Hematopathology — MCQs
On this page
CD19 positive, CD22 positive, CD103 positive monoclonal B-cells with bright kappa positivity were found to comprise 60% of the peripheral blood lymphoid cells on flow cytometric analysis in a 55-year-old man with massive splenomegaly and a total leucocyte count of 3.3 x 10^9/L. Which one of the following is the most likely diagnosis?
Which of the following statements about stored blood is false?
ADAMTS13 is associated with which of the following disorders?
An infant presents with bony pain and dermatitis on the scalp. Skull X-ray and electron microscopy of a biopsy from a lesion are provided. What is the most probable diagnosis?
Which of the following is NOT a cause of Disseminated Intravascular Coagulation (DIC)?
All are seen in Thalassemia major EXCEPT?
"Autosplenectomy" is a feature seen in:
What is the characteristic finding in chronic myeloid leukemia?
Auer rods are specific for which of the following conditions?
Plasmacytoid lymphomas may be associated with which immunoglobulin?
Hematopathology Indian Medical PG Practice Questions and MCQs
Question 481: CD19 positive, CD22 positive, CD103 positive monoclonal B-cells with bright kappa positivity were found to comprise 60% of the peripheral blood lymphoid cells on flow cytometric analysis in a 55-year-old man with massive splenomegaly and a total leucocyte count of 3.3 x 10^9/L. Which one of the following is the most likely diagnosis?
- A. Splenic lymphoma with villous lymphocytes
- B. Mantle cell lymphoma
- C. B-cell prolymphocytic leukemia
- D. Hairy cell leukemia (Correct Answer)
Explanation: ### Explanation **Hairy Cell Leukemia (HCL)** is the most likely diagnosis based on the classic triad of clinical and immunophenotypic findings presented: 1. **Clinical Presentation:** The patient is a middle-aged male (55 years) with **massive splenomegaly** and **pancytopenia** (suggested by the low TLC of 3.3 x 10⁹/L). Unlike most leukemias, HCL typically presents with a low white cell count due to splenic sequestration and bone marrow fibrosis [1]. 2. **Immunophenotype (The "Gold Standard"):** The presence of **CD103** is highly specific for HCL. While CD19 and CD22 confirm a B-cell lineage, the bright expression of surface light chains (kappa) and the positivity of CD103 are diagnostic hallmarks. --- ### Why the other options are incorrect: * **A. Splenic Lymphoma with Villous Lymphocytes (SLVL):** While it presents with splenomegaly, it is typically **CD103 negative**. It often expresses CD11c but lacks the specific HCL marker profile. * **B. Mantle Cell Lymphoma (MCL):** MCL is characterized by **CD5 positivity** and **CD23 negativity**. It would not express CD103 and is associated with t(11;14) and Cyclin D1 overexpression. * **C. B-cell Prolymphocytic Leukemia (B-PLL):** This presents with a **very high TLC** (usually >100 x 10⁹/L) and prominent nucleoli in cells. It does not express CD103. --- ### High-Yield Clinical Pearls for NEET-PG: * **Classic Markers:** CD11c, CD25, **CD103**, and **CD123** (The "HCL Four"). * **Annexin A1:** The most specific immunohistochemical marker for HCL. * **BRAF V600E Mutation:** Present in nearly 100% of classic HCL cases. * **Bone Marrow:** Often results in a **"Dry Tap"** due to increased reticulin fibrosis; biopsy shows a **"Fried Egg" appearance** [1]. * **TRAP Stain:** Historically used (Tartrate-Resistant Acid Phosphatase), but now largely replaced by flow cytometry. * **Treatment:** Highly sensitive to Cladribine (2-CdA). **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. 612.
Question 482: Which of the following statements about stored blood is false?
- A. It can be stored for up to 40 days.
- B. It is a good source of platelets. (Correct Answer)
- C. Potassium levels increase during storage.
- D. Factors V and VIII are deficient in stored blood.
