General Pathology — MCQs

A 49-year-old female presents with shortness of breath and hilar lymphadenopathy on chest x-ray. Biopsy of a lymph node reveals granulomas, highly suggestive of sarcoidosis. Which of the following histological findings must be present in the biopsy material to support the diagnosis of granulomatous inflammation?

Q979Medium

Which of the following is characteristic of a dental cyst?

Q980Easy

What is most important for diapedesis?

General Pathology Indian Medical PG Practice Questions and MCQs

Question 971: Pseudoepitheliomatous hyperplasia is a feature of:

A. Myoblastoma
B. Blastomycosis
C. Papillary hyperplasia
D. All of the above (Correct Answer)

Explanation: **Explanation:** **Pseudoepitheliomatous Hyperplasia (PEH)** is a benign clinicopathological entity characterized by reactive, irregular hyperplasia of the overlying squamous epithelium [1]. It histologically mimics squamous cell carcinoma (SCC) due to the presence of downward-proliferating rete ridges, but it lacks the cellular atypia and disordered maturation seen in malignancy [1]. **Why "All of the Above" is Correct:** PEH is not a primary disease but a secondary reaction to various stimuli, including chronic inflammation, infections, and certain tumors. * **Myoblastoma (Granular Cell Tumor):** This is a classic high-yield association. In nearly 50% of cases, the overlying epithelium shows PEH, which is often misdiagnosed as SCC on superficial biopsies. * **Blastomycosis:** Deep fungal infections (like Blastomycosis, Coccidioidomycosis, and Histoplasmosis) are potent triggers for PEH. The intense inflammatory response to the fungi stimulates epithelial proliferation. * **Papillary Hyperplasia:** Chronic irritation (e.g., inflammatory papillary hyperplasia of the palate due to ill-fitting dentures) leads to reactive epithelial thickening and PEH. **High-Yield Clinical Pearls for NEET-PG:** * **Differential Diagnosis:** The most critical distinction is between PEH and **Squamous Cell Carcinoma**. PEH lacks significant nuclear pleomorphism and atypical mitoses [1]. * **Other Causes of PEH:** * **Infections:** Tuberculosis verrucosa cutis, Leishmaniasis, and Orf. * **Tumors:** Spitz nevus, Dermatofibroma, and Keratoacanthoma. * **Chronic Conditions:** Venous stasis ulcers and Pyoderma gangrenosum. * **Key Histological Feature:** Look for "islands" of epithelium that appear to be invading the dermis but maintain a well-differentiated appearance with an intact basement membrane. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1000-1002.

Question 972: Which of the following is associated with cystic hygroma?

A. Marfan syndrome
B. Turner syndrome (Correct Answer)
C. Down syndrome
D. Noonan syndrome

Explanation: **Explanation:** **Cystic hygroma** (also known as macrocystic lymphatic malformation) is a congenital malformation of the lymphatic system characterized by large, fluid-filled sacs, most commonly occurring in the neck or axilla [1]. It results from a failure of the lymphatic channels to communicate with the venous system, leading to lymph accumulation. **Why Turner Syndrome is the correct answer:** Cystic hygroma is a classic phenotypic feature of **Turner syndrome (45, XO)**. In these patients, the failure of lymphatic drainage in the neck leads to the formation of a cystic hygroma during fetal development. As the hygroma regresses or resolves postnatally, it leaves behind redundant skin, resulting in the characteristic **"webbed neck"** (pterygium colli) seen in Turner patients. **Analysis of Incorrect Options:** * **Marfan Syndrome:** This is a connective tissue disorder (FBN1 mutation) primarily associated with cystic medial necrosis of the aorta, ectopia lentis, and arachnodactyly. It is not typically associated with lymphatic malformations. * **Down Syndrome (Trisomy 21):** While Down syndrome is associated with increased **nuchal translucency** on first-trimester ultrasound [3], it is less frequently associated with true large cystic hygromas compared to Turner syndrome. * **Noonan Syndrome:** Often called "male Turner syndrome" due to phenotypic similarities (like webbed neck and short stature), it is an autosomal dominant disorder. While it can present with lymphatic issues, Turner syndrome remains the most high-yield and classic association for cystic hygroma in exams. **High-Yield Pearls for NEET-PG:** * **Most common site:** Posterior triangle of the left side of the neck [1]. * **Transillumination:** Cystic hygromas are **brilliantly transilluminant** (unlike hemangiomas). * **Associated Karyotypes:** Turner syndrome (45, XO) is the most common; also seen in Trisomies 13, 18, and 21 [2]. * **Complication:** If large, it can cause hydrops fetalis and fetal demise. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 524-525. [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. 92-93. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 170-171.

