Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 641: A 14-year-old boy presents with gingival bleeding, oral ulcers, anemia, hepatomegaly, and no lymphadenopathy. His total leukocyte count is one lakh cells per mm³. What is the most likely diagnosis?

A. Acute myeloid leukemia (Correct Answer)
B. Chronic monocytic leukemia
C. Chronic lymphoblastic leukemia
D. Chronic myeloid leukemia

Explanation: **Explanation:** The clinical presentation of a young patient with **gingival bleeding, oral ulcers, and anemia** suggests acute bone marrow failure and extramedullary involvement. The presence of a high total leukocyte count (1 lakh/mm³) indicates a leukemic state [1], [2]. **Why Acute Myeloid Leukemia (AML) is correct:** AML, specifically the monocytic subtypes (**FAB M4 and M5**), is classically associated with **gingival hyperplasia and infiltration**, leading to bleeding and oral ulcers [3]. The absence of lymphadenopathy is more characteristic of AML than Acute Lymphoblastic Leukemia (ALL) [3]. In a pediatric/adolescent patient, a rapid onset of symptoms with significant hepatomegaly and a very high TLC (hyperleukocytosis) strongly points toward an acute process [1], [3]. **Why other options are incorrect:** * **Chronic Monocytic Leukemia:** This is not a standard WHO classification; it is usually part of Chronic Myelomonocytic Leukemia (CMML), which typically affects elderly patients and presents more indolently. * **Chronic Lymphoblastic Leukemia (CLL):** This is a disease of the elderly (median age >60). It presents with significant lymphadenopathy (which is absent here) and would not typically cause gingival ulcers. * **Chronic Myeloid Leukemia (CML):** While CML presents with a high TLC and hepatosplenomegaly, it usually features massive splenomegaly rather than gingival hypertrophy [4]. It also lacks the acute symptoms of mucosal ulcers and bleeding unless it has progressed to a Blast Crisis [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Gingival Hypertrophy:** Always think of AML-M4 (Myelomonocytic) or AML-M5 (Monocytic) [2], [3]. * **Auer Rods:** Pathognomonic for AML (specifically M1, M2, M3, and M4) [2]. * **Hyperleukocytosis (TLC >100,000):** Increases the risk of leukostasis (respiratory distress or CNS symptoms) [4]. * **DIC:** Most commonly associated with AML-M3 (Acute Promyelocytic Leukemia) [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 607-608. [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. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 608-610. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612.

Question 642: Acute hemolytic transfusion reactions are typically caused by antibodies directed against which of the following blood group antigens?

A. Rh
B. Kell
C. Duffy
D. All of the above (Correct Answer)

Explanation: **Explanation:** Acute Hemolytic Transfusion Reactions (AHTR) occur when a recipient’s pre-existing antibodies (IgM or IgG) attack the donor’s red blood cells (RBCs) immediately or within 24 hours of transfusion [2]. This leads to intravascular or extravascular hemolysis. **Why "All of the above" is correct:** While **ABO incompatibility** is the most common and severe cause of AHTR (due to naturally occurring IgM antibodies), antibodies against **minor blood group antigens** can also trigger these reactions [1]. * **Rh system (Option A):** Anti-D, Anti-C, or Anti-E antibodies are potent triggers for hemolysis [1]. * **Kell system (Option B):** The K antigen is highly immunogenic; anti-K antibodies are a frequent cause of severe hemolytic reactions. * **Duffy system (Option C):** Anti-Fya and Anti-Fyb antibodies are known to cause both acute and delayed hemolytic reactions. Since antibodies against Rh, Kell, and Duffy antigens are all clinically significant and capable of causing acute hemolysis, "All of the above" is the most accurate choice. **Clinical Pearls for NEET-PG:** * **Most Common Cause of AHTR:** Clerical error leading to ABO incompatibility [2]. * **Mechanism:** Type II Hypersensitivity reaction. * **Classic Triad:** Fever/chills, flank pain, and hemoglobinuria (red/dark urine). * **Delayed Hemolytic Transfusion Reaction (DHTR):** Most commonly associated with the **Kidd (Jk)** blood group system. * **Duffy Antigen & Malaria:** The Duffy antigen serves as a receptor for *Plasmodium vivax*. Individuals who are Duffy-negative (common in African populations) are resistant to *P. vivax* infection. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 673-674.

