Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1101: A 40-year-old male presented with massive splenomegaly and mild hepatic enlargement. Peripheral blood film shows cells with hair-like projections that are positive for CD25 and CD103, and negative for CD23. What is the likely diagnosis?

A. Precursor B-cell neoplasm
B. Peripheral B-cell neoplasm (Correct Answer)
C. Precursor T-cell neoplasm
D. Peripheral T-cell neoplasm

Explanation: The clinical presentation and immunophenotype described are classic for **Hairy Cell Leukemia (HCL)**. ### **1. Why Option B is Correct** Hairy Cell Leukemia is a mature (peripheral) B-cell neoplasm [2]. The diagnosis is established by: * **Clinical Features:** Massive splenomegaly (due to red pulp infiltration) and "dry tap" on bone marrow aspiration (due to reticulin fibrosis) [1]. * **Morphology:** Lymphocytes with characteristic "hair-like" cytoplasmic projections [1]. * **Immunophenotype:** HCL cells express mature B-cell markers (CD19, CD20, CD22) and specific markers: **CD103** (most specific), **CD25**, **CD11c**, and **Annexin A1**. Since these are mature cells that have exited the bone marrow/thymus, they are classified as **Peripheral B-cell neoplasms** [2]. ### **2. Why Other Options are Incorrect** * **Option A (Precursor B-cell):** These are B-lymphoblastic leukemias/lymphomas (B-ALL). They typically present in children with bone marrow failure and express immature markers like **TdT** and **CD10**, which are absent in HCL [2]. * **Options C & D (T-cell neoplasms):** HCL is of B-lineage. T-cell neoplasms would express markers like CD3, CD4, or CD8. While Hairy Cell Leukemia-Variant (HCL-V) exists, the presence of CD25 and the classic "hairy" morphology strongly point toward the B-cell lineage. ### **3. High-Yield Clinical Pearls for NEET-PG** * **TRAP Stain:** Historically, HCL is positive for Tartrate-Resistant Acid Phosphatase (TRAP), though flow cytometry is now the gold standard. * **BRAF V600E Mutation:** Present in nearly 100% of classic HCL cases. * **Treatment:** Highly sensitive to purine analogs like **Cladribine** (2-CdA). * **Monocytopenia:** A very characteristic laboratory finding in HCL. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 612. [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. 596-598.

Question 1102: Which of the following organ involvements is not commonly observed with CNS involvement in a patient with Diffuse Large B-cell Lymphoma (DLBCL)?

A. Ovary (Correct Answer)
B. Testis
C. Kidney
D. Adrenal

Explanation: In Diffuse Large B-cell Lymphoma (DLBCL), certain extranodal sites are notorious for their association with a high risk of secondary Central Nervous System (CNS) relapse. This clinical pattern is often referred to as "sanctuary site" involvement. **Explanation of the Correct Answer:** * **Ovary (Option A):** While DLBCL can involve the female reproductive tract, the **ovary is not classically associated with a high risk of CNS involvement.** In contrast, the "triad" of high-risk extranodal sites for CNS spread in DLBCL includes the **testis, kidney, and adrenal glands.** Therefore, ovarian involvement does not carry the same prognostic weight for CNS prophylaxis as the other options. **Explanation of Incorrect Options:** * **Testis (Option B):** Primary or secondary testicular DLBCL has the strongest association with CNS relapse (up to 15-20% risk). The blood-testis barrier and blood-brain barrier share similar physiological properties, making both "sanctuary sites" where chemotherapy penetration is poor. * **Kidney & Adrenal (Options C & D):** Involvement of these retroperitoneal organs is a well-documented independent risk factor for CNS dissemination. Patients with renal or adrenal involvement are typically considered for CNS-directed prophylaxis (e.g., intrathecal methotrexate). **High-Yield Clinical Pearls for NEET-PG:** * **CNS-IPI Score:** This is used to predict CNS relapse risk. It includes the 5 standard IPI factors (Age, LDH, Stage, Performance Status, Extranodal sites >1) plus **Kidney/Adrenal involvement.** * **Sanctuary Sites:** Testis and CNS are the primary sanctuary sites in lymphomas due to physiological barriers. * **Most Common Extranodal Site:** The **Stomach** is the most common overall extranodal site for DLBCL, but it does not carry the same high CNS risk as the testis or adrenals. [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. 563-564.

