Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 751: In beta thalassemia, what change occurs to the beta and alpha globin chains?

A. Increase in beta chain, decrease in alpha chain
B. Decrease in beta chain, increase in alpha chain (Correct Answer)
C. Decrease in beta chain, decrease in alpha chain
D. Increase in beta chain, increase in alpha chain

Explanation: ### Explanation **Underlying Medical Concept:** Beta-thalassemia is a quantitative hemoglobinopathy caused by mutations (usually point mutations) in the $\beta$-globin gene on chromosome 11 [3]. This leads to **reduced ($\beta^+$) or absent ($\beta^0$) synthesis of $\beta$-globin chains** [3], [5]. The hallmark of the disease is the **relative excess of $\alpha$-globin chains** [1], [2]. Since $\alpha$-chains have no $\beta$-chains to pair with to form Hemoglobin A ($\alpha_2\beta_2$), they precipitate within red cell precursors as insoluble inclusions [1]. These inclusions cause membrane damage, leading to ineffective erythropoiesis in the bone marrow and extravascular hemolysis in the spleen. **Analysis of Options:** * **Option B (Correct):** Accurately reflects the primary defect (decreased $\beta$-chain) and the resulting secondary imbalance (relative increase/excess of $\alpha$-chains). * **Option A:** Incorrect; $\beta$-chains are never increased in thalassemia. * **Option C:** Incorrect; while $\beta$-chains decrease, $\alpha$-chains are produced at normal rates, leading to a relative excess, not a decrease. * **Option D:** Incorrect; this does not describe any form of thalassemia. **High-Yield NEET-PG Pearls:** * **Peripheral Smear:** Microcytic hypochromic anemia with **target cells** and basophilic stippling. * **Diagnosis:** Gold standard is **Hb Electrophoresis/HPLC**. In $\beta$-thalassemia minor, look for **increased HbA2 (>3.5%)**. * **Mentzer Index:** (MCV/RBC count) **<13** suggests Thalassemia; **>13** suggests Iron Deficiency Anemia. * **Skeletal Changes:** "Crew-cut" appearance on skull X-ray and "chipmunk facies" due to compensatory extramedullary hematopoiesis [4]. * **Complication:** Secondary hemochromatosis (iron overload) due to repeated transfusions and increased intestinal absorption [2], [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 647-648. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 648. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 646-647. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 648-649. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 650.

Question 752: Which tumor is associated with polycythemia vera?

A. Sarcoma
B. Pituitary adenoma
C. Cerebellar haemangioblastoma (Correct Answer)
D. None of the above

Explanation: ### Explanation The correct answer is **C. Cerebellar haemangioblastoma.** **Underlying Medical Concept:** The association between certain tumors and polycythemia is due to the **ectopic production of Erythropoietin (EPO)**. This leads to **Secondary Polycythemia**, characterized by an increased red cell mass driven by high EPO levels (unlike Polycythemia Vera, which is a primary myeloproliferative neoplasm with low EPO levels) [2]. Cerebellar haemangioblastoma is a classic example of a tumor that secretes EPO. **Analysis of Options:** * **Cerebellar Haemangioblastoma (Correct):** This is a benign, highly vascular tumor often associated with **Von Hippel-Lindau (VHL) syndrome** [1]. The tumor cells produce erythropoietin, leading to erythrocytosis in approximately 10-20% of cases. * **Sarcoma (Incorrect):** While some rare soft tissue tumors might theoretically interfere with systemic processes, sarcomas are not classically associated with ectopic EPO production or polycythemia. * **Pituitary Adenoma (Incorrect):** Pituitary tumors typically secrete hormones like GH, ACTH, or Prolactin. While ACTH-secreting tumors (Cushing’s Disease) can cause mild polycythemia due to cortisol's effect on the bone marrow, it is not a primary or classic association compared to haemangioblastoma. **High-Yield Clinical Pearls for NEET-PG:** * **"Potentially Erythropoietin-Producing Tumors" (The "H-R-H-L-U" Mnemonic):** 1. **H**emangioblastoma (Cerebellum) 2. **R**enal Cell Carcinoma (Most common association) 3. **H**epatocellular Carcinoma (Hepatoma) 4. **L**eiomyoma (Uterine fibroids) 5. **U**rothelial/Ovarian tumors (Rarely) * **Distinction:** In **Primary Polycythemia (Polycythemia Vera)**, EPO levels are **low** (due to feedback inhibition). In **Secondary Polycythemia** (caused by these tumors), EPO levels are **high** [2]. * **VHL Syndrome Triad:** Retinal hemangiomas, Cerebellar hemangioblastomas, and Renal Cell Carcinoma [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 726-727. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 663-664.

