Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1201: A 70-year-old male has a pathologic fracture of the femur. X-rays show a lytic lesion with a circumscribed, punched-out appearance. Curettage from the fracture site is most likely to show which of the following?

A. Diminished and thinned trabecular bone
B. Sheets of atypical plasma cells (Correct Answer)
C. Metastatic prostatic adenocarcinoma
D. Malignant cells forming osteoid bone

Explanation: ### Explanation The clinical presentation of an elderly male with a **pathologic fracture** [1] and characteristic **"punched-out" lytic lesions** on X-ray [2] is a classic description of **Multiple Myeloma (MM)**. **1. Why "Sheets of atypical plasma cells" is correct:** Multiple Myeloma is a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells in the bone marrow [2]. These cells secrete cytokines (like IL-6 and RANK-L) that activate osteoclasts, leading to bone resorption. Histologically, curettage of these lesions reveals dense sheets of atypical plasma cells (plasmacytes) with eccentric nuclei, "clock-face" chromatin, and a prominent perinuclear clear zone (Golgi zone) [3]. **2. Analysis of Incorrect Options:** * **Option A (Diminished and thinned trabecular bone):** This describes **Osteoporosis**. While it causes pathologic fractures in the elderly, it presents with generalized bone loss rather than focal, circumscribed "punched-out" lytic lesions. * **Option C (Metastatic prostatic adenocarcinoma):** Prostate cancer typically produces **osteoblastic (sclerotic)** lesions, which appear radio-dense (white) on X-ray, not lytic (dark). * **Option D (Malignant cells forming osteoid bone):** This is the hallmark of **Osteosarcoma**. While it causes bone destruction, it is characterized by the production of malignant osteoid and usually occurs in a younger age group (bimodal distribution) with a "sunburst" appearance or Codman’s triangle on X-ray. **3. High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** **C**alcium (Hypercalcemia), **R**enal insufficiency, **A**nemia, **B**one lesions [1]. * **Diagnosis:** Bone marrow biopsy showing >10% plasma cells [3]; M-spike on Serum Protein Electrophoresis (SPEP) [2]. * **Urine:** Bence-Jones proteins (detected by sulfosalicylic acid test, not standard dipstick) [2]. * **Blood:** Rouleaux formation on peripheral smear due to high globulin levels [3]. * **Radiology:** Skull X-rays often show "raindrop" lytic lesions [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. 608-609. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 617-618.

Question 1202: Mycosis cells are altered:

A. T Lymphocytes (Correct Answer)
B. Monocytes
C. B lymphocytes
D. Eosinophils

Explanation: Mycosis Fungoides (MF) is the most common type of Cutaneous T-cell Lymphoma (CTCL) [1]. The "Mycosis cells" mentioned in the question refer to the malignant cells characteristic of this condition. 1. Why T Lymphocytes are correct: The neoplastic cells in Mycosis Fungoides are specifically CD4+ T-helper lymphocytes [2]. These cells exhibit epidermotropism, meaning they have a unique affinity for the epidermis. Under the microscope, these altered T-cells often display a "cerebriform" nucleus (convoluted, brain-like appearance) [1]. When these malignant T-cells aggregate within the epidermis, they form pathognomonic structures known as Pautrier microabscesses [2]. 2. Why other options are incorrect: * Monocytes: While monocytes are part of the inflammatory infiltrate in many skin conditions, they are not the primary neoplastic cell in MF. * B Lymphocytes: B-cell lymphomas can involve the skin (e.g., Marginal zone lymphoma), but Mycosis Fungoides is strictly a T-cell malignancy [1]. * Eosinophils: Eosinophils may be present in the background of the skin biopsy due to cytokine release (IL-5) by the malignant T-cells, but they are reactive cells, not the "Mycosis cells" themselves. High-Yield Clinical Pearls for NEET-PG: * Sézary Syndrome: This is the leukemic phase of MF, characterized by a triad of erythroderma, lymphadenopathy, and circulating malignant T-cells (Sézary cells) with cerebriform nuclei [1]. * Staging: MF typically progresses through three stages: Patch $\rightarrow$ Plaque $\rightarrow$ Tumor [2,3]. * Immunophenotype: Usually CD3+, CD4+, and CD8-. A loss of normal T-cell markers (like CD7) is a common diagnostic clue. **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. 613-614. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 564-565. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, p. 1162.