Question 1103: Translocation of the bcr-abl gene is characteristically seen in which of the following conditions?

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

Explanation: The **bcr-abl** fusion gene is the hallmark of **Chronic Myeloid Leukemia (CML)** [1]. It results from a reciprocal translocation between chromosomes 9 and 22, denoted as **t(9;22)(q34;q11)** [1]. This shortened chromosome 22 is famously known as the **Philadelphia (Ph) chromosome** [1]. 1. **Why CML is correct:** The translocation fuses the *ABL1* proto-oncogene (Ch 9) with the *BCR* gene (Ch 22) [2]. This creates a chimeric protein with **constitutive tyrosine kinase activity**, which drives uncontrolled proliferation of the myeloid lineage [2]. It is present in >95% of CML cases. 2. **Why other options are incorrect:** * **Acute Myeloid Leukemia (AML):** While rare variants exist, the classic translocations for AML are t(8;21) in M3 or t(15;17) in APL (PML-RARA). * **Chronic Lymphatic Leukemia (CLL):** Characterized typically by deletions (13q, 11q, 17p) or Trisomy 12, not the bcr-abl translocation. * **Acute Lymphatic Leukemia (ALL):** While t(9;22) occurs in ~25% of adult ALL and ~5% of pediatric ALL, it is not the *characteristic* or defining feature of the disease as it is for CML. In ALL, it signifies a poor prognosis. **High-Yield Clinical Pearls for NEET-PG:** * **Protein Product:** The most common CML variant produces a **p210** protein; the ALL variant often produces a **p190** protein. * **Treatment:** The discovery of bcr-abl led to the development of **Imatinib (Gleevec)**, a tyrosine kinase inhibitor that revolutionized CML therapy. * **Diagnosis:** Gold standard is identifying the translocation via **FISH** or **RT-PCR**. * **Leukocyte Alkaline Phosphatase (LAP) Score:** Characteristically **decreased** in CML (helps differentiate it from a Leukemoid reaction). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 225-226. [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. 624-625.

Question 1104: Pappenheimer bodies are composed of:

A. Copper
B. Iron (Correct Answer)
C. Lead
D. Zinc

Explanation: **Explanation:** **Pappenheimer bodies** are abnormal basophilic granules found in red blood cells. They are composed of **ferritin (iron) aggregates** that have not been incorporated into hemoglobin [1]. 1. **Why Iron is Correct:** Under normal conditions, iron is transported to the mitochondria for heme synthesis. When there is iron overload or impaired utilization (as seen in Sideroblastic anemia), non-heme iron accumulates in the mitochondria. On a peripheral smear stained with **Wright-Giemsa**, these appear as small, irregular, dark-blue granules usually located at the periphery of the cell. Their identity as iron is confirmed using the **Prussian Blue (Perls') stain**, where they are referred to as **Siderotic granules**. 2. **Why Other Options are Incorrect:** * **Copper:** While copper deficiency can lead to sideroblastic-like changes, the bodies themselves are not made of copper. * **Lead:** Lead poisoning inhibits heme synthesis and causes **Basophilic Stippling**, which consists of **ribosomal precipitates (RNA)**, not iron. * **Zinc:** Excess zinc can cause a secondary copper deficiency, but it does not form intra-erythrocytic inclusions. **Clinical Pearls for NEET-PG:** * **Differential Diagnosis:** Pappenheimer bodies are most commonly seen in **Sideroblastic anemia**, **Splenectomy** (due to loss of splenic "pitting"), and **Hemolytic anemias**. * **Staining Distinction:** * **Wright-Giemsa:** Called Pappenheimer bodies. * **Prussian Blue:** Called Siderotic granules. * **Comparison:** Do not confuse with **Howell-Jolly bodies** (DNA remnants) or **Heinz bodies** (Denatured hemoglobin, seen in G6PD deficiency). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 658-659.

Question 1105: All of the following infections may be transmitted by blood transfusion, except?

