Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1231: Which of the following findings is NOT typically seen in hemolytic anemia?

A. Hemosiderosis
B. Hemochromatosis (Correct Answer)
C. Cholelithiasis
D. None of the above

Explanation: **Explanation:** In hemolytic anemia, the premature destruction of red blood cells (RBCs) leads to the release of hemoglobin and subsequent iron overload. However, there is a distinct pathological difference between **Hemosiderosis** and **Hemochromatosis**. **Why Hemochromatosis is the correct answer:** Hemochromatosis (specifically Hereditary Hemochromatosis) is a primary genetic disorder of iron metabolism characterized by excessive intestinal iron absorption leading to systemic iron deposition and, crucially, **associated tissue damage and organ dysfunction** (e.g., cirrhosis, diabetes, skin pigmentation) [4]. While chronic hemolysis can lead to "Secondary Hemochromatosis" due to repeated blood transfusions, it is not a *typical* or inherent finding of the hemolytic process itself. In the context of this question, the term usually refers to the primary disease state involving organ damage. **Analysis of other options:** * **A. Hemosiderosis:** This is a hallmark of hemolytic anemia. It refers to the deposition of iron in the form of hemosiderin within macrophages (spleen, liver, bone marrow) and parenchymal cells [3]. Unlike hemochromatosis, it generally does not imply functional organ damage. * **C. Cholelithiasis:** Chronic hemolysis leads to increased production of bilirubin (unconjugated) [1]. This results in a high concentration of bilirubin in the bile, leading to the formation of **pigment stones** (calcium bilirubinate), a very common complication in conditions like Hereditary Spherocytosis or Sickle Cell Anemia [2]. **NEET-PG High-Yield Pearls:** * **Pigment Stones:** Black, small, and radiopaque (due to calcium salts) [1]. * **Haptoglobin:** The most sensitive marker for hemolysis (levels will be decreased) [3]. * **Reticulocytosis:** A compensatory response of the bone marrow to hemolysis, often seen as polychromasia on a peripheral smear [1], [2]. * **Urine findings:** Hemoglobinuria and Hemosiderinuria are seen in *intravascular* hemolysis, but not typically in *extravascular* hemolysis [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 640. [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. 639-640. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 854-855.

Question 1232: Gandy-Gandy bodies are typically seen in chronic venous congestion of which of the following organs?

A. Lung
B. Spleen (Correct Answer)
C. Kidney
D. Liver

Explanation: **Explanation:** **Gandy-Gamna bodies** (also known as Gamna-Gandy bodies or Siderofibrotic nodules) are a classic histopathological finding in the **Spleen**. 1. **Mechanism (Why Spleen is correct):** In conditions causing chronic venous congestion of the spleen (most commonly **Portal Hypertension**), there is increased pressure leading to focal hemorrhages within the splenic parenchyma. As the blood breaks down, deposits of **hemosiderin** (iron) and **calcium** form on the fibrous connective tissue and elastic fibers [1]. Microscopically, these appear as yellow-brown or rust-colored nodules consisting of fibrous tissue, iron, and calcium salts. 2. **Analysis of Incorrect Options:** * **Lung:** Chronic venous congestion of the lung (often due to left heart failure) leads to the formation of **Heart Failure Cells** (hemosiderin-laden macrophages in the alveoli), not Gandy-Gamna bodies. * **Liver:** Chronic venous congestion here results in the **"Nutmeg Liver"** appearance due to centrilobular necrosis and congestion, but it does not typically form siderofibrotic nodules. * **Kidney:** Congestion in the kidney leads to dusky, enlarged organs but lacks the specific fibro-calcific and iron-laden reaction seen in the spleen. **High-Yield Clinical Pearls for NEET-PG:** * **Staining:** Gandy-Gamna bodies stain positive with **Prussian Blue** (for iron) and **Von Kossa** (for calcium). * **Common Associations:** Portal hypertension (due to Cirrhosis), Sickle Cell Anemia, and Splenic Lymphoma. * **Radiology:** On MRI, they appear as multiple low-signal intensity foci (due to the paramagnetic effect of iron) on T2-weighted sequences, often referred to as the "tobacco-fleck" appearance. **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. 630-634.

Question 1233: Intravascular hemolysis occurs in which of the following conditions?