Question 973: Which of the following structures is seen in all except?

A. Follicular carcinoma of thyroid (Correct Answer)
B. Papillary carcinoma of thyroid
C. Serous cystadenoma of ovary
D. Meningioma

Explanation: The question refers to the presence of **Psammoma bodies**, which are characteristic histological findings in specific tumors [1]. ### **Understanding the Concept: Psammoma Bodies** Psammoma bodies are concentric, laminated calcified structures representing a form of **dystrophic calcification**. They occur when single necrotic cells serve as a focus for calcium salt deposition. ### **Explanation of Options** * **A. Follicular Carcinoma of Thyroid (Correct):** This tumor is characterized by a microfollicular pattern and vascular/capsular invasion [3]. It **does not** typically exhibit Psammoma bodies. Their absence is a key histological differentiator from Papillary carcinoma. * **B. Papillary Carcinoma of Thyroid:** This is the most common site for Psammoma bodies [2]. They are found in the cores of the papillae and are a high-yield diagnostic marker for this malignancy. * **C. Serous Cystadenoma/Cystadenocarcinoma of Ovary:** Psammoma bodies are frequently seen in serous tumors of the ovary (both benign and malignant), where they indicate a slow-growing process. * **D. Meningioma:** Specifically the **psammomatous variant** of meningioma is loaded with these calcifications, which can sometimes be visualized on CT scans as hyperdense areas. ### **NEET-PG High-Yield Pearls** To remember the common causes of Psammoma bodies, use the mnemonic **"PSaMMoma"**: * **P** – **P**apillary carcinoma of thyroid * **S** – **S**erous cystadenocarcinoma of ovary * **M** – **M**esothelioma * **M** – **M**eningioma **Note:** While Follicular carcinoma lacks them, **Hurthle cell variants** [4] and **Medullary thyroid carcinoma** (associated with Amyloid) also typically do not show Psammoma bodies. **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. 134-135. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1099. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1100-1101. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1096-1097.

Question 974: What is considered the most severe form of Ehlers-Danlos syndrome?

A. Type 1
B. Type 2
C. Type 4 (Correct Answer)
D. Type 8

Explanation: **Explanation:** **Ehlers-Danlos Syndrome (EDS)** is a heterogeneous group of inherited connective tissue disorders characterized by defects in collagen synthesis [1]. **Why Type 4 is Correct:** **Type 4 (Vascular Type)** is considered the most severe and life-threatening form of EDS. It results from a mutation in the **COL3A1 gene**, leading to deficient synthesis of **Type III collagen**. Since Type III collagen is a major structural component of blood vessels and hollow organs, patients are predisposed to spontaneous **rupture of large arteries** (e.g., aorta), **bowel perforation**, and **uterine rupture** during pregnancy [1]. These catastrophic events often lead to sudden death at a young age. **Analysis of Incorrect Options:** * **Type 1 & 2 (Classical Type):** These are caused by mutations in **Type V collagen** (COL5A1, COL5A2). While they present with significant skin hyperextensibility, "cigarette paper" scarring, and joint hypermobility, they are generally not life-threatening [1]. * **Type 8 (Periodontal Type):** This is a rare variant characterized primarily by severe early-onset periodontitis leading to premature loss of teeth and skin fragility, but it lacks the fatal systemic complications of the vascular type. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most EDS types are Autosomal Dominant (including Types 1, 2, and 4). * **Kyphoscoliotic Type (Type 6):** Notable for lysyl hydroxylase deficiency; presents with ocular fragility (corneal rupture) [1]. * **Key Clinical Triad:** Hyperextensible skin, hypermobile joints, and fragile tissues (poor wound healing) [1]. * **Vascular EDS Sign:** Translucent skin with visible underlying veins and characteristic "aged" facial features (acrogeria). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 154-156.