Question 643: Hematopoietic stem cells differ from progenitor stem cells in that they can:

A. Form terminally differentiated cells
B. Have a role in bone marrow regeneration (Correct Answer)
C. Produce growth factors
D. Have receptors for anchoring proteins

Explanation: ### Explanation The fundamental difference between **Hematopoietic Stem Cells (HSCs)** and **Progenitor Cells** lies in the property of **self-renewal** [2]. **Why the Correct Answer is Right:** HSCs are pluripotent cells characterized by their ability to undergo asymmetric division [1]. This allows them to maintain their own population (self-renewal) while simultaneously giving rise to differentiated progeny [2]. Because HSCs can replenish the entire hematopoietic system indefinitely, they are essential for **bone marrow regeneration** following injury, chemotherapy, or in the context of a bone marrow transplant [1]. Progenitor cells, while proliferative, have a limited lifespan and lack the capacity for long-term self-renewal; they eventually exhaust themselves. **Analysis of Incorrect Options:** * **A. Form terminally differentiated cells:** Both HSCs and progenitor cells eventually lead to the formation of terminally differentiated cells (like RBCs, WBCs, and platelets). This is a shared feature, not a differentiating one [1]. * **C. Produce growth factors:** Growth factors (like EPO, G-CSF) are primarily produced by the bone marrow stroma, macrophages, or distant organs (kidneys/liver), rather than the stem cells themselves. * **D. Have receptors for anchoring proteins:** Both HSCs and progenitors possess adhesion molecules (like VLA-4 or CXCR4) to anchor themselves within the osteoblastic or vascular niches of the bone marrow. **NEET-PG High-Yield Pearls:** * **Marker of HSCs:** **CD34+** is the most specific marker used for identifying and harvesting stem cells for transplant. * **Negative Marker:** HSCs are typically **Lin-** (lack lineage-specific markers like CD3, CD19, or CD14). * **Niche:** The **Osteoblastic niche** (endosteum) is associated with HSC quiescence, while the **Vascular niche** is associated with HSC proliferation and differentiation. * **Homing:** The interaction between **SDF-1** (on stroma) and **CXCR4** (on HSCs) is critical for stem cell "homing" to the bone marrow. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 588-589. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 311-312.

Question 644: A 55-year-old male presents with renal failure, bone pain for 7 years, and osteolytic lesions on X-ray. Serum electrophoresis shows an M spike and 35% plasma cells with aberrant protein expression. What is the diagnosis?

A. MGUS
B. Multiple myeloma (Correct Answer)
C. Smoldering myeloma
D. Plasma cell leukemia

Explanation: The diagnosis is **Multiple Myeloma (MM)**. This case presents the classic "CRAB" features (Calcium elevation, Renal failure, Anemia, and Bone lesions) associated with a neoplastic proliferation of plasma cells [1], [2]. ### **Why Multiple Myeloma is Correct?** According to the International Myeloma Working Group (IMWG) criteria, a diagnosis of MM requires: 1. **Clonal bone marrow plasma cells ≥10%** (Patient has 35%). 2. **Evidence of end-organ damage (CRAB features):** The patient exhibits renal failure and symptomatic osteolytic lesions (bone pain) [2]. 3. **Monoclonal (M) protein** in serum or urine, confirmed here by the M-spike on electrophoresis [1], [4]. ### **Why Other Options are Incorrect:** * **MGUS (Monoclonal Gammopathy of Undetermined Significance):** Requires serum M-protein <3 g/dL, bone marrow plasma cells <10%, and **no** end-organ damage (CRAB). * **Smoldering Myeloma:** Characterized by M-protein ≥3 g/dL or plasma cells 10–60%, but crucially, it lacks end-organ damage (asymptomatic) [3]. * **Plasma Cell Leukemia:** A rare, aggressive variant defined by an absolute plasma cell count of >2 x 10⁹/L or >20% plasma cells in the **peripheral blood** smear [5]. ### **NEET-PG High-Yield Pearls:** * **Most common site of involvement:** Vertebral column [1]. * **Radiology:** "Punched-out" lytic lesions; avoid Bone Scans (they detect osteoblastic activity, while MM is osteolytic) [2]. * **Peripheral Smear:** **Rouleaux formation** (due to decreased zeta potential from paraproteins) [5]. * **Urine:** Bence-Jones proteins (light chains) precipitate at 40–60°C and redissolve at 100°C [1]. * **Histology:** "Flame cells" (IgA myeloma) and "Mott cells" (grape-like cytoplasmic inclusions). **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] 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. [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. [4] 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. [5] 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 645: Poor prognosis in Acute Myeloid Leukemia (AML) is indicated by which of the following?

