5.chronic inflammation dr ashutosh kumar
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Chronic inflammation involves prolonged active inflammation, tissue destruction, and repair that lasts weeks to months. It is caused by persistent infections, prolonged exposure to toxic agents, or autoimmune disorders. Chronic inflammation is characterized by mononuclear cell infiltration, ongoing tissue damage, and attempts at healing through angiogenesis and fibrosis. A granuloma forms as a cellular attempt to contain a difficult to eradicate offending agent, consisting of aggregated macrophages surrounded by lymphocytes and occasionally plasma cells. Systemic effects of inflammation include fever, acute phase protein production, leukocytosis, and symptoms like anorexia and somnolence.
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Chronic inflammation 2-1-2
Chronic inflammation is inflammation of prolonged duration that involves ongoing active inflammation, tissue injury, and simultaneous healing. It can be caused by persistent infections, prolonged exposure to toxic agents, or autoimmunity. Morphologically, it is characterized by infiltration of mononuclear cells like macrophages, lymphocytes, and plasma cells, as well as ongoing tissue destruction and attempts at repair through angiogenesis and fibrosis. Chronic inflammation involves recruitment and accumulation of macrophages from the blood and their activation, leading to effects like increased cytokine production. Other cells like mast cells, lymphocytes, plasma cells, and eosinophils may also be present. Granulomatous inflammation features collections of macrophages that form granulomas. Chronic inflammation can also cause systemic effects through the acute
Chronic inflammation /orthodontic courses by Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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Inflammation by Ahmad
The document defines inflammation and its advantages and disadvantages. It discusses the players involved in the inflammatory response, including circulating cells, vascular wall cells, and the extracellular matrix. It describes acute and chronic inflammation, distinguishing their features. Chronic inflammation arises from acute inflammation when the stimulus cannot be resolved. It involves macrophages, lymphocytes, eosinophils, and mast cells and can be granulomatous or non-granulomatous.
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The document discusses the players and process of inflammation, describing how circulating cells, proteins, vascular wall cells and the extracellular matrix respond to inflammatory stimuli through chemical mediators, and defines chronic inflammation as prolonged inflammation from weeks to years where injury and healing occur simultaneously, detailing the cells and mediators involved like macrophages, lymphocytes, eosinophils and mast cells.
2. inflammation cellular events dr ashutosh kumar
The document discusses the process of acute inflammation and the cellular events involved. It describes how leukocytes are recruited to the site of injury through a process called chemotaxis. It then outlines the steps of phagocytosis - adherence, ingestion, digestion. It discusses the mechanisms used by phagocytes to kill and degrade microbes, including both oxygen-dependent and oxygen-independent processes. Finally, it briefly mentions some genetic defects and acquired conditions that can cause defects in leukocyte function.
Inflammation acute and chronic
The document summarizes inflammation and its processes. It describes the sequence of events in acute inflammation, from vasodilation to resolution. It lists chemical mediators involved like histamine, cytokines, and eicosanoids. Acute inflammation can resolve completely, form scar tissue, or progress to chronic inflammation. Chronic inflammation involves lymphocytes, macrophages and plasma cells and can be caused by persistent infection, prolonged insult, or autoimmunity.
Vascular and cellular events in inflammation
This document summarizes the vascular and cellular events that occur during acute inflammation. It discusses the features of acute inflammation including extravasation of neutrophils and exudate formation. It then describes the vascular events such as transient vasoconstriction, vasodilation, increased vascular permeability and cellular events including adhesion, chemotaxis, and phagocytosis. Specifically, it outlines the steps of adhesion including selectins, immunoglobins, integrins and CD31/PECAM-1 involvement and the mechanisms of appearance of adhesion molecules. It also discusses the chemotactic agents and receptors that mediate chemotaxis as well as the process of phagocytosis including recognition, engulfment and killing of bacteria via oxygen-dependent and independent
Chronic inflammation in 2 parts /orthodontic courses by Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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Chronic inflammation 2-1-2
Chronic inflammation is inflammation of prolonged duration that involves ongoing active inflammation, tissue injury, and simultaneous healing. It can be caused by persistent infections, prolonged exposure to toxic agents, or autoimmunity. Morphologically, it is characterized by infiltration of mononuclear cells like macrophages, lymphocytes, and plasma cells, as well as ongoing tissue destruction and attempts at repair through angiogenesis and fibrosis. Chronic inflammation involves recruitment and accumulation of macrophages from the blood and their activation, leading to effects like increased cytokine production. Other cells like mast cells, lymphocytes, plasma cells, and eosinophils may also be present. Granulomatous inflammation features collections of macrophages that form granulomas. Chronic inflammation can also cause systemic effects through the acute
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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2. inflammation cellular events dr ashutosh kumar
The document discusses the process of acute inflammation and the cellular events involved. It describes how leukocytes are recruited to the site of injury through a process called chemotaxis. It then outlines the steps of phagocytosis - adherence, ingestion, digestion. It discusses the mechanisms used by phagocytes to kill and degrade microbes, including both oxygen-dependent and oxygen-independent processes. Finally, it briefly mentions some genetic defects and acquired conditions that can cause defects in leukocyte function.