Question 975: Granulomatous inflammatory reaction is caused by all of the following organisms, EXCEPT:

A. M. Tuberculosis
B. M. Leprae
C. Yersinia pestis
D. Mycoplasma (Correct Answer)

Explanation: **Explanation:** A **granuloma** is a distinctive pattern of chronic inflammation characterized by a focal collection of activated macrophages (epithelioid cells), often surrounded by a collar of lymphocytes and plasma cells [2]. It is a Type IV hypersensitivity reaction triggered by agents that are difficult to eradicate [4]. **Why Mycoplasma is the correct answer:** * **Mycoplasma pneumoniae** typically causes **atypical pneumonia**, characterized by interstitial inflammation. The histological hallmark is a peribronchial and perivascular infiltration of lymphocytes and plasma cells, not granuloma formation. It lacks a cell wall and does not trigger the chronic macrophage activation required for a granulomatous response. **Analysis of incorrect options:** * **M. Tuberculosis:** The classic cause of **caseating granulomas** [1]. The cell wall contains mycolic acids (cord factor) that resist phagocytosis, leading to the formation of Ghon complexes. * **M. Leprae:** Causes leprosy, characterized by granulomatous inflammation. In **Tuberculoid leprosy**, well-formed non-caseating granulomas are seen; in **Lepromatous leprosy**, foamy macrophages (Virchow cells) predominate due to a poor T-cell response. * **Yersinia pestis:** While the acute phase of Plague is suppurative, *Yersinia* species (especially *Y. pseudotuberculosis* and *Y. enterocolitica*) are well-known causes of **necrotizing granulomas** in lymph nodes (stellate abscesses). **NEET-PG High-Yield Pearls:** 1. **Non-infectious causes of granulomas:** Sarcoidosis (non-caseating), Berylliosis, and Foreign body reactions (e.g., Talc, Sutures) [3]. 2. **Stellate Granulomas:** Classically seen in **Cat Scratch Disease** (*Bartonella henselae*), Lymphogranuloma venereum (LGV), and Tularemia. 3. **Schistosomiasis:** The most common cause of granulomatous inflammation worldwide (parasitic). 4. **Langhans Giant Cells:** Characterized by peripherally arranged nuclei in a horseshoe pattern, typical of TB granulomas [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 384-385. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [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. 198-200. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360.

Question 976: Pulp chamber is absent in which of the following conditions?

A. Dentinogenesis imperfecta (Correct Answer)
B. Amelogenesis imperfecta
C. Craniofacial dysostosis
D. None of the above

Explanation: **Explanation:** The correct answer is **Dentinogenesis Imperfecta (DI)**. **1. Why Dentinogenesis Imperfecta is correct:** Dentinogenesis imperfecta is a hereditary defect of dentin formation (specifically involving the DSPP gene). The hallmark of this condition is the **obliteration of the pulp chamber and root canals**. This occurs because the odontoblasts are functionally abnormal, leading to the continuous, rapid, and irregular deposition of dentin (circumpulpal dentin) until the entire pulp space is filled. Radiographically, this presents as "opalescent teeth" with bulbous crowns, cervical constriction (bell-shaped), and absent pulp chambers. **2. Why other options are incorrect:** * **Amelogenesis Imperfecta:** This is a defect of **enamel** formation, not dentin. While the enamel may be thin, pitted, or hypoplastic, the underlying dentin and the pulp chamber remain structurally normal. * **Craniofacial Dysostosis (Crouzon Syndrome):** This is a genetic disorder characterized by premature fusion of skull bones (craniosynostosis). While it causes midface hypoplasia and dental crowding, it does not inherently cause the obliteration of the pulp chambers. **3. Clinical Pearls for NEET-PG:** * **Shields Classification:** DI is divided into Type I (associated with Osteogenesis Imperfecta), Type II (isolated DI - most common), and Type III (Brandywine type - features "shell teeth" with enlarged pulps, the exception to the rule). * **Radiographic Triad for DI:** Bulbous crowns, constricted necks (cervical constriction), and **obliterated pulp chambers**. * **Differential Diagnosis:** Dentin Dysplasia Type I also shows pulp obliteration, but the teeth typically have "half-moon" shaped pulp remains and short, blunted roots.

Question 977: Which statement is true about fragile-X syndrome?

A. It is caused by a trinucleotide repeat sequence. (Correct Answer)
B. It is associated with chromosome breaks.
C. It involves a mitochondrial mutation.
D. It is characterized by the absence of the centromere.

