Hematopathology — MCQs

A 56-year-old woman with a history of breast cancer treated 5 years ago with lumpectomy and radiation, but no chemotherapy, presents with bone pain, fatigue, and weakness. Her complete blood count shows severe anemia, decreased white blood cells, and thrombocytopenia. Examination of a peripheral blood smear reveals a few nucleated red cells, an occasional blast cell, and myelocyte. What is the likely cause of these hematologic abnormalities?

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 1151: Increase in MCHC is associated with which of the following?

A. Iron deficiency anemia
B. Megaloblastic anemia
C. Anemia of chronic disease
D. Hereditary spherocytosis (Correct Answer)

Explanation: **Explanation:** **MCHC (Mean Corpuscular Hemoglobin Concentration)** represents the average concentration of hemoglobin in a given volume of packed red blood cells. It is one of the most stable red cell indices, typically ranging between 32–36 g/dL. **Why Hereditary Spherocytosis (HS) is correct:** In HS, a defect in RBC membrane proteins (like spectrin or ankyrin) leads to the loss of membrane fragments [1]. This results in a decreased surface-area-to-volume ratio, forcing the cell into a spherical shape [1],[2]. Because the cell shrinks (loses membrane) but retains its full complement of hemoglobin, the hemoglobin becomes "concentrated." **Hereditary Spherocytosis is the only clinical condition where the MCHC is characteristically elevated (>36 g/dL).** **Why other options are incorrect:** * **Iron Deficiency Anemia (IDA):** Characterized by impaired hemoglobin synthesis, leading to **decreased MCHC** (hypochromic) and decreased MCV (microcytic). * **Megaloblastic Anemia:** While the MCV is high (macrocytic), the MCHC remains **normal**. The cells are larger, but the hemoglobin concentration within that volume is not increased. * **Anemia of Chronic Disease (ACD):** Usually presents as normocytic, normochromic anemia. The MCHC is typically **normal**, though it may decrease in long-standing cases. **High-Yield Clinical Pearls for NEET-PG:** * **MCHC >36 g/dL:** Highly specific for Hereditary Spherocytosis. * **Gold Standard Test for HS:** Eosin-5-maleimide (EMA) binding test (Flow cytometry). * **Screening Test:** Osmotic Fragility Test (increased fragility) [2]. * **Peripheral Smear:** Look for microspherocytes (small, dark cells lacking central pallor) [2]. * **Hyperchromia:** True hyperchromia does not exist (cells cannot be "over-filled" with Hb); an elevated MCHC is almost always due to relative dehydration or membrane loss. [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. 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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638.

Question 1152: Which of the following cytogenetic abnormalities is associated with the worst prognosis in Acute Myeloid Leukemia (AML)?

A. t(8;21)
B. inv(16)
C. Normal cytogenetics
D. Monosomy 7 (Correct Answer)

Explanation: ### Explanation In Acute Myeloid Leukemia (AML), cytogenetics is the single most important predictor of treatment response and overall survival. The prognosis is categorized into Favorable, Intermediate, and Adverse (Poor) risk groups [1]. **Why Monosomy 7 is the Correct Answer:** **Monosomy 7 (-7)** or a deletion of the long arm of chromosome 7 (**7q-**) is a hallmark of the **Adverse/Poor Risk** category. It is frequently associated with complex karyotypes, therapy-related AML (t-AML), and AML arising from myelodysplastic syndrome (MDS). These cases typically show poor response to standard induction chemotherapy and a high rate of relapse, necessitating hematopoietic stem cell transplantation (HSCT) in first remission. **Analysis of Incorrect Options:** * **A. t(8;21):** This involves the *RUNX1-RUNX1T1* fusion. It is a **Favorable Risk** cytogenetic abnormality, often associated with the presence of Auer rods and a high rate of complete remission [1]. * **B. inv(16):** This involves the *CBFB-MYH11* fusion. Along with t(8;21), it belongs to the "Core Binding Factor" (CBF) leukemias. It is a **Favorable Risk** abnormality, often characterized by abnormal bone marrow eosinophils (AML-M4eo) [1]. * **C. Normal Cytogenetics:** This represents the **Intermediate Risk** group. Prognosis in this group is further refined by molecular markers; for example, *NPM1* mutations (without *FLT3-ITD*) improve prognosis, while *FLT3-ITD* mutations worsen it [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Best Prognosis:** t(15;17) [APML], followed by t(8;21) and inv(16). * **Worst Prognosis:** Monosomy 7, Monosomy 5, 17p deletions, and complex karyotypes (≥3 abnormalities). * **Molecular Marker Tip:** *NPM1* and *CEBPA* mutations are generally favorable; *FLT3-ITD* and *TP53* mutations are unfavorable. * **APML (M3):** Associated with t(15;17) and DIC; treated with ATRA and Arsenic Trioxide. **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 1153: Which of the following is positive in Follicular lymphoma?