Question 1203: Which of the following conditions is associated with an increased Erythrocyte Sedimentation Rate (ESR)?

A. Sickle cell anemia
B. Multiple myeloma (Correct Answer)
C. Polycythemia vera
D. Thalassemia

Explanation: **Explanation:** The **Erythrocyte Sedimentation Rate (ESR)** is a non-specific marker of inflammation that measures how quickly red blood cells (RBCs) sink to the bottom of a tube. This process is primarily governed by the formation of **Rouleaux** (stacks of RBCs). **1. Why Multiple Myeloma is Correct:** In Multiple Myeloma, there is a neoplastic proliferation of plasma cells leading to high levels of monoclonal immunoglobulins (paraproteins) [2]. These large, positively charged proteins neutralize the negative surface charge (**Zeta potential**) of RBCs, which normally keeps them apart. Once the charge is neutralized, RBCs clump together to form Rouleaux [1]. These aggregates have a lower surface-area-to-volume ratio than individual cells, causing them to sediment much faster, resulting in a **markedly elevated ESR** (often >100 mm/hr). **2. Why the other options are incorrect:** * **Sickle cell anemia:** The abnormally shaped (sickled) cells cannot stack into Rouleaux. This hinders sedimentation, leading to a **decreased ESR**. * **Polycythemia vera:** An increase in the concentration of RBCs increases the viscosity of the blood, which creates internal friction and slows down the settling process, leading to a **decreased ESR**. * **Thalassemia:** Similar to sickle cell, the presence of microcytic and abnormally shaped cells (poikilocytosis) interferes with proper Rouleaux formation, typically resulting in a **low ESR**. **High-Yield Clinical Pearls for NEET-PG:** * **Factors increasing ESR:** Pregnancy, Anemia (except those with abnormal shapes), Macrocytosis, Aging, and Acute phase reactants (Fibrinogen is the most potent). * **Factors decreasing ESR:** Afibrinogenemia, Spherocytosis (low surface area), and extreme Leukocytosis. * **Key Rule:** Any condition that alters the shape of the RBC (making it non-discoid) will generally decrease the ESR. **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 1204: Which laboratory tests are typically affected in Von Willebrand disease?

A. Bleeding Time (BT) and Partial Thromboplastin Time (PTT) (Correct Answer)
B. Prothrombin Time (PT) and Partial Thromboplastin Time (PTT)
C. Prothrombin Time (PT)
D. Clotting Time (CT)

Explanation: **Explanation:** Von Willebrand Disease (vWD) is the most common inherited bleeding disorder, characterized by a deficiency or dysfunction of **Von Willebrand Factor (vWF)**. To understand the lab findings, one must remember the dual role of vWF: 1. **Platelet Adhesion:** vWF acts as a bridge between platelet GpIb receptors and subendothelial collagen [1]. A deficiency impairs primary hemostasis, leading to a **prolonged Bleeding Time (BT)**. 2. **Carrier for Factor VIII:** vWF stabilizes Factor VIII in the circulation, protecting it from rapid degradation [1]. Low levels of vWF lead to a secondary decrease in Factor VIII. Since Factor VIII is part of the intrinsic pathway, its deficiency results in a **prolonged Partial Thromboplastin Time (PTT)**. **Analysis of Options:** * **Option A (Correct):** Reflects the defect in both primary hemostasis (BT) and the intrinsic coagulation pathway (PTT). * **Option B & C (Incorrect):** Prothrombin Time (PT) measures the extrinsic and common pathways (Factors VII, X, V, II, I). These are unaffected in vWD; thus, PT is characteristically **normal**. * **Option D (Incorrect):** Clotting Time is a non-specific, insensitive test for secondary hemostasis and is not the standard diagnostic parameter for vWD. **NEET-PG High-Yield Pearls:** * **Ristocetin Cofactor Assay:** This is the "Gold Standard" diagnostic test; it measures vWF-induced platelet agglutination. * **Platelet Count:** Usually **normal** in vWD (except in Type 2B, where mild thrombocytopenia may occur). * **Treatment:** Desmopressin (DDAVP) is used as it releases stored vWF from Weibel-Palade bodies in endothelial cells. * **Inheritance:** Most types are Autosomal Dominant. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 669-670.

Question 1205: Which metabolic abnormality is seen in multiple myeloma?