A. Hereditary spherocytosis
B. Autoimmune hemolytic anemia
C. Paroxysmal nocturnal hemoglobinuria (Correct Answer)
D. Thalassemia

Explanation: ### Explanation Hemolysis is categorized based on the site of red blood cell (RBC) destruction: **Intravascular** (within the blood vessels) or **Extravascular** (within the splenic or hepatic sinusoids) [1]. **Correct Answer: C. Paroxysmal Nocturnal Hemoglobinuria (PNH)** PNH is a classic example of intravascular hemolysis [2]. It is caused by an acquired mutation in the **PIGA gene**, leading to a deficiency of **GPI-anchored proteins** (CD55 and CD59) on the RBC membrane [2]. These proteins normally protect cells from complement-mediated attack. Their absence allows the **Complement Membrane Attack Complex (MAC)** to punch holes directly into the RBCs within the circulation, releasing hemoglobin directly into the plasma [2]. **Why the other options are incorrect:** * **A. Hereditary Spherocytosis:** This is a prototype of **extravascular hemolysis**. Molecular defects in membrane proteins (ankyrin, spectrin) result in spherical RBCs that are inflexible. These cells are trapped and destroyed by **splenic macrophages** [3]. * **B. Autoimmune Hemolytic Anemia (AIHA):** Most cases (Warm AIHA) involve IgG-coated RBCs being partially "nibbled" by splenic macrophages, leading to extravascular destruction [3]. (Note: Cold Agglutinin Disease can rarely cause intravascular hemolysis, but AIHA is generally classified as extravascular). * **D. Thalassemia:** This is a quantitative globin chain defect. The primary mechanism is **ineffective erythropoiesis** (destruction in bone marrow) and **extravascular hemolysis** as the spleen removes RBCs containing Heinz-like inclusions. **High-Yield Clinical Pearls for NEET-PG:** * **Intravascular Markers:** Low haptoglobin, high LDH, **hemoglobinuria**, and **hemosiderinuria** [1]. * **Extravascular Markers:** Splenomegaly and jaundice (unconjugated hyperbilirubinemia) [1]. * **PNH Triad:** Hemolytic anemia, pancytopenia, and venous thrombosis (e.g., Budd-Chiari syndrome) [2]. * **Gold Standard Test for PNH:** Flow cytometry (detecting absence of CD55/CD59) [2]. **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, pp. 650-651. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603.

Question 1234: Which of the following is true about Burkitt's lymphoma?

A. Associated with t(14;18)
B. Expresses BCL-2
C. Shows a starry sky pattern on histology (Correct Answer)
D. Slowly progressing

Explanation: **Explanation:** Burkitt’s Lymphoma (BL) is a highly aggressive B-cell neoplasm characterized by the rapid proliferation of lymphoid cells [1]. **1. Why Option C is Correct:** The hallmark histological feature of BL is the **"Starry Sky" appearance**. This pattern is created by numerous pale-colored, tingible-body macrophages (the "stars") scattered amidst a dense background of small, dark, monomorphic neoplastic B-cells (the "sky") [1]. These macrophages are busy phagocytosing apoptotic debris resulting from the exceptionally high turnover rate of the tumor cells [1]. **2. Why the Other Options are Incorrect:** * **Option A:** BL is associated with **t(8;14)**, involving the translocation of the *c-MYC* gene to the Ig heavy chain locus. **t(14;18)** is characteristic of Follicular Lymphoma (involving *BCL-2*) [3]. * **Option B:** BL typically **does not express BCL-2** (it is BCL-2 negative). The absence of this anti-apoptotic protein, combined with high *c-MYC* expression, contributes to the high rate of apoptosis seen in the tumor [3]. * **Option D:** BL is one of the **fastest-growing human tumors** with a Ki-67 proliferation index of nearly 100% [1]. It is rapidly progressive, not slow [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Variants:** Endemic (African; associated with EBV, involves the jaw), Sporadic (Abdominal involvement), and Immunodeficiency-associated (HIV) [2]. * **Immunophenotype:** CD19+, CD20+, CD10+, and BCL-6+. * **Genetics:** Overexpression of **c-MYC** (transcription factor) is the primary driver. * **Morphology:** Cells have "oil red O" positive cytoplasmic lipid vacuoles. **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. [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. 605-606. [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. 602-604.

Question 1235: Which of the following is NOT a feature of histiocytosis?

