Hematology — MCQs
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In iron deficiency anemia, all are true except?
A 47-year-old man with a history of sickle cell disease has had numerous hospitalizations requiring the placement of intravenous lines. The patient has poor peripheral venous access, and a catheter is placed in the right subclavian vein. The patient subsequently develops right arm discomfort and swelling, and a temperature of 40.1°C with chills. Multiple blood cultures are taken, and gram-positive cocci are isolated. The organism is catalase-positive and grows on mannitol salt agar, but does not turn the agar yellow; the colonies are gamma-hemolytic on a sheep blood agar plate. Which of the following organisms is the most likely cause of this patient's symptoms?
A patient with Hodgkin's lymphoma presents with a single cervical lymph node. Biopsy showed the lymphocyte-predominant variant. Which of the following is the most appropriate treatment?
Which of the following statements regarding the treatment of Chronic Lymphocytic Leukemia (CLL) is true?
A 60-year-old male patient complains of bleeding gums and loss of appetite. Histopathologic examination reveals basophilic leukocytosis. What condition might this patient have?
A 57-year-old man, with a history of chronic alcohol ingestion, is admitted to the hospital with acute alcoholic intoxication and lobar pneumonia. Physical examination reveals pallor; a large, tender liver; and consolidation of the right lower lobe. Laboratory data include hemoglobin of 7 g/dL, WBC of 4000/mL, and platelet count of 85,000/mL. Which of the following is the most likely factor for the anemia?
A 45-year-old man complains of recurrent nausea and abdominal distress. A gastric biopsy shows atrophy of the mucosa in the fundus and body, with marked lymphocytic infiltration. Blood studies show severe macrocytic anemia with a mean corpuscular volume of 110 mm3. In addition, numerous hypersegmented neutrophils are appreciated on a blood smear. Which of the following is the MOST likely pathogenetic mechanism of this patient's anemia?
A patient diagnosed with deep vein thrombosis is being treated with heparin. Which of the following tests will you order to adjust its dosage?
A 70-year-old woman, previously in good health, is found to have an asymptomatic monoclonal immunoglobulin peak on serum electrophoresis. Her physical examination is normal, as is her CBC, electrolytes, renal function, and calcium level. A skeletal survey does not reveal any osteolytic lesions, and a bone-marrow aspirate reveals 5% plasma cells. Which of the following is the most likely diagnosis?
Which of the following is NOT true regarding Waldenström's macroglobulinemia?
Hematology Indian Medical PG Practice Questions and MCQs
Question 211: In iron deficiency anemia, all are true except?
- A. Corpuscular volume is reduced
- B. MCHC is increased (Correct Answer)
- C. Increased total iron binding capacity
- D. Serum ferritin is reduced
Explanation: In Iron Deficiency Anemia (IDA), the body lacks sufficient iron to produce hemoglobin. This leads to a **Microcytic Hypochromic** anemia [1]. ### Why Option B is the Correct Answer (The "Except") **MCHC (Mean Corpuscular Hemoglobin Concentration)** represents the average concentration of hemoglobin in a given volume of packed red cells. In IDA, hemoglobin synthesis is impaired more significantly than the reduction in cell size. Consequently, the cells become "hypochromic" (pale), and the **MCHC is decreased**, not increased. An increased MCHC is rare and typically seen in Hereditary Spherocytosis. ### Explanation of Other Options * **A. Corpuscular volume is reduced:** True. Due to deficient hemoglobin synthesis, RBCs undergo extra divisions in the bone marrow, resulting in smaller cells (**Microcytosis**; MCV <80 fL) [3]. * **C. Increased TIBC:** True. Total Iron Binding Capacity (TIBC) is a measure of Transferrin levels. In IDA, the liver increases Transferrin production to maximize the transport of any available iron. * **D. Serum ferritin is reduced:** True. Serum ferritin reflects total body iron stores. It is the **earliest laboratory marker** to decrease in IDA [2]. ### NEET-PG High-Yield Pearls * **Gold Standard Diagnosis:** Bone marrow aspiration (Perls' Prussian blue stain) showing absent haemosiderin in macrophages [2]. * **Best Initial Screening Test:** Serum Ferritin (Low). * **Red Cell Distribution Width (RDW):** Characteristically **increased** in IDA (Anisocytosis), helping differentiate it from Thalassemia trait (where RDW is often normal). * **Mentzer Index:** MCV/RBC count >13 suggests IDA; <13 suggests Thalassemia.