Question 753: Which of the following types of anemia is associated with a raised MCV and normal MCHC?

A. Sideroblastic anemia
B. Vitamin B12 and Folic acid deficiency (Correct Answer)
C. Beta thalassemia
D. Iron deficiency anemia

Explanation: ### Explanation **Correct Answer: B. Vitamin B12 and Folic acid deficiency** **1. Why it is correct:** Vitamin B12 and Folic acid are essential cofactors for DNA synthesis (specifically thymidine synthesis) [1]. Deficiency leads to **nuclear-cytoplasmic asynchrony**, where the nucleus matures slowly while the cytoplasm grows at a normal rate [1]. This results in the formation of abnormally large red blood cell precursors called megaloblasts [1]. Consequently, the mature RBCs released into the circulation are larger than normal, leading to a **raised Mean Corpuscular Volume (MCV > 100 fL)**. Since hemoglobin synthesis (cytoplasmic maturation) remains unaffected, the concentration of hemoglobin within these large cells remains within the normal range, resulting in a **normal Mean Corpuscular Hemoglobin Concentration (MCHC)** [1]. This is the classic presentation of **Megaloblastic Macrocytic Anemia**. **2. Why the other options are incorrect:** * **Iron Deficiency Anemia (D):** This is the prototype of **Microcytic Hypochromic anemia**. Lack of iron impairs hemoglobin synthesis, leading to small cells (Low MCV) with low hemoglobin concentration (Low MCHC). * **Beta Thalassemia (C):** This is a quantitative defect in globin chain synthesis. It also presents as **Microcytic Hypochromic anemia** (Low MCV, Low MCHC). * **Sideroblastic Anemia (A):** This involves a defect in heme synthesis (protoporphyrin production). It typically presents as a **Microcytic Hypochromic anemia**, often characterized by a dimorphic blood picture and ring sideroblasts in the bone marrow. **3. High-Yield Clinical Pearls for NEET-PG:** * **Hypersegmented Neutrophils:** The earliest peripheral blood sign of megaloblastic anemia (defined as >5% neutrophils with 5 lobes or a single neutrophil with ≥6 lobes) [1]. * **Pancytopenia:** Severe B12/Folate deficiency can cause ineffective hematopoiesis affecting all three cell lines. * **Neurological Symptoms:** Subacute Combined Degeneration (SCD) of the spinal cord is seen in **Vitamin B12 deficiency** (due to methylmalonic acid accumulation) but **NOT** in Folate deficiency. * **Schilling Test:** Historically used to differentiate the cause of B12 deficiency (e.g., Pernicious anemia vs. malabsorption). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 592-595.

Question 754: Which of the following statements is true regarding the cytochemistry of ALL?

A. PAS positive (Block positivity) (Correct Answer)
B. Myeloperoxidase positive
C. Sudan Black B positive
D. Non-specific esterase positive

Explanation: In Hematopathology, cytochemistry is a vital tool for differentiating Acute Lymphoblastic Leukemia (ALL) from Acute Myeloid Leukemia (AML). **1. Why Option A is Correct:** **Periodic Acid-Schiff (PAS)** stains glycogen. In ALL, the lymphoblasts often show a characteristic **"block positivity"** or "coarse granular" pattern. This occurs because the glycogen is clustered in large chunks within the cytoplasm against a clear background. This is a classic diagnostic hallmark for the L1 and L2 subtypes of ALL (FAB classification). **2. Why the Other Options are Incorrect:** * **Myeloperoxidase (MPO):** This is the most sensitive and specific marker for the **myeloid lineage**. It is found in the primary granules of myeloid cells. ALL is characteristically **MPO negative**. * **Sudan Black B (SBB):** This stain detects phospholipids and sterols in the membranes of primary and secondary granules. Like MPO, it is positive in AML and **negative in ALL**. * **Non-specific Esterase (NSE):** This stain (e.g., alpha-naphthyl acetate esterase) is used to identify cells of the **monocytic lineage**. It is strongly positive in Acute Monocytic Leukemia (AML-M4 and M5) but negative in ALL. **3. High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard:** While cytochemistry is high-yield for exams, **Immunophenotyping (Flow Cytometry)** is the current gold standard for diagnosing ALL (look for TdT, CD10, CD19, and CD3) [1]. * **TdT (Terminal Deoxynucleotidyl Transferase):** A specialized DNA polymerase that is positive in >95% of ALL cases but negative in AML. * **Acid Phosphatase:** Shows **focal polar (paranuclear) positivity** specifically 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. 596-600.

