Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 101: Which of the following statements is true of hereditary spherocytosis (HS)?

A. Pigment-type gallstones are common. (Correct Answer)
B. Diagnosis can be made in the neonatal period easily by examination of a blood film.
C. Intravascular hemolysis is a common feature.
D. Autosomal recessive inheritance is seen in the majority of cases.

Explanation: ### Explanation: Hereditary Spherocytosis (HS) **Correct Answer: A. Pigment-type gallstones are common.** **1. Why Option A is Correct:** Hereditary Spherocytosis is characterized by a defect in red blood cell (RBC) membrane proteins (most commonly **Ankyrin**), leading to the formation of spherical, fragile erythrocytes. These spherocytes are prematurely trapped and destroyed in the **splenic cords (extravascular hemolysis)**. The chronic breakdown of hemoglobin results in a constant state of hyperbilirubinemia (unconjugated) [1]. Over time, the excess bilirubin precipitates in the gallbladder, leading to the formation of **calcium bilirubinate (pigment) gallstones** in up to 50% of patients [2]. **2. Why Other Options are Incorrect:** * **Option B:** Diagnosis in the neonatal period is **difficult**. Normal neonates often have a higher number of physiological spherocytes, making blood film interpretation unreliable. Furthermore, the characteristic osmotic fragility test may yield inconclusive results in newborns. * **Option C:** HS is the classic example of **extravascular hemolysis**. The RBCs are destroyed by splenic macrophages, not within the blood vessels [2]. Therefore, features of intravascular hemolysis (like hemoglobinuria or low haptoglobin) are typically absent. * **Option D:** In approximately **75% of cases**, HS follows an **Autosomal Dominant** inheritance pattern. Autosomal recessive forms exist but are less common and usually present with more severe clinical manifestations. **3. NEET-PG High-Yield Pearls:** * **Most common molecular defect:** Ankyrin (followed by Band 3 and Spectrin). * **Gold Standard Test:** Eosin-5-maleimide (EMA) binding test (Flow cytometry). * **Classic Lab Findings:** Increased **MCHC** (>36 g/dL), increased RDW, and a positive Osmotic Fragility Test [2]. * **Treatment of Choice:** Splenectomy (indicated in moderate to severe cases, usually deferred until after age 6 to reduce sepsis risk) [2]. Post-splenectomy, **Howell-Jolly bodies** appear on the blood film. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 640. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598.

Question 102: Which of the following is NOT an intrinsic cause of hemolytic anemia?

A. G6PD deficiency
B. Hereditary spherocytosis
C. Hypersplenism (Correct Answer)
D. Pyruvate kinase deficiency

Explanation: **Explanation:** Hemolytic anemias are broadly classified into **Intrinsic (Intracorpuscular)** and **Extrinsic (Extracorpuscular)** causes. **Why Hypersplenism is the correct answer:** Hypersplenism is an **extrinsic** cause of hemolysis. In this condition, the red blood cells (RBCs) themselves are structurally and enzymatically normal, but they are prematurely destroyed or sequestered due to an overactive or enlarged spleen. The pathology lies in the environment surrounding the RBC, not within the cell itself. **Analysis of incorrect options (Intrinsic Causes):** * **G6PD Deficiency:** An X-linked recessive **enzymopathy** where the RBC lacks protection against oxidative stress, leading to intrinsic hemolysis [1]. * **Hereditary Spherocytosis:** A **membranopathy** caused by defects in anchor proteins (like Ankyrin or Spectrin), making the RBC intrinsically fragile [1]. * **Pyruvate Kinase Deficiency:** The most common glycolytic pathway **enzymopathy**, leading to ATP depletion and rigid RBCs that are destroyed intrinsically. **NEET-PG High-Yield Pearls:** 1. **The Rule of Thumb:** Almost all intrinsic hemolytic anemias are **hereditary** (G6PD, Spherocytosis, Sickle Cell), with the notable exception of **Paroxysmal Nocturnal Hemoglobinuria (PNH)**, which is acquired. 2. **Extrinsic Causes:** These are usually **acquired** and include Microangiopathic Hemolytic Anemia (MAHA), Autoimmune Hemolytic Anemia (AIHA), infections (Malaria), and Hypersplenism [3]. 3. **G6PD Key Finding:** Look for **Heinz bodies** (denatured hemoglobin) and **Bite cells** (degmacytes) on a peripheral smear [1]. 4. **Hereditary Spherocytosis Key Test:** The **Osmotic Fragility Test** is the classic diagnostic tool [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. 640-643. [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. 602-603.

