Hematopathology — MCQs

A 17-year-old woman's urine becomes red after being given sulfonamides for a urinary tract infection. Both urine and serum test positive for free hemoglobin, and the urine red cell count is 1.2 million/mm3. A peripheral blood smear shows normocytic and normochromic red cells and a few "bite cells." Deficiency of which of the following substances is most likely responsible for these symptoms?

Q460Medium

The autohemolysis test is positive in which of the following conditions?

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 451: Cold haemagglutinin is associated with which type of antibody?

A. Anti-IgM
B. Anti-IgG
C. Anti-IgA
D. Donath-Landsteiner antibody (Correct Answer)

Explanation: **Explanation:** The question refers to **Paroxysmal Cold Hemoglobinuria (PCH)**, a rare form of autoimmune hemolytic anemia. The hallmark of this condition is the **Donath-Landsteiner antibody**, which is a unique biphasic hemolysin. **Why the correct answer is right:** The Donath-Landsteiner antibody is an **IgG antibody** (specifically anti-P specificity) that exhibits a unique temperature-dependent behavior. It binds to red blood cells (RBCs) at low temperatures (cold phase) and fixes complement. When the blood returns to core body temperature (warm phase), the complement cascade is activated, leading to intravascular hemolysis. Despite being an IgG, it is clinically classified as a "cold" antibody because it requires cold exposure for initial binding. **Why the incorrect options are wrong:** * **Anti-IgM:** While most "Cold Agglutinin Diseases" (associated with *Mycoplasma* or Mononucleosis) involve IgM antibodies, the specific term "Cold haemagglutinin" in the context of classic biphasic hemolysis refers to the Donath-Landsteiner antibody. * **Anti-IgG/Anti-IgA:** Warm Autoimmune Hemolytic Anemia (WAIHA) is typically mediated by IgG (and rarely IgA) that reacts at 37°C [1]. These do not require a cold phase for binding or hemolysis. **High-Yield Clinical Pearls for NEET-PG:** * **PCH Etiology:** Historically associated with late-stage Syphilis; currently more common in children following viral infections (e.g., Measles, Mumps, Flu). * **Specificity:** Donath-Landsteiner antibodies almost always have **Anti-P antigen** specificity. * **Diagnostic Test:** The **Donath-Landsteiner Test** confirms the diagnosis by demonstrating hemolysis only after a sample is chilled and then warmed. * **Comparison:** Remember: **Cold Agglutinin Disease = IgM** (Extravascular); **PCH = IgG/Donath-Landsteiner** (Intravascular). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603.

Question 452: What is the normal platelet count?

A. D1C
B. Shaken baby syndrome (Correct Answer)
C. Microangiopathic hemolytic anaemia
D. Splenomegaly

Explanation: The question asks for a condition associated with a specific clinical presentation (implied by the options, despite the phrasing "normal platelet count"). In the context of pediatric pathology and forensic medicine, **Shaken Baby Syndrome (SBS)**, now often referred to as Abusive Head Trauma (AHT), is a critical high-yield topic. ### **Explanation of the Correct Answer** **Shaken Baby Syndrome (B)** is characterized by a classic clinical triad: **subdural hemorrhage, retinal hemorrhages, and encephalopathy (brain swelling).** While these patients may present with bruising or intracranial bleeding [2], their **platelet count and coagulation profile are typically normal.** This is a crucial diagnostic point used to rule out medical causes of bleeding, such as idiopathic thrombocytopenic purpura (ITP) or hemophilia, thereby pointing toward non-accidental trauma [1]. ### **Analysis of Incorrect Options** * **DIC (A):** Disseminated Intravascular Coagulation is a consumptive coagulopathy. It is characterized by a **low platelet count** (thrombocytopenia), prolonged PT/aPTT, and decreased fibrinogen [3]. * **Microangiopathic Hemolytic Anaemia (C):** MAHA (seen in HUS or TTP) involves the mechanical destruction of RBCs and the consumption of platelets in microthrombi, leading to significant **thrombocytopenia** [3]. * **Splenomegaly (D):** An enlarged spleen leads to **sequestration** of platelets. Up to 90% of the body's platelets can be trapped in an enlarged spleen, resulting in a low peripheral platelet count. ### **High-Yield Clinical Pearls for NEET-PG** * **The Triad of SBS:** Subdural hematoma, Retinal hemorrhage, and Diffuse axonal injury/Cerebral edema. * **Radiology:** Look for "metaphyseal corner fractures" (bucket-handle fractures) and posterior rib fractures, which are highly specific for child abuse. * **Normal Lab Values:** In suspected child abuse, always check CBC and Coagulation profile; a **normal platelet count** and **normal PT/aPTT** help exclude systemic bleeding disorders [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. 665-667. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 132. [3] 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 453: Cryoprecipitate is rich in which of the following factors?

