Inflammation and Repair — MCQs

Inflammation and Repair Indian Medical PG Practice Questions and MCQs

Question 221: Which one of the following statements best describes the process called chemotaxis?

A. Abnormal fusion of phagosomes to primary lysosomes
B. Attachment of chemicals to extracellular material to increase phagocytosis
C. Dilation of blood vessels by chemotherapeutic drugs
D. Movement of cells toward a certain site or source (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Movement of cells toward a certain site or source** **Concept:** Chemotaxis is the process of **unidirectional movement** of leukocytes (such as neutrophils and macrophages) along a chemical gradient toward the site of injury [1]. After leukocytes exit the bloodstream (emigration), they are guided by substances known as **chemoattractants** [2]. These substances bind to specific G protein-coupled receptors (GPCRs) on the leukocyte surface, triggering actin polymerization at the leading edge of the cell, which results in "crawling" toward the stimulus [1]. **Analysis of Incorrect Options:** * **Option A:** This describes the defect seen in **Chediak-Higashi Syndrome**, where a mutation in the LYST gene leads to disordered intracellular trafficking and failure of phagolysosome formation. * **Option B:** This describes **Opsonization** [1]. Opsonins (like IgG or C3b) coat microbes to make them more "appetizing" and easily recognized by phagocytic cells [1]. * **Option C:** This is a distractor. While vasodilation occurs during inflammation (mediated by histamine/prostaglandins), it is not related to the term "chemotaxis." **NEET-PG High-Yield Pearls:** 1. **Exogenous Chemoattractants:** The most common are bacterial products, particularly those with **N-formylmethionine** termini. 2. **Endogenous Chemoattractants:** * **C5a** (Complement system) * **Leukotriene B4 (LTB4)** (Arachidonic acid metabolite) * **IL-8** (A major chemokine for neutrophils) 3. **Sequence of Leukocyte Events:** Margination → Rolling (Selectins) → Adhesion (Integrins) → Transmigration (PECAM-1) → **Chemotaxis** [2]. 4. **Nature of Movement:** It is an active, energy-dependent process involving the cytoskeleton (actin filaments) [1]. **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. 190-191. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89.

Question 222: Which antibody is least commonly seen in keloids?

A. IgG
B. IgM
C. IgE (Correct Answer)
D. None of the above

Explanation: **Explanation:** Keloids are characterized by an exaggerated healing response resulting in excessive collagen deposition (primarily Type I and Type III) that extends beyond the boundaries of the original wound. Immunological studies of keloid tissue have demonstrated the presence of various immunoglobulins, suggesting an immune-mediated component in their pathogenesis. **Why IgE is the correct answer:** Research analyzing the immunological profile of keloids has consistently shown that **IgG and IgM** are the predominant antibodies found within the lesional tissue. These antibodies are often found in association with antinuclear antibodies (ANA) or as part of immune complexes within the extracellular matrix. **IgE**, however, is typically associated with Type I hypersensitivity (allergic) reactions and parasitic infections. It is **least commonly** detected or found in negligible amounts in keloid tissue compared to the other classes. **Analysis of Incorrect Options:** * **IgG:** This is the most abundant antibody found in keloids. It is often localized in the perivascular areas and the collagen fibers, suggesting a chronic inflammatory stimulus. * **IgM:** This is frequently detected alongside IgG in keloid specimens. Its presence indicates an active, ongoing immune response within the fibroproliferative lesion. **NEET-PG High-Yield Pearls:** * **Collagen Type:** Keloids contain thick, wavy "glassy" collagen bundles (mostly **Type I and III**). * **Boundaries:** Unlike hypertrophic scars, keloids **extend beyond** the site of original injury and rarely regress spontaneously. * **Genetics:** Higher incidence in individuals with darker skin pigmentation (African, Asian, and Hispanic populations). * **Common Sites:** Presternal area, deltoid, and earlobes. * **Treatment:** Intralesional corticosteroids (Triamcinolone) are the first-line medical therapy.

Question 223: Which of the following types of necrosis is seen in blood vessels due to immune complex-mediated damage?