Question 212: A 47-year-old man with a history of sickle cell disease has had numerous hospitalizations requiring the placement of intravenous lines. The patient has poor peripheral venous access, and a catheter is placed in the right subclavian vein. The patient subsequently develops right arm discomfort and swelling, and a temperature of 40.1°C with chills. Multiple blood cultures are taken, and gram-positive cocci are isolated. The organism is catalase-positive and grows on mannitol salt agar, but does not turn the agar yellow; the colonies are gamma-hemolytic on a sheep blood agar plate. Which of the following organisms is the most likely cause of this patient's symptoms?
- A. Enterococcus faecalis
- B. Staphylococcus aureus
- C. Staphylococcus epidermidis (Correct Answer)
- D. Streptococcus agalactiae
Explanation: ### Explanation This clinical scenario describes a **catheter-related bloodstream infection (CRBSI)** in a patient with poor venous access. The diagnosis is reached by systematically analyzing the microbiological characteristics provided: 1. **Gram-positive cocci & Catalase-positive:** This narrows the differential to the *Staphylococcus* genus (distinguishing them from *Streptococcus* and *Enterococcus*, which are catalase-negative). 2. **Mannitol Salt Agar (MSA) growth without yellow color:** MSA is both selective and differential. While all Staphylococci can grow on it, only *Staphylococcus aureus* ferments mannitol to produce acid, turning the phenol red indicator **yellow**. A negative result (pink/red agar) indicates **Coagulase-Negative Staphylococci (CoNS)** [1]. 3. **Gamma-hemolysis:** This confirms a non-hemolytic organism, consistent with *S. epidermidis*. **Staphylococcus epidermidis** is the most common cause of prosthetic valve endocarditis and infections related to indwelling medical devices (catheters, shunts, prostheses) due to its ability to produce a **polysaccharide biofilm**, which protects it from host immune responses and antibiotics [1]. #### Analysis of Incorrect Options: * **A. Enterococcus faecalis:** These are catalase-negative and typically show variable hemolysis (often gamma), but they do not typically grow on MSA in the same manner as Staphylococci. * **B. Staphylococcus aureus:** While it is catalase-positive, it **ferments mannitol**, turning MSA yellow, and typically shows **beta-hemolysis** on blood agar [1]. * **D. Streptococcus agalactiae (GBS):** These are catalase-negative and typically show narrow-zone beta-hemolysis. #### NEET-PG High-Yield Pearls: * **Biofilm formation:** The primary virulence factor for *S. epidermidis* is the production of an extracellular polysaccharide matrix (slime/biofilm). * **Novobiocin Sensitivity:** *S. epidermidis* is Novobiocin **sensitive**, whereas *S. saprophyticus* (another CoNS) is Novobiocin **resistant** [1]. * **Treatment:** Most strains are methicillin-resistant (MRSE) due to the *mecA* gene; **Vancomycin** is the drug of choice.
Question 213: A patient with Hodgkin's lymphoma presents with a single cervical lymph node. Biopsy showed the lymphocyte-predominant variant. Which of the following is the most appropriate treatment?
- A. Chemotherapy with Radiotherapy
- B. Chemotherapy only
- C. Radiotherapy only (Correct Answer)
- D. No treatment needed
Explanation: **Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLPHL)** is a distinct clinical entity from Classical Hodgkin Lymphoma (cHL) [1]. It is characterized by an indolent (slow-growing) course and typically presents as localized (Stage I or II) peripheral lymphadenopathy, most commonly in the cervical, axillary, or inguinal regions [1]. 1. **Why Radiotherapy only is correct:** For patients with **early-stage (Stage IA or IIA)** NLPHL without bulky disease, **Involved-Field Radiation Therapy (IFRT)** or Involved-Site Radiation Therapy (ISRT) is the gold standard [2]. Because the disease is highly radiosensitive and has a very low risk of distant spread in early stages, local control with radiotherapy alone achieves excellent long-term survival (often >90%), sparing the patient from the systemic toxicities of chemotherapy [2]. 2. **Why other options are incorrect:** * **Chemotherapy (with or without RT):** While effective, combined modality therapy (e.g., ABVD or CHOP + RT) is generally reserved for advanced stages (III/IV) or patients with "B symptoms" and bulky disease. Using it for a single node is considered "over-treatment." * **No treatment needed:** Although indolent, NLPHL is a progressive malignancy and requires active management to prevent local growth or transformation into aggressive Large B-cell Lymphoma. **NEET-PG High-Yield Pearls:** * **Cell Marker:** NLPHL is **CD20+** and **CD45+**, but usually **CD15- and CD30-** (the opposite of Classical HL). * **Pathology:** Look for **"Popcorn cells"** (L&H cells) instead of typical Reed-Sternberg cells [1]. * **Prognosis:** It has the best prognosis among all Hodgkin variants but carries a 3-5% risk of transformation to Diffuse Large B-Cell Lymphoma (DLBCL). * **Treatment Note:** For advanced NLPHL, the **R-CHOP** regimen is often preferred over ABVD due to the CD20 positivity [3].