Question 103: Bone infarcts are seen in which of the following conditions?

A. Iron deficiency anemia
B. Thalassemia
C. Sickle cell anemia (Correct Answer)
D. Hereditary spherocytosis

Explanation: **Sickle Cell Anemia (SCA)** is the correct answer due to the fundamental pathophysiology of the disease [1]. In SCA, a point mutation (Glu → Val at the 6th position of the β-globin chain) leads to the formation of HbS [2]. Under conditions of hypoxia, acidosis, or dehydration, HbS polymerizes, causing RBCs to adopt a "sickle" shape [2]. These rigid cells increase blood viscosity and adhere to the vascular endothelium, leading to **Vaso-occlusive Crises (VOC)**. When this occurs in the microvasculature of the bone marrow, it results in **bone infarction** (osteonecrosis) [1]. Common sites include the femoral head (leading to Avascular Necrosis) and the small bones of the hands and feet (Hand-Foot Syndrome/Dactylitis) [3]. **Why other options are incorrect:** * **Iron Deficiency Anemia:** This is a microcytic hypochromic anemia caused by lack of iron. It affects hemoglobin synthesis but does not cause vascular occlusion or tissue infarction. * **Thalassemia:** While this involves ineffective erythropoiesis and massive marrow expansion (leading to "crew-cut" appearance on X-ray), it is not characterized by vaso-occlusion or bone infarcts [4]. * **Hereditary Spherocytosis:** This is a membrane defect (spectrin/ankyrin deficiency) leading to extravascular hemolysis in the spleen. It does not involve the sickling mechanism required for vascular infarction. **High-Yield Clinical Pearls for NEET-PG:** * **Fish-mouth vertebra:** A classic radiological sign in SCA caused by chronic bone infarctions of the vertebral endplates. * **Salmonella Osteomyelitis:** Patients with SCA are uniquely predisposed to *Salmonella* bone infections due to functional asplenia and gut infarctions. * **Autosplenectomy:** Repeated splenic infarcts in SCA lead to a shrunken, fibrotic spleen (Howell-Jolly bodies seen on peripheral smear) [3], [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 652-654. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 645-646. [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 104: Which of the following is NOT true about follicular lymphoma?

A. CD20 positive
B. CD5 positive (Correct Answer)
C. BC1-1 positive in follicular lymphoma whereas BCL-2 positive in mantle cell lymphoma
D. Translocation of (14:18)

Explanation: **Follicular Lymphoma (FL)** is a common low-grade B-cell non-Hodgkin lymphoma derived from germinal center B-cells [1], [2]. Understanding its immunophenotype and genetics is crucial for NEET-PG. ### **Explanation of the Correct Answer** * **Option B (CD5 positive) is NOT true:** CD5 is a T-cell marker that is aberrantly expressed in specific B-cell malignancies, namely **Mantle Cell Lymphoma (MCL)** and **Small Lymphocytic Lymphoma (SLL/CLL)** [3], [4]. Follicular Lymphoma is characteristically **CD5 negative**. ### **Analysis of Other Options** * **Option A (CD20 positive):** FL is a B-cell neoplasm; therefore, it strongly expresses pan-B-cell markers like CD19, CD20, and CD79a [3]. * **Option C (BCL-2 vs. BCL-1):** This option highlights a key diagnostic distinction. FL is characterized by **BCL-2 protein overexpression** (which inhibits apoptosis) [1], [2]. In contrast, Mantle Cell Lymphoma is characterized by **BCL-1 (Cyclin D1)** overexpression [3]. * **Option D (t(14;18)):** This is the cytogenetic hallmark of FL. The translocation moves the *BCL-2* gene (chromosome 18) to the *IgH* locus (chromosome 14), leading to constitutive expression of the anti-apoptotic BCL-2 protein [1], [2]. ### **High-Yield Clinical Pearls for NEET-PG** * **Immunophenotype:** FL is CD10+, BCL-2+, BCL-6+, and **CD5- / CD23-**. * **Morphology:** Shows a nodular/follicular growth pattern [1]. Unlike reactive follicles, neoplastic follicles in FL **lack tingible body macrophages** and have a narrowed or absent mantle zone [1], [2]. * **Grading:** Based on the number of **centroblasts** per high-power field (Mann and Berard system). * **Transformation:** FL can transform into a more aggressive **Diffuse Large B-Cell Lymphoma (DLBCL)**, known as Richter’s transformation (though this term is more commonly used for CLL). **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. 602-604. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 561-562. [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. 610-612. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 562-563.