Question 755: Proliferation and survival of myeloma cells are dependent on which of the following cytokines?

A. IL-1
B. IL-6 (Correct Answer)
C. IL-2
D. IL-5

Explanation: **Explanation:** **Multiple Myeloma (MM)** is a plasma cell neoplasm characterized by the clonal proliferation of malignant plasma cells in the bone marrow. The survival, growth, and proliferation of these myeloma cells are critically dependent on the bone marrow microenvironment. **Why IL-6 is the Correct Answer:** **Interleukin-6 (IL-6)** is the most important growth factor for myeloma cells. It is produced by both the bone marrow stromal cells and the myeloma cells themselves (autocrine and paracrine loops). IL-6 acts by activating the JAK/STAT3 and PI3K/Akt pathways, which prevent apoptosis and promote the cell cycle. Clinically, high serum levels of IL-6 correlate with a poor prognosis and increased disease activity. **Analysis of Incorrect Options:** * **IL-1 (Osteoclast Activating Factor):** While IL-1 (specifically IL-1β) is produced by myeloma cells, its primary role is to stimulate osteoclasts, leading to the characteristic "punched-out" lytic bone lesions. It is not the primary survival/proliferation factor. * **IL-2:** This is a T-cell growth factor produced by Th1 cells. It is primarily involved in the proliferation of T-lymphocytes and NK cells, not plasma cells. * **IL-5:** This cytokine is mainly involved in the proliferation and activation of **eosinophils**. It plays a role in allergic responses and parasitic infections. **High-Yield Clinical Pearls for NEET-PG:** * **M-Spike:** Found on Serum Protein Electrophoresis (SPEP), usually due to IgG (most common) or IgA [1]. * **CRAB Criteria:** **C**alcium elevation, **R**enal insufficiency, **A**nemia, and **B**one lesions [1]. * **Diagnosis:** Bone marrow biopsy showing >10% clonal plasma cells [2]. * **Prognostic Marker:** **Beta-2 microglobulin** is the most useful prognostic marker in MM (reflects tumor burden). **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] 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.

Question 756: Diagnosis of Hodgkin's disease is based on all of the following, except:

A. Reed-Sternberg cells
B. Reactive cellular background
C. Atypical cells in background (Correct Answer)
D. CD30 positivity

Explanation: **Explanation:** The diagnosis of **Hodgkin Lymphoma (HL)** is unique in hematopathology because the neoplastic cells (Reed-Sternberg cells) constitute only a tiny fraction (1–5%) of the total tumor mass [1]. The bulk of the lesion is composed of a **non-neoplastic, reactive inflammatory background** [1]. 1. **Why "Atypical cells in background" is the correct answer:** In Hodgkin Lymphoma, the background consists of **benign, mature reactive cells** (lymphocytes, plasma cells, eosinophils, and histiocytes) [2]. If the background cells themselves were "atypical" or neoplastic, the diagnosis would shift toward **Non-Hodgkin Lymphoma (NHL)**, where the majority of the cellular population is malignant. 2. **Analysis of Incorrect Options:** * **Reed-Sternberg (RS) cells:** These are the hallmark neoplastic giant cells (often with "owl-eye" nuclei) required for the diagnosis of classical HL [1], [3]. * **Reactive cellular background:** This is a diagnostic requirement. The RS cells secrete cytokines (like IL-5) that recruit the characteristic inflammatory milieu [1]. * **CD30 positivity:** This is a key immunophenotypic marker for Classical Hodgkin Lymphoma (along with CD15). **High-Yield Clinical Pearls for NEET-PG:** * **RS Cell Variants:** *L&H cells (Popcorn cells)* are seen in Nodular Lymphocyte Predominant HL (CD20+, CD45+, but CD15-/CD30-). *Lacunar cells* are characteristic of the Nodular Sclerosis subtype [3]. * **Immunophenotype:** Classical HL is typically **CD15+, CD30+, and CD45-**. * **Prognosis:** Lymphocyte Predominant has the best prognosis; Lymphocyte Depleted has the worst [4]. * **Bimodal Age Distribution:** HL typically shows peaks in the 20s and after age 50 [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. 614-616. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 616-618. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 616. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 559-560.

