General Pathology — MCQs

General Pathology Indian Medical PG Practice Questions and MCQs

Question 1041: RET gene mutation is associated with which malignancy?

A. Pheochromocytoma
B. Medullary carcinoma thyroid (Correct Answer)
C. Lymphoma
D. Renal cell carcinoma

Explanation: The **RET proto-oncogene**, located on chromosome 10q11.2, encodes a receptor tyrosine kinase essential for the development of neural crest-derived cells. **Why Medullary Carcinoma Thyroid (MCT) is correct:** MCT arises from the parafollicular C-cells of the thyroid [1]. Gain-of-function mutations in the *RET* gene are the hallmark of this malignancy. It is seen in: * **Sporadic MCT (75%):** Somatic *RET* mutations are found in about 50% of cases. * **Familial MCT (25%):** Germline *RET* mutations are present in nearly 100% of cases, occurring as part of **Multiple Endocrine Neoplasia (MEN) syndromes 2A and 2B**, or Familial MCT [2]. **Analysis of Incorrect Options:** * **Pheochromocytoma:** While *RET* mutations are associated with pheochromocytoma (as part of MEN 2A/2B), it is not the primary malignancy defined by this gene in isolation [2]. MCT is the most consistent feature across all *RET*-associated syndromes. * **Lymphoma:** Associated with genes like *c-MYC* (Burkitt), *BCL-2* (Follicular), or *BCL-6*. * **Renal Cell Carcinoma:** Primarily associated with the *VHL* gene (Clear cell variant) or *MET* proto-oncogene (Papillary variant) [2]. **High-Yield Clinical Pearls for NEET-PG:** 1. **MEN 2A:** MCT + Pheochromocytoma + Parathyroid Hyperplasia [2]. 2. **MEN 2B:** MCT + Pheochromocytoma + Mucosal Neuromas + Marfanoid habitus [2]. 3. **Prophylactic Thyroidectomy:** In children with known germline *RET* mutations, the thyroid is removed early because MCT penetrance is nearly 100%. 4. **Hirschsprung Disease:** Loss-of-function mutations in *RET* are associated with this congenital condition (failure of neural crest migration). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1102-1103. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1137.

Question 1042: Internucleosomal cleavage of DNA is characteristic of which of the following?

A. Reversible cell injury
B. Irreversible cell injury
C. Necrosis
D. Apoptosis (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Apoptosis** **Underlying Concept:** Internucleosomal cleavage of DNA is the biochemical hallmark of **apoptosis** (programmed cell death) [2]. During the execution phase of apoptosis, specific enzymes called **Caspase-Activated DNases (CAD)** are activated [2]. these enzymes cleave the DNA at the vulnerable linker regions between nucleosomes. Since nucleosomes are spaced at regular intervals of approximately 180–200 base pairs, this degradation results in DNA fragments of consistent, repeating sizes. When visualized via agarose gel electrophoresis, this produces a characteristic **"DNA Ladder" pattern**. **Why other options are incorrect:** * **A & B (Reversible/Irreversible Injury):** These are broad stages of cell damage [1]. While irreversible injury leads to cell death, the specific pattern of internucleosomal cleavage is unique to the apoptotic pathway, not a general feature of all injury. * **C (Necrosis):** In necrosis, DNA degradation is random and chaotic due to the uncontrolled release of lysosomal enzymes (DNases) [3]. This results in a diffuse, non-specific distribution of DNA fragment sizes, which appears as a **"Smear" pattern** on gel electrophoresis, rather than a ladder. **High-Yield Pearls for NEET-PG:** * **DNA Laddering:** Pathognomonic for Apoptosis. * **DNA Smearing:** Characteristic of Necrosis. * **Morphological Hallmark of Apoptosis:** Chromatin condensation (pyknosis) is the most characteristic morphological feature, but internucleosomal cleavage is the biochemical hallmark. * **Annexin V:** A marker used to detect apoptosis (binds to Phosphatidylserine flipped to the outer membrane) [4]. * **Councilman bodies:** Apoptotic hepatocytes seen in Viral Hepatitis. **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. 101-102. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 64-65. [3] 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. 102-103. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 67-69.