A. Hyponatremia
B. Hypokalemia
C. Hypercalcemia (Correct Answer)
D. Hyperphosphatemia

Explanation: **Explanation:** **Multiple Myeloma (MM)** is a neoplastic proliferation of plasma cells in the bone marrow [1]. The hallmark of the disease is the activation of osteoclasts, leading to extensive bone destruction [2]. **Why Hypercalcemia is Correct:** In MM, malignant plasma cells secrete cytokines known as **Osteoclast Activating Factors (OAFs)**, primarily **RANK-ligand (RANKL)**, IL-1 (Osteoclast Activating Factor), and TNF-beta. These factors stimulate osteoclasts to resorb bone, leading to "punched-out" lytic lesions [3]. As the bone matrix breaks down, calcium is released into the bloodstream, resulting in **hypercalcemia** [3]. This is a critical component of the **CRAB** criteria (Calcium elevation, Renal insufficiency, Anemia, and Bone lesions) used for diagnosis [1]. **Why Other Options are Incorrect:** * **Hyponatremia & Hypokalemia:** These are not characteristic features of MM. While electrolyte imbalances can occur secondary to renal failure, they are not direct metabolic hallmarks of the disease process itself. In fact, MM can sometimes cause a "pseudohyponatremia" due to high protein levels, but this is an analytical artifact, not a true metabolic state. * **Hyperphosphatemia:** While it can occur if there is significant renal failure, it is not the primary metabolic abnormality associated with the plasma cell pathology. **High-Yield Clinical Pearls for NEET-PG:** * **M-Spike:** Seen on Serum Protein Electrophoresis (SPEP), usually due to IgG (most common) or IgA [1]. * **Bence-Jones Proteins:** Free light chains (Kappa/Lambda) found in urine [1]; they precipitate at 40-60°C and redissolve at 100°C. * **Blood Film:** Characterized by **Rouleaux formation** due to decreased zeta potential between RBCs caused by high globulin levels [2]. * **Bone Scan:** Often **negative** because there is no osteoblastic activity (bone scans detect new bone formation, not destruction). Skeletal surveys or MRI are preferred [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 617-618. [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, p. 608.

Question 1206: Which of the following statements are true about blood transfusion reactions?

A. Complement mediated severe hemolysis
B. Renal blood flow is decreased (Correct Answer)
C. Transfusion should not be stopped
D. Death is not seen

Explanation: This question pertains to **Acute Hemolytic Transfusion Reactions (AHTR)**, typically caused by ABO incompatibility. ### **Explanation of the Correct Option** **B. Renal blood flow is decreased:** In an acute hemolytic reaction, the binding of antibodies to donor RBCs triggers the complement cascade and the release of inflammatory cytokines (like TNF-α and IL-1). This leads to systemic hypotension and shock. Simultaneously, free hemoglobin released from lysed RBCs has a potent **vasoconstrictive effect** (by scavenging Nitric Oxide) and can cause direct tubular toxicity [1]. The combination of systemic hypotension and renal vasoconstriction leads to a significant **decrease in renal blood flow**, often resulting in Acute Tubular Necrosis (ATN) and oliguric renal failure [2]. ### **Analysis of Incorrect Options** * **A. Complement mediated severe hemolysis:** While this statement is technically true for AHTR, in the context of multiple-choice questions where only one "best" physiological consequence is sought among distractors, the focus is often on the systemic complications like renal failure or DIC. [1] (Note: If this were a "Multiple True/False" type, A would be correct; however, in standard NEET-PG patterns, B represents the critical pathological outcome). * **C. Transfusion should not be stopped:** This is clinically dangerous. The **first and most crucial step** in managing any suspected transfusion reaction is to **stop the transfusion immediately** to prevent further antigen-antibody interaction. * **D. Death is not seen:** AHTR is a life-threatening emergency. Death can occur due to profound shock, Disseminated Intravascular Coagulation (DIC), or acute renal failure. ### **High-Yield Clinical Pearls for NEET-PG** * **Most common cause of AHTR:** Clerical/Administrative error (wrong unit to wrong patient). * **Pathophysiology:** Type II Hypersensitivity reaction. * **Classic Triad:** Fever, chills, and flank pain (due to renal ischemia). * **Key Lab Finding:** Hemoglobinuria (pink/red urine) and a positive Direct Antiglobulin Test (DAT/Coombs) [1]. * **Management:** Stop transfusion, aggressive IV hydration to maintain urine output, and cardiorespiratory support. **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] 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. 150-151.