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The document summarizes inflammation and its processes. It describes the sequence of events in acute inflammation, from vasodilation to resolution. It lists chemical mediators involved like histamine, cytokines, and eicosanoids. Acute inflammation can resolve completely, form scar tissue, or progress to chronic inflammation. Chronic inflammation involves lymphocytes, macrophages and plasma cells and can be caused by persistent infection, prolonged insult, or autoimmunity.
Vascular and cellular events in inflammation
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Chronic inflammation in 2 parts /orthodontic courses by Indian dental academy
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offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Acute inflammation
Acute inflammation is a protective process that helps eliminate harmful stimuli and promote tissue repair. It is characterized by increased blood flow, vascular permeability, and migration of white blood cells. The major signs of acute inflammation are heat, redness, swelling, pain, and loss of function. Key events in acute inflammation include changes in blood vessels that allow fluid and cells to move between blood vessels and tissues. White blood cells like neutrophils are recruited to destroy pathogens and initiate repair.
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This document provides an overview of inflammation and its mediators. It begins with introductions to the history and definitions of inflammation. The causes and cardinal signs of inflammation are then discussed. The document outlines the types of inflammatory reactions including acute and chronic inflammation. It then provides details on the vascular and cellular events in acute inflammation. The remainder of the document focuses on the various chemical mediators involved in inflammation, including vasoactive amines, arachidonic acid metabolites, cytokines, chemokines, lysosomal constituents, and other mediators. It also discusses inflammatory cells and the outcomes and resolution of inflammation.
chronic inflammation
Chronic inflammation is a prolonged host response to persistent stimuli that involves lymphocytes, macrophages, plasma cells, and mast cells. It is characterized by infiltration of mononuclear cells and macrophages, tissue destruction by inflammatory cells, and attempts at healing through fibrosis and angiogenesis. Chronic inflammation can result from acute inflammation turning persistent, infections, hypersensitivity, or prolonged toxic exposure. It causes diseases like atherosclerosis, tuberculosis, and rheumatoid arthritis. Granulomatous inflammation is a form of chronic inflammation seen in diseases like tuberculosis that involves collections of epithelioid macrophages and giant cells forming granulomas.
Pathology cptr2 ( acute & chronic inflammation)
The document summarizes inflammation and its processes. It describes the sequence of events in acute inflammation, from vasodilation to resolution. It lists chemical mediators involved like histamine, cytokines, and eicosanoids. Acute inflammation can resolve completely, form scar tissue, or progress to chronic inflammation. Chronic inflammation involves lymphocytes, macrophages and plasma cells and can be caused by persistent infection, prolonged insult, or autoimmunity.
Chronic inflammation
Chronic inflammation can last for months or years and is driven by macrophages and lymphocytes. It can be caused by persistent infections, autoimmune reactions, and foreign bodies. Activated macrophages and T cells secrete cytokines and growth factors that lead to tissue damage and fibrosis over time. Macrophages and T cells also interact and stimulate each other, prolonging the inflammatory response. Granulomas are clusters of macrophages that form in response to chronic inflammation and surround foreign materials to isolate them.
Chronic inflammation
Chronic inflammation is inflammation that lasts for weeks or months. It can be caused by persistent infections, immune-mediated diseases, or toxic agents. The key features are infiltration by mononuclear cells like macrophages and lymphocytes, ongoing tissue destruction, and attempts at healing through fibrosis and new blood vessel formation. Activated macrophages play a major role by releasing factors that cause further tissue injury and scar formation. Granulomatous inflammation is a pattern of chronic inflammation seen in some infectious and noninfectious conditions. It involves the formation of granulomas, which are microscopic aggregations of macrophages that form giant cells and are surrounded by lymphocytes in an attempt to contain hard to eliminate agents.