A. Factor II
B. Factor V
C. Factor VII
D. Factor VIII (Correct Answer)

Explanation: **Explanation:** Cryoprecipitate is the cold-insoluble fraction of plasma obtained by thawing fresh frozen plasma (FFP) at 1–6°C. It is a concentrated source of specific coagulation proteins. **Why Factor VIII is correct:** Cryoprecipitate is specifically enriched with five key components: **Factor VIII** (anti-hemophilic factor), **Von Willebrand Factor (vWF)**, **Fibrinogen** (Factor I), **Factor XIII**, and **Fibronectin**. It contains approximately 80–120 units of Factor VIII per bag, making it a traditional treatment for Hemophilia A and Von Willebrand disease (though recombinant factors are now preferred). **Why other options are incorrect:** * **Factor II (Prothrombin), Factor VII, and Factor IX:** These are Vitamin K-dependent factors. They remain in the supernatant (cryo-poor plasma) during the thawing process and are not concentrated in the cryoprecipitate. These factors are best replaced using **Prothrombin Complex Concentrate (PCC)** or **FFP**. * **Factor V:** This is a labile factor found in FFP but is not significantly concentrated in cryoprecipitate. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Indication:** Currently, the most common clinical use of cryoprecipitate is **hypofibrinogenemia** (e.g., in DIC or massive hemorrhage) because it provides a high concentration of Fibrinogen in a small volume. * **Storage:** It is stored at **-18°C or colder** and has a shelf life of 1 year. Once thawed, it must be transfused within 6 hours (or 4 hours if pooled). * **Dosage:** One unit of cryoprecipitate typically raises the fibrinogen level by 5–10 mg/dL in an average adult. * **Mnemonic:** Remember **"8-1-13-vWF"** (Factors 8, 1, 13, and vWF).

Question 454: All of the following are true of beta-thalassemia major, except?

A. Splenomegaly
B. Target cells on peripheral smear
C. Microcytic hypochromic anemia
D. Increased osmotic fragility (Correct Answer)

Explanation: **Explanation:** In **$\beta$-thalassemia major**, there is a total or near-total deficiency of $\beta$-globin chain synthesis, leading to an excess of unpaired $\alpha$-chains [1]. These $\alpha$-chains precipitate, causing ineffective erythropoiesis and hemolysis [1]. **Why "Increased Osmotic Fragility" is the Correct (False) Statement:** In thalassemia, the red blood cells (RBCs) are microcytic and hypochromic, meaning they have a **decreased** volume-to-surface area ratio (they are "flatter"). Because these cells have "extra" membrane relative to their hemoglobin content, they can withstand more fluid influx before bursting. Therefore, $\beta$-thalassemia major is characterized by **decreased osmotic fragility**. *Note: Increased osmotic fragility is a hallmark of Hereditary Spherocytosis.* **Analysis of Incorrect Options:** * **A. Splenomegaly:** This is a classic feature. It occurs due to both extramedullary hematopoiesis and the sequestration/destruction of damaged RBCs by the splenic macrophages [1]. * **B. Target Cells:** These are characteristic of thalassemia. They form because the reduction in hemoglobin creates a redundant cell membrane that bunches up in the center, resembling a "bullseye." * **C. Microcytic Hypochromic Anemia:** This is the fundamental morphological finding in thalassemia due to defective hemoglobin synthesis [2]. **High-Yield Clinical Pearls for NEET-PG:** * **X-ray finding:** "Crew-cut" or "Hair-on-end" appearance of the skull due to compensatory marrow expansion [1]. * **Hb Electrophoresis:** Shows markedly increased **HbF** (up to 90%) and variable HbA2, with little to no HbA [1]. * **Mentzer Index:** (MCV/RBC count) < 13 suggests Thalassemia; > 13 suggests Iron Deficiency Anemia. * **Complication:** Secondary hemochromatosis (iron overload) due to repeated transfusions is a major cause of mortality [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. 648-649. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 590-591.

Question 455: Spherocytosis in a peripheral blood smear is seen in which of the following conditions?