Explanation: **Explanation** The correct answer is **B**, as stored blood is **not** a good source of platelets. Platelets are highly sensitive to temperature; they lose their viability and functional integrity within 24–48 hours when stored at the standard blood bank refrigeration temperature (2°C to 6°C) [1]. For effective transfusion, platelets must be stored at room temperature (20°C to 24°C) with continuous agitation and have a shelf life of only 5 days. **Analysis of other options:** * **Option A (Storage duration):** Using modern CPDA-1 (Citrate Phosphate Dextrose Adenine) anticoagulant-preservative solutions, whole blood can be stored for up to **35 days**. With the addition of additive solutions like SAGM (Saline Adenine Glucose Mannitol), the shelf life extends to **42 days**. Thus, "up to 40 days" is a clinically valid statement. * **Option C (Potassium levels):** During storage, the "storage lesion" occurs. The sodium-potassium pump in RBC membranes fails due to ATP depletion, causing potassium to leak out of the cells into the plasma. Therefore, **hyperkalemia** is a classic finding in stored blood. * **Option D (Coagulation factors):** Factors V and VIII are "labile factors." Their activity declines rapidly (significantly reduced within 24–48 hours) at refrigerated temperatures [2]. Consequently, stored blood is deficient in these factors compared to Fresh Frozen Plasma (FFP). **High-Yield NEET-PG Pearls:** * **Storage Lesion:** Includes decreased pH, decreased 2,3-DPG (shifting the oxygen dissociation curve to the **left**), increased Potassium, and increased Lactate. * **Citrate Toxicity:** Massive transfusion of stored blood can lead to hypocalcemia because the citrate anticoagulant chelates the recipient's ionized calcium. * **Temperature:** Whole blood/RBCs are stored at **2–6°C**, while Platelets are stored at **20–24°C**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 581-582. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626.
Question 483: ADAMTS13 is associated with which of the following disorders?
- A. Thrombotic thrombocytopenic purpura (TTP) (Correct Answer)
- B. Churg-Strauss syndrome
- C. Wegener's granulomatosis
- D. Membranous nephropathy
Explanation: **Explanation:** **ADAMTS13** (A Disintegrin And Metalloproteinase with a ThromboSpondin type 1 motif, member 13) is a plasma enzyme responsible for cleaving large **von Willebrand Factor (vWF) multimers** into smaller, less prothrombotic fragments. 1. **Why Option A is Correct:** **Thrombotic Thrombocytopenic Purpura (TTP)** is caused by a deficiency or inhibition of ADAMTS13 (either due to genetic mutations or acquired autoantibodies) [1]. Without this enzyme, "ultralarge" vWF multimers accumulate in the blood, causing spontaneous platelet aggregation and microthrombi formation. This leads to microangiopathic hemolytic anemia (MAHA) and consumptive thrombocytopenia [2]. 2. **Why Other Options are Incorrect:** * **Churg-Strauss Syndrome (EGPA):** A small-vessel vasculitis characterized by asthma, eosinophilia, and p-ANCA positivity. It is not related to vWF processing. * **Wegener’s Granulomatosis (GPA):** A necrotizing granulomatous vasculitis associated with c-ANCA (anti-PR3) antibodies, primarily affecting the respiratory tract and kidneys. * **Membranous Nephropathy:** A glomerular disease caused by immune complex deposition (often anti-PLA2R antibodies), leading to nephrotic syndrome, unrelated to ADAMTS13. **NEET-PG High-Yield Pearls:** * **The TTP Pentad:** Microangiopathic Hemolytic Anemia (Schistocytes), Thrombocytopenia, Fever, Renal failure, and Neurological symptoms (Mnemonic: **FAT RN**) [1]. * **Diagnosis:** Decreased ADAMTS13 activity (<10%) is the definitive marker. * **Treatment:** **Plasmapheresis (Plasma Exchange)** is the gold standard as it removes autoantibodies and replenishes the ADAMTS13 enzyme. * **Schistocytes:** Always look for "helmet cells" on a peripheral smear in TTP questions [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 947-948. [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.
Question 484: An infant presents with bony pain and dermatitis on the scalp. Skull X-ray and electron microscopy of a biopsy from a lesion are provided. What is the most probable diagnosis?
- A. Multiple myeloma
- B. Thalassemia
- C. Langerhans cell histiocytosis (Correct Answer)
- D. Acute myeloid leukemia
Explanation: ***Langerhans cell histiocytosis*** - **Classic triad** in infants includes **bony lytic lesions**, **scalp dermatitis**, and **diabetes insipidus**, with skull X-ray showing characteristic **punched-out lesions**. - Electron microscopy reveals pathognomonic **Birbeck granules** (tennis racket-shaped organelles) within Langerhans cells, confirming the diagnosis. *Multiple myeloma* - Primarily affects **adults over 60 years**, making it extremely rare in infants and children. - Presents with **hypercalcemia**, **renal dysfunction**, and **anemia** rather than scalp dermatitis. *Thalassemia* - Characterized by **hemolytic anemia**, **splenomegaly**, and **growth retardation** due to defective hemoglobin synthesis. - Does not cause **lytic bone lesions** or **dermatitis**; instead shows **extramedullary hematopoiesis**. *Acute myeloid leukemia* - Presents with **pancytopenia**, **bleeding**, and **infections** due to bone marrow infiltration by malignant cells. - Does not typically cause **punched-out skull lesions** or **scalp dermatitis** seen in this case.