A. Inversion 16
B. Translocation 15;17 (t15;17)
C. Normal cytogenetics
D. Monosomy 7 (Correct Answer)

Explanation: **Explanation:** In Acute Myeloid Leukemia (AML), cytogenetics is the most significant independent prognostic factor for determining clinical outcome and treatment strategy. [1] **Why Monosomy 7 is the Correct Answer:** Monosomy 7 (-7) and Deletion 7q (7q-) are classified under the **adverse/poor risk category**. These chromosomal abnormalities are often associated with complex karyotypes, prior exposure to alkylating agents (therapy-related AML), or evolution from Myelodysplastic Syndrome (MDS). Patients with Monosomy 7 typically show poor response to standard induction chemotherapy and have high relapse rates, often requiring hematopoietic stem cell transplantation (HSCT). **Analysis of Incorrect Options:** * **Inversion 16 [inv(16)]:** This is a hallmark of AML-M4eo (with abnormal eosinophils). It is categorized as a **favorable prognosis** marker with high rates of complete remission. [1] * **Translocation 15;17 [t(15;17)]:** This defines Acute Promyelocytic Leukemia (APL/M3). It carries a **favorable prognosis** due to its high sensitivity to All-trans Retinoic Acid (ATRA) and Arsenic Trioxide. [1] * **Normal Cytogenetics:** This is classified as **Intermediate-risk**. While not as favorable as inv(16), it carries a significantly better prognosis than Monosomy 7. **High-Yield Clinical Pearls for NEET-PG:** * **Favorable Prognosis:** t(8;21), t(15;17), inv(16), and NPM1 mutation (without FLT3-ITD). [1] * **Poor Prognosis:** Monosomy 7, Monosomy 5, del(5q), t(6;9), 11q23 (MLL gene) rearrangements, and **FLT3-ITD** mutations. [1] * **Most common cytogenetic abnormality in AML:** Normal karyotype (~40-50% of cases). * **Auer Rods:** Most commonly seen in t(15;17) and t(8;21). [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. 620.

Question 646: High mitotic activity with rapid cellular turnover and characteristic "Starry sky" appearance is seen in which of the following conditions?

A. Follicular lymphoma
B. Diffuse lymphoma
C. Burkitt's lymphoma (Correct Answer)
D. Hodgkin's lymphoma

Explanation: **Explanation:** **Burkitt’s Lymphoma (Correct Answer):** Burkitt’s lymphoma is a highly aggressive B-cell neoplasm characterized by a **"Starry sky" appearance** on histopathology [1]. This pattern is created by a dense background of small, monotonous malignant B-cells (the "dark sky") interspersed with numerous **tingible body macrophages** (the "stars") [1]. These macrophages contain ingested apoptotic debris, a direct result of the tumor's exceptionally high mitotic index and rapid cellular turnover. It is classically associated with the **t(8;14)** translocation, leading to the overexpression of the **c-MYC** oncogene. **Incorrect Options:** * **Follicular Lymphoma:** Characterized by a nodular growth pattern mimicking germinal centers [3]. It typically shows a low mitotic rate and is associated with **t(14;18)** and BCL-2 overexpression, which inhibits apoptosis rather than promoting rapid turnover [3]. * **Diffuse Large B-cell Lymphoma (DLBCL):** While aggressive, it lacks the specific, uniform "starry sky" pattern. It shows large, pleomorphic cells with prominent nucleoli [2]. * **Hodgkin’s Lymphoma:** Defined by the presence of **Reed-Sternberg (RS) cells** (owl-eye appearance) against a background of non-neoplastic inflammatory cells. It does not exhibit the diffuse, high-turnover starry sky morphology. **High-Yield NEET-PG Pearls:** * **Variants:** Endemic (African, associated with EBV, involves the jaw), Sporadic (involves ileocecum), and Immunodeficiency-associated (HIV). * **Cytogenetics:** t(8;14) is most common; also t(2;8) and t(8;22). * **Immunophenotype:** CD19+, CD20+, CD10+, and BCL-6+. Crucially, it is **BCL-2 negative**. * **Ki-67 index:** Typically approaches **100%**, reflecting the rapid growth [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. 606. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 604-605. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 602-604.