A. Antigen processing cells
B. CD1a marker present
C. CD127 marker (Correct Answer)
D. Osteolytic lesions

Explanation: **Explanation:** Histiocytosis, specifically **Langerhans Cell Histiocytosis (LCH)**, is a group of idiopathic disorders characterized by the abnormal proliferation of mature histiocytes (Langerhans cells) [1]. **Why Option C is correct:** **CD127** (Interleukin-7 receptor alpha) is a marker typically associated with **lymphocytes** (T-cells and B-cell progenitors), not histiocytes. In LCH, the characteristic immunophenotype includes positivity for **CD1a, S100, and CD207 (Langerin)** [1]. Therefore, CD127 is not a feature of this condition. **Analysis of Incorrect Options:** * **Option A (Antigen processing cells):** Langerhans cells are specialized dendritic cells found in the skin and mucosa [1]. Their primary physiological role is to act as **antigen-presenting cells (APCs)**, capturing and processing antigens to present them to T-lymphocytes. * **Option B (CD1a marker):** CD1a is a highly specific surface marker used in immunohistochemistry to identify Langerhans cells, making it a hallmark diagnostic feature of LCH [1]. * **Option D (Osteolytic lesions):** LCH frequently involves the bone (most commonly the skull, femur, and ribs). These present radiographically as "punched-out" **osteolytic lesions** without a sclerotic rim, often leading to pathological fractures or "floating teeth" in the jaw. **High-Yield Clinical Pearls for NEET-PG:** * **Electron Microscopy:** Look for **Birbeck Granules**, which are pathognomonic "tennis-racket" shaped cytoplasmic organelles [1]. * **Key Markers:** CD1a (+), S100 (+), and **Langerin/CD207 (+)**. Langerin is the most specific marker as it constitutes the Birbeck granule [1]. * **Clinical Triad (Hand-Schüller-Christian disease):** Calvarial bone defects, diabetes insipidus, and exophthalmos. * **BRAF V600E Mutation:** Seen in approximately 50% of LCH cases, highlighting its neoplastic nature [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. 629-630.

Question 1236: A 22-year-old African American male, with no prior history of signs or symptoms of sickle cell anemia, wants to know if he has sickle cell trait. Which laboratory method can be used to detect the presence of hemoglobin S?

A. Coombs' test
B. Osmotic fragility test
C. Metabisulfite test (Correct Answer)
D. Sucrose hemolysis test

Explanation: ### Explanation **Correct Option: C. Metabisulfite test** The **Sodium Metabisulfite test** (Sickling test) is a screening method used to detect the presence of Hemoglobin S (HbS). The underlying principle is that sodium metabisulfite is a reducing agent that lowers oxygen tension. In deoxygenated conditions, HbS polymerizes, causing the red blood cells to take on a characteristic **sickle shape**, which can be visualized under a light microscope [1]. This test is positive in both Sickle Cell Anemia (HbSS) and Sickle Cell Trait (HbAS). **Analysis of Incorrect Options:** * **A. Coombs' test:** Used to detect antibodies or complement on the surface of RBCs (Direct) or in the serum (Indirect). It is the gold standard for diagnosing **Autoimmune Hemolytic Anemia (AIHA)**. * **B. Osmotic fragility test:** Measures the resistance of RBCs to hemolysis in varying concentrations of hypotonic saline. It is the classic screening test for **Hereditary Spherocytosis**. * **D. Sucrose hemolysis test:** Also known as the Sugar Water test, it was historically used to screen for **Paroxysmal Nocturnal Hemoglobinuria (PNH)** by demonstrating increased sensitivity of RBCs to complement-mediated lysis. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** While the metabisulfite test and Solubility test (using Sodium dithionite) are screening tools, **Hemoglobin Electrophoresis** or **HPLC** is the definitive method to quantify HbS and differentiate between trait and disease. * **Sickle Cell Trait (HbAS):** Typically asymptomatic with a normal peripheral smear [1]. Sickling only occurs under extreme conditions (e.g., severe hypoxia or high altitudes). * **Metabisulfite Test Limitation:** It cannot distinguish between Sickle Cell Disease and Sickle Cell Trait; both will show a positive result. * **False Negatives:** Can occur in infants <6 months due to high levels of HbF, which inhibits sickling. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599.

Question 1237: All of the following are features of Hemophagocytic Lymphohistiocytosis (HLH), except?