Question 485: Which of the following is NOT a cause of Disseminated Intravascular Coagulation (DIC)?
- A. Falciparum malaria
- B. Trauma
- C. Carcinoma of the pancreas
- D. Acute myeloid leukemia M1 subtype (Correct Answer)
Explanation: **Explanation:** Disseminated Intravascular Coagulation (DIC) is a thrombohemorrhagic disorder characterized by the systemic activation of the coagulation cascade. The correct answer is **Acute myeloid leukemia M1 subtype** because it is not typically associated with DIC. **1. Why M1 is the correct answer:** In the context of Acute Myeloid Leukemia (AML), DIC is classically and most strongly associated with the **M3 subtype (Acute Promyelocytic Leukemia)** [1]. In M3, the primary granules of the malignant promyelocytes contain procoagulant substances and tissue factor-like molecules that, when released, trigger massive activation of the clotting cascade. The **M1 subtype (AML without maturation)** lacks these specialized granules and is therefore not a standard cause of DIC. **2. Analysis of other options:** * **Falciparum malaria:** Severe malaria causes DIC through widespread endothelial damage and the release of procoagulant material from ruptured infected erythrocytes. * **Trauma:** Major trauma, especially involving the brain (release of thromboplastin), leads to the systemic entry of tissue factor, a potent initiator of the extrinsic pathway [2]. * **Carcinoma of the pancreas:** Mucin-secreting adenocarcinomas (pancreas, prostate, lung) can trigger DIC because mucin acts as a direct activator of Factor X [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of DIC:** Sepsis (Gram-negative organisms releasing endotoxins) [2]. * **Obstetric cause:** Abruptio placentae (release of tissue thromboplastin from the placenta) [2]. * **Laboratory Hallmark:** Elevated **D-dimer** (most specific) and prolonged PT/APTT with low fibrinogen levels [3]. * **Blood Smear:** Presence of **Schistocytes** (fragmented RBCs) due to microangiopathic hemolytic anemia (MAHA) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, 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. 671-672. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 624-626.
Question 486: All are seen in Thalassemia major EXCEPT?
- A. Macrocytic anemia (Correct Answer)
- B. Transfusion dependency
- C. Hepato-splenomegaly
- D. Target cells
Explanation: **Explanation:** **Thalassemia Major** is a genetic disorder characterized by the complete absence or severe reduction of $\beta$-globin chain synthesis [1]. This leads to an imbalance between $\alpha$ and non-$\alpha$ chains, resulting in ineffective erythropoiesis and hemolysis. **1. Why "Macrocytic Anemia" is the correct answer (The Exception):** Thalassemia is a classic cause of **Microcytic Hypochromic Anemia** (MCV < 80 fL) [2]. The defect in globin chain synthesis leads to reduced hemoglobin production per cell, making the RBCs smaller (microcytic) and paler (hypochromic) [2]. Macrocytic anemia (MCV > 100 fL) is typically seen in Vitamin B12/Folate deficiency or liver disease, not in Thalassemia. **2. Analysis of Incorrect Options:** * **Transfusion dependency:** Due to severe anemia (Hb often <7 g/dL) and ineffective erythropoiesis, patients require lifelong regular blood transfusions to survive and suppress excessive bone marrow expansion [1],[3]. * **Hepato-splenomegaly:** This occurs due to two mechanisms: **Extramedullary hematopoiesis** (the body attempting to produce RBCs outside the bone marrow) and **sequestration/destruction** of abnormal RBCs in the spleen [4]. * **Target cells (Codocytes):** These are a hallmark peripheral smear finding in Thalassemia. They occur due to a relative excess of cell membrane compared to the reduced hemoglobin content, giving the cell a "bullseye" appearance. **Clinical Pearls for NEET-PG:** * **Mentzer Index:** (MCV/RBC count) < 13 suggests Thalassemia; > 13 suggests Iron Deficiency Anemia. * **X-ray findings:** "Crew-cut" or "Hair-on-end" appearance of the skull due to marrow expansion [4]. * **Hb Analysis:** HPLC or Electrophoresis shows absent or markedly reduced HbA, with significantly increased **HbF** [1]. * **Complication:** Secondary **hemosiderosis** (iron overload) is the leading cause of mortality, often resulting in heart failure or endocrine dysfunction [1],[4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 648. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 590-591. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 650. [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.