A. Post-transfusion reactions
B. Hereditary spherocytosis
C. Hemolytic disease of the newborn
D. All of the above (Correct Answer)

Explanation: **Explanation:** Spherocytes are erythrocytes that are spherical rather than biconcave, appearing smaller, denser, and lacking central pallor on a peripheral smear [2]. They form when a portion of the red cell membrane is lost, forcing the cell to adopt the minimum surface area for its volume [1], [3]. **Analysis of Options:** * **Hereditary Spherocytosis (HS):** This is the classic cause. Genetic defects in membrane proteins (Ankyrin, Spectrin, or Band 3) lead to vertical instability of the lipid bilayer [3]. This results in the shedding of membrane vesicles, creating spherical cells that are sequestered and destroyed in the spleen [3]. * **Post-transfusion Reactions:** In delayed hemolytic transfusion reactions or ABO incompatibility, recipient antibodies coat donor RBCs. Splenic macrophages "nibble" away the antibody-coated membrane (partial phagocytosis), resulting in spherocyte formation [1]. * **Hemolytic Disease of the Newborn (HDN):** Specifically in **ABO incompatibility** (Mother O, Baby A or B), maternal IgG antibodies cross the placenta and bind to fetal RBCs. Similar to transfusion reactions, splenic macrophages remove portions of the membrane, leading to prominent spherocytosis [1]. (Note: Spherocytes are rare in Rh incompatibility). **Conclusion:** Since all three conditions involve the loss of RBC membrane surface area leading to a spherical shape, **Option D** is correct. **High-Yield Clinical Pearls for NEET-PG:** * **MCHC:** Spherocytosis is the only condition where Mean Corpuscular Hemoglobin Concentration (MCHC) is typically **increased** (>36 g/dL). * **Diagnostic Test:** The **Osmotic Fragility Test** is increased in HS [2]. The most specific modern test is the **EMA Binding test** (Flow cytometry). * **Coombs Test:** Used to differentiate causes. HS is **Coombs negative**, while Immune-mediated causes (Transfusion reactions, HDN, AIHA) are **Coombs positive**. * **Other causes:** Spherocytes are also seen in Thermal injury (burns), Clostridial sepsis, and Snake venom poisoning. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 602-603. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641.

Question 456: Necrotizing ragged ulceration with no apparent inflammatory response is indicative of which of the following conditions?

A. Leukocytosis
B. Polycythemia vera
C. Sickle cell anemia
D. Agranulocytosis (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Agranulocytosis** **Mechanism and Pathophysiology:** Agranulocytosis is characterized by a severe reduction in the number of circulating granulocytes (neutrophils, basophils, and eosinophils), typically with a neutrophil count below **500 cells/µL**. Neutrophils are the primary mediators of the acute inflammatory response and are essential for containing bacterial and fungal infections. In the absence of these cells, the body cannot mount a typical inflammatory reaction (which usually involves pus formation and localized swelling). Consequently, infections—most commonly in the oral cavity (gingiva, floor of the mouth, or pharynx)—manifest as deep, **necrotizing, ragged ulcers**. These ulcers are covered by gray-green or black necrotic membranes but, crucially, show **no apparent inflammatory response** (lack of leukocytic infiltration) on histopathology. **Analysis of Incorrect Options:** * **A. Leukocytosis:** This refers to an *increase* in white blood cell count [1]. This would typically result in a robust inflammatory response and pus formation at the site of infection. * **B. Polycythemia Vera:** This is a myeloproliferative neoplasm characterized by an excess of red blood cells. While it increases blood viscosity and risk of thrombosis, it does not inherently cause necrotizing ulcers without inflammation. * **C. Sickle Cell Anemia:** While patients are prone to infections (due to autosplenectomy) and chronic leg ulcers, these ulcers are usually ischemic in nature and do not present with the specific "ragged necrotizing" pattern devoid of inflammation characteristic of agranulocytosis. **High-Yield Clinical Pearls for NEET-PG:** * **Common Causes:** Most frequently drug-induced (e.g., Clozapine, Carbamazepine, Propylthiouracil, and Methimazole) [2]. * **Clinical Presentation:** Patients often present with "Agranulocytic Angina"—severe necrotizing sore throat and high-grade fever. * **Morphology:** The most striking feature is the presence of overwhelming bacterial colonies (due to lack of host defense) at the site of ulceration. * **Treatment:** Immediate withdrawal of the offending drug and administration of G-CSF (Granulocyte Colony-Stimulating Factor). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 592. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 590-592.

Question 457: ADAMTS13 deficiency is associated with which disease?