Question 757: What is the preservative used in coagulation studies?

A. Calcium citrate
B. EDTA (Correct Answer)
C. Sodium bromide
D. Thrombin

Explanation: **Explanation:** The correct answer is **EDTA (Ethylenediaminetetraacetic acid)**. **Why EDTA is the correct answer:** In the context of general hematology and specific platelet-related coagulation studies, EDTA is the standard anticoagulant. It works by **chelating ionized calcium** ($Ca^{2+}$), which is Factor IV in the coagulation cascade [1]. By removing available calcium, it prevents the activation of the clotting mechanism [1]. EDTA is preferred for routine blood counts because it preserves the morphology of blood cells and prevents platelet aggregation. **Analysis of Incorrect Options:** * **A. Calcium citrate:** This is a distractor. While **Sodium Citrate** (3.2%) is the gold standard for PT/APTT tests because its effects are reversible by adding calcium, *Calcium* citrate would actually promote clotting rather than preserve the sample. * **C. Sodium bromide:** This is not used as an anticoagulant in clinical pathology. Bromide salts were historically used as sedatives but have no role in coagulation studies. * **D. Thrombin:** Thrombin is a potent **pro-coagulant** (Factor IIa). It converts fibrinogen to fibrin [1]. Adding thrombin would cause the blood to clot immediately, making it the opposite of a preservative. **High-Yield Clinical Pearls for NEET-PG:** * **Sodium Citrate (Blue top):** Used for PT, APTT, and D-dimer. The ratio is strictly **1:9** (1 part citrate to 9 parts blood). * **EDTA (Purple top):** Best for CBC and HbA1c. It can cause "Platelet Satellitism" (an in-vitro artifact), leading to a falsely low platelet count (Pseudothrombocytopenia). * **Heparin (Green top):** Acts by activating Antithrombin III. It is the best anticoagulant for **Osmotic Fragility Tests** and arterial blood gas (ABG) analysis. * **Sodium Fluoride (Grey top):** Used for blood glucose; it is an antiglycolytic agent (inhibits enolase), not primarily a coagulation preservative. **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 758: A patient with previously normal hemoglobin suffered sudden massive acute hemorrhage. Which of the following changes is LEAST likely to occur?

A. High reticulocyte count
B. High neutrophil count
C. High packed cell volume
D. Low mean corpuscular volume (Correct Answer)

Explanation: ### Explanation The correct answer is **D. Low mean corpuscular volume (MCV)**. In the setting of **sudden massive acute hemorrhage**, the body loses whole blood (both cells and plasma) simultaneously [1]. Therefore, the remaining red blood cells (RBCs) are initially normocytic and normochromic. **1. Why "Low MCV" is the least likely:** A low MCV (microcytosis) is a hallmark of **chronic blood loss**, which leads to iron deficiency over time [2]. In an acute setting, there has not been enough time for iron stores to deplete or for the bone marrow to produce smaller, hemoglobin-deficient cells [2]. Thus, the MCV remains within the normal range (80–100 fL). **2. Analysis of other options:** * **High reticulocyte count (A):** Within 3–5 days of acute blood loss, the bone marrow responds to increased erythropoietin levels by releasing immature RBCs (reticulocytes) into the peripheral blood to compensate for the loss. * **High neutrophil count (B):** Acute hemorrhage triggers a "stress response." Adrenaline and cortisol cause demargination of neutrophils from the vessel walls into the circulation, leading to a transient **leukocytosis**. * **High packed cell volume (C):** While PCV eventually drops due to hemodilution (fluid shifting from interstitium to vessels), an **initial** transient rise in PCV can occur due to splenic contraction (releasing stored RBCs) and sympathetic-mediated vasoconstriction. However, compared to microcytosis, this is a more plausible acute physiological response. ### NEET-PG Clinical Pearls * **Immediate Phase:** In the first few hours of acute hemorrhage, Hb and Hematocrit may appear **normal** because both cells and plasma are lost in equal proportions. * **Hemodilution:** It takes 24–72 hours for the full drop in Hb/PCV to manifest as interstitial fluid moves into the intravascular space. * **Morphology:** Acute blood loss results in **Normocytic Normochromic Anemia**, whereas chronic blood loss results in **Microcytic Hypochromic Anemia** [1, 2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 590-591.