A. Parvovirus B-19
B. Dengue virus (Correct Answer)
C. Cytomegalovirus
D. Hepatitis G virus

Explanation: **Explanation:** The core concept tested here is the **transmissibility of pathogens via blood products**. For an infection to be routinely transmitted by blood transfusion, the pathogen must have a significant period of asymptomatic viremia in the donor's blood [2]. **Why Dengue Virus is the correct answer:** While Dengue virus causes a high-grade viremia, it is an **acute, symptomatic febrile illness**. Donors are typically symptomatic during the viremic phase, leading to self-exclusion or deferral during pre-donation screening [1]. Furthermore, Dengue is an arbovirus primarily transmitted via the *Aedes aegypti* mosquito; while rare case reports of transfusion-transmitted dengue exist in endemic areas, it is **not** considered a standard transfusion-transmitted infection (TTI) in the context of medical examinations compared to the other options. **Analysis of Incorrect Options:** * **Parvovirus B-19:** This is a small, non-enveloped DNA virus that is highly resistant to inactivation. It is frequently transmitted via blood products (especially clotting factor concentrates) and can cause transient aplastic crisis in recipients with hemolytic anemias. * **Cytomegalovirus (CMV):** CMV resides within leukocytes (monocytes and neutrophils). It is a major TTI, particularly dangerous for immunocompromised recipients and neonates [3]. This is why "leukoreduction" is performed to make blood "CMV-safe." * **Hepatitis G Virus (HGV/GBV-C):** HGV is a flavivirus known to be transmitted via blood and blood products. Although it is often a co-infection with HCV and is generally non-pathogenic, it remains a transmissible agent through transfusion. **High-Yield Clinical Pearls for NEET-PG:** * **Most common infection transmitted by blood transfusion:** Hepatitis B (HBV) is historically significant, but in many modern settings, bacterial contamination (especially *Staphylococcus epidermidis* in platelets) is a more frequent complication. * **CMV Prevention:** Leukocyte depletion (leukoreduction) is the gold standard for preventing CMV transmission. * **Window Period:** The time between infection and the ability of a test to detect it. Nucleic Acid Testing (NAT) has significantly reduced this period for HIV, HBV, and HCV. **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. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 66-67. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 367-368.

Question 1106: Which of the following leukemias is associated with a "convent girl" appearance?

A. Chronic myelogenous leukemia
B. Chronic lymphocytic leukemia (Correct Answer)
C. Hairy cell leukemia
D. Diffuse large B cell lymphoma

Explanation: **Explanation:** **Chronic Lymphocytic Leukemia (CLL)** is the correct answer. The term **"convent girl" appearance** refers to the characteristic morphology of the mature neoplastic lymphocytes seen on a peripheral blood smear. These cells exhibit a dense, clumped chromatin pattern often described as **"soccer-ball" nuclei** [1]. The metaphor "convent girl" (or "monk’s hood") arises because the dark, condensed chromatin is tightly packed, resembling the modest, uniform appearance of students in a convent or the hooded habit of a nun. Additionally, CLL is famously associated with **Smudge cells** (Basket cells), which are fragile lymphocytes that rupture during the preparation of the slide [1]. **Analysis of Incorrect Options:** * **A. Chronic Myelogenous Leukemia (CML):** Characterized by a "myelocyte bulge" and a full spectrum of myeloid cells (neutrophils, metamyelocytes, myelocytes) and basophilia, not the uniform clumped chromatin of CLL [3]. * **C. Hairy Cell Leukemia:** Associated with "hairy" cytoplasmic projections and a **"fried egg" appearance** in bone marrow biopsies, not convent girl morphology [2]. * **D. Diffuse Large B-cell Lymphoma (DLBCL):** Features large, atypical cells with prominent nucleoli and dispersed chromatin, representing a high-grade transformation rather than the mature, condensed appearance of CLL. **High-Yield Clinical Pearls for NEET-PG:** * **Immunophenotype:** CLL is characteristically **CD5+, CD19+, CD20+ (weak), and CD23+** [1]. * **Richter Transformation:** The progression of CLL into DLBCL (occurs in ~5-10% of cases). * **Prognostic Marker:** Deletion 13q (good prognosis); ZAP-70 expression or Unmutated IgVH (poor prognosis). * **Smudge Cells:** Can be minimized by adding a drop of **albumin** to the blood sample before making the smear. **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. 602. [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. 612. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612.