Question 487: "Autosplenectomy" is a feature seen in:
- A. Hereditary spherocytosis
- B. Sickle cell anemia (Correct Answer)
- C. G6PD deficiency
- D. Thalassemia minor
Explanation: **Explanation:** **Autosplenectomy** refers to the progressive fibrosis and shrinkage of the spleen due to repeated episodes of splenic infarction [1]. **Why Sickle Cell Anemia (SCA) is the correct answer:** In SCA, deoxygenation causes hemoglobin S (HbS) to polymerize, leading to the "sickling" of red blood cells [3]. These rigid, sickle-shaped cells become trapped in the narrow splenic sinusoids, causing **vaso-occlusion** [2]. In early childhood, this leads to splenomegaly (due to congestion); however, repeated micro-infarctions over time result in extensive scarring, fibrosis, and calcification [4]. By adulthood, the spleen becomes a small, non-functional fibrous remnant [2]. This process is termed autosplenectomy. A classic radiological sign associated with this is **Gamna-Gandy bodies** (siderofibrotic nodules). **Why other options are incorrect:** * **Hereditary Spherocytosis:** Characterized by **splenomegaly** (enlargement), as the spleen actively traps and destroys spherical RBCs. It does not undergo infarction-led shrinkage. * **G6PD Deficiency:** Typically presents as episodic hemolysis triggered by oxidative stress. It does not cause chronic splenic infarction or autosplenectomy. * **Thalassemia Minor:** Usually asymptomatic or presents with mild anemia; it does not lead to the vaso-occlusive crises required for autosplenectomy. (Note: Thalassemia Major often causes massive splenomegaly). **High-Yield Clinical Pearls for NEET-PG:** * **Howell-Jolly Bodies:** These nuclear remnants are seen on a peripheral smear post-autosplenectomy, indicating splenic dysfunction [4]. * **Infection Risk:** Autosplenectomy increases susceptibility to **encapsulated organisms** (*S. pneumoniae, H. influenzae, N. meningitidis*) [1]. * **Salmonella Osteomyelitis:** Patients with SCA and autosplenectomy have a uniquely high predisposition to this infection. * **Radiology:** On X-ray, an autosplenectomized spleen may appear as a small, shrunken, calcified mass in the left upper quadrant. **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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599. [4] 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 488: What is the characteristic finding in chronic myeloid leukemia?
- A. Reduced score of alkaline phosphatase in granulocytes (Correct Answer)
- B. Reduced score of acid phosphatase in granulocytes
- C. Total lack of platelets
- D. Total lack of neutrophils
Explanation: **Explanation:** **1. Why Option A is correct:** The hallmark of Chronic Myeloid Leukemia (CML) is the **Leukocyte Alkaline Phosphatase (LAP) score**, also known as the Neutrophil Alkaline Phosphatase (NAP) score. In CML, the mature-appearing neutrophils are biochemically abnormal and deficient in this enzyme. Therefore, a **low or zero LAP score** is a critical diagnostic marker used to differentiate CML from a **Leukemoid Reaction** (where the LAP score is characteristically elevated). **2. Why the other options are incorrect:** * **Option B:** Acid phosphatase is the marker used for **Hairy Cell Leukemia** (specifically the Tartrate-Resistant Acid Phosphatase or TRAP stain), not CML. * **Option C:** CML is a myeloproliferative neoplasm. Instead of a lack of platelets, patients often present with **thrombocytosis** (elevated platelet count) or a normal count [2]. Thrombocytopenia only typically occurs during the "Blast Crisis" phase. * **Option D:** CML is characterized by a massive **increase in neutrophils** and their precursors (the "myeloid bulge"), not a lack of them. **3. High-Yield Clinical Pearls for NEET-PG:** * **Cytogenetics:** Associated with **t(9;22)**, forming the **Philadelphia (Ph) chromosome** and the **BCR-ABL1** fusion gene (tyrosine kinase activity) [1]. * **Peripheral Smear:** Shows a "full spectrum" of myeloid cells (myeloblasts to mature neutrophils) with a characteristic peak in **myelocytes and segmented neutrophils** [3]. * **Basophilia:** An increase in basophils is a classic finding in CML; a rising basophil count often signals disease progression. * **Splenomegaly:** Usually the most common physical finding (often massive) [2], [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 624. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 625-626. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612.
Question 489: Auer rods are specific for which of the following conditions?
