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Questions and Answers
What is the primary purpose of inflammation?
What is the primary purpose of inflammation?
What is the role of opsonins in the process of phagocytosis?
What is the role of opsonins in the process of phagocytosis?
Which of the following is NOT a classical sign of inflammation?
Which of the following is NOT a classical sign of inflammation?
In which type of inflammation is tissue destruction more prominent?
In which type of inflammation is tissue destruction more prominent?
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Which type of reactive species is primarily involved in the oxidative burst during the microbial killing process?
Which type of reactive species is primarily involved in the oxidative burst during the microbial killing process?
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Why are neutrophils predominant in acute inflammation?
Why are neutrophils predominant in acute inflammation?
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What are the five Rs of the inflammatory response?
What are the five Rs of the inflammatory response?
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What effect do lysosomal enzymes released during phagocytosis have?
What effect do lysosomal enzymes released during phagocytosis have?
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Which cells are primarily involved in the acute inflammatory response?
Which cells are primarily involved in the acute inflammatory response?
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Which of the following triggers can initiate acute inflammation?
Which of the following triggers can initiate acute inflammation?
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Which condition exemplifies a genetic defect in leukocyte adhesion?
Which condition exemplifies a genetic defect in leukocyte adhesion?
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What is a primary function of chemical mediators in acute inflammation?
What is a primary function of chemical mediators in acute inflammation?
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What is the consequence of prolonged or inappropriate inflammatory reactions?
What is the consequence of prolonged or inappropriate inflammatory reactions?
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What role do histamine and serotonin play during acute inflammation?
What role do histamine and serotonin play during acute inflammation?
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What is a key component of the vascular response in acute inflammation?
What is a key component of the vascular response in acute inflammation?
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What is the effect of the complement system in the process of inflammation?
What is the effect of the complement system in the process of inflammation?
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Which mediator is primarily responsible for the regulation of the inflammatory response?
Which mediator is primarily responsible for the regulation of the inflammatory response?
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What immediate effect does the release of chemical mediators have on the surrounding tissue?
What immediate effect does the release of chemical mediators have on the surrounding tissue?
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What effect does inflammation have on the healing process?
What effect does inflammation have on the healing process?
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Which type of cells synthesize cytokines during the inflammatory process?
Which type of cells synthesize cytokines during the inflammatory process?
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What causes increased vascular permeability during acute inflammation?
What causes increased vascular permeability during acute inflammation?
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What is characterized by the absence of prominent cellular response and has a yellow, straw-like color?
What is characterized by the absence of prominent cellular response and has a yellow, straw-like color?
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During the margination process, which of the following occurs?
During the margination process, which of the following occurs?
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Which type of fluid is characterized by having a high protein concentration and often contains inflammatory cells?
Which type of fluid is characterized by having a high protein concentration and often contains inflammatory cells?
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Which mechanism leads to the development of stasis during inflammation?
Which mechanism leads to the development of stasis during inflammation?
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Which of the following is NOT a major family of adhesion molecules involved in the adhesion process?
Which of the following is NOT a major family of adhesion molecules involved in the adhesion process?
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In terms of leukocyte migration, what is the role of chemotaxis?
In terms of leukocyte migration, what is the role of chemotaxis?
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What effect does increased vascular permeability have on blood viscosity?
What effect does increased vascular permeability have on blood viscosity?
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What type of injury results in leukocyte-dependent injury during inflammation?
What type of injury results in leukocyte-dependent injury during inflammation?
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What role do vasoactive mediators play in the process of inflammation?
What role do vasoactive mediators play in the process of inflammation?
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Study Notes
Inflammation: A Protective Response
- Inflammation is a complex process involving tissue and microcirculation in response to injury or infection.
- Key features include:
- Release of inflammatory mediators
- Movement of fluids and leukocytes from blood to tissues
- Aims to eliminate the cause of injury, remove altered cells, and initiate healing.
- While beneficial, inflammation can cause harm if excessive, prolonged, or misdirected (e.g., autoimmune reactions).
- Components of the inflammatory response:
- Circulating cells and proteins
- Blood vessel wall
- Extracellular matrix and cells
The Five Rs of Inflammation
- Recognition: Immune cells detect the injurious agent.
- Recruitment: Leukocytes are drawn to the site of inflammation.
- Removal: The injurious agent is eliminated.
- Regulation: The inflammatory response is controlled.
- Resolution: Tissue repair and restoration of function occur.
Types of Inflammation
-
Acute inflammation:
- Short duration
- Fluid accumulation (edema)
- Presence of neutrophils (multinuclear cells)
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Chronic inflammation:
- Long duration
- Tissue destruction
- Presence of macrophages and lymphocytes (mononuclear cells)
- Overlap: Acute and chronic inflammation can exist simultaneously.
Acute Inflammation: Classical Signs
- Redness (rubor)
- Swelling (tumor)
- Heat (calor)
- Pain (dolor)
- Loss of function (functio laesa)
Stimuli Triggering Acute Inflammation
- Infections
- Tissue necrosis
- Foreign bodies
- Physical and chemical agents
Vascular Response in Acute Inflammation
- Vasodilation: Widening of blood vessels leads to increased blood flow, causing redness (rubor) and heat (calor).
