses:** These are often obliterated by the expanding marrow, except for the ethmoid sinuses. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 644-649.

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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