Question 214: Which of the following statements regarding the treatment of Chronic Lymphocytic Leukemia (CLL) is true?
- A. Treatment should be offered to all patients with CLL.
- B. Treatment can be withheld in asymptomatic patients with CLL. (Correct Answer)
- C. Treatment for CLL is curative.
- D. Combination chemotherapy should be administered to patients with CLL above 50 years of age.
Explanation: The management of Chronic Lymphocytic Leukemia (CLL) is unique because it is often an indolent malignancy [1]. Unlike many other cancers, early intervention in asymptomatic patients does not improve overall survival [1]. **1. Why Option B is Correct:** The standard of care for CLL is the **"Watch and Wait"** strategy. Treatment is only initiated when the patient becomes symptomatic or shows evidence of progressive disease (based on the **iwCLL criteria**). These criteria include "B-symptoms" (fever, night sweats, weight loss), symptomatic lymphadenopathy/splenomegaly, or progressive bone marrow failure (anemia/thrombocytopenia) [1]. **2. Why the Other Options are Incorrect:** * **Option A:** Treatment is not offered to all. Roughly 1/3 of patients never require treatment, 1/3 present with stable disease that later progresses, and 1/3 require immediate therapy [1]. * **Option C:** Current therapies (including BTK inhibitors like Ibrutinib or BCL-2 inhibitors like Venetoclax) are highly effective at inducing remission but are **not curative** [1]. The only potentially curative treatment is Allogeneic Stem Cell Transplant, which is reserved for very high-risk, fit patients [1]. * **Option D:** Age alone does not dictate the use of combination chemotherapy. In fact, modern management has shifted away from chemotherapy (like FCR) toward **targeted oral therapies**, especially in older patients or those with comorbidities [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Absolute Lymphocyte Count >5000/µL for >3 months + Flow cytometry showing **CD5+, CD19+, CD20+(weak), and CD23+** B-cells. * **Peripheral Smear:** Characterized by **Smudge cells** (Gumprecht shadows). * **Prognosis:** **Deletion 17p** (TP53 mutation) is the most significant poor prognostic marker and predicts resistance to standard chemotherapy. * **Richter Transformation:** The sudden transformation of CLL into an aggressive Diffuse Large B-cell Lymphoma (DLBCL).
Question 215: A 60-year-old male patient complains of bleeding gums and loss of appetite. Histopathologic examination reveals basophilic leukocytosis. What condition might this patient have?
- A. Hodgkin lymphoma
- B. Systemic lupus erythematosus
- C. Chronic myeloid leukemia (Correct Answer)
- D. Bordetella pertussis infection
Explanation: The presence of **basophilic leukocytosis** (basophilia) is a hallmark diagnostic clue for **Chronic Myeloid Leukemia (CML)**. In clinical practice and for the NEET-PG exam, an absolute basophil count >2% is highly suggestive of a myeloproliferative neoplasm, and CML is the most common cause. **Why CML is correct:** CML is a myeloproliferative disorder characterized by the uncontrolled proliferation of the myeloid lineage. It typically presents with a massive shift to the left in the white cell line. Basophilia is a classic feature of CML and is often used as a marker for disease progression; an increasing basophil count often signals a transition from the Chronic Phase to the Accelerated Phase or Blast Crisis [1]. **Why other options are incorrect:** * **Hodgkin Lymphoma:** While it can cause eosinophilia, basophilia is not a characteristic feature. It typically presents with painless lymphadenopathy and Reed-Sternberg cells. * **Systemic Lupus Erythematosus (SLE):** SLE is an autoimmune condition usually associated with cytopenias (leukopenia, anemia, thrombocytopenia) rather than leukocytosis or basophilia. * **Bordetella pertussis:** This infection is famous for causing a marked **lymphocytosis** (absolute increase in lymphocytes), not basophilia. **High-Yield Clinical Pearls for NEET-PG:** * **Philadelphia Chromosome:** t(9;22) resulting in the *BCR-ABL1* fusion gene is the cytogenetic hallmark of CML [1]. * **LAP Score:** Leukocyte Alkaline Phosphatase (LAP) score is **decreased** in CML (helps differentiate it from a Leukemoid reaction where the score is increased). * **Drug of Choice:** Imatinib (Tyrosine Kinase Inhibitor) [1]. * **Splenomegaly:** CML is a common cause of massive splenomegaly [2].