Question 1043: Progressive cellular damage, including to DNA, can lead to which of the following outcomes?

A. Necrosis or Apoptosis (Correct Answer)
B. Atrophy
C. Metaplasia
D. Calcification

Explanation: **Explanation:** **Why the correct answer is right:** Cellular injury occurs when a stressor exceeds the cell's ability to adapt. When damage is **progressive and irreversible**, especially involving critical components like **DNA** or mitochondrial membranes, the cell can no longer maintain homeostasis [1]. * **Apoptosis:** If the DNA damage is detected by sensors (like p53) and is beyond repair, the cell initiates a programmed suicide pathway (Apoptosis) to prevent the propagation of mutations [1]. * **Necrosis:** If the damage is sudden, severe, or causes massive ATP depletion and membrane rupture, the cell undergoes accidental, unregulated death (Necrosis) [3]. Thus, progressive cellular damage is the fundamental precursor to cell death [3]. **Why incorrect options are wrong:** * **Atrophy:** This is an **adaptive response** where a cell decreases in size and organelle content to survive under diminished nutrient supply or disuse. It is not a result of progressive DNA damage. * **Metaplasia:** This is a **reversible change** where one adult cell type is replaced by another (e.g., Squamous metaplasia in smokers). It is an adaptation to chronic irritation, not a direct outcome of lethal DNA damage. * **Calcification:** This is a **consequence** of cell injury (Dystrophic) or hypercalcemia (Metastatic). While Dystrophic calcification occurs in necrotic tissues, it is a secondary mineral deposition rather than the primary cellular outcome of DNA damage [4]. **High-Yield NEET-PG Pearls:** * **The "Point of No Return":** Irreversible injury is characterized by **mitochondrial dysfunction** (inability to generate ATP) and **profound membrane damage** (lysosomal and plasma membranes) [2]. * **DNA Damage Sensor:** **p53** is the "Guardian of the Genome." It arrests the cell cycle in G1 for repair; if repair fails, it triggers apoptosis via the BAX/BAK (pro-apoptotic) proteins. * **Morphological Hallmark:** The appearance of **myelin figures** and **amorphous densities** in the mitochondrial matrix are classic electron microscopy findings of irreversible cell injury. **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. 101-102. [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. 102-103. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 49-50. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 77.

Question 1044: Acute graft-versus-host disease (GVHD) reaction occurs in all of the following organs except:

A. Liver
B. Adrenals (Correct Answer)
C. Gut
D. Skin

Explanation: **Explanation:** Acute Graft-versus-Host Disease (GVHD) occurs when immunocompetent T-cells from a donor graft (the "graft") recognize the recipient's (the "host") HLA antigens as foreign and initiate an immune attack [1]. This typically occurs within 100 days of a hematopoietic stem cell transplant. **Why Adrenals is the Correct Answer:** Acute GVHD characteristically targets specific epithelial "barrier" organs [1]. The **Adrenals** are not a target organ for acute GVHD. The immune-mediated damage is primarily directed at tissues that are highly regenerative or possess specific antigen-presenting environments. **Analysis of Incorrect Options:** * **Skin (Option D):** This is the most common organ involved [1]. It typically presents as a maculopapular rash, often starting on the palms, soles, and neck, which can progress to generalized erythroderma or toxic epidermal necrolysis-like lesions [1]. * **Gut (Option C):** The gastrointestinal tract is a major target. Patients present with profuse watery diarrhea, abdominal pain, and mucosal ulceration due to crypt cell necrosis [1]. * **Liver (Option A):** Involvement manifests as cholestatic jaundice [1]. The T-cells target the bile duct epithelium, leading to elevated alkaline phosphatase and bilirubin levels. **High-Yield Clinical Pearls for NEET-PG:** * **The "Triad" of Acute GVHD:** Skin (Rash), Liver (Jaundice), and Gut (Diarrhea) [1]. * **Pathological Hallmark:** Presence of **"Satellite Cell Necrosis"** (lymphocytes surrounding a necrotic keratinocyte) in the skin or **crypt abscesses** in the gut. * **Chronic GVHD:** Occurs after 100 days and resembles autoimmune disorders like Systemic Sclerosis (Scleroderma) or Sjögren’s syndrome. * **Prevention:** Depletion of donor T-cells before transfusion can prevent GVHD but may increase the risk of graft failure or leukemia recurrence (loss of Graft-versus-Leukemia effect). **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. 182-183.