Explanation: **Explanation:** **1. Why Option A is Correct:** Fragile-X syndrome is the most common cause of inherited intellectual disability. It is caused by a **trinucleotide repeat expansion** of the **CGG** sequence in the **FMR1 gene** located on the X chromosome (Xq27.3) [1]. In normal individuals, there are about 6–50 repeats; however, in affected individuals, this expands to over 200 repeats (full mutation) [1]. This expansion leads to hypermethylation of the promoter region, resulting in transcriptional silencing of the FMR1 gene and a deficiency of the Fragile X Mental Retardation Protein (FMRP) [1]. **2. Why Other Options are Incorrect:** * **Option B:** While the name "Fragile-X" comes from the appearance of a "break" or gap in the long arm of the X chromosome when cultured in folate-deficient medium, there is **no actual physical breakage** of the chromosome in vivo. It is a staining artifact representing non-staining chromatin. * **Option C:** Mitochondrial mutations involve maternal inheritance and typically affect high-energy tissues (e.g., MELAS, LHON). Fragile-X follows an **X-linked dominant** pattern with variable expressivity and anticipation [1]. * **Option D:** The centromere is present and functional; the defect is localized to the distal long arm (q) of the X chromosome [1]. **3. NEET-PG High-Yield Clinical Pearls:** * **Clinical Triad:** Intellectual disability, **macro-orchidism** (post-pubertal), and long face with large everted ears. * **Genetics:** Shows **Anticipation** (severity increases in successive generations) and the **Sherman Paradox** (anomalous inheritance pattern) [1]. * **Premutation (55-200 repeats):** Associated with Fragile X-associated Tremor/Ataxia Syndrome (FXTAS) and Premature Ovarian Failure [1]. * **Diagnosis:** PCR is used for premutations; **Southern Blot analysis** is the gold standard for detecting full mutations and methylation status [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 177-181. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 186-187.

Question 978: A 49-year-old female presents with shortness of breath and hilar lymphadenopathy on chest x-ray. Biopsy of a lymph node reveals granulomas, highly suggestive of sarcoidosis. Which of the following histological findings must be present in the biopsy material to support the diagnosis of granulomatous inflammation?

A. Asteroid bodies
B. Caseous necrosis
C. Epithelioid histiocytes (Correct Answer)
D. Fibroblast proliferation

Explanation: ### Explanation The correct answer is **C. Epithelioid histiocytes.** #### 1. Why Epithelioid Histiocytes are Correct A **granuloma** is a specific pattern of chronic inflammation characterized by a focal collection of **activated macrophages**, which transform into **epithelioid histiocytes** [1], [2]. These cells are the "sine qua non" (essential requirement) of granulomatous inflammation. They have abundant pink granular cytoplasm and indistinct cell boundaries, resembling epithelial cells [1]. Their presence, often surrounded by a rim of lymphocytes and occasional multinucleated giant cells, is what defines a lesion as granulomatous [1]. #### 2. Analysis of Incorrect Options * **A. Asteroid bodies:** These are star-shaped eosinophilic inclusions found within the giant cells of sarcoidosis. While highly characteristic of sarcoidosis, they are **not required** to define a granuloma and can be seen in other conditions like foreign body granulomas. * **B. Caseous necrosis:** This is a feature of "caseating" granulomas, most typically seen in **Tuberculosis**. Sarcoidosis is characterized by **non-caseating** granulomas [3]. Therefore, caseous necrosis is not a prerequisite for granulomatous inflammation in general. * **D. Fibroblast proliferation:** While fibroblasts may surround older granulomas (healing by fibrosis), they are a non-specific feature of many types of chronic inflammation and repair, not a defining component of a granuloma [1]. #### 3. NEET-PG High-Yield Pearls * **Definition:** A granuloma is a collection of epithelioid histiocytes [2]. * **Sarcoidosis Hallmark:** Non-caseating granulomas + Schaumann bodies (laminated calcium/protein concretions) + Asteroid bodies. * **Key Cytokine:** **IFN-γ** (Interferon-gamma), secreted by Th1 cells, is the most important cytokine for activating macrophages into epithelioid cells [1]. * **Differential:** Always rule out TB (Acid-fast bacilli stain) before diagnosing sarcoidosis, as both present with hilar lymphadenopathy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109. [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. 198-200. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 700-701.