A. Bcl 2 (Correct Answer)
B. Bcl 6
C. Bcl 1
D. Bcl 10

Explanation: **Explanation:** **Follicular Lymphoma (FL)** is a B-cell neoplasm derived from germinal center B-cells [1, 2]. The hallmark of FL is the chromosomal translocation **t(14;18)(q32;q21)** [4]. This translocation moves the **BCL2 gene** from chromosome 18 to the Immunoglobulin Heavy chain (IgH) locus on chromosome 14 [1, 2]. This leads to the constitutive overexpression of the Bcl-2 protein, which is an **anti-apoptotic** molecule [2]. In a normal germinal center, B-cells are Bcl-2 negative to allow for the apoptosis of cells with low-affinity antibodies; however, in FL, the overexpression of Bcl-2 prevents cell death, leading to the accumulation of neoplastic cells [1, 3]. **Analysis of Options:** * **Bcl-2 (Option A):** Correct. It is the diagnostic marker for FL. Note that while Bcl-2 is positive in the neoplastic follicles of FL, it is negative in the reactive follicles of follicular hyperplasia [3]. * **Bcl-6 (Option B):** While often expressed in FL (as it is a germinal center marker), Bcl-2 is the definitive diagnostic hallmark associated with the t(14;18) translocation. * **Bcl-1 (Option C):** Also known as **Cyclin D1**, this is the characteristic marker for **Mantle Cell Lymphoma**, associated with t(11;14). * **Bcl-10 (Option D):** This marker is associated with **MALT lymphoma** (Mucosa-Associated Lymphoid Tissue), specifically those involving t(1;14). **High-Yield Pearls for NEET-PG:** * **Immunophenotype of FL:** CD19+, CD20+, CD10+, Bcl-2+, Bcl-6+, but **CD5- and CD23-** (helps differentiate from CLL/SLL). * **Grading:** Based on the number of **centroblasts** per high-power field (Mann and Berard classification). * **Transformation:** FL can transform into a more aggressive **Diffuse Large B-Cell Lymphoma (DLBCL)**, known as Richter’s transformation (though more common in 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, p. 604. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311.

Question 1154: Leukemoid reaction is seen in which of the following conditions?

A. Acute infection (Correct Answer)
B. Erythroleukemia
C. Myelomatosis
D. Hemorrhage

Explanation: **Explanation:** A **Leukemoid Reaction** is defined as a reactive, non-neoplastic increase in the total leukocyte count (typically >50,000/mm³), characterized by a significant "shift to the left" (presence of immature precursors like myelocytes and metamyelocytes). 1. **Why Acute Infection is Correct:** Severe bacterial infections (e.g., pneumonia, sepsis) are the most common cause [1]. The body’s bone marrow responds to inflammatory cytokines by rapidly releasing mature and immature neutrophils into the peripheral blood [2]. A key diagnostic feature is a **high Leukocyte Alkaline Phosphatase (LAP) score**, which distinguishes it from Chronic Myeloid Leukemia (CML), where the LAP score is low. 2. **Why Other Options are Incorrect:** * **Erythroleukemia (AML-M6):** This is a neoplastic condition (malignancy) involving erythroid and myeloid precursors. Leukemoid reactions are by definition reactive and non-malignant. * **Myelomatosis (Multiple Myeloma):** This is a plasma cell dyscrasia. While it involves the bone marrow, it typically presents with plasma cell infiltration and monoclonal protein spikes, not a massive reactive neutrophilia. * **Hemorrhage:** While acute hemorrhage can cause a mild leukocytosis, it rarely reaches the threshold of a leukemoid reaction [1]. **High-Yield Clinical Pearls for NEET-PG:** * **LAP/NAP Score:** Increased in Leukemoid reaction; Decreased in CML and Paroxysmal Nocturnal Hemoglobinuria (PNH). * **Morphology:** Look for **Döhle bodies**, toxic granulations, and cytoplasmic vacuolation in neutrophils—these are hallmarks of a leukemoid reaction. * **Other Causes:** Apart from infection, it can be seen in severe hemolysis and certain solid tumors (paraneoplastic) [1]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 580-581. [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. 592.