A. Coagulative necrosis
B. Liquefactive necrosis
C. Fibrinoid necrosis (Correct Answer)
D. Caseous necrosis

Explanation: **Explanation:** **Correct Answer: C. Fibrinoid Necrosis** Fibrinoid necrosis is a specialized form of cell death typically seen in immune-mediated vascular damage [3]. It occurs when **antigen-antibody complexes** (Type III Hypersensitivity) are deposited in the walls of arteries [3], [4]. These complexes, along with leaked plasma proteins (like fibrin), create a bright pink, amorphous, "fibrin-like" appearance under H&E staining [1]. This is a hallmark of conditions like **Polyarteritis Nodosa (PAN)** [2], Systemic Lupus Erythematosus (SLE) [3], and Malignant Hypertension [1]. **Why other options are incorrect:** * **A. Coagulative Necrosis:** The most common type of necrosis, usually caused by ischemia/infarcts in solid organs (except the brain). The cell architecture is preserved for a few days. * **B. Liquefactive Necrosis:** Characterized by the digestion of dead cells into a liquid viscous mass. It is typically seen in focal bacterial/fungal infections (abscesses) and **CNS infarcts**. * **D. Caseous Necrosis:** A "cheese-like" friable white appearance seen classically in **Tuberculosis**. Microscopically, it presents as a structureless, granular debris surrounded by a granulomatous inflammatory border. **High-Yield Clinical Pearls for NEET-PG:** * **Malignant Hypertension:** Along with immune complexes, extreme high blood pressure can also cause fibrinoid necrosis in arterioles [1]. * **Aschoff Bodies:** Fibrinoid necrosis is a key component of Aschoff bodies seen in Rheumatic Heart Disease. * **Staining:** Fibrinoid material stains intensely acidic (eosinophilic) on H&E and bright red with Mallory's phosphotungstic acid hematoxylin (PTAH) stain. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 277-278. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 517-518. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 514-515. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 278-279.

Question 224: What is the primary role of P-selectin in the process of inflammation?

A. Rolling of leukocytes along the endothelium (Correct Answer)
B. Stable adhesion of leukocytes to the endothelium
C. Directing leukocytes to specific lymphoid tissues
D. Passage of leukocytes through the endothelial barrier

Explanation: **Explanation:** The recruitment of leukocytes from the blood vessel to the site of injury occurs in a series of well-defined steps. **P-selectin** (along with E-selectin) is a cell adhesion molecule expressed on activated endothelial cells that mediates the initial step of **Rolling (Option A)** [1]. Selectins bind to sialylated oligosaccharides (like **Sialyl-Lewis X**) on leukocyte surfaces [1]. These bonds have a high "off-rate," meaning they break and reform easily under the force of blood flow, causing the leukocyte to tumble or "roll" slowly along the vessel wall [3]. **Analysis of Incorrect Options:** * **Option B (Stable Adhesion):** This step is mediated by **Integrins** (e.g., VLA-4, LFA-1) on leukocytes binding to **Immunoglobulin superfamily** ligands (e.g., VCAM-1, ICAM-1) on the endothelium [3]. * **Option C (Homing to Lymphoid Tissues):** This is primarily the role of **L-selectin**, which is expressed on leukocytes and helps them home to high endothelial venules (HEVs) in lymph nodes [1]. * **Option D (Transmigration/Diapedesis):** This describes the passage through the endothelial barrier, which is primarily mediated by **PECAM-1 (CD31)** [2]. **High-Yield NEET-PG Pearls:** * **Storage:** P-selectin is pre-stored in **Weibel-Palade bodies** of endothelial cells and **Alpha-granules** of platelets. It can be rapidly redistributed to the cell surface by mediators like histamine or thrombin. * **Deficiency:** A deficiency in Sialyl-Lewis X (the ligand for selectins) leads to **Leukocyte Adhesion Deficiency (LAD) Type 2**, characterized by recurrent infections and a lack of pus formation [2]. * **Mnemonic:** **P**-selectin = **P**latelets and **P**assive rolling. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 87-89. [3] 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.

Question 225: What is scar tissue called?