Question 105: All of the following are major complications of massive blood transfusion except?

A. Hyperthermia (Correct Answer)
B. Hyperkalemia
C. Coagulopathy
D. Hypocalcemia

Explanation: **Explanation:** Massive blood transfusion (MBT) is defined as the replacement of one total blood volume within 24 hours or 10 units of PRBCs within 24 hours. The correct answer is **Hyperthermia** because MBT typically causes **Hypothermia**, not hyperthermia. **1. Why Hyperthermia is the Exception:** Blood products are stored at 1–6°C. Rapid infusion of large volumes of cold blood overwhelms the body’s thermoregulatory mechanisms, leading to **hypothermia**. This can shift the oxygen-dissociation curve to the left and worsen coagulopathy. **2. Analysis of Other Options:** * **Hyperkalemia (B):** During storage, RBCs undergo a "storage lesion" where intracellular potassium leaks into the plasma due to the failure of the Na+/K+ ATPase pump at low temperatures. Infusing old blood rapidly leads to elevated serum potassium. * **Coagulopathy (C):** This occurs due to "dilutional thrombocytopenia" and a deficiency of labile clotting factors (Factors V and VIII), which are not present in stored PRBCs [1]. [2] * **Hypocalcemia (D):** Citrate is used as an anticoagulant in blood bags. In MBT, the liver cannot metabolize the excess citrate quickly enough. Citrate binds to the patient's ionized calcium, leading to hypocalcemia (Citrate toxicity). **Clinical Pearls for NEET-PG:** * **Acid-Base Balance:** MBT initially causes **metabolic acidosis** (due to the acidic preservative and lactic acid in stored blood) but later results in **metabolic alkalosis** as citrate is metabolized into bicarbonate. * **2,3-DPG:** Stored blood has depleted 2,3-DPG, causing a **left shift** in the oxygen-dissociation curve (increased O2 affinity, decreased delivery to tissues). * **TRALI:** The leading cause of transfusion-related fatalities. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 628-631. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626.

Question 106: What is the cause of congestive splenomegaly?

A. Visceral Leishmaniasis
B. Budd-Chiari Syndrome (Correct Answer)
C. Gaucher's Disease
D. Hodgkin's Lymphoma

Explanation: **Explanation:** **Congestive splenomegaly** occurs when there is chronic venous outflow obstruction, leading to increased pressure in the splenic vein (portal hypertension). This back-pressure causes the splenic sinusoids to become engorged with blood, eventually leading to fibrosis [1] and the formation of **Gamna-Gandy bodies** (siderofibrotic nodules). * **Why Budd-Chiari Syndrome is correct:** This syndrome involves the obstruction of hepatic venous outflow (at the level of hepatic veins or the inferior vena cava) [3]. This leads to post-hepatic portal hypertension, which directly causes passive congestion of the spleen [2]. Other common causes include cirrhosis and right-sided heart failure. **Analysis of Incorrect Options:** * **Visceral Leishmaniasis (Kala-azar):** Causes massive splenomegaly primarily due to **hyperplasia of the mononuclear phagocytic system** (reticuloendothelial hyperplasia) as macrophages become laden with Amastigote forms (LD bodies). * **Gaucher’s Disease:** This is a lysosomal storage disorder where the accumulation of glucocerebroside in "Gaucher cells" leads to **infiltrative splenomegaly**. * **Hodgkin’s Lymphoma:** Splenomegaly here is due to **neoplastic infiltration** by Reed-Sternberg cells and associated inflammatory cells. **NEET-PG High-Yield Pearls:** 1. **Gamna-Gandy Bodies:** Small, brown nodules containing iron and calcium deposits in the splenic connective tissue; pathognomonic for chronic congestive splenomegaly. 2. **Massive Splenomegaly (>1000g):** Classically seen in Chronic Myeloid Leukemia (CML), Myelofibrosis, Visceral Leishmaniasis, and Malaria [1]. 3. **Splenic Infarcts:** Common in massive splenomegaly; typically appear as wedge-shaped, pale areas (subcapsular) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 632-634. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 834-835. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 869-870.

