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Questions and Answers
What is primarily responsible for the migration of leukocytes through interendothelial spaces during inflammation?
What is primarily responsible for the migration of leukocytes through interendothelial spaces during inflammation?
Which of the following cytokines is NOT primarily involved in acute inflammation?
Which of the following cytokines is NOT primarily involved in acute inflammation?
Which mechanism helps eliminate microbes during the process of phagocytosis?
Which mechanism helps eliminate microbes during the process of phagocytosis?
Which substance produced by macrophages is NOT involved in the process of tissue injury during inflammation?
Which substance produced by macrophages is NOT involved in the process of tissue injury during inflammation?
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What is a characteristic feature of chronic inflammation?
What is a characteristic feature of chronic inflammation?
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Which of the following is primarily a feature of granulomatous inflammation?
Which of the following is primarily a feature of granulomatous inflammation?
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What is the primary role of Fibrin formation during acute inflammation?
What is the primary role of Fibrin formation during acute inflammation?
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Which of the following cytokines is particularly noted for amplifying and prolonging the inflammatory response?
Which of the following cytokines is particularly noted for amplifying and prolonging the inflammatory response?
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Which of the following conditions is most likely to lead to chronic inflammation?
Which of the following conditions is most likely to lead to chronic inflammation?
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How do ROS (reactive oxygen species) contribute to inflammation?
How do ROS (reactive oxygen species) contribute to inflammation?
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What role do cytokines such as TNF and IL-1 play in systemic inflammation?
What role do cytokines such as TNF and IL-1 play in systemic inflammation?
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Which type of inflammation is characterized by watery, protein-poor fluid effusions?
Which type of inflammation is characterized by watery, protein-poor fluid effusions?
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What type of cells are primarily responsible for removing fibrinous exudates during fibrinous inflammation?
What type of cells are primarily responsible for removing fibrinous exudates during fibrinous inflammation?
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Which cell type is characteristic of labile tissues, which continuously divide?
Which cell type is characteristic of labile tissues, which continuously divide?
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What is required for tissue regeneration to occur intact, without scar formation?
What is required for tissue regeneration to occur intact, without scar formation?
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In which situation does septic shock typically occur?
In which situation does septic shock typically occur?
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What characterizes induced pluripotent stem (iPS) cells?
What characterizes induced pluripotent stem (iPS) cells?
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What is a potential result of excessive extracellular matrix (ECM) production during wound healing?
What is a potential result of excessive extracellular matrix (ECM) production during wound healing?
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What happens during ulceration as a form of inflammation?
What happens during ulceration as a form of inflammation?
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Which of the following is NOT a characteristic of stable tissues?
Which of the following is NOT a characteristic of stable tissues?
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What is the primary role of inflammation in response to tissue injury?
What is the primary role of inflammation in response to tissue injury?
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Which component is primarily responsible for the vascular reaction during acute inflammation?
Which component is primarily responsible for the vascular reaction during acute inflammation?
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What characterizes the cellular infiltrate in acute inflammation?
What characterizes the cellular infiltrate in acute inflammation?
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What feature distinguishes chronic inflammation from acute inflammation?
What feature distinguishes chronic inflammation from acute inflammation?
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Which of the following processes is NOT part of the steps of inflammatory response?
Which of the following processes is NOT part of the steps of inflammatory response?
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What does increased vascular permeability during acute inflammation allow?
What does increased vascular permeability during acute inflammation allow?
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Which mediators are involved in the process of vasodilation during inflammation?
Which mediators are involved in the process of vasodilation during inflammation?
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What outcome may arise from persistent injury during acute inflammation?
What outcome may arise from persistent injury during acute inflammation?
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Which of the following is NOT a classic sign of acute inflammation?
Which of the following is NOT a classic sign of acute inflammation?
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What happens during the regulation phase of the inflammatory response?
What happens during the regulation phase of the inflammatory response?
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Study Notes
Inflammation
- Host response to foreign invaders and necrotic tissue, but it is itself capable of causing tissue damage.
- A protective response, aimed at removing the initial cause of cell injury, necrotic cells, and tissues.
- Can have harmful effects, contributing to conditions like anaphylactic shock, rheumatoid arthritis, and atherosclerosis.
Main Components of Inflammation
- Vascular Reaction: Increased blood flow and vascular permeability.
- Cellular Response: Recruitment of leukocytes to the site of injury.
Steps of the Inflammatory Response
- Recognition of the injurious agent.
- Recruitment of leukocytes.
- Removal of the agent.
- Regulation (control) of the response.
- Resolution (repair).
Features of Acute Inflammation
- Fast onset, within minutes or hours.
- Main cellular infiltrate includes neutrophils.
- Usually mild and self-limited tissue injury.
- Prominent local and systemic signs.
Acute Inflammation
- Short duration, lasting from a few minutes to a few days.
- Characterized by:
- Vasodilation: Increased blood flow (hyperemia).
- Increased Vascular Permeability: Leakage of plasma proteins (exudation).
- Leukocyte Emigration: Neutrophils migrate towards the site of injury.
Outcomes of Acute Inflammation
- Elimination of the noxious stimulus, followed by repair.
- Persistent injury, resulting in chronic inflammation.
Signs of Inflammation
- Heat: Calor
- Redness: Rubor
- Swelling: Tumor
- Pain: Dolor
- Loss of Function: Functio laesa
Leukocyte Recruitment
- Leukocytes are recruited from the blood into the extravascular tissue.
- A multi-step process involving:
- Loose attachment and rolling on endothelium (mediated by selectins).
- Firm attachment to endothelium (mediated by integrins).
- Migration through interendothelial spaces.