Question 216: A 57-year-old man, with a history of chronic alcohol ingestion, is admitted to the hospital with acute alcoholic intoxication and lobar pneumonia. Physical examination reveals pallor; a large, tender liver; and consolidation of the right lower lobe. Laboratory data include hemoglobin of 7 g/dL, WBC of 4000/mL, and platelet count of 85,000/mL. Which of the following is the most likely factor for the anemia?
- A. Hemolysis
- B. Hemobilia
- C. Vitamin B12 deficiency
- D. Toxic marrow suppression (Correct Answer)
Explanation: The patient presents with **pancytopenia** (anemia, mild leukopenia, and thrombocytopenia) in the setting of acute alcohol intoxication and infection. In chronic alcoholics, the most common cause of sudden hematologic decline is **Toxic Marrow Suppression**. **1. Why Toxic Marrow Suppression is correct:** Alcohol is a direct bone marrow toxin. Acute heavy ingestion can cause a transient but significant suppression of all three cell lines (erythroid, myeloid, and megakaryocytic). This effect is often exacerbated by concurrent infection (lobar pneumonia), which further stresses the marrow. While alcoholics often have folate deficiency, the acute nature of this presentation and the presence of pancytopenia strongly point toward the direct toxic effects of ethanol on hematopoiesis. **2. Why the other options are incorrect:** * **A. Hemolysis:** While alcoholics can develop Zieve’s syndrome (hemolysis, jaundice, and hyperlipidemia), there is no evidence of jaundice or schistocytes here to suggest hemolysis as the primary cause. * **B. Hemobilia:** This refers to bleeding into the biliary tree (usually post-trauma or procedure). It presents with the triad of biliary colic, jaundice, and GI bleeding, which does not fit this clinical picture. * **C. Vitamin B12 deficiency:** Alcoholics are much more prone to **Folate deficiency** than B12 deficiency. B12 stores last for years, whereas folate stores are depleted in weeks. Furthermore, B12 deficiency would not explain the acute drop during intoxication. **Clinical Pearls for NEET-PG:** * **MCV in Alcoholics:** The most common cause of macrocytosis (high MCV) in alcoholics is **direct ethanol toxicity**, even before folate deficiency or liver disease develops. * **Sideroblastic Anemia:** Alcohol can interfere with heme synthesis, leading to ringed sideroblasts in the bone marrow. * **Thrombocytopenia:** This is the most common hematologic abnormality in alcoholics, caused by both direct toxicity and splenic sequestration (if portal hypertension is present).
Question 217: A 45-year-old man complains of recurrent nausea and abdominal distress. A gastric biopsy shows atrophy of the mucosa in the fundus and body, with marked lymphocytic infiltration. Blood studies show severe macrocytic anemia with a mean corpuscular volume of 110 mm3. In addition, numerous hypersegmented neutrophils are appreciated on a blood smear. Which of the following is the MOST likely pathogenetic mechanism of this patient's anemia?