Question 647: A patient being investigated for anemia has a dry marrow tap. Peripheral smear reveals tear drop cells. What is the likely diagnosis?

A. Leukemia
B. Lymphoma
C. Myelofibrosis (Correct Answer)
D. Polycythemia rubra vera

Explanation: ### Explanation The combination of a **dry marrow tap** and **tear drop cells (dacrocytes)** on a peripheral smear is a classic presentation of **Primary Myelofibrosis (PMF)** [1]. **1. Why Myelofibrosis is correct:** In Myelofibrosis, there is extensive deposition of collagen (fibrosis) in the bone marrow, stimulated by cytokines like TGF-β released from neoplastic megakaryocytes [1, 2]. This fibrosis makes the marrow rigid, resulting in a **"dry tap"** (failure to aspirate marrow). As red blood cells attempt to squeeze through the fibrotic marrow and the distorted vasculature of the spleen (extramedullary hematopoiesis), they undergo mechanical stretching, resulting in **tear drop cells (dacrocytes)** [2]. **2. Why other options are incorrect:** * **Leukemia:** While some leukemias (like Hairy Cell Leukemia) can cause a dry tap, the hallmark of leukemia is the presence of blasts. Tear drop cells are not a characteristic feature. * **Lymphoma:** Lymphoma primarily involves lymph nodes. While it can infiltrate the marrow, it rarely causes a dry tap or significant dacrocytosis unless secondary fibrosis occurs. * **Polycythemia Rubra Vera (PRV):** PRV is characterized by an increased red cell mass (panmyelosis). While it can progress to a "spent phase" (post-polycythemic myelofibrosis), the primary diagnosis for the described classic triad is Myelofibrosis [3]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Leukoerythroblastic Picture:** The presence of immature RBCs (nucleated) and immature WBCs in the peripheral smear is highly suggestive of myelofibrosis [2]. * **Splenomegaly:** PMF often presents with massive splenomegaly due to extramedullary hematopoiesis [1, 2]. * **JAK2 Mutation:** Present in approximately 50-60% of PMF cases [1]. * **Silver Stain:** Reticulin stain is used to grade the severity of marrow fibrosis. * **Other causes of Dry Tap:** Hairy cell leukemia, Aplastic anemia, and Metastatic carcinoma to the bone. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, 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. 628-629. [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. 627-628.

Question 648: Which one of the following platelet counts is usually associated with an increased incidence of spontaneous bleeding?

A. Greater than 80,000/mm³
B. 40,000/mm³
C. 20,000/mm³
D. Less than 20,000/mm³ (Correct Answer)

Explanation: **Explanation:** The risk of bleeding in thrombocytopenia is inversely proportional to the platelet count. The correct answer is **Less than 20,000/mm³** because this threshold represents the critical level where the body’s primary hemostatic mechanisms are severely compromised, leading to **spontaneous bleeding** (bleeding without preceding trauma) [2]. * **Why D is correct:** While the normal platelet count is 1.5–4.5 lakh/mm³, clinical symptoms usually do not manifest until levels drop significantly. At counts **<20,000/mm³**, patients are at high risk for spontaneous petechiae, ecchymoses, and life-threatening intracranial or gastrointestinal hemorrhages [1], [2]. This is the standard trigger for prophylactic platelet transfusion in many clinical protocols. * **Why A, B, and C are incorrect:** * **>80,000/mm³:** Hemostasis is typically adequate for most surgical procedures. * **40,000/mm³ to 20,000/mm³:** Patients may experience excessive bleeding following **trauma or surgery**, but spontaneous bleeding is uncommon in this range [3]. **Clinical Pearls for NEET-PG:** 1. **Safe Zone:** Platelet counts >50,000/mm³ are generally sufficient to prevent major bleeding during minor surgeries. 2. **Bleeding Time (BT):** In thrombocytopenia, BT is prolonged, but it is not a reliable predictor of bleeding risk compared to the absolute platelet count. 3. **Morphology:** Large platelets (Megathrombocytes) on a peripheral smear suggest peripheral destruction (e.g., ITP) [3], whereas small platelets suggest marrow failure or Wiskott-Aldrich syndrome. 4. **Spontaneous Intracranial Hemorrhage:** The risk becomes extreme when the count falls below **5,000–10,000/mm³** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 665-666. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 619-620. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 666-667.