Question 1155: Popkorn cells are found in which of the following conditions?

A. Hodgkin's Lymphoma (Correct Answer)
B. Non-Hodgkin's lymphoma
C. Multiple myeloma
D. Iron deficiency anemia

Explanation: **Explanation:** **Popcorn cells** (also known as **L&H cells**—Lymphocytic and Histiocytic variants) are the characteristic diagnostic hallmark of **Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLPHL)**, a specific subtype of Hodgkin Lymphoma [1]. 1. **Why Option A is Correct:** Popcorn cells are large, neoplastic B-cells with multi-lobed, folded nuclei resembling a kernel of popped corn [1]. Unlike the "classic" Reed-Sternberg (RS) cells found in other subtypes, popcorn cells are **CD20+** and **CD45+**, but typically **CD15- and CD30-**. Their presence in a background of small B-lymphocytes confirms the diagnosis of NLPHL [1]. 2. **Why Other Options are Incorrect:** * **Non-Hodgkin Lymphoma (NHL):** While NHL involves various malignant B or T cells (e.g., "flower cells" in HTLV-1 or "buttock cells" in Follicular Lymphoma), the specific "popcorn" morphology is unique to the NLPHL subtype of Hodgkin's. * **Multiple Myeloma:** This is a plasma cell dyscrasia characterized by "clock-face" nuclei, perinuclear halos (hof), and occasionally **Mott cells** or **Russell bodies**, but not popcorn cells. * **Iron Deficiency Anemia:** This is a microcytic hypochromic anemia characterized by peripheral smear findings like **pencil cells** (elliptocytes) and target cells, not neoplastic giant cells. **NEET-PG High-Yield Pearls:** * **Classic RS Cell:** Found in Mixed Cellularity and Nodular Sclerosis; markers are **CD15+ and CD30+**. * **Lacunar Cells:** Characteristic of **Nodular Sclerosis** HL (seen in formalin-fixed tissue). * **Mummy Cells:** Degenerated RS cells with pyknotic nuclei. * **NLPHL Prognosis:** Generally carries an excellent prognosis but has a risk of transformation into Diffuse Large B-Cell Lymphoma (DLBCL) [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. 614-618.

Question 1156: A 40-year-old female presented with the following findings: Hb 9.8 gm%, TLC 15,700/cumm, Platelet count 3 lac/cumm. Peripheral smear showed increased neutrophils with 14% blasts, 15% myelocytes and metamyelocytes with some dysplasia. Cytogenetic study revealed t(8;21). What is your diagnosis?

A. AML (Correct Answer)
B. CML
C. MDS
D. ALL

Explanation: **Explanation:** The key to this diagnosis lies in the cytogenetic finding of **t(8;21)**. According to the WHO classification of myeloid neoplasms, the presence of specific recurrent genetic abnormalities—namely **t(8;21), inv(16), or t(15;17)**—is diagnostic of **Acute Myeloid Leukemia (AML)** regardless of the blast count [1]. While the peripheral smear shows 14% blasts (which is below the traditional 20% threshold), the genetic marker overrides the blast percentage requirement. **Why other options are incorrect:** * **CML (Chronic Myeloid Leukemia):** Characterized by the Philadelphia chromosome **t(9;22)** and a "myelocyte bulge." While this patient has myelocytes and metamyelocytes, the t(8;21) is pathognomonic for AML (specifically AML-M2 in the FAB classification). * **MDS (Myelodysplastic Syndrome):** Although dysplasia is mentioned, the presence of t(8;21) automatically upgrades the diagnosis to AML [1]. MDS typically presents with cytopenias, not leukocytosis [2]. * **ALL (Acute Lymphoblastic Leukemia):** This involves a proliferation of lymphoblasts. The presence of myelocytes, metamyelocytes, and t(8;21) (a myeloid marker) points exclusively to a myeloid lineage [1]. **High-Yield Pearls for NEET-PG:** * **WHO Exception Rule:** AML can be diagnosed with <20% blasts if t(8;21), inv(16), or t(15;17) is present [1]. * **AML with t(8;21):** Often associated with **RUNX1-RUNX1T1** fusion gene, good prognosis, and the presence of **Auer rods** [1]. * **Morphology:** Frequently shows large blasts with prominent granules and "maturation" (presence of myelocytes/metamyelocytes), which can mimic CML or MDS [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. 620-621. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.

Question 1157: What is the specific type of cells found in infectious mononucleosis?