Question 1107: Bone marrow aspiration is not indicated in which of the following conditions?

A. Thalassemia major (Correct Answer)
B. Megaloblastic anemia
C. Idiopathic thrombocytopenic purpura
D. Pure red cell aplasia

Explanation: **Explanation:** The diagnosis of **Thalassemia major** is primarily established through peripheral blood smear examination (showing microcytic hypochromic anemia with target cells and nucleated RBCs [1]) and confirmed via **Hb Electrophoresis or HPLC** (showing high HbF and absent/low HbA [3]). Bone marrow aspiration in Thalassemia merely shows erythroid hyperplasia [2], which is a non-specific finding common to all hemolytic anemias. Therefore, it is not indicated for diagnosis or management. **Analysis of Incorrect Options:** * **Megaloblastic Anemia:** BMA is indicated to demonstrate **megaloblastic erythropoiesis** (sieve-like chromatin) and giant metamyelocytes, especially when the diagnosis is unclear from serum B12/Folate levels. * **Idiopathic Thrombocytopenic Purpura (ITP):** While the diagnosis is clinical, BMA is often performed (especially in elderly or atypical cases) to rule out leukemia and to confirm the presence of **increased or normal megakaryocytes**, ensuring the marrow is functioning despite peripheral destruction. * **Pure Red Cell Aplasia (PRCA):** BMA is essential to confirm the diagnosis by demonstrating a selective and near-complete **absence of erythroid precursors** while granulopoiesis and megakaryocytes remain normal [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Dry Tap on BMA:** Most commonly seen in Myelofibrosis, Hairy Cell Leukemia, and Aplastic Anemia [5]. * **Indications for Bone Marrow Biopsy (Trephine) over Aspiration:** Granulomatous lesions, metastatic deposits, and staging of lymphomas. * **HPLC (High-Performance Liquid Chromatography):** The current "Gold Standard" for diagnosing hemoglobinopathies like Thalassemia and Sickle Cell Anemia. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 600-601. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 648-649. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 648. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 595-596. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 662-663.

Question 1108: Activated protein C resistance disorder is due to inactivation of which factor?

A. Factor 8
B. Factor 5 (Correct Answer)
C. Factor 13
D. Factor 4

Explanation: **Explanation:** **Activated Protein C (APC) Resistance** is most commonly caused by a specific genetic mutation known as **Factor V Leiden** [1]. In a normal physiological state, Protein C is activated to APC, which acts as a natural anticoagulant by degrading and inactivating **Factor Va** and Factor VIIIa. In patients with Factor V Leiden, a point mutation (substitution of arginine by glutamine at position 506) alters the cleavage site on the Factor V molecule. This makes Factor V resistant to inactivation by APC. Consequently, Factor Va remains active in the circulation for longer periods, leading to a hypercoagulable state and an increased risk of venous thromboembolism (VTE) [1]. **Analysis of Incorrect Options:** * **Option A (Factor 8):** While APC does normally inactivate Factor VIIIa, "APC Resistance" specifically refers to the inherited defect in the Factor V molecule that prevents its degradation. * **Option C (Factor 13):** Factor XIII is the fibrin-stabilizing factor responsible for cross-linking fibrin clots. It is not the target of the APC resistance mechanism. * **Option D (Factor 4):** Platelet Factor 4 (PF4) is involved in heparin-induced thrombocytopenia (HIT) and platelet aggregation, but it has no role in the Protein C anticoagulant pathway. **High-Yield Clinical Pearls for NEET-PG:** * **Factor V Leiden** is the **most common** inherited cause of hypercoagulability (thrombophilia) in Caucasians [1]. * **Inheritance:** Autosomal Dominant. * **Screening Test:** Functional APC resistance assay (clotting-based). * **Confirmatory Test:** Genetic testing (PCR) for the G1691A mutation in the Factor V gene. * **Clinical Presentation:** Recurrent Deep Vein Thrombosis (DVT) and pulmonary embolism. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 281-282.

Question 1109: A patient with postpartum hemorrhage had about 2 liters of blood loss. Investigation revealed normal PT and a prolonged aPTT. Which test is used to differentiate between coagulation factor deficiency and a factor inhibitor?