- A. Autoantibodies to intrinsic factor (Correct Answer)
- B. Chronic blood loss
- C. Deficient iron absorption
- D. Helicobacter pylori infection
Explanation: ### Explanation **Correct Option: A. Autoantibodies to intrinsic factor** The clinical presentation describes **Pernicious Anemia (PA)**, a classic cause of Vitamin B12 deficiency [1]. The biopsy findings of **atrophic gastritis** (atrophy of the fundus and body) with lymphocytic infiltration indicate an autoimmune destruction of **gastric parietal cells** [2]. These cells are responsible for secreting **Intrinsic Factor (IF)**, which is essential for B12 absorption in the terminal ileum. * **Hematological findings:** Macrocytic anemia (MCV >100 fL) and **hypersegmented neutrophils** (≥5 lobes) are hallmark features of megaloblastic anemia caused by impaired DNA synthesis [1], [3]. * **Pathogenesis:** Type I antibodies block the binding of B12 to IF, while Type II antibodies block the binding of the IF-B12 complex to ileal receptors. **Why other options are incorrect:** * **B & C (Chronic blood loss/Deficient iron absorption):** These lead to **Microcytic Hypochromic anemia** (low MCV), not macrocytic anemia [3]. Gastric atrophy can decrease acid (achlorhydria) and impair iron absorption, but the presence of hypersegmented neutrophils specifically points toward megaloblastic (B12/Folate) deficiency. * **D (Helicobacter pylori):** While *H. pylori* causes chronic antral gastritis, autoimmune gastritis (Pernicious Anemia) typically spares the antrum and involves the **fundus and body** [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Absorption:** Vitamin B12 is absorbed in the **Terminal Ileum**; Iron in the **Duodenum**; Folate in the **Jejunum**. * **Schilling Test:** Historically used to differentiate B12 malabsorption causes (now largely replaced by antibody testing). * **Neurological Symptoms:** B12 deficiency causes **Subacute Combined Degeneration (SCD)** of the spinal cord (dorsal columns and corticospinal tracts), which distinguishes it from Folate deficiency. * **Gastric Cancer Risk:** Patients with Pernicious Anemia have a 3x increased risk of gastric adenocarcinoma and carcinoid tumors.
Question 218: A patient diagnosed with deep vein thrombosis is being treated with heparin. Which of the following tests will you order to adjust its dosage?
- A. Platelet count
- B. Prothrombin time
- C. Bleeding time
- D. Activated partial thromboplastin time (Correct Answer)
Explanation: The correct answer is **Activated partial thromboplastin time (aPTT)**. **1. Why aPTT is correct:** Unfractionated Heparin (UFH) exerts its anticoagulant effect by binding to Antithrombin III, which subsequently inactivates Thrombin (Factor IIa) and Factor Xa [1]. The aPTT measures the integrity of the **intrinsic and common pathways** of the coagulation cascade [2]. Since heparin primarily affects these pathways, the aPTT is the standard laboratory test used to monitor its therapeutic efficacy and adjust dosages to ensure the patient remains within the "therapeutic window" (typically 1.5 to 2.5 times the control value) [3]. **2. Why other options are incorrect:** * **Platelet count:** While heparin can cause Heparin-Induced Thrombocytopenia (HIT), platelet counts are used to monitor for this *complication*, not to adjust the anticoagulant dosage itself. * **Prothrombin time (PT/INR):** This test monitors the **extrinsic pathway** and is the standard for monitoring **Warfarin** therapy, not heparin [3]. * **Bleeding time:** This measures platelet function and vascular integrity; it is not a reliable or specific indicator for heparin's anticoagulant effect. **3. Clinical Pearls for NEET-PG:** * **Low Molecular Weight Heparin (LMWH):** Unlike UFH, LMWH (e.g., Enoxaparin) does not require routine monitoring. If monitoring is necessary (e.g., in renal failure or pregnancy), the **Anti-Factor Xa assay** is used. * **Antidote:** The specific neutralizer for heparin overdose is **Protamine sulfate**. * **Mechanism:** Heparin acts as a catalyst, increasing the activity of Antithrombin III by 1000-fold [1].
Question 219: A 70-year-old woman, previously in good health, is found to have an asymptomatic monoclonal immunoglobulin peak on serum electrophoresis. Her physical examination is normal, as is her CBC, electrolytes, renal function, and calcium level. A skeletal survey does not reveal any osteolytic lesions, and a bone-marrow aspirate reveals 5% plasma cells. Which of the following is the most likely diagnosis?