Question 107: Howell-Jolly bodies may be seen after which procedure?

A. Hepatectomy
B. Splenectomy (Correct Answer)
C. Pancreatectomy
D. Cholecystectomy

Explanation: **Explanation:** **Howell-Jolly bodies** are small, round, basophilic nuclear remnants (clusters of DNA) found inside circulating erythrocytes [1]. **1. Why Splenectomy is the Correct Answer:** Under normal physiological conditions, during the maturation of red blood cells in the bone marrow, the nucleus is expelled. However, small fragments of DNA sometimes remain. As these cells pass through the splenic sinusoids, the **splenic macrophages** identify and remove these inclusions via a process known as "pitting" [1]. Following a **splenectomy** (or in cases of functional asplenia, such as Sickle Cell Anemia), this filtering mechanism is lost, allowing erythrocytes with Howell-Jolly bodies to persist in the peripheral circulation [2]. **2. Why Other Options are Incorrect:** * **Hepatectomy:** While the liver contains Kupffer cells (macrophages), it does not possess the specialized "pitting" microcirculation of the splenic cords required to remove nuclear remnants. * **Pancreatectomy & Cholecystectomy:** These procedures involve the removal of organs belonging to the endocrine/digestive systems. Neither the pancreas nor the gallbladder plays a role in erythrocyte "quality control" or the removal of intracellular inclusions. **3. NEET-PG High-Yield Pearls:** * **Stain:** Howell-Jolly bodies are visible on routine **Wright-Giemsa** or **Leishman** stains. * **Differential Diagnosis:** They must be distinguished from **Heinz bodies** (denatured hemoglobin), which require **Supravital stains** (e.g., Crystal Violet) to be visualized. * **Clinical Significance:** Their presence on a peripheral smear is a hallmark of **asplenia** or **hyposplenism** [1]. * **Other Post-Splenectomy Findings:** Look for Pappenheimer bodies (iron granules), Heinz bodies, and target cells (codocytes) [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 570-571. [2] 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 108: Which of the following findings is seen in the peripheral smear of a patient who has undergone splenectomy?

A. Howell-Jolly bodies (Correct Answer)
B. Eosinophilia
C. Macrocytosis
D. Thrombocytopenia

Explanation: **Explanation:** The spleen acts as the body’s primary "quality control" organ for erythrocytes. It performs two critical functions: **pitting** (removing inclusions from red cells without destroying the cell) and **culling** (removing aged or deformed cells). **1. Why Howell-Jolly bodies are correct:** Howell-Jolly bodies are small, round, basophilic nuclear remnants (DNA clusters) that normally remain in a small fraction of maturing RBCs [1]. In a healthy individual, the splenic macrophages "pit" these remnants out. Following a splenectomy, this filtration mechanism is lost, allowing RBCs with these inclusions to circulate in the peripheral blood [1]. **2. Analysis of Incorrect Options:** * **Eosinophilia:** Splenectomy typically leads to transient **lymphocytosis and monocytosis**, but not specifically eosinophilia. * **Macrocytosis:** This refers to increased MCV (seen in Vitamin B12/Folate deficiency). Splenectomy does not alter the size of the RBCs, only their morphology (e.g., presence of inclusions). * **Thrombocytopenia:** Post-splenectomy, patients actually develop **thrombocytosis** (increased platelet count). The spleen normally sequesters about one-third of the body's platelets; removing it releases this pool into circulation. **3. High-Yield Clinical Pearls for NEET-PG:** Other characteristic peripheral smear findings post-splenectomy include: * **Pappenheimer bodies:** Siderotic (iron) granules. * **Heinz bodies:** Denatured hemoglobin (seen with supravital stains). * **Target cells (Codocytes):** Due to an increase in the surface area-to-volume ratio. * **Acanthocytes:** Irregularly spiked cells. * **Risk:** Patients are at lifelong risk of **OPSI (Overwhelming Post-Splenectomy Infection)**, primarily from encapsulated organisms like *S. pneumoniae*, *H. influenzae*, and *N. meningitidis* [2]. Vaccination is mandatory [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. 644-645. [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. 631-632.