A. Downey cells (Correct Answer)
B. Raquet cells
C. Arbiskov cells
D. None of the above

Explanation: **Explanation:** **Infectious Mononucleosis (IM)**, caused primarily by the **Epstein-Barr Virus (EBV)**, is characterized by the presence of **Downey cells** (Option A) in the peripheral blood smear. These are **atypical T-lymphocytes** (specifically CD8+ cytotoxic T-cells) that have been activated to respond against EBV-infected B-cells [1]. Morphologically, Downey cells are larger than normal lymphocytes, possessing an abundant, "ballpoint-pen" blue cytoplasm that appears to "hug" or indent around adjacent red blood cells (scalloping) [1]. **Analysis of Incorrect Options:** * **Raquet cells (Option B):** These are characteristic of **Rhabdomyosarcoma**. They are tadpole or racquet-shaped cells with a single nucleus and a long cytoplasmic process containing cross-striations. * **Arbiskov cells (Option C):** This is a distractor term and does not represent a recognized pathological cell type in standard hematopathology. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of IM:** Fever, pharyngitis, and lymphadenopathy (typically posterior cervical) [1]. * **Paul-Bunnell Test:** A classic heterophile antibody test used for diagnosis (positive in EBV-induced IM). * **Splenic Rupture:** A rare but serious complication; patients are advised to avoid contact sports for 3–4 weeks. * **Ampicillin Rash:** Patients with IM who are mistakenly treated with Ampicillin or Amoxicillin often develop a characteristic maculopapular rash. * **Downey Classification:** Downey cells are categorized into three types (Type I, II, and III), with Type II being the most common "atypical" form seen in IM. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 369-370.

Question 1158: A patient presents with cervical lymphadenopathy. Biopsy demonstrates a nodular lymphoma with follicle formation. This lesion would most likely be associated with which of the following?

A. bcr-abl hybrid
B. bcl-2 activation (Correct Answer)
C. c-myc activation
D. t(8, 14)

Explanation: ### Explanation The clinical presentation of cervical lymphadenopathy and a biopsy showing **nodular lymphoma with follicle formation** is characteristic of **Follicular Lymphoma (FL)**. **1. Why the Correct Answer is Right:** Follicular Lymphoma is defined by the translocation **t(14;18)** [1]. This translocation moves the **BCL-2 gene** from chromosome 18 to the immunoglobulin heavy chain (IgH) locus on chromosome 14 [1], [2]. This results in the overexpression of the BCL-2 protein, which is an **anti-apoptotic** molecule [2]. In a normal germinal center, B-cells undergo apoptosis if they do not bind antigen; however, in FL, BCL-2 overexpression prevents this programmed cell death, leading to the accumulation of neoplastic B-cells [1]. **2. Why the Other Options are Incorrect:** * **A. bcr-abl hybrid:** This is the hallmark of **Chronic Myeloid Leukemia (CML)**, resulting from the t(9;22) Philadelphia chromosome. It creates a constitutively active tyrosine kinase. * **C. c-myc activation:** This is associated with **Burkitt Lymphoma**. It involves the translocation of the c-myc proto-oncogene (chromosome 8), usually to the IgH locus (chromosome 14) [4]. * **D. t(8, 14):** This is the specific translocation seen in **Burkitt Lymphoma**, leading to c-myc overexpression and a "starry sky" appearance, not a nodular follicular pattern [4]. **High-Yield NEET-PG Pearls:** * **Follicular Lymphoma:** Most common indolent (slow-growing) Non-Hodgkin Lymphoma. * **Histology:** Back-to-back follicles lacking tingible body macrophages (unlike reactive hyperplasia) [1]. * **Immunophenotype:** CD10+, CD19+, CD20+, and **BCL-2+** [2]. * **Transformation:** Can transform into a more aggressive **Diffuse Large B-Cell Lymphoma (DLBCL)** (Richter’s transformation) [3]. **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] 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. [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, p. 606.

Question 1159: What is the shelf life of platelets?