A. Immune Thrombocytopenic Purpura (ITP)
B. Thrombotic Thrombocytopenic Purpura (TTP) (Correct Answer)
C. Hemolytic Uremic Syndrome (HUS)
D. Paroxysmal Nocturnal Hemoglobinuria (PNH)

Explanation: **Explanation:** **Thrombotic Thrombocytopenic Purpura (TTP)** is caused by a deficiency of **ADAMTS13**, a metalloproteinase responsible for cleaving large von Willebrand Factor (vWF) multimers [1]. When ADAMTS13 is deficient (due to autoantibodies or genetic mutations), "ultra-large" vWF multimers persist in the circulation [1]. These multimers cause spontaneous platelet aggregation and microthrombi formation, leading to microangiopathic hemolytic anemia (MAHA) and consumptive thrombocytopenia. **Analysis of Incorrect Options:** * **Immune Thrombocytopenic Purpura (ITP):** Caused by anti-platelet antibodies (usually against GpIIb/IIIa) leading to splenic destruction of platelets. ADAMTS13 levels are normal. * **Hemolytic Uremic Syndrome (HUS):** While clinically similar to TTP, classic HUS is caused by **Shiga toxin** (from *E. coli* O157:H7), which damages endothelial cells [1]. ADAMTS13 levels are typically normal [1]. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** A stem cell disorder caused by a mutation in the **PIGA gene**, leading to a deficiency of GPI-anchored proteins (CD55/CD59) and complement-mediated hemolysis. **High-Yield Clinical Pearls for NEET-PG:** * **The TTP Pentad:** Fever, Anemia (MAHA), Thrombocytopenia, Neurological symptoms, and Renal failure (Mnemonic: **FAT RN**) [1]. * **Diagnosis:** Schistocytes (fragmented RBCs) on peripheral smear and reduced ADAMTS13 activity (<10%). * **Treatment:** **Plasmapheresis (Plasma Exchange)** is the gold standard as it removes antibodies and replenishes ADAMTS13. * **Note:** PT and APTT are usually **normal** in TTP/HUS, distinguishing them from DIC. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 947-948.

Question 458: Which of the following is NOT included in the myeloproliferative neoplasms?

A. Angiogenic myeloid metaplasia
B. Thrombocythemia
C. Erythroleukemia (Correct Answer)
D. Megaloblastic hyperplasia

Explanation: **Explanation:** The **Myeloproliferative Neoplasms (MPNs)** are a group of clonal hematopoietic stem cell disorders characterized by the proliferation of one or more myeloid lineages (erythroid, granulocytic, or megakaryocytic) with relatively normal maturation [1]. **Why Erythroleukemia is the Correct Answer:** **Erythroleukemia (AML-M6)** is classified under **Acute Myeloid Leukemia (AML)**, not MPNs. While MPNs involve the overproduction of mature, functional cells, AML is characterized by a "maturation arrest," leading to the accumulation of immature **blasts** (≥20% in bone marrow). Erythroleukemia specifically involves a neoplastic proliferation of erythroid precursors. **Analysis of Other Options:** * **A. Angiogenic Myeloid Metaplasia:** This is an older term for **Primary Myelofibrosis (PMF)** [2]. It is a classic MPN characterized by marrow fibrosis and extramedullary hematopoiesis (myeloid metaplasia) [1]. * **B. Thrombocythemia:** Specifically **Essential Thrombocythemia (ET)**, this is a classic MPN characterized by a sustained increase in platelet count and megakaryocytic hyperplasia in the bone marrow [1], [2]. * **D. Megaloblastic Hyperplasia:** While this term usually refers to Vitamin B12/Folate deficiency, in the context of older nomenclature for MPNs (like Di Guglielmo syndrome), it was sometimes associated with the erythroid phase of myeloproliferative processes. However, in modern MCQ patterns, if the question implies "Polycythemia Vera" or "Myeloid metaplasia" variants, the other three are traditionally grouped as MPNs, whereas Erythroleukemia is strictly an AML. **NEET-PG High-Yield Pearls:** 1. **Classic MPNs:** Chronic Myeloid Leukemia (CML), Polycythemia Vera (PV), Essential Thrombocythemia (ET), and Primary Myelofibrosis (PMF) [2]. 2. **Genetic Markers:** **JAK2 V617F** mutation is seen in >95% of PV cases and ~50-60% of ET and PMF [2]. CML is defined by the **Philadelphia chromosome t(9;22)** [2]. 3. **Transformation:** MPNs have a high risk of transforming into **Acute Myeloid Leukemia** (Blast Crisis). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615. [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. 624.

Question 459: A 17-year-old woman's urine becomes red after being given sulfonamides for a urinary tract infection. Both urine and serum test positive for free hemoglobin, and the urine red cell count is 1.2 million/mm3. A peripheral blood smear shows normocytic and normochromic red cells and a few "bite cells." Deficiency of which of the following substances is most likely responsible for these symptoms?