Question 759: Which X-linked recessive disease in males presents with a clotting defect?

A. Hemophilia A (Correct Answer)
B. Idiopathic Thrombocytopenic Purpura (ITP)
C. Von-Willebrand disease
D. None of the above

Explanation: ### Explanation **Correct Answer: A. Hemophilia A** **Medical Concept:** Hemophilia A is a classic **X-linked recessive** bleeding disorder caused by a deficiency or dysfunction of **Coagulation Factor VIII** [1]. Because the gene is located on the X chromosome, the disease primarily affects males, while females are typically asymptomatic carriers [2]. Factor VIII is a critical cofactor in the intrinsic pathway of the coagulation cascade; its deficiency leads to a failure in fibrin clot formation, resulting in a **clotting defect** characterized by deep-seated bleeds (e.g., hemarthrosis) [1]. **Analysis of Incorrect Options:** * **B. Idiopathic Thrombocytopenic Purpura (ITP):** This is an **acquired autoimmune** disorder where antibodies are directed against platelets. It is not hereditary or X-linked. It presents as a **platelet defect** (mucocutaneous bleeding) rather than a clotting factor defect. * **C. Von-Willebrand Disease (vWD):** This is the most common inherited bleeding disorder, but it follows an **Autosomal Dominant** inheritance pattern (most types). While it involves a deficiency of vWF (which stabilizes Factor VIII), it is not X-linked. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Hemophilia A and B (Christmas Disease) are both **X-linked recessive** [2]. * **Laboratory Findings:** Characterized by a **prolonged Activated Partial Thromboplastin Time (aPTT)** with a **normal Prothrombin Time (PT)** and normal bleeding time. * **Mixing Study:** The prolonged aPTT will **correct** when the patient's plasma is mixed with normal plasma (distinguishing it from Factor VIII inhibitors). * **Clinical Presentation:** Hallmark is **Hemarthrosis** (bleeding into joints, commonly the knee) and intramuscular hematomas [1]. * **Treatment:** Recombinant Factor VIII concentrate; Desmopressin (dDAVP) can be used in mild cases to release stored vWF and Factor VIII. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 670-671. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 151.

Question 760: Which of the following is NOT a B cell marker?

A. CD-15 (Correct Answer)
B. CD-19
C. CD-21
D. CD-24

Explanation: **Explanation:** The correct answer is **CD-15** because it is a marker primarily associated with **granulocytes** (neutrophils) and **Reed-Sternberg (RS) cells** in Classical Hodgkin Lymphoma [3]. It is not expressed on B-lymphocytes. **Analysis of Options:** * **CD-15 (Correct Answer):** Also known as Lewis X, it is a carbohydrate adhesion molecule. In hematopathology, it is a high-yield marker for **Classical Hodgkin Lymphoma** (alongside CD-30) [3]. It is also found on mature myeloid cells but is absent in B-cell lineages. * **CD-19 (Incorrect):** This is the most reliable and "pan-B cell" marker. It is expressed from the earliest stages of B-cell commitment (pro-B cell) until the plasma cell stage (where it is often lost) [1]. * **CD-21 (Incorrect):** Also known as Complement Receptor 2 (CR2), it is expressed on mature B cells and follicular dendritic cells [1]. It serves as the receptor for the **Epstein-Barr Virus (EBV)** [1], [2]. * **CD-24 (Incorrect):** This is a glycosylphosphatidylinositol (GPI)-anchored glycoprotein expressed on the surface of B-lineage cells from the pre-B to the mature B-cell stage. **NEET-PG High-Yield Pearls:** 1. **Pan-B cell markers:** CD-19, CD-20, CD-22, and CD-79a [1], [2]. 2. **Classical Hodgkin Lymphoma Profile:** RS cells are typically **CD-15+, CD-30+, and CD-45 negative.** 3. **CD-21 Fact:** It is the specific cell surface receptor that allows EBV to infect B-cells, leading to conditions like Infectious Mononucleosis and Burkitt Lymphoma [2]. 4. **Plasma Cell Markers:** CD-138 (Syndecan-1) and CD-38 are the primary markers used to identify plasma cells, as they often lose traditional B-cell markers like CD-19 and CD-20 [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. 598. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 199-200. [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. 616.

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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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