Question 1207: All of the following conditions may be associated with pancytopenia and splenomegaly, except?

A. Aplastic Anemia (Correct Answer)
B. Hairy Cell Leukemia
C. Myelofibrosis
D. Hypersplenism

Explanation: **Explanation:** The hallmark of **Aplastic Anemia** is pancytopenia resulting from bone marrow failure (hypocellular marrow). Because the pathology is a primary failure of production rather than peripheral destruction or infiltration, there is **no splenomegaly** [1]. In fact, the presence of a palpable spleen in a patient with pancytopenia should lead a clinician to look for diagnoses other than aplastic anemia. **Analysis of Options:** * **Hairy Cell Leukemia (B):** This is a classic cause of "massive splenomegaly" and pancytopenia. The pancytopenia occurs due to bone marrow infiltration and splenic sequestration. * **Myelofibrosis (C):** In the fibrotic stage, the marrow fails (pancytopenia), leading to compensatory **Extramedullary Hematopoiesis (EMH)**. This results in significant hepatosplenomegaly. * **Hypersplenism (D):** This is a functional state where an enlarged spleen (due to portal hypertension, storage disorders, etc.) excessively sequesters and destroys circulating blood cells, leading to pancytopenia [2]. **NEET-PG High-Yield Pearls:** 1. **Rule of Thumb:** If pancytopenia is present **without** splenomegaly, think Aplastic Anemia, PNH, or Vitamin B12 deficiency. 2. **Rule of Thumb:** If pancytopenia is present **with** splenomegaly, think Hairy Cell Leukemia, Myelofibrosis, Kala-azar, or Gaucher’s disease. 3. **Bone Marrow Finding:** In Aplastic Anemia, the marrow is replaced by fat cells ("Dry tap" is not common here; rather, a "fatty marrow" is seen on biopsy) [1]. 4. **Hairy Cell Leukemia** is uniquely associated with "Dry tap" on aspiration and TRAP (Tartrate-Resistant Acid Phosphatase) positivity. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 662-663. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 604-605.

Question 1208: Which of the following are true about aplastic anemia?

A. Splenomegaly
B. Nucleated RBCs in peripheral blood (Correct Answer)
C. Reticulocytopenia
D. Thrombocytopenia and Neutropenia

Explanation: **Explanation:** Aplastic anemia is a bone marrow failure syndrome characterized by **pancytopenia** and a **hypocellular bone marrow**, where hematopoietic stem cells are replaced by fat [1]. **Why Option B is the Correct Answer (in the context of "False" statements):** In classic aplastic anemia, the peripheral blood smear shows a "clean" background. Because the bone marrow is "empty" (hypocellular), there is no compensatory erythropoiesis. Therefore, **nucleated RBCs (NRBCs) and immature white cells are characteristically absent.** If NRBCs or a leucoerythroblastic picture are present, one must suspect bone marrow infiltration (Myelophthisic anemia) or MDS rather than aplastic anemia [3]. *(Note: In many standard MCQ formats, this question asks "Which of the following is NOT true," as B is a negative finding, while C and D are classic features.)* **Analysis of Other Options:** * **C. Reticulocytopenia:** Correct feature. Since the marrow cannot produce new cells, the corrected reticulocyte count is significantly low (<1%) [1]. * **D. Thrombocytopenia and Neutropenia:** Correct features. Aplastic anemia presents as pancytopenia [1]. Neutropenia leads to recurrent infections, and thrombocytopenia leads to mucosal bleeding/petechiae. * **A. Splenomegaly:** Characteristically **absent** in aplastic anemia [1]. Its presence should prompt a search for alternative diagnoses like leukemia or hypersplenism. **NEET-PG High-Yield Pearls:** 1. **Gold Standard Diagnosis:** Bone marrow biopsy showing >70% fat content ("Dry tap" is common on aspiration). 2. **Most Common Cause:** Idiopathic (T-cell mediated destruction of stem cells) [2]. 3. **Drugs:** Chloramphenicol, Sulfonamides, and Gold salts are notorious triggers [2]. 4. **Fanconi Anemia:** The most common inherited cause; look for thumb anomalies and DNA cross-link sensitivity (Diepoxybutane test) [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. 662-663. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 595-596. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 589-590.