A. Alpha-chain of hemoglobin
B. Beta-chain of hemoglobin
C. Glucose-6-phosphate dehydrogenase (Correct Answer)
D. Glycoprotein IIb/IIIa

Explanation: **Explanation:** The clinical presentation of acute hemolysis (red urine, hemoglobinuria, and hemoglobinemia) triggered by **sulfonamides** in a young patient is a classic manifestation of **Glucose-6-phosphate dehydrogenase (G6PD) deficiency**. [1] **1. Why G6PD Deficiency is Correct:** G6PD is the rate-limiting enzyme in the pentose phosphate pathway, responsible for producing **NADPH**. NADPH is essential for maintaining a pool of reduced **glutathione**, which protects red blood cells (RBCs) from oxidative stress. [2] When exposed to oxidative triggers like sulfonamides, fava beans, or infections, hemoglobin precipitates into **Heinz bodies**. As these cells pass through the splenic sinusoids, macrophages pluck out these inclusions, resulting in the characteristic **"bite cells"** seen on the peripheral smear. [1] **2. Why the Other Options are Incorrect:** * **Options A & B (Alpha/Beta-chains):** Deficiencies in hemoglobin chains lead to **Thalassemias**. [2] These typically present with microcytic hypochromic anemia and target cells, not acute episodic hemolysis triggered by drugs. * **Option D (Glycoprotein IIb/IIIa):** This is a surface receptor on platelets required for aggregation. Deficiency leads to **Glanzmann Thrombasthenia**, a bleeding disorder characterized by mucosal bleeding and a normal platelet count, not hemolysis. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked recessive (more common in males; females are usually asymptomatic carriers unless skewed lyonization occurs). * **Morphology:** Heinz bodies (Supravital stains like Crystal Violet) and Bite cells (Degmacytes). [1] * **Triggers:** SSS (Sulfonamides, Septra/TMP-SMX, Sepsis), Antimalarials (Primaquine), and Fava beans. * **Timing:** Hemolysis typically occurs 2–3 days after exposure. [1] * **Diagnosis:** Enzyme assays should not be performed during an acute episode, as young reticulocytes have higher G6PD levels, potentially yielding a false-normal result. [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. 642-643. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638.

Question 460: The autohemolysis test is positive in which of the following conditions?

A. Beta thalassemia
B. Hereditary spherocytosis (Correct Answer)
C. Vitamin E deficiency
D. Sickle cell disease

Explanation: ### Explanation **Hereditary Spherocytosis (HS)** is the correct answer because the autohemolysis test is a classic diagnostic tool for this condition. In HS, a defect in red cell membrane proteins (like spectrin or ankyrin) leads to a decreased surface-area-to-volume ratio [1]. When these cells are incubated at 37°C for 48 hours, they lose membrane lipids more rapidly than normal cells, leading to increased fragility and spontaneous lysis (**autohemolysis**). A key diagnostic feature is that this hemolysis is **significantly corrected by the addition of glucose**, as the cells require ATP to fuel the cation pumps that maintain osmotic stability. **Why the other options are incorrect:** * **Beta Thalassemia:** This is a quantitative defect in globin chain synthesis. While osmotic fragility may be altered (usually decreased due to target cells), the autohemolysis test is not a standard or positive diagnostic feature. * **Vitamin E Deficiency:** This leads to oxidative stress and hemolytic anemia (especially in neonates), but it does not show the characteristic glucose-corrected autohemolysis seen in membrane defects like HS. * **Sickle Cell Disease:** This is caused by a structural hemoglobinopathy (HbS) [3]. While these cells are fragile, the primary pathology is polymerization of hemoglobin under hypoxic conditions, not a primary membrane protein deficiency detectable by the autohemolysis test [3]. **Clinical Pearls for NEET-PG:** * **Gold Standard:** While the autohemolysis test was historically important, the **Eosin-5-maleimide (EMA) binding test** (flow cytometry) is now the preferred screening test for HS. * **Osmotic Fragility Test (OFT):** HS shows *increased* osmotic fragility (cells burst in less hypotonic solutions) [2]. * **Triad of HS:** Anemia, Jaundice, and Splenomegaly. * **Peripheral Smear:** Look for microspherocytes (small, dark RBCs lacking central pallor) and an increased **MCHC** (>36 g/dL) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599.

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Anemias: Classification and Approach

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Hemolytic Anemias

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Myeloproliferative Neoplasms

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Myelodysplastic Syndromes

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Acute Leukemias

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Chronic Leukemias

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Lymphomas and Lymphoid Neoplasms

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Plasma Cell Disorders

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Bleeding Disorders

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Thrombotic Disorders

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