Question 109: All of the following are true regarding Hereditary Spherocytosis, EXCEPT:

A. Cholesterol gallstones (Correct Answer)
B. Mild to moderate anemia
C. Normocytic anemia
D. Increased MCHC

Explanation: **Explanation:** Hereditary Spherocytosis (HS) is an autosomal dominant disorder caused by defects in red cell membrane proteins (most commonly **Ankyrin**, followed by Spectrin), leading to the formation of spherical, fragile erythrocytes. **Why Option A is the Correct Answer (The Exception):** In HS, there is chronic extravascular hemolysis occurring in the spleen. This results in an excess production of unconjugated bilirubin [1]. Consequently, patients develop **Pigment gallstones (calcium bilirubinate)**, not cholesterol gallstones [1], [2]. Cholesterol stones are typically associated with metabolic factors like obesity or female gender, whereas pigment stones are a hallmark of chronic hemolytic anemias [1]. **Analysis of Other Options:** * **B. Mild to moderate anemia:** Most patients present with a compensated or mild-to-moderate hemolytic state [2]. Severe anemia is rare unless triggered by an aplastic crisis (Parvovirus B19) [2]. * **C. Normocytic anemia:** While cells appear smaller (microspherocytes), the Mean Corpuscular Volume (MCV) is usually within the normal range or slightly low, classifying it as a normocytic anemia [2]. * **D. Increased MCHC:** This is a **high-yield diagnostic marker**. Due to membrane loss and subsequent cellular dehydration, the hemoglobin becomes more concentrated. An MCHC >36 g/dL is highly suggestive of HS. **Clinical Pearls for NEET-PG:** * **Gold Standard Test:** Cryohemolysis test or Eosin-5-maleimide (EMA) binding test (Flow cytometry). * **Screening Test:** Osmotic Fragility Test (increased fragility) [2]. * **Peripheral Smear:** Characterized by microspherocytes (loss of central pallor) [2]. * **Treatment of Choice:** Splenectomy (indicated in moderate to severe cases to reduce hemolysis) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 640. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598.

Question 110: Which of the following is NOT a cause of pancytopenia with hypocellular marrow?

A. Acquired aplastic anemia
B. Fanconi's anaemia
C. Some myelodysplasia
D. Aleukemic leukemia (Correct Answer)

Explanation: Pancytopenia is defined as a reduction in all three peripheral blood cell lines (RBCs, WBCs, and platelets). To differentiate the causes, clinicians look at the bone marrow cellularity. **1. Why Aleukemic Leukemia is the correct answer:** In **Aleukemic Leukemia**, the peripheral blood shows pancytopenia because the abnormal cells (blasts) remain confined to the bone marrow. However, the bone marrow itself is typically **hypercellular** or packed with malignant blasts [1]. It is a "space-occupying" lesion where the marrow is crowded, preventing the release of mature cells into the circulation. This distinguishes it from "hypocellular" causes where the marrow is empty [1]. **2. Analysis of incorrect options (Causes of Hypocellular Marrow):** * **Acquired Aplastic Anemia:** This is the prototype of pancytopenia with a **hypocellular/empty marrow**, where hematopoietic stem cells are replaced by fat cells due to immune-mediated destruction [1], [2]. * **Fanconi’s Anemia:** This is an inherited (autosomal recessive) DNA repair defect leading to progressive bone marrow failure and **hypocellularity** [2]. * **Some Myelodysplastic Syndromes (MDS):** While most MDS cases are hypercellular [3], a specific subtype known as **Hypoplastic MDS** (seen in ~10-15% of cases) presents with pancytopenia and a hypocellular marrow, mimicking aplastic anemia. **Clinical Pearls for NEET-PG:** * **Pancytopenia + Hypercellular Marrow:** Think of Megaloblastic anemia (most common cause in India), Aleukemic leukemia, and most MDS. * **Pancytopenia + Hypocellular Marrow:** Think of Aplastic anemia, Hypoplastic MDS, and Fanconi’s anemia. * **Dry Tap on Bone Marrow Aspiration:** Commonly seen in Myelofibrosis, Hairy Cell Leukemia, and sometimes Aleukemic Leukemia due to packed marrow. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 662-663. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 595-596. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.

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Hemolytic Anemias

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Chronic Leukemias

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Plasma Cell Disorders

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Bleeding Disorders

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Thrombotic Disorders

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