A. Granulation tissue
B. Keloid (Correct Answer)
C. Callus
D. All of the above

Explanation: **Explanation:** The correct answer is **B. Keloid**. **1. Why Keloid is correct:** A keloid is a specific type of **hypertrophic scar tissue** that results from an excessive accumulation of collagen (primarily Type I and Type III) during the repair process [1]. Unlike normal scars, keloids extend beyond the boundaries of the original wound and do not regress spontaneously [1], [2]. They represent an aberration in the remodeling phase of wound healing, where the balance between collagen synthesis and degradation is lost. **2. Why other options are incorrect:** * **A. Granulation tissue:** This is the highly vascularized, pink, soft tissue that forms during the *early* stages of wound healing. It consists of new capillaries (angiogenesis), fibroblasts, and inflammatory cells. It is a precursor to a scar, not the scar tissue itself. * **C. Callus:** This term refers to the specialized repair tissue formed during the healing of a **bone fracture**. While it is a form of "repair," it is specific to osseous tissue and involves fibrocartilage and mineralized bone, rather than the fibrous connective tissue typically referred to as a "scar" in soft tissue. **3. NEET-PG High-Yield Pearls:** * **Keloid vs. Hypertrophic Scar:** Keloids extend *beyond* the wound margins and have thick "glassy" collagen (collagen bundles) [1]. Hypertrophic scars stay *within* the wound boundaries and often regress over time. * **Collagen Transition:** During wound maturation, Type III collagen (found in granulation tissue) is replaced by **Type I collagen** (the main component of mature scars). * **Genetic Predisposition:** Keloids are significantly more common in individuals with darker skin pigmentation (African, Asian, or Hispanic descent) [2]. * **Common Sites:** The sternum, earlobes, and deltoid region are high-risk areas for keloid formation. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 121. [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. 106-107.

Question 226: Liquefactive necrosis is seen in which of the following organs?

A. Heart
B. Brain (Correct Answer)
C. Lungs
D. Spleen

Explanation: **Explanation:** Liquefactive necrosis is characterized by the transformation of the tissue into a liquid, viscous mass. This occurs when the rate of enzymatic digestion of cells exceeds the rate of protein denaturation. **Why the Brain is the Correct Answer:** In the **Central Nervous System (CNS)**, hypoxic injury (infarction) uniquely results in liquefactive necrosis rather than coagulative necrosis [1]. This is primarily due to the brain's high lipid content and the relative lack of a supportive connective tissue framework. When brain cells die, they are rapidly digested by lysosomal enzymes released by neurons and microglia, resulting in a fluid-filled cavity [1]. **Analysis of Incorrect Options:** * **A. Heart:** Ischemic injury to the myocardium leads to **Coagulative Necrosis**. The cell proteins denature, preserving the basic structural outline of the tissue for several days (ghost cells). * **C. Lungs:** While the lungs can undergo liquefactive necrosis during a bacterial abscess, the standard pattern for pulmonary infarction is **Coagulative Necrosis**. (Note: Tuberculosis in the lungs causes Caseous Necrosis). * **D. Spleen:** Like most solid visceral organs, ischemia in the spleen leads to **Coagulative Necrosis**, typically resulting in wedge-shaped pale infarcts. **High-Yield Clinical Pearls for NEET-PG:** * **Two main scenarios for Liquefactive Necrosis:** 1. Brain Infarcts; 2. Abscesses (due to pyogenic bacterial or fungal infections). * **Coagulative Necrosis** is the most common pattern of necrosis in all solid organs **except** the brain. * **Wet Gangrene** is a form of liquefactive necrosis superimposed on coagulative necrosis, usually seen in the limbs or bowel. * **Enzymatic Fat Necrosis** is specifically associated with Acute Pancreatitis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1268-1269.

Question 227: Which of the following is NOT considered a cardinal sign of inflammation?