Cell-Derived Mediators of Inflammation
- Vasoactive Amines: Histamine and serotonin, causing vasodilation and increased vascular permeability.
-
Arachidonic Acid Metabolites: Prostaglandins and leukotrienes, involved in vascular reactions, leukocyte chemotaxis, and other reactions of inflammation.
- Lipoxins antagonize prostaglandins and leukotrienes.
- Cytokines: TNF, IL-1, IL-6, and chemokines, mediate leukocyte recruitment and migration.
- Reactive Oxygen Species (ROS): Microbial killing and tissue injury.
- Nitric Oxide (NO): Vasodilation and microbial killing.
- Lysosomal Enzymes: Microbial killing and tissue injury.
Plasma Protein-Derived Mediators of Inflammation
- Complement Proteins: Activated by microbes or antibodies, lead to chemotaxis, opsonization, and cell killing.
- Coagulation Proteins: Activated factor XII triggers the clotting, kinin, and complement cascades.
- Kinins: Mediated by proteolytic cleavage of precursors, causing vascular reactions and pain.
Sequence of Events in Acute Inflammation
- Increased Blood Flow: Vasodilation leads to erythema and warmth.
- Exudation: Increased vascular permeability leads to protein-rich extravascular fluid (tissue edema).
- Leukocyte Adhesion and Migration: Leukocytes, primarily neutrophils, adhere to the endothelium and migrate to the site of injury.
- Phagocytosis and Degradation: Leukocytes eliminate the offending agent.
Beneficial Effects of Acute Inflammation
- Dilution of toxins.
- Exudation of protective antibodies.
- Fibrin formation, delaying bacterial spread.
- Exudation of plasma mediators, including complement, coagulation, fibrinolytic, and kinin systems.
- Exudation of nutrients.
- Promotion of immunity.
Outcomes of Acute Inflammation
- Complete Resolution: Tissue returns to normal.
- Fibrosis: Occurs when inflammation is in tissues that do not regenerate, after substantial tissue destruction, or with extensive fibrinous exudates.
- Abscess Formation: Focal collection of pus caused by deep seeding of microorganisms or secondary infection.
- Progression to Chronic Inflammation: Persistent injury leads to chronic inflammation.
Chronic Inflammation
- Longer duration, lasting days or years.
- Characterized by:
- Infiltration by mononuclear cells (monocytes, lymphocytes, and macrophages).
- Tissue destruction.
- Tissue repair (vascular proliferation and fibrosis).
Causes of Chronic Inflammation
- Persistent infections.
- Prolonged exposure to toxic agents.
- Autoimmune disorders.
Features of Chronic Inflammation
- Prolonged host response to a persistent stimulus.
- Often caused by microbes that resist elimination, immune responses against self and environmental antigens, or toxic substances.
- Characterized by persistent inflammation, tissue injury, attempted repair by scarring, and an immune response.
- Cellular infiltrate includes activated macrophages, lymphocytes, and plasma cells, often with prominent fibrosis.
Granulomatous Inflammation
- Aggregation of activated macrophages, often with epithelioid appearance.
- Causes:
- Bacterial infection (e.g., tuberculosis, leprosy, syphilis).
- Parasitic infection (e.g., bilharziasis).
- Fungal infection (e.g., histoplasmosis).
- Inorganic metals (e.g., silica, berylliosis).
- Foreign body.
- Unknown (e.g., sarcoidosis)
Systemic Effects of Inflammation
- Fever: Cytokines (TNF, IL-1) stimulate prostaglandin production in the hypothalamus.
- Production of Acute-Phase Proteins: C-reactive protein, stimulated by cytokines (IL-6, others) acting on liver cells.
- Leukocytosis: Cytokines (CSFs) stimulate leukocyte production in the bone marrow.
Septic Shock
- Severe infections can lead to septic shock, with decreased blood pressure, disseminated intravascular coagulation, and metabolic abnormalities.
- Induced by high levels of TNF.
Cell Proliferation, the Cell Cycle, and Stem Cells
- Regeneration of tissues is driven by proliferation of uninjured cells and replacement from stem cells.
- Cell proliferation occurs when quiescent cells enter the cell cycle.
- The cell cycle is regulated by stimulators and inhibitors.
- Tissues are classified into labile, stable, and permanent, based on the proliferative capacity of their cells.
Extracellular Matrix and Tissue Repair
- The ECM consists of the interstitial matrix and basement membranes.
- Provides mechanical support, acts as a substrate for cell growth, and regulates cell proliferation and differentiation.
- An intact ECM is essential for tissue regeneration.
- If damaged, repair can only be accomplished by scar formation.
Morphologic Patterns of Acute and Chronic Inflammation
- Serous Inflammation: Watery, protein-poor fluid derived from serum or mesothelial cells.
- Fibrinous Inflammation: Meshwork of threads or an amorphous coagulum, often replaced by fibrosis.
- Suppurative (Purulent) Inflammation: Presence of pus, consisting of neutrophils, necrotic cells, and fluid.
- Ulceration: Erosion of an epithelial surface by necrosis with associated inflammation.
Cutaneous Wound Healing
- Can heal by primary union (first intention) or secondary union (second intention).
- Secondary healing involves more extensive scarring and wound contraction.
- Many conditions can alter wound healing, including infection and diabetes.
- Excessive production of ECM can cause keloids.
- Persistent stimulation of collagen synthesis leads to fibrosis.
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Description
This quiz covers the fundamental concepts of inflammation, including its purpose, mechanisms, and components. You'll explore the steps of the inflammatory response and the characteristics distinguishing acute inflammation from other types of inflammation. Test your knowledge on how the body reacts to injury and infection.