Question 649: Apheresis is defined as:

A. Selective separation of components of blood (Correct Answer)
B. Preventing blood transfusion infections
C. Separation of platelets from plasma
D. Isolating organisms from mixed culture

Explanation: **Explanation:** **Apheresis** (derived from the Greek word *aphaeresis*, meaning "to take away") is a medical technology in which the blood of a donor or patient is passed through an apparatus that **selectively separates one or more specific components** (such as plasma, platelets, or leukocytes) and returns the remainder to the circulation. * **Why Option A is correct:** The core principle of apheresis is the selective removal of a specific blood constituent based on density or size using centrifugation or membrane filtration. It allows for the collection of large volumes of a single component from a single donor (e.g., Single Donor Platelets). * **Why Option B is incorrect:** While apheresis products are "leukoreduced" (reducing CMV transmission or febrile reactions), the primary definition is the separation process, not infection prevention. * **Why Option C is incorrect:** This describes *Plateletpheresis*, which is merely one specific subtype of apheresis. The term apheresis itself is broader and encompasses the separation of any component (RBCs, WBCs, or Plasma). * **Why Option D is incorrect:** This refers to microbiological techniques (e.g., subculturing), which is unrelated to hematological blood processing. **High-Yield Clinical Pearls for NEET-PG:** 1. **Plasmapheresis:** Used therapeutically in conditions like **Guillain-Barré Syndrome**, **Myasthenia Gravis**, and **TTP** (to remove autoantibodies or toxins). 2. **Leukapheresis:** Indicated in cases of extreme hyperleukocytosis (e.g., AML/CML with leukostasis). 3. **Erythrocytapheresis:** Used in severe Sickle Cell Disease to exchange HbS for HbA. 4. **Anticoagulation:** **Citrate** is the most common anticoagulant used during the apheresis procedure; watch for signs of hypocalcemia in the donor.

Question 650: All of the following cause intravascular hemolysis, except?

A. Mismatched blood transfusion
B. Snake bite
C. Thalassemia (Correct Answer)
D. Paroxysmal Nocturnal Hemoglobinuria (PNH)

Explanation: Hemolysis is classified into two types based on the site of red blood cell (RBC) destruction: **Intravascular** (within the blood vessels) and **Extravascular** (within the splenic sinusoids or liver). [2] **Why Thalassemia is the Correct Answer:** Thalassemia is a classic example of **extravascular hemolysis**. In $\beta$-thalassemia, there is a deficiency of $\beta$-globin chains leading to a relative excess of $\alpha$-chains. These unpaired $\alpha$-chains form insoluble precipitates (Heinz bodies) that damage the RBC membrane. As these deformed cells pass through the splenic cords, they are recognized as abnormal by splenic macrophages and destroyed. This results in splenomegaly, a hallmark of extravascular hemolysis. **Analysis of Incorrect Options:** * **Mismatched Blood Transfusion:** This triggers an acute Type II hypersensitivity reaction. Complement activation leads to the formation of Membrane Attack Complexes (MAC), causing immediate **intravascular** osmotic lysis of donor RBCs. * **Snake Bite:** Certain venoms (e.g., Cobra or Viper) contain phospholipases and hemolysins that directly dissolve RBC membranes within the circulation, causing massive **intravascular** hemolysis. * **PNH:** This is an acquired stem cell defect (PIGA gene mutation) leading to a deficiency of GPI-anchored proteins (CD55/CD59). Without these regulators, the alternative complement pathway causes direct **intravascular** lysis of RBCs, typically at night. [1] **NEET-PG High-Yield Pearls:** * **Intravascular Hemolysis Markers:** Low Haptoglobin, Hemoglobinuria, Hemosiderinuria, and elevated LDH. [2] * **Extravascular Hemolysis Markers:** Splenomegaly and Jaundice (unconjugated hyperbilirubinemia); Hemoglobinuria is usually absent. [2] * **Other Extravascular Causes:** Hereditary Spherocytosis, Sickle Cell Anemia, and Warm Autoimmune Hemolytic Anemia (AIHA). [3] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-651. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 639-640. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603.

Practice by Chapter

Anemias: Classification and Approach

Practice Questions

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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