Question 1045: What is the inheritance pattern of familial retinoblastoma?

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

Explanation: **Explanation** The correct answer is **B. Autosomal dominant**, although the question provided indicates D. In the context of medical examinations like NEET-PG, it is crucial to distinguish between the **genotypic inheritance** (how it is passed through generations) and the **cellular mechanism** (how the mutation acts at a molecular level). **1. Why Autosomal Dominant is the correct inheritance pattern:** Familial Retinoblastoma follows an **Autosomal Dominant** pattern of inheritance with high penetrance (approx. 90%) [1]. This is because an individual inheriting one defective copy of the *RB1* gene (located on chromosome 13q14) from a parent has a very high probability of acquiring a "second hit" (somatic mutation) in the remaining wild-type allele, leading to tumor formation [2]. **2. Analysis of Options:** * **Autosomal Dominant (Correct):** Pedigree analysis shows the disease appearing in every generation, affecting both males and females equally. [1] * **Autosomal Recessive (Incorrect):** While the *RB1* gene is a "recessive oncogene" at the **cellular level** (both alleles must be lost for cancer to develop—Knudson’s Two-Hit Hypothesis), the **inheritance pattern** is dominant [1]. * **X-linked Recessive/Dominant (Incorrect):** The *RB1* gene is located on Chromosome 13, which is an autosome, not a sex chromosome [2]. **3. Clinical Pearls for NEET-PG:** * **Knudson’s Two-Hit Hypothesis:** Familial cases have one germline mutation (1st hit) and one somatic mutation (2nd hit). Sporadic cases require two independent somatic mutations [2]. * **Clinical Presentation:** Familial cases are typically **bilateral**, multifocal, and present at an earlier age compared to sporadic (unilateral) cases. * **Associated Tumors:** Patients with germline *RB1* mutations have a high risk of developing **Osteosarcoma** later in life. * **Pathology:** Look for **Flexner-Wintersteiner rosettes** (pathognomonic) on histopathology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 298-300. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 300.

Question 1046: In Marfan's syndrome, the defect is in which of the following?

A. Fibrillin I (Correct Answer)
B. Fibrillin II
C. Collagen
D. Elastin

Explanation: **Explanation:** **Marfan’s Syndrome** is an autosomal dominant disorder of connective tissue caused by a mutation in the **FBN1 gene** located on chromosome **15q21**. 1. **Why Fibrillin-I is correct:** The FBN1 gene encodes **Fibrillin-I**, a glycoprotein that serves as a major structural component of microfibrils. These microfibrils act as a scaffold for the deposition of elastin. Furthermore, Fibrillin-I normally sequesters **TGF-β** (Transforming Growth Factor beta) [1]. A defect leads to excessive TGF-β signaling, which causes abnormal vascular remodeling and bone overgrowth, explaining the skeletal and cardiovascular manifestations [1]. 2. **Why other options are incorrect:** * **Fibrillin-II:** Mutations in the FBN2 gene (chromosome 5) lead to **Congenital Contractural Arachnodactyly (Beals Syndrome)**, characterized by "crumpled" ears and joint contractures, but without the life-threatening aortic complications of Marfan’s. * **Collagen:** Defects in collagen synthesis or structure are characteristic of **Ehlers-Danlos Syndrome (EDS)** and **Osteogenesis Imperfecta**, not Marfan’s. * **Elastin:** While elastin is associated with fibrillin, primary mutations in the elastin gene (ELN) are linked to **Williams Syndrome** and supravalvular aortic stenosis. **High-Yield Clinical Pearls for NEET-PG:** * **Cardiovascular:** Most common cause of death is **Aortic Dissection** (due to cystic medial necrosis). Mitral Valve Prolapse (MVP) is also common. * **Ocular:** **Ectopia lentis** (dislocation of the lens) typically occurs **upward and outward** (Superior-temporal). * **Skeletal:** Arachnodactyly (long fingers), pectus excavatum, and high-arched palate [1]. * **Diagnosis:** Based on the **Ghent Criteria**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 153-154.