A. Fever
B. Splenomegaly
C. Hyperferritinemia
D. Hyperfibrinogenemia (Correct Answer)

Explanation: **Explanation:** Hemophagocytic Lymphohistiocytosis (HLH) is a reactive condition marked by cytopenias and signs and symptoms of systemic inflammation related to macrophage activation [1]. The diagnosis is based on the **HLH-2004 trial criteria**, which require meeting 5 out of 8 specific clinical and laboratory findings. **Why Option D is the Correct Answer:** In HLH, there is massive activation of macrophages. these macrophages release plasminogen activators, leading to increased plasmin levels. Plasmin cleaves fibrinogen, resulting in **Hypofibrinogenemia** (low fibrinogen levels, typically <150 mg/dL), not hyperfibrinogenemia. This is often associated with elevated D-dimers and features of Disseminated Intravascular Coagulation (DIC) [3]. **Analysis of Incorrect Options:** * **A. Fever:** This is a cardinal feature caused by the systemic release of pyrogenic cytokines like IL-1, IL-6, and TNF-alpha. * **B. Splenomegaly:** Infiltration of the spleen by activated lymphocytes and macrophages leads to organomegaly [1]. Splenomegaly is a major manifestation in disorders involving the mononuclear phagocyte system [2]. * **C. Hyperferritinemia:** This is a highly sensitive marker for HLH. Ferritin levels often exceed 500 ng/mL (and frequently >3,000 ng/mL). It reflects the extreme degree of macrophage activation. **High-Yield Clinical Pearls for NEET-PG:** * **HLH-2004 Diagnostic Criteria (Need 5/8):** Fever, Splenomegaly, Cytopenias (affecting ≥2 lineages), Hypertriglyceridemia and/or **Hypofibrinogenemia**, Hemophagocytosis (in bone marrow, spleen, or lymph nodes), Low/Absent NK cell activity, Hyperferritinemia, and High soluble CD25 (sIL-2 receptor). * **Pathognomonic Finding:** "Hemophagocytosis"—macrophages engulfing erythrocytes, leukocytes, or platelets (though its absence does not rule out HLH) [1]. * **Primary HLH:** Associated with *PRF1* (Perforin) mutations. * **Secondary HLH:** Often triggered by EBV infection or malignancies (e.g., NK/T-cell lymphoma). **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. 593-594. [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. 631-632. [3] 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 1238: Disseminated Intravascular Coagulation (DIC) is most commonly seen in which AML subtype?

A. M2
B. M3 (Correct Answer)
C. M4
D. M5

Explanation: **Explanation:** **Correct Answer: B. M3 (Acute Promyelocytic Leukemia - APL)** The association between AML-M3 and **Disseminated Intravascular Coagulation (DIC)** is a classic high-yield medical fact [1]. In APL, the malignant cells are arrested at the promyelocyte stage. These promyelocytes contain numerous **primary granules and Auer rods** which are rich in **Tissue Factor (TF)** and procoagulant enzymes [2]. When these cells die or are treated with chemotherapy, they release these substances into the circulation, triggering the extrinsic coagulation cascade and leading to life-threatening DIC [2]. **Analysis of Incorrect Options:** * **A. M2 (AML with maturation):** This is the most common subtype of AML overall. While it is associated with the t(8;21) translocation and chloromas (granulocytic sarcomas), it does not typically present with primary DIC [1]. * **C. M4 (Acute Myelomonocytic Leukemia):** This subtype involves both granulocytic and monocytic differentiation. It is frequently associated with **inv(16)** and is known for gingival hypertrophy, but not specifically for DIC [1]. * **D. M5 (Acute Monocytic Leukemia):** This subtype is strongly associated with **extramedullary involvement**, such as gingival hyperplasia, skin infiltration (leukemia cutis), and CNS involvement [2]. **Clinical Pearls for NEET-PG:** * **Cytogenetics:** M3 is characterized by **t(15;17)**, which involves the *PML-RARA* fusion gene [1]. * **Morphology:** Look for "Faggot cells" (cells containing bundles of Auer rods) in the peripheral smear [3]. * **Treatment:** The standard of care is **All-trans Retinoic Acid (ATRA)**, which induces the differentiation of promyelocytes into mature neutrophils, thereby reducing the risk of DIC. * **Emergency:** DIC in M3 is often exacerbated by the initiation of standard cytotoxic chemotherapy; hence, ATRA should be started immediately upon suspicion. **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. 620. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 608-610. [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. 621-622.