A. Pain
B. Swelling
C. Redness
D. Absence of functional loss (Correct Answer)

Explanation: The cardinal signs of inflammation, first described by **Aulus Cornelius Celsus** in the 1st century AD, are the hallmark clinical features of acute inflammation [1]. **Explanation of the Correct Answer:** The correct answer is **D (Absence of functional loss)** because **Loss of Function (*Functio Laesa*)** is actually the fifth cardinal sign of inflammation [1]. It was added later by **Rudolf Virchow** (the father of modern pathology). Therefore, the *absence* of functional loss contradicts the established clinical presentation of inflammation. **Analysis of Incorrect Options:** * **A. Pain (*Dolor*):** Caused by the release of chemical mediators like bradykinin and prostaglandins (PGE2), which sensitize nerve endings, and by the pressure exerted by inflammatory edema [2]. * **B. Swelling (*Tumor*):** Results from increased vascular permeability, leading to the accumulation of extravascular fluid (exudate) in the interstitial space. * **C. Redness (*Rubor*):** Occurs due to vasodilation and increased blood flow (hyperemia) to the injured area [1]. **NEET-PG High-Yield Pearls:** 1. **The Five Signs:** *Rubor* (Redness), *Tumor* (Swelling), *Calor* (Heat), *Dolor* (Pain), and *Functio Laesa* (Loss of function) [1]. 2. **Mediator of Pain:** Prostaglandin **PGE2** and **Bradykinin** are the primary mediators responsible for the "Dolor" component [2]. 3. **Mediator of Fever:** **IL-1 and TNF-̑** (produced by macrophages) act on the hypothalamus to induce fever [2]. 4. **Vascular Hallmark:** The most characteristic feature of acute inflammation is **increased vascular permeability**, leading to edema [2]. **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. 183-186. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101.

Question 228: A keloid scar is primarily composed of which type of tissue?

A. Dense collagen (Correct Answer)
B. Loose fibrous tissue
C. Granulomatous tissue
D. Loose areolar tissue

Explanation: ### Explanation **Correct Option: A. Dense Collagen** A keloid is a pathological result of an aberrant wound-healing process characterized by the excessive accumulation of extracellular matrix components, specifically **Type I and Type III collagen**. Histologically, keloids are defined by thick, eosinophilic, hyalinized bundles of **dense collagen** that are arranged haphazardly [1]. Unlike hypertrophic scars, keloids extend beyond the boundaries of the original wound and rarely regress spontaneously [1]. **Why the other options are incorrect:** * **B. Loose fibrous tissue:** This is characteristic of early stages of wound healing or normal dermis. In keloids, the fibrous tissue is abnormally thickened and densely packed, not loose [2]. * **C. Granulomatous tissue:** This refers to a specific type of chronic inflammation (e.g., TB, Sarcoidosis) characterized by collections of activated macrophages (epithelioid cells) and multinucleated giant cells. Keloids are a disorder of repair, not granulomatous inflammation. * **D. Loose areolar tissue:** This is a type of connective tissue found in the hypodermis and around blood vessels, providing flexibility. It lacks the dense, structural rigidity found in a keloid scar. **High-Yield Clinical Pearls for NEET-PG:** * **Collagen Type:** Keloids contain a high ratio of Type III to Type I collagen initially, but eventually, dense Type I collagen predominates. * **Genetic Predisposition:** More common in individuals with darker skin pigmentation (African, Asian, or Hispanic descent) [2]. * **Common Sites:** Presternal area, back, and earlobes. * **Key Distinction:** **Hypertrophic scars** stay within the wound boundary and contain parallel collagen bundles; **Keloids** extend beyond the boundary and contain disorganized, thick collagen bundles [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 121. [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. 106-107.

Question 229: Following surgery, the wound heals in a linear fashion without any complication. This type of healing is called?