Question 1047: What is the term for a cell's capacity to differentiate into diverse lineages?

A. Transdifferentiation (Correct Answer)
B. Dedifferentiation
C. Metaplasia
D. Developmental plasticity

Explanation: **Explanation:** The correct answer is **Transdifferentiation (Option A)**. This is a process where a fully differentiated (mature) somatic cell transforms into another mature somatic cell of a different lineage without reverting to an undifferentiated state. In the context of stem cell biology, it specifically refers to the capacity of a stem cell of one tissue lineage to differentiate into cells of an entirely different lineage (e.g., hematopoietic stem cells becoming hepatocytes). **Analysis of Options:** * **Dedifferentiation (Option B):** This refers to a process where a mature cell reverts to a less differentiated, more primitive stage (often seen in regeneration or certain malignancies). It is a "backward" step in development, unlike transdifferentiation which is a "sideways" switch. * **Metaplasia (Option C):** While similar, metaplasia is a reversible change where one adult cell type is *replaced* by another adult cell type (e.g., Squamous metaplasia in the bronchus). Transdifferentiation is often considered the underlying cellular mechanism that drives metaplasia. * **Developmental Plasticity (Option D):** This is a broad umbrella term describing the ability of cells to change their fate in response to environmental cues [2]. While transdifferentiation is a *form* of plasticity, the specific term for the capacity to cross lineage boundaries is transdifferentiation [1]. **NEET-PG High-Yield Pearls:** * **Classic Example:** The transformation of esophageal squamous epithelium to columnar epithelium (Barrett’s Esophagus) is a clinical manifestation of metaplasia driven by transdifferentiation. * **Stem Cell Niche:** The microenvironment that surrounds stem cells and dictates their differentiation path via signaling molecules [3]. * **Therapeutic Potential:** Transdifferentiation is a major focus in regenerative medicine, aiming to reprogram cells (e.g., fibroblasts into insulin-producing beta cells) without the use of embryonic stem cells. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 39-40. [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. 84-85. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 38-39.

Question 1048: What accumulates in tissues in hemochromatosis?

A. Iron (Correct Answer)
B. Copper
C. Ceruloplasmin
D. Lipofuschin

Explanation: **Explanation:** **Hemochromatosis** is a disorder of iron metabolism characterized by excessive intestinal iron absorption, leading to the systemic deposition of **Iron** (in the form of hemosiderin) within parenchymal cells of organs such as the liver, pancreas, heart, and joints [1]. This iron overload causes oxidative stress and lipid peroxidation, eventually leading to tissue fibrosis and organ failure [2]. **Analysis of Options:** * **Iron (Correct):** In hereditary hemochromatosis (most commonly due to *HFE* gene mutations), the lack of hepcidin regulation leads to uncontrolled iron entry into the plasma, causing toxic accumulation in tissues [1]. * **Copper:** Accumulation of copper is the hallmark of **Wilson Disease**, not hemochromatosis [1, 3]. * **Ceruloplasmin:** This is the primary copper-carrying protein in the blood. Its levels are typically *decreased* in Wilson Disease; it does not accumulate in tissues [3]. * **Lipofuscin:** Known as the "wear-and-tear" pigment, lipofuscin is an insoluble brownish-yellow pigment representing polymers of lipids and phospholipids complexed with protein. It accumulates due to free radical injury and lipid peroxidation, typically associated with aging or atrophy, rather than iron overload. **NEET-PG High-Yield Pearls:** * **Classic Triad:** "Bronze diabetes" (Skin pigmentation, Diabetes mellitus, and Cirrhosis). * **Diagnosis:** Best initial screening test is **Transferrin saturation** (elevated); Gold standard for quantification is **MRI** or liver biopsy with **Prussian Blue stain** [1]. * **Treatment:** Repeated phlebotomy is the mainstay of therapy [2]. * **Complication:** Patients have a significantly increased risk (up to 200-fold) of developing **Hepatocellular Carcinoma (HCC)** [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 854-855, 858. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 854. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 394-395.