A. Less than 5 days (Correct Answer)
B. Less than 3 weeks
C. Less than 5 weeks
D. Less than 2 years

Explanation: **Explanation:** **1. Why Option A is Correct:** Platelets are unique among blood components because they must be stored at **room temperature (20–24°C)** with continuous agitation to maintain their viability and function. Because they are stored at room temperature, there is a significantly high risk of **bacterial proliferation**. To minimize the risk of transfusion-transmitted bacterial infections (sepsis), the shelf life is strictly limited to **5 days**. Some newer technologies (like pathogen reduction or large-volume delayed sampling) may extend this to 7 days in specific settings, but for examination purposes, 5 days remains the standard. **2. Why Incorrect Options are Wrong:** * **Option B (3 weeks):** This corresponds to the shelf life of Whole Blood or Packed Red Blood Cells (PRBCs) collected in **CPD (Citrate Phosphate Dextrose)** anticoagulant, which is 21 days. * **Option C (5 weeks):** This corresponds to the shelf life of PRBCs collected in **CPDA-1** (35 days) or those using additive solutions like SAGM (42 days). * **Option D (2 years):** This refers to the storage of **Fresh Frozen Plasma (FFP)** or Cryoprecipitate when stored at temperatures below -65°C. **3. High-Yield Clinical Pearls for NEET-PG:** * **Storage Temperature:** Platelets = 20–24°C; PRBCs = 2–6°C; FFP = < -18°C. * **Agitation:** Continuous agitation is required for platelets to prevent pH drop and aggregation. * **Bacterial Sepsis:** Platelets are the blood component most commonly associated with transfusion-related sepsis (most common organism: *Staphylococcus epidermidis*). * **Dose Effect:** One unit of Random Donor Platelets (RDP) typically raises the platelet count by 5,000–10,000/µL in an average adult.

Question 1160: A 56-year-old woman with a history of breast cancer treated 5 years ago with lumpectomy and radiation, but no chemotherapy, presents with bone pain, fatigue, and weakness. Her complete blood count shows severe anemia, decreased white blood cells, and thrombocytopenia. Examination of a peripheral blood smear reveals a few nucleated red cells, an occasional blast cell, and myelocyte. What is the likely cause of these hematologic abnormalities?

A. Chloramphenicol toxicity
B. Diphyllobothrium latum infestation
C. Megaloblastic anemia
D. Myelophthisic anemia (Correct Answer)

Explanation: ### Explanation The clinical presentation of a patient with a history of malignancy (breast cancer) presenting with pancytopenia and a **leukoerythroblastic blood picture** (nucleated RBCs, immature white cells like myelocytes, and occasional blasts) is classic for **Myelophthisic Anemia**. [1] **1. Why Myelophthisic Anemia is Correct:** Myelophthisic anemia occurs due to the infiltration of the bone marrow by non-hematopoietic tissue, most commonly **metastatic adenocarcinoma** (breast, prostate, lung). This "space-occupying" lesion disrupts the marrow architecture and the blood-bone marrow barrier. Consequently, immature precursors (nucleated RBCs and immature WBCs) are prematurely released into the peripheral circulation, creating a leukoerythroblastic smear [1]. The displacement of normal hematopoietic stem cells leads to pancytopenia. **2. Why Incorrect Options are Wrong:** * **Chloramphenicol toxicity:** Typically causes **Aplastic Anemia**. While it presents with pancytopenia, the peripheral smear is "empty" (no immature cells or nucleated RBCs) because the marrow is hypocellular, not infiltrated. * **Diphyllobothrium latum:** This fish tapeworm competes for **Vitamin B12**, leading to megaloblastic anemia. It does not typically cause a leukoerythroblastic picture. * **Megaloblastic anemia:** While it can cause pancytopenia and macro-ovalocytes, the hallmark is **hypersegmented neutrophils**, not the presence of myelocytes and nucleated RBCs seen in marrow infiltration. **3. High-Yield Clinical Pearls for NEET-PG:** * **Leukoerythroblastic Picture:** Defined as the presence of immature myeloid cells and nucleated RBCs in the peripheral blood [2]. It is the hallmark of Myelophthisic anemia. * **Tear-drop cells (Dacrocytes):** Frequently seen on the smear in myelophthisic anemia as RBCs are squeezed through the distorted marrow sinuses [2]. * **Common Causes:** Metastatic cancer (most common), Granulomatous diseases (TB), and Myelofibrosis [1]. * **Diagnosis:** Bone marrow biopsy is essential to visualize the infiltrating secondary cells or fibrosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 589-590. [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.

Practice by Chapter

Anemias: Classification and Approach

Practice Questions

Hemolytic Anemias

Practice Questions

Myeloproliferative Neoplasms

Practice Questions

Myelodysplastic Syndromes

Practice Questions

Acute Leukemias

Practice Questions

Chronic Leukemias

Practice Questions

Lymphomas and Lymphoid Neoplasms

Practice Questions

Plasma Cell Disorders

Practice Questions

Bleeding Disorders

Practice Questions

Thrombotic Disorders

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free