A. Primary healing (Correct Answer)
B. Secondary healing
C. Delayed primary healing
D. Reepithelialization

Explanation: ### Explanation **Correct Answer: A. Primary healing (Healing by First Intention)** **Why it is correct:** Primary healing occurs when wound edges are clean, uninfected, and closely apposed, typically seen in **surgically incised wounds** closed with sutures, staples, or adhesive strips [1, 2]. Because the tissue loss is minimal, the wound heals in a **linear fashion** with a very small scar [4]. The process involves rapid epithelial regeneration and minimal formation of granulation tissue [2]. **Why the other options are incorrect:** * **B. Secondary healing (Second Intention):** This occurs in wounds with extensive tissue loss, irregular edges, or infection (e.g., large ulcers or abscesses) [3]. It involves significant granulation tissue formation and **wound contraction** (mediated by myofibroblasts), resulting in a larger, irregular scar [1]. * **C. Delayed primary healing (Third Intention):** This is a hybrid approach where a wound is initially left open (due to contamination or edema) and closed surgically after a few days once the infection is controlled. * **D. Reepithelialization:** This is a specific *component* of the healing process where epithelial cells migrate across the wound surface [3]. While it occurs in primary healing, it does not describe the entire clinical pattern of "linear healing" following surgery. **High-Yield Clinical Pearls for NEET-PG:** * **The Hallmark of Secondary Healing:** Wound contraction is the defining feature that distinguishes it from primary healing [3]. * **Tensile Strength:** At the end of 1 week (when sutures are removed), wound strength is ~10% [2, 5]. It reaches ~70-80% by 3 months but **never** returns to 100% of the original pre-wound strength [5]. * **Key Cell Type:** **Myofibroblasts** are responsible for wound contraction in secondary healing [1]. * **Type of Collagen:** Initially, Type III collagen is deposited; it is later replaced by **Type I collagen** (stronger) during the remodeling phase. **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. 105-106. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 117-119. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 119. [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. 106-107. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 119-121.

Question 230: A 10-year-old male child complains of pain and swelling in the left foot after an injury while playing. What mediates the migration of leukocytes to the site of injury?

A. Cytokines
B. Histamine
C. Chemokines (Correct Answer)
D. Prostaglandins

Explanation: ### Explanation **Correct Answer: C. Chemokines** Leukocyte migration to the site of injury is a multi-step process known as the **Leukocyte Adhesion Cascade** [2]. While selectins and integrins handle rolling and adhesion [4], **chemokines** (chemoattractant cytokines) are the primary mediators responsible for the **directed movement (chemotaxis)** of leukocytes [3]. They create a chemical gradient that guides leukocytes through the vessel wall (diapedesis) and toward the focus of inflammation. Common examples include **IL-8** (for neutrophils) and **MCP-1** (for monocytes) [1]. **Analysis of Incorrect Options:** * **A. Cytokines:** This is a broad category of signaling proteins. While some cytokines (like TNF and IL-1) induce the expression of adhesion molecules on endothelium [4], they do not directly mediate the "migration" or directional movement as specifically as chemokines do [1]. * **B. Histamine:** Released primarily by mast cells, histamine is the chief mediator of the **immediate transient response**, causing vasodilation and increased vascular permeability (leading to edema), but it does not guide leukocyte migration [1]. * **D. Prostaglandins:** These arachidonic acid metabolites are primarily involved in inducing **vasodilation, pain, and fever** [1]. They do not act as chemoattractants. **NEET-PG High-Yield Pearls:** * **Chemotactic Agents:** Remember the "Big Four" for Neutrophils: **C5a, LTB4, IL-8, and Bacterial products** (N-formyl methionine) [1]. * **Steps of Migration:** 1. *Rolling:* Mediated by Selectins (P and E) [4]. 2. *Adhesion:* Mediated by Integrins (ICAM-1, VCAM-1) [4]. 3. *Transmigration:* Mediated by **PECAM-1 (CD31)** [3]. 4. *Chemotaxis:* Mediated by Chemokines [3]. * **Clinical Correlation:** Deficiencies in these processes lead to **Leukocyte Adhesion Deficiency (LAD)**, characterized by delayed umbilical cord separation and recurrent infections without pus formation [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 101. [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, pp. 87-89. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 87.

Practice by Chapter

Acute Inflammation: Vascular Events

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Acute Inflammation: Cellular Events

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Chemical Mediators of Inflammation

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Chronic Inflammation

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Granulomatous Inflammation

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Systemic Effects of Inflammation

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Wound Healing

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Tissue Regeneration

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Fibrosis and Repair

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Resolution of Inflammation

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