Question 1049: Gastrin is a biochemical marker for which of the following tumours?

A. Medullary carcinoma of thyroid
B. Pancreatic neuroendocrine tumour (Correct Answer)
C. Pheochromocytoma
D. Gastrointestinal stromal tumor

Explanation: **Explanation:** **Gastrin** is a peptide hormone primarily produced by the G-cells of the gastric antrum. In a pathological context, it serves as a specific biochemical marker for **Gastrinomas** [1], which are a type of **Pancreatic Neuroendocrine Tumour (PanNET)**. These tumours (often located in the "Gastrinoma Triangle") secrete excessive gastrin, leading to **Zollinger-Ellison Syndrome (ZES)**, characterized by refractory peptic ulcers and severe diarrhea [1]. **Analysis of Options:** * **Medullary Carcinoma of Thyroid (MCT):** The classic biochemical marker is **Calcitonin**. Carceaembryonic Antigen (CEA) is also used for monitoring. * **Pheochromocytoma:** This tumour of the adrenal medulla secretes catecholamines. The diagnostic markers are urinary and plasma **Metanephrines** and Vanillylmandelic acid (VMA). * **Gastrointestinal Stromal Tumor (GIST):** This is a mesenchymal tumour, not a neuroendocrine one. Its hallmark is the expression of **CD117 (c-KIT)** and **DOG1** on immunohistochemistry. **High-Yield Clinical Pearls for NEET-PG:** * **Zollinger-Ellison Syndrome:** Suspect this when ulcers are multiple, distal to the duodenum, or recur after treatment [1]. * **MEN1 Syndrome:** Gastrinomas are the most common functional pancreatic neuroendocrine tumours associated with Multiple Endocrine Neoplasia Type 1 (The 3 P’s: Pituitary, Parathyroid, Pancreas) [1]. * **Diagnostic Test:** The **Secretin Stimulation Test** is the provocative test of choice; secretin causes a paradoxical *increase* in serum gastrin levels in gastrinoma patients. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1124-1125.

Question 1050: What is the characteristic shape of Birbeck granules?

A. Hockeystick
B. Bat
C. Ball
D. Tennis racket (Correct Answer)

Explanation: **Explanation:** **Birbeck granules** are the pathognomonic ultrastructural hallmark of **Langerhans Cell Histiocytosis (LCH)**. These are rod-shaped, pentalaminar cytoplasmic organelles with a central striated line and a bulbous end, giving them a classic **tennis racket** appearance under electron microscopy [1]. They are formed by the invagination of the cell membrane and are associated with the protein **Langerin (CD207)**, which is involved in antigen processing [1]. **Analysis of Options:** * **Option D (Tennis racket):** This is the correct description. The "handle" of the racket is the rod-like portion, and the "head" is the dilated vesicular end [1]. * **Option A (Hockeystick):** This is a distractor. While some granules might appear slightly curved, "tennis racket" is the standard medical descriptor. * **Option B (Bat):** Incorrect. This does not describe the specific pentalaminar structure seen on EM. * **Option C (Ball):** Incorrect. Birbeck granules are elongated rods, not spherical structures. **High-Yield Clinical Pearls for NEET-PG:** * **Cell of Origin:** Langerhans cells (dendritic cells of the skin/monocyte-macrophage lineage). * **Immunohistochemistry (IHC) Markers:** LCH cells are characteristically positive for **S-100**, **CD1a**, and **Langerin (CD207)** [1]. CD207 is the most specific marker. * **Clinical Presentation:** Can range from a solitary bone lesion (Eosinophilic Granuloma) to multisystem involvement (Letterer-Siwe disease). * **Radiology:** Often presents as "punched-out" lytic lesions in the skull. **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. 630.

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