- Increased vascular permeability: Endothelial cells lining blood vessels become leaky, allowing fluids and proteins to escape into the interstitial space, resulting in swelling (tumor).
Mechanisms for Increased Vascular Permeability
- Endothelial cell contraction: Mediated by vasoactive mediators (e.g., histamine, leukotrienes), causing temporary gaps between endothelial cells, primarily in venules.
- Direct injury: Damage to endothelial cells by toxins, burns, or chemicals, affecting arterioles, capillaries, and venules.
- Leukocyte-dependent injury: Leukocytes contribute to damage, leading to sustained permeability, primarily in venules and pulmonary capillaries.
- Increased transcytosis: Transcellular transport of fluid is enhanced, predominantly in venules, driven by vascular endothelium-derived growth factor.
Exudate: Inflammatory Fluid
- Exudate: Protein-rich fluid in inflammatory sites with a high specific gravity (> 1.015).
- Transudate: Fluid with low protein content and specific gravity (< 1.015).
- Edema: Fluid accumulation in the extravascular compartment and interstitial tissues.
- Effusion: Excess fluid within body cavities (e.g., peritoneum, pleura).
Types of Exudates
- Serous exudate: Clear, straw-colored fluid with minimal cellular response.
- Serosanguineous exudate: Serous fluid with red blood cells, giving it a reddish tinge.
- Fibrinous exudate: Contains high levels of fibrin, often seen in more severe inflammation.
- Purulent exudate: Contains pus, a mixture of dead leukocytes, cellular debris, and microorganisms.
Leukocyte Cellular Events: Journey to Inflammation
- Margination: Leukocytes accumulate along the periphery of blood vessels.
- Adhesion and Rolling: Leukocytes bind to endothelial cells via adhesion molecules (e.g., selectins, integrins), initially rolling and then firmly adhering.
- Transmigration (Diapedesis): Leukocytes squeeze between endothelial cells and penetrate the basement membrane.
- Chemotaxis: Leukocytes are attracted to the site of injury by chemical signals (chemotactic factors), which can be exogenous (e.g., bacterial products) or endogenous (e.g., C5a, LTB4, IL-8).
Leukocyte Activation, Phagocytosis, and Degranulation
- Phagocytosis: Leukocytes engulf and destroy microbes and cellular debris.
- Opsonization: Host proteins (opsonins) like IgG and C3b coat microbes, enhancing their phagocytosis.
- Microbial killing: Leukocytes use oxygen-based radicals (reactive oxygen species) and lysosomal enzymes to kill pathogens.
Leukocyte-Induced Tissue Injury
- Lysosomal enzymes released by leukocytes can cause collateral damage to tissues, contributing to inflammation.
Predominance of Neutrophils in Acute Inflammation
- Neutrophils are abundant in the blood and respond rapidly to chemokines.
- They adhere tightly to endothelial cells and are short-lived in tissues.
Defects in Leukocyte Function
-
Genetic defects:
- Leukocyte adhesion deficiency (LAD-1 syndrome): Lack of integrins, impairing adhesion to endothelial cells.
- Chediak-Higashi disease: Defective phagolysosome function, hindering microbial killing.
- Chronic granulomatous diseases: Defective microbicidal activity, resulting in persistent inflammation.
Chemical Mediators of Acute Inflammation
- Plasma-derived mediators: Synthesized by the liver and activated during inflammation (e.g., complement system, kinin system, clotting system).
- Cell-derived mediators: Produced locally by cells at the site of inflammation (e.g., histamine, prostaglandins, cytokines).
Sources and Effects of Chemical Mediators
- Triggered by microbial products and tissue damage.
- Bind to specific receptors on target cells, initiating various responses.
- May act on multiple cells and exhibit different effects on different cell types.
- Action is tightly regulated, with rapid inactivation or decay.
Examples of Chemical Mediators
- Plasma proteins: Complement system, kinin system, clotting system.
- Amines: Histamine, serotonin (vasodilation, increased vascular permeability).
- Arachidonic acid metabolites: Prostaglandins and leukotrienes (vascular reactions, leukocyte chemotaxis).
- Cytokines: Proteins produced by various cells, mediating leukocyte recruitment and migration (e.g., TNF, IL-1, chemokines).
- Reactive oxygen species: Microbial killing and tissue injury.
- Nitric oxide: Vasodilation, microbial killing.
- Lysosomal enzymes: Antimicrobial activity and tissue injury.
- Other: Platelet-activating factor (PAF).
Beneficial Effects of Inflammatory Exudate: Protective Mechanisms
- Dilution of toxins.
- Delivery of protective antibodies.
- Fibrin formation to promote clotting and wound healing.
- Activation of plasma mediator systems.
- Provision of nutrients for cells.
- Promotion of immunity.
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Description
Test your knowledge on inflammation, its features, and the protective responses it triggers in the body. This quiz covers key elements such as the Five Rs of inflammation, types of inflammation, and the role of immune cells. Explore how inflammation aids in healing and its potential risks when misdirected.