Recovery from bacterial infections
Recovery from infection involves multiple lines of defense. The innate immune system provides the first response through physical and chemical barriers that prevent pathogen entry. If a pathogen breaches these barriers, pattern recognition receptors recognize molecular signatures to activate phagocytes and the complement system for removal. The adaptive immune system provides long-lasting protection through antigen-specific B and T cells that respond to future infections. Different immune strategies like antibodies, T lymphocytes, and cytotoxic T cells help eliminate pathogens specifically.
Systemic effects of acute inflammation and granuloma
Inflammation is the protective immune response to tissue injury or infection. It involves movement of fluid and immune cells into injured tissues and is characterized by redness, swelling, heat, pain, and loss of function. The systemic inflammatory response causes fever, increased pulse and blood pressure, and changes in white blood cell counts. Chronic inflammation lasts longer and involves macrophages and lymphocytes, often leading to fibrosis, proliferation of blood vessels, and necrosis. Granulomatous inflammation forms structures called granulomas, which contain giant cells, to wall off long-term infections or foreign materials.
Lecture 50 chronic inflammation.ppt 4.11.11
This document provides an overview of chronic inflammation and granulomatous inflammation. It defines chronic inflammation as inflammation of prolonged duration that involves simultaneous active inflammation, tissue destruction, and attempts at repair. Chronic inflammation can arise from persistent infections, immune-mediated diseases, or prolonged exposure to toxic substances. Key cells involved include macrophages, lymphocytes, and plasma cells. Chronic inflammation is characterized by infiltration of mononuclear cells, tissue destruction, and attempts at repair through fibrosis. Granulomatous inflammation features microscopic granulomas composed of activated macrophages surrounded by lymphocytes. Tuberculosis is provided as an example of a disease involving granulomatous inflammation.
11,12
Acute inflammation is the body's initial protective response to harmful stimuli or damaged tissue. It is characterized by vascular changes such as increased blood flow and vascular permeability, as well as the recruitment of immune cells like neutrophils to the site of injury. A variety of chemical mediators are involved in regulating the inflammatory response, including histamine, prostaglandins, cytokines, free radicals, and components of the complement system. Acute inflammation can resolve with repair of the damaged tissue, result in fibrosis or scarring if damage is extensive, or progress to a chronic inflammatory state.
Difference between acute and chronic inflammation
Acute inflammation is the early response of the body to short-term adverse stimuli and is not specific, involving dendritic cells, Kupffer cells, histiocytes, resistant macrophages, and mast cells in response to physical or chemical damage or pathogen invasion. Chronic inflammation is the prolonged inflammatory response lasting months or years, is specific involving acquired immunity, and responds to prolonged irritation by microorganisms through fibrosis and angiogenesis involving macrophages, neutrophils and lymphocytes.
Inflammation
This document summarizes the key aspects of inflammation. It defines inflammation as the body's protective response to injury. The classic signs of inflammation are described as heat, redness, swelling, pain, and loss of function. The mechanisms of inflammation are explained, including vasodilation, exudation, edema, and emigration of cells. Different chemical mediators that contribute to inflammation are also outlined.
MID2163 TOPIC 3
Inflammation is the body's response to injury or infection and is characterized by redness, swelling, heat, pain, and loss of function. It involves increased blood flow, exudation of fluid, and emigration of leukocytes. The goals are to remove harmful stimuli, limit tissue damage, and initiate repair. Acute inflammation is short-lived and has beneficial effects like fighting infection, but can also cause harmful tissue swelling and pain.
Inflammation
This document summarizes the key aspects of inflammation. It begins by defining inflammation and describing the cardinal signs. It then discusses the etiological factors, types of inflammation (acute vs chronic), and the haemodynamic and cellular events in acute inflammation. Specifically, it outlines the vascular changes, increased permeability, exudation of leukocytes, and process of phagocytosis. It also discusses the chemical mediators of inflammation like histamine, kinins, cytokines, prostaglandins, and the resolution of inflammation. Finally, it concludes that inflammation is an important immune response but better understanding its pathways could aid in treating diseases.