Question 1239: The typical bone marrow finding in Idiopathic Thrombocytopenic Purpura (ITP) is:

A. Absent megakaryocytes
B. Foam cells
C. Increased megakaryocytes (Correct Answer)
D. Fragmented megakaryocytes

Explanation: **Explanation:** **1. Why "Increased Megakaryocytes" is correct:** Idiopathic Thrombocytopenic Purpura (ITP) is an autoimmune disorder characterized by the production of IgG antibodies against platelet surface glycoproteins (most commonly GpIIb/IIIa). This leads to the premature destruction of platelets in the spleen [2]. In response to this peripheral destruction and the resulting thrombocytopenia, the bone marrow undergoes **compensatory hyperplasia**. Therefore, the marrow typically shows an **increased number of megakaryocytes** (megakaryocytosis) as it attempts to ramp up platelet production to meet the demand [1]. **2. Why other options are incorrect:** * **A. Absent megakaryocytes:** This is characteristic of Aplastic Anemia or Amegakaryocytic Thrombocytopenia, where the primary defect is in the marrow production rather than peripheral destruction. * **B. Foam cells:** These are lipid-laden macrophages typically seen in storage disorders like Niemann-Pick disease or Gaucher disease, not in ITP. * **D. Fragmented megakaryocytes:** While megakaryocytes in ITP may appear "immature" or show "non-lobulated" nuclei (sometimes called "smooth" megakaryocytes), "fragmented" is not a standard pathological description for ITP. **3. NEET-PG High-Yield Pearls:** * **Mechanism:** Type II Hypersensitivity reaction. * **Morphology:** Megakaryocytes in ITP often appear "immature" with single nuclei and scant cytoplasm (increased "young" forms). * **Clinical Rule:** ITP is a diagnosis of exclusion [2]. The spleen is typically **not enlarged**; if splenomegaly is present, consider other diagnoses [1]. * **Treatment:** First-line treatment is Corticosteroids. Splenectomy is considered for refractory cases because the spleen is both the site of antibody production and platelet destruction [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 620-621. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 666-667.

Question 1240: Splenomegaly may be a feature of which of the following conditions?

A. Megaloblastic anemia
B. Sickle cell anemia (Correct Answer)
C. Thalassemia
D. G6PD deficiency

Explanation: **Explanation:** The correct answer is **Sickle Cell Anemia (SCA)**. While this may seem counterintuitive due to the classic teaching of "autosplenectomy," it is a crucial distinction for NEET-PG. **1. Why Sickle Cell Anemia is Correct:** In the **early stages** of Sickle Cell Anemia (especially in children), the spleen is frequently enlarged [3]. This is due to **sequestration** of sickled red blood cells within the splenic cords and congestion of the red pulp [2]. It is only after repeated infarctions over several years that the spleen undergoes progressive fibrosis and shrinkage, eventually leading to **autosplenectomy** (shrunken, calcified spleen) by adulthood [1], [3]. Therefore, splenomegaly is a definitive feature of the disease's natural history. **2. Analysis of Other Options:** * **Megaloblastic Anemia:** Splenomegaly is generally **absent**. It is a maturation defect (ineffective erythropoiesis) rather than a primary hemolytic process that taxes the spleen. * **Thalassemia:** While Thalassemia major causes massive splenomegaly due to extramedullary hematopoiesis, the question asks for a condition where splenomegaly is a "feature." In the context of standard MCQ patterns, SCA is often highlighted for its unique biphasic splenic involvement (enlargement followed by atrophy). * **G6PD Deficiency:** This typically causes **episodic intravascular hemolysis** [4]. Since the destruction occurs primarily within the blood vessels (due to oxidative stress), the spleen does not usually enlarge [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Autosplenectomy:** Associated with **Howell-Jolly bodies** on peripheral smear (signifying splenic dysfunction) [3]. * **Splenic Sequestration Crisis:** A life-threatening complication in pediatric SCA patients where the spleen rapidly enlarges, leading to hypovolemic shock. * **Massive Splenomegaly:** Remember the mnemonic **"CML"** (Chronic Myeloid Leukemia, Malaria, Leishmaniasis/Kala-azar) and Myelofibrosis [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. 631-632. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 645-646. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 644-645. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 642-643.

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Anemias: Classification and Approach

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Hemolytic Anemias

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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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