- A. monoclonal gammopathy of uncertain significance (MGUS) (Correct Answer)
- B. multiple myeloma
- C. Waldenstrom macroglobulinemia
- D. amyloidosis
Explanation: ### Explanation The patient presents with an incidental finding of a monoclonal (M) protein spike without any associated end-organ damage. This clinical picture is classic for **Monoclonal Gammopathy of Undetermined Significance (MGUS)**. **1. Why MGUS is the Correct Answer:** MGUS is defined by a triad of specific criteria, all of which are met in this case: * **M-protein level:** < 3 g/dL. * **Bone marrow plasma cells:** < 10% (this patient has 5%). * **Absence of CRAB features:** No **C**alcium elevation, **R**enal insufficiency, **A**nemia, or **B**one lesions. Since the patient is asymptomatic with normal labs and a skeletal survey, MGUS is the most likely diagnosis. **2. Why the Other Options are Incorrect:** * **Multiple Myeloma:** Requires ≥10% clonal plasma cells in the bone marrow AND evidence of end-organ damage (CRAB features). This patient has only 5% plasma cells and no CRAB features. * **Waldenstrom Macroglobulinemia:** This is a lymphoplasmacytic lymphoma characterized by an IgM M-spike and bone marrow infiltration by lymphoplasmacytic cells. It typically presents with hyperviscosity symptoms, hepatosplenomegaly, or lymphadenopathy, which are absent here. * **Amyloidosis:** While associated with monoclonal proteins, it presents with systemic symptoms like macroglossia, nephrotic syndrome, restrictive cardiomyopathy, or hepatomegaly. **3. NEET-PG High-Yield Pearls:** * **Risk of Progression:** MGUS progresses to Multiple Myeloma at a rate of approximately **1% per year**. * **Management:** MGUS does not require chemotherapy. The standard of care is **"Watchful Waiting"** with periodic monitoring of serum electrophoresis. * **Smoldering Myeloma:** Defined as M-protein ≥ 3 g/dL OR bone marrow plasma cells 10–60%, but still **without** CRAB features. * **Most Common Type:** IgG is the most common isotype found in MGUS.
Question 220: Which of the following is NOT true regarding Waldenström's macroglobulinemia?
- A. Lymphadenopathy is usually present.
- B. Blood viscosity is increased.
- C. IgM immunoglobulin is increased.
- D. Hypercalcemia is present. (Correct Answer)
Explanation: Waldenström’s Macroglobulinemia (WM) is a **lymphoplasmacytic lymphoma** characterized by the infiltration of the bone marrow by neoplastic cells that secrete a monoclonal **IgM** protein [1]. **Why Option D is the Correct Answer:** Unlike Multiple Myeloma (MM), Waldenström’s Macroglobulinemia is typically **not** associated with lytic bone lesions or significant bone destruction [1]. Consequently, **hypercalcemia and renal failure (due to light chains) are rare** in WM. If a patient presents with high IgM and lytic lesions, the diagnosis is more likely "IgM Myeloma" rather than WM. **Analysis of Incorrect Options:** * **Option A (Lymphadenopathy):** WM is a lymphoma. Unlike Multiple Myeloma, patients frequently present with organomegaly, including **lymphadenopathy and hepatosplenomegaly** (in ~20-40% of cases) [1]. * **Option B (Blood Viscosity):** IgM is a large pentameric molecule. High levels significantly increase serum viscosity, leading to **Hyperviscosity Syndrome** (headache, visual disturbances, and mucosal bleeding) [1]. * **Option C (IgM Increase):** By definition, WM involves a monoclonal gammopathy of the **IgM** class (usually >3 g/dL) [1]. **NEET-PG High-Yield Pearls:** 1. **Genetic Marker:** Over 90% of WM patients possess the **MYD88 L265P mutation**. 2. **Clinical Triad:** Hyperviscosity, lymphadenopathy/splenomegaly, and anemia [1]. 3. **Diagnosis:** Bone marrow biopsy shows **lymphoplasmacytic infiltration** (CD19+, CD20+, CD22+, CD10-, CD5-). 4. **Dutcher Bodies:** Periodic acid–Schiff (PAS)-positive intranuclear inclusions of immunoglobulins are a classic pathological finding. 5. **Treatment:** Plasmapheresis is the immediate treatment for symptomatic hyperviscosity; Rituximab-based regimens are used for definitive therapy [1].
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
Practice Questions
Thalassemias
Practice Questions
Platelet Disorders
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Coagulation Disorders
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Thrombotic Disorders
Practice Questions
Leukemias
Practice Questions
Lymphomas
Practice Questions
Multiple Myeloma and Plasma Cell Disorders
Practice Questions
Myeloproliferative Neoplasms
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Transfusion Medicine
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Hematopoietic Stem Cell Transplantation
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