A. Tissue thromboplastin inhibition time
B. Ecarin clotting time
C. Dilute Russel viper venom time
D. Mixing studies (Correct Answer)

Explanation: **Explanation:** The correct answer is **Mixing studies (Option D)**. In a patient with isolated prolonged aPTT (normal PT), the primary differential diagnosis is either a **factor deficiency** (e.g., Factor VIII, IX, XI, or XII) or the presence of a **circulating inhibitor** (e.g., Factor VIII inhibitor or Lupus Anticoagulant) [1]. **Mixing Studies (1:1 Mix):** This test involves mixing the patient's plasma with normal pooled plasma (which contains 100% of all clotting factors). [2] * **Correction:** If the aPTT normalizes, it indicates a **factor deficiency** (as the normal plasma provides the missing factors). [2] * **No Correction:** If the aPTT remains prolonged, it indicates an **inhibitor** (as the inhibitor in the patient's plasma neutralizes the factors in the normal plasma). [2] * *Clinical Context:* In postpartum hemorrhage, the sudden development of an inhibitor (Acquired Hemophilia A/Factor VIII inhibitor) is a rare but life-threatening possibility [1]. **Incorrect Options:** * **A. Tissue thromboplastin inhibition time:** Used primarily to screen for Lupus Anticoagulant, not to differentiate deficiency from inhibitors. [2] * **B. Ecarin clotting time:** Used to monitor Direct Thrombin Inhibitors (like Dabigatran); it is unaffected by heparin. * **C. Dilute Russell Viper Venom Time (dRVVT):** A specific confirmatory test for Lupus Anticoagulant, which acts by directly activating Factor X. **High-Yield Pearls for NEET-PG:** 1. **Isolated prolonged aPTT:** Think Factors VIII, IX, XI, XII, or Heparin. [3] 2. **Isolated prolonged PT:** Think Factor VII deficiency or early Warfarin use. 3. **Prolonged PT and aPTT:** Think common pathway (X, V, II, I), Vitamin K deficiency, or Liver disease. [1] 4. **Mixing study failure to correct after incubation (37°C for 1-2 hours):** Highly suggestive of a specific factor inhibitor (like Factor VIII) rather than Lupus Anticoagulant. [1] **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 622-626. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 664-665. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 670-671.

Question 1110: The mode of inheritance in hemophilia is

A. Autosomal dominant
B. Autosomal recessive
C. X linked dominant
D. X linked recessive (Correct Answer)

Explanation: **Explanation:** **Hemophilia A (Factor VIII deficiency)** and **Hemophilia B (Factor IX deficiency)** are classic examples of **X-linked recessive** inheritance [1]. The genes for these clotting factors are located on the X chromosome. Because males have only one X chromosome (XY), a single defective copy results in the disease [1]. Females (XX) are typically asymptomatic carriers because their second, normal X chromosome provides sufficient factor levels; they only manifest the disease if both X chromosomes are affected or due to extreme "Lyonization" (X-inactivation) [2]. **Analysis of Incorrect Options:** * **Autosomal Dominant:** This pattern requires only one copy of a mutant gene on a non-sex chromosome to express the disease (e.g., Von Willebrand Disease Type 1) [3]. Hemophilia does not follow this, as it predominantly affects males. * **Autosomal Recessive:** This requires two copies of the mutant gene (e.g., Sickle Cell Anemia). While rare factor deficiencies (like Factor VII or X) are autosomal recessive [4], Hemophilia A and B are not. * **X-linked Dominant:** In this pattern, both males and females are affected if they carry one copy of the gene (e.g., Alport Syndrome). Hemophilia is recessive because carriers are generally healthy. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** "Criss-cross inheritance" is seen (Grandfather to grandson via carrier daughter). * **Clinical Feature:** Characterized by **Hemarthrosis** (bleeding into joints) and delayed bleeding after trauma. * **Lab Findings:** Isolated **prolonged aPTT** with a normal PT and normal bleeding time. * **Mixing Study:** The prolonged aPTT **corrects** when mixed with normal plasma (distinguishes it from factor inhibitors). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, p. 151. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 670-671. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 149-150. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 53-54.

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Hemolytic Anemias

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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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