Question 979: Which of the following is characteristic of a dental cyst?

A. Occurs from the reduced enamel epithelium
B. Replaces the tooth to which it is attached
C. Is frequently seen with a missing tooth on the X-ray
D. Has a cystic lining of stratified squamous epithelium (Correct Answer)

Explanation: **Explanation:** A **Dental Cyst** (also known as a **Radicular Cyst** or Periapical Cyst) is the most common inflammatory odontogenic cyst. It typically forms at the apex of a non-vital (necrotic) tooth due to inflammation following dental caries or pulpitis [1]. **1. Why Option D is correct:** The hallmark histological feature of a dental cyst is a lumen lined by **non-keratinized stratified squamous epithelium**. This lining is derived from the **Rest Cells of Malassez** (remnants of Hertwig’s epithelial root sheath) found in the periodontal ligament, which proliferate in response to inflammatory cytokines. **2. Why other options are incorrect:** * **Option A:** This describes a **Dentigerous Cyst** (Follicular Cyst). Dentigerous cysts originate from the reduced enamel epithelium and surround the crown of an unerupted tooth. * **Option B:** This describes an **Odontogenic Keratocyst (OKC)** or a Primordial Cyst. A dental cyst is attached to the root of an existing tooth rather than replacing it. * **Option C:** A "missing tooth" on an X-ray associated with a radiolucency is characteristic of a **Dentigerous Cyst** (where the tooth is impacted/unerupted). In a dental cyst, the involved tooth is present in the oral cavity but is non-vital. **NEET-PG High-Yield Pearls:** * **Rushton Bodies:** Eosinophilic, linear, or arch-shaped calcifications often found within the epithelial lining of radicular cysts. * **Radiology:** Appears as a well-defined unilocular radiolucency at the periapical region. * **Cholesterol Clefts:** Frequently seen in the cyst wall with associated multinucleated giant cells. * **Key Distinction:** Radicular cyst = Non-vital tooth; Dentigerous cyst = Unerupted tooth. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Head and Neck, pp. 741-742.

Question 980: What is most important for diapedesis?

A. PECAM (Correct Answer)
B. Selectins
C. Integrins
D. Mucin-like glycoprotein

Explanation: **Explanation:** **Diapedesis** (also known as Transmigration) is the process by which leukocytes squeeze through endothelial intercellular junctions to reach the site of injury [1]. **1. Why PECAM-1 is the Correct Answer:** The key molecule mediating this specific step is **PECAM-1 (Platelet Endothelial Cell Adhesion Molecule-1)**, also known as **CD31** [1]. It is expressed on both the leukocytes and the endothelial cell junctions [2]. The homophilic interaction (PECAM-1 binding to PECAM-1) acts like a "zipper," allowing the leukocyte to traverse the endothelial barrier without causing a permanent leak. **2. Why Other Options are Incorrect:** * **Selectins (E, P, and L-selectin):** These are responsible for the initial **Rolling** phase [3]. They have low-affinity interactions with Sialyl-Lewis X ligands, causing the leukocyte to slow down. * **Integrins (e.g., LFA-1, VLA-4):** These mediate **Firm Adhesion** [3]. Once activated by chemokines, integrins bind tightly to ligands like ICAM-1 and VCAM-1 on the endothelium, stopping the rolling leukocyte. * **Mucin-like glycoproteins (e.g., GlyCam-1, PSGL-1):** These serve as ligands for selectins and are primarily involved in the **Rolling** phase. **Clinical Pearls for NEET-PG:** * **Sequence of Extravasation:** Rolling (Selectins) → Activation (Chemokines) → Adhesion (Integrins) → Diapedesis (PECAM-1) [2]. * **Site of Diapedesis:** It occurs predominantly in the **systemic post-capillary venules** [2]. * **LAD Type 1:** Caused by a deficiency in **Integrins** (specifically CD18/β2 chain), leading to impaired firm adhesion and recurrent infections without pus formation [1]. * **LAD Type 2:** Caused by a defect in **Sialyl-Lewis X** (ligand for selectins), leading to impaired rolling. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Migration in the tissues toward a chemotactic stimulus, pp. 86-87. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87.

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