- A. Acute myeloid leukemia (Correct Answer)
- B. Acute lymphocytic leukemia
- C. Chronic lymphocytic leukemia
- D. Hodgkin's lymphoma
Explanation: **Explanation:** **Auer rods** are pathognomonic laboratory findings in **Acute Myeloid Leukemia (AML)**. They are elongated, needle-shaped, pink-to-red cytoplasmic inclusions formed by the fusion and crystallization of primary azurophilic granules [2]. Their presence indicates a neoplastic proliferation of the myeloid lineage, specifically signifying that the blast cells are **myeloblasts**. 1. **Why Option A is correct:** Auer rods contain peroxidase, lysosomal enzymes, and crystalline proteins. They are most commonly seen in AML subtypes M1, M2, M3, and M4 (FAB classification) [2]. In **Acute Promyelocytic Leukemia (AML-M3)**, cells may contain bundles of Auer rods known as **"faggot cells,"** which can trigger Disseminated Intravascular Coagulation (DIC) upon lysis [1]. 2. **Why Options B, C, and D are incorrect:** * **Acute Lymphocytic Leukemia (ALL):** Auer rods are **never** found in lymphoblasts [2]. Their absence is a key morphological feature used to differentiate ALL from AML. * **Chronic Lymphocytic Leukemia (CLL):** This is a mature B-cell neoplasm characterized by "smudge cells," not immature blasts or myeloid granules. * **Hodgkin’s Lymphoma:** This is a nodal malignancy characterized by **Reed-Sternberg (RS) cells** (owl-eye appearance), not circulating myeloid inclusions. **High-Yield Clinical Pearls for NEET-PG:** * **Staining:** Auer rods are **Myeloperoxidase (MPO) positive** and Sudan Black B positive. * **Pathognomonic:** If you see an Auer rod, the diagnosis is AML until proven otherwise. * **Exception:** While specific to myeloid lineage, they can occasionally be seen in high-grade Myelodysplastic Syndromes (MDS) like RAEB-2, but never in lymphoid malignancies. **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] 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 490: Plasmacytoid lymphomas may be associated with which immunoglobulin?
- A. IgG
- B. IgM (Correct Answer)
- C. IgA
- D. IgE
Explanation: ### Explanation **Correct Option: B (IgM)** The term **Plasmacytoid lymphoma** (most commonly referring to **Lymphoplasmacytic Lymphoma - LPL**) is a mature B-cell neoplasm characterized by a mixture of small B-lymphocytes, plasmacytoid lymphocytes, and plasma cells [1]. The hallmark of LPL is the secretion of a monoclonal protein, which in the vast majority of cases is **IgM** [3]. When LPL involves the bone marrow and is associated with a serum IgM monoclonal gammopathy, it is clinically defined as **Waldenström Macroglobulinemia (WM)** [1]. The high molecular weight of IgM (a pentamer) leads to increased blood viscosity, resulting in the classic "Hyperviscosity Syndrome" (visual disturbances, neurological symptoms, and mucosal bleeding) [3]. **Why Incorrect Options are Wrong:** * **IgG and IgA (Options A & C):** While these are the most common immunoglobulins associated with **Multiple Myeloma**, they are rarely associated with LPL [2]. If an LPL-like morphology secretes IgG or IgA, it is termed a "non-IgM LPL," which is clinically distinct and much rarer [1]. * **IgE (Option D):** IgE-mediated monoclonal gammopathies are extremely rare in clinical practice and are not a characteristic feature of plasmacytoid lymphomas [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Genetic Marker:** Over 90% of LPL/Waldenström cases carry the **MYD88 L265P mutation**. * **Morphology:** Look for **Dutcher bodies** (PAS-positive intranuclear inclusions) and **Russell bodies** (intracytoplasmic inclusions), which represent accumulated immunoglobulins. * **Clinical Presentation:** Unlike Multiple Myeloma, LPL/WM typically presents with **hepatosplenomegaly and lymphadenopathy**, but lacks "CRAB" features (specifically, bone lytic lesions and hypercalcemia are rare) [1]. * **Diagnosis:** Bone marrow biopsy shows an interstitial, diffuse, or paratrabecular infiltration by lymphoplasmacytic cells. **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. 609-610. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617. [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. 606-607.
Practice by Chapter
Anemias: Classification and Approach
Practice Questions
Hemolytic Anemias
Practice Questions
Myeloproliferative Neoplasms
Practice Questions
Myelodysplastic Syndromes
Practice Questions
Acute Leukemias
Practice Questions
Chronic Leukemias
Practice Questions
Lymphomas and Lymphoid Neoplasms
Practice Questions
Plasma Cell Disorders
Practice Questions
Bleeding Disorders
Practice Questions
Thrombotic Disorders
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free