Chronic inflammation
Chronic inflammation is defined as prolonged inflammation and tissue destruction occurring simultaneously. It can result from acute inflammation persisting, recurrent acute attacks, or starting de novo from low pathogenicity organisms. Features include mononuclear cell infiltration, tissue destruction, and proliferative changes like granulation tissue formation and fibrosis. Examples given are tuberculosis, leprosy, and actinomycosis. Granulomas are characteristic of chronic granulomatous inflammation and are composed of epithelioid cells, giant cells, lymphocytes, and may show caseation necrosis.
Acute And Chronic Inflammation
Acute inflammation is the immediate response to tissue injury and involves vasodilation, increased vascular permeability leading to edema, and leukocyte emigration. The key events in acute inflammation are vascular changes, leukocyte migration into tissues, and the release of chemical mediators. Chronic inflammation is a prolonged inflammatory response involving lymphocytes, macrophages and plasma cells that can lead to tissue destruction and attempts at repair through fibrosis. [/SUMMARY]
Inflammation
Inflammation is the body's immediate response to damage to its tissues and cells by pathogens, noxious stimuli such as chemicals, or physical injury. Acute inflammation is a short-term response that usually results in healing: leukocytes infiltrate the damaged region, removing the stimulus and repairing the tissue. Chronic inflammation, by contrast, is a prolonged, dysregulated and maladaptive response that involves active inflammation, tissue destruction and attempts at tissue repair. Such persistent inflammation is associated with many chronic human conditions and diseases, including allergy, atherosclerosis, cancer, arthritis and autoimmune diseases.
Patho inflammation
This document discusses inflammation and healing. It defines inflammation as the local response of living tissues to injury. The causes of inflammation can be exogenous, such as physical or chemical agents, or endogenous like circulation disorders or metabolic products. The classic signs of inflammation are redness, swelling, heat, and pain. Acute inflammation involves rapid onset and short duration, while chronic inflammation has insidious onset and longer duration. Acute inflammation is characterized by increased blood flow, vascular permeability, and leukocyte infiltration. Chronic inflammation features infiltration by mononuclear cells like macrophages and lymphocytes, along with simultaneous tissue destruction and healing.
Acute and chronic inflammation(1)
Acute inflammation is an immediate protective response to injury that involves vasodilation, increased vascular permeability, and leukocyte migration. It is characterized by redness, warmth, swelling and pain. If the injury persists, acute inflammation can progress to chronic inflammation, a prolonged response involving lymphocytes, macrophages and plasma cells that can lead to tissue destruction and attempts at repair through fibrosis. The key events and mediators of acute inflammation include histamine release, complement activation, kinin system activation, leukotriene and prostaglandin production, and cytokine signaling.
Acute inflammation
The document discusses acute inflammation. It defines inflammation and lists its causes. Acute inflammation is characterized by rapid onset and short duration. It involves vascular events like vasodilation, increased permeability and cellular events like recruitment and migration of leukocytes to the site of injury via adhesion molecules. Leukocytes recognize and remove microbes via phagocytosis and intracellular killing to resolve the inflammatory response.
Chronic inflammation & repair
Chronic inflammation is characterized by prolonged inflammation, simultaneous tissue injury and healing, and infiltration by mononuclear cells. It occurs in persistent infections, prolonged exposure to toxic agents, and autoimmune conditions. The macrophage plays a prominent role in chronic inflammation through recruitment, proliferation, differentiation, and release of inflammatory mediators and proteins. Granulomatous inflammation forms aggregations of activated macrophages that appear in response to bacteria, parasites, fungi, dusts, and foreign materials. Chronic inflammation involves ongoing tissue damage, repair through angiogenesis and fibrosis, and macrophage-driven processes.
Inflammation
1. The cellular events of inflammation involve the adhesion of leukocytes to endothelial cells, their migration through blood vessels into tissues, and chemotaxis towards inflammatory stimuli.
2. Phagocytosis is the process by which phagocytes engulf pathogens or debris through opsonization, engulfment, degranulation, and degradation. Phagocytes release reactive oxygen species and enzymes to kill pathogens intracellularly.
3. The resolution of acute inflammation involves demolition of exudates by macrophages, with complete healing and return to normal tissue, or formation of granulation tissue and fibrosis if resolution is delayed. Prolonged inflammation can result in suppuration and abscess formation.