Question 1209: Howell-Jolly bodies are seen in which of the following conditions?

A. Iron deficiency anemia
B. Hemolytic anemia (Correct Answer)
C. Polycythemia vera
D. Multiple myeloma

Explanation: **Explanation:** **Howell-Jolly bodies** are small, round, basophilic (purple-blue) nuclear remnants (DNA) found within erythrocytes [1]. Normally, as red blood cells mature in the bone marrow, they expel their nuclei. Any remaining nuclear fragments are typically "pitted" or removed by the **splenic macrophages** as the cells pass through the splenic sinusoids. **Why Hemolytic Anemia is correct:** In certain types of hemolytic anemia, particularly **Sickle Cell Anemia**, the spleen undergoes repeated infarction leading to **autosplenectomy** (functional asplenia) [1]. Without a functional spleen to filter these cells, Howell-Jolly bodies persist in the peripheral blood. They are also seen in other hemolytic states where erythropoiesis is accelerated or when a splenectomy has been performed (e.g., in Hereditary Spherocytosis). **Analysis of Incorrect Options:** * **A. Iron deficiency anemia:** Characterized by microcytic hypochromic RBCs and pencil cells, but not nuclear remnants. * **C. Polycythemia vera:** A myeloproliferative neoplasm characterized by an absolute increase in RBC mass; it does not typically involve nuclear maturation defects or splenic dysfunction. * **D. Multiple myeloma:** A plasma cell dyscrasia characterized by "Rouleaux formation" due to high paraproteins, not Howell-Jolly bodies. **NEET-PG High-Yield Pearls:** * **Stain:** Howell-Jolly bodies are visible on routine **Wright-Giemsa** or Leishman stains. * **Differential Diagnosis:** Must be distinguished from **Heinz bodies** (denatured hemoglobin), which require **supravital stains** (like Brilliant Cresyl Blue) to be seen. * **Classic Association:** Post-splenectomy status is the most common cause [1]. If seen in a child with anemia, think **Sickle Cell Anemia** (autosplenectomy) [1]. * **Other conditions:** Also seen in Megaloblastic anemia due to dyserythropoiesis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 644-645.

Question 1210: What test helps differentiate between leukemia and leukemoid reaction?

A. Leukocyte alkaline phosphatase (Correct Answer)
B. Presence of immature cells
C. Total leukocyte count
D. Erythrocyte sedimentation rate

Explanation: **Explanation:** The differentiation between a **Leukemoid Reaction** (an exaggerated white blood cell response to infection or stress) and **Chronic Myeloid Leukemia (CML)** is a classic high-yield topic in hematopathology. **1. Why Leukocyte Alkaline Phosphatase (LAP) is the correct answer:** The LAP score (also known as the Neutrophil Alkaline Phosphatase or NAP score) measures the enzyme activity within the secondary granules of mature neutrophils. * In a **Leukemoid Reaction**, the neutrophils are functionally normal and "stressed," leading to an **increased LAP score**. * In **CML**, the malignant cells are biochemically defective despite appearing mature; thus, the **LAP score is characteristically low or zero**. **2. Why other options are incorrect:** * **Presence of immature cells:** Both conditions show a "left shift" (myelocytes, metamyelocytes, and band forms) [2]. While CML typically shows a more significant "myelocytic bulge," immature cells alone are not pathognomonic. * **Total Leukocyte Count (TLC):** Both can present with massive leukocytosis (>50,000 cells/mm³). While CML counts often exceed 100,000, there is significant overlap, making it unreliable for differentiation. * **Erythrocyte Sedimentation Rate (ESR):** ESR is a non-specific marker of inflammation and can be elevated in both malignancy and infection. **High-Yield Clinical Pearls for NEET-PG:** * **LAP Score Trends:** * **Decreased:** CML, Paroxysmal Nocturnal Hemoglobinuria (PNH), Hypophosphatasia. * **Increased:** Leukemoid reaction, Polycythemia Vera, Pregnancy, and Down Syndrome. * **Confirmatory Test:** If LAP is low, the definitive gold standard to diagnose CML is identifying the **Philadelphia chromosome t(9;22)** or the **BCR-ABL1** fusion gene via FISH or PCR [3]. * **Morphology:** Look for **Döhle bodies** and toxic granulations in neutrophils to favor a Leukemoid reaction [1]. Basophilia, however, strongly favors CML [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, p. 592. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612. [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.

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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