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Acute inflammation
Acute inflammation is a protective process that helps eliminate harmful stimuli and promote tissue repair. It is characterized by increased blood flow, vascular permeability, and migration of white blood cells. The major signs of acute inflammation are heat, redness, swelling, pain, and loss of function. Key events in acute inflammation include changes in blood vessels that allow fluid and cells to move between blood vessels and tissues. White blood cells like neutrophils are recruited to destroy pathogens and initiate repair.
Inflammation Seminar by Dr Pratik
This document provides an overview of inflammation and its mediators. It begins with introductions to the history and definitions of inflammation. The causes and cardinal signs of inflammation are then discussed. The document outlines the types of inflammatory reactions including acute and chronic inflammation. It then provides details on the vascular and cellular events in acute inflammation. The remainder of the document focuses on the various chemical mediators involved in inflammation, including vasoactive amines, arachidonic acid metabolites, cytokines, chemokines, lysosomal constituents, and other mediators. It also discusses inflammatory cells and the outcomes and resolution of inflammation.
chronic inflammation
Chronic inflammation is a prolonged host response to persistent stimuli that involves lymphocytes, macrophages, plasma cells, and mast cells. It is characterized by infiltration of mononuclear cells and macrophages, tissue destruction by inflammatory cells, and attempts at healing through fibrosis and angiogenesis. Chronic inflammation can result from acute inflammation turning persistent, infections, hypersensitivity, or prolonged toxic exposure. It causes diseases like atherosclerosis, tuberculosis, and rheumatoid arthritis. Granulomatous inflammation is a form of chronic inflammation seen in diseases like tuberculosis that involves collections of epithelioid macrophages and giant cells forming granulomas.
Pathology cptr2 ( acute & chronic inflammation)
The document summarizes inflammation and its processes. It describes the sequence of events in acute inflammation, from vasodilation to resolution. It lists chemical mediators involved like histamine, cytokines, and eicosanoids. Acute inflammation can resolve completely, form scar tissue, or progress to chronic inflammation. Chronic inflammation involves lymphocytes, macrophages and plasma cells and can be caused by persistent infection, prolonged insult, or autoimmunity.
Chronic inflammation
Chronic inflammation can last for months or years and is driven by macrophages and lymphocytes. It can be caused by persistent infections, autoimmune reactions, and foreign bodies. Activated macrophages and T cells secrete cytokines and growth factors that lead to tissue damage and fibrosis over time. Macrophages and T cells also interact and stimulate each other, prolonging the inflammatory response. Granulomas are clusters of macrophages that form in response to chronic inflammation and surround foreign materials to isolate them.
Chronic inflammation
Chronic inflammation is inflammation that lasts for weeks or months. It can be caused by persistent infections, immune-mediated diseases, or toxic agents. The key features are infiltration by mononuclear cells like macrophages and lymphocytes, ongoing tissue destruction, and attempts at healing through fibrosis and new blood vessel formation. Activated macrophages play a major role by releasing factors that cause further tissue injury and scar formation. Granulomatous inflammation is a pattern of chronic inflammation seen in some infectious and noninfectious conditions. It involves the formation of granulomas, which are microscopic aggregations of macrophages that form giant cells and are surrounded by lymphocytes in an attempt to contain hard to eliminate agents.
Recovery from bacterial infections
Recovery from infection involves multiple lines of defense. The innate immune system provides the first response through physical and chemical barriers that prevent pathogen entry. If a pathogen breaches these barriers, pattern recognition receptors recognize molecular signatures to activate phagocytes and the complement system for removal. The adaptive immune system provides long-lasting protection through antigen-specific B and T cells that respond to future infections. Different immune strategies like antibodies, T lymphocytes, and cytotoxic T cells help eliminate pathogens specifically.
Systemic effects of acute inflammation and granuloma
Inflammation is the protective immune response to tissue injury or infection. It involves movement of fluid and immune cells into injured tissues and is characterized by redness, swelling, heat, pain, and loss of function. The systemic inflammatory response causes fever, increased pulse and blood pressure, and changes in white blood cell counts. Chronic inflammation lasts longer and involves macrophages and lymphocytes, often leading to fibrosis, proliferation of blood vessels, and necrosis. Granulomatous inflammation forms structures called granulomas, which contain giant cells, to wall off long-term infections or foreign materials.
Lecture 50 chronic inflammation.ppt 4.11.11
This document provides an overview of chronic inflammation and granulomatous inflammation. It defines chronic inflammation as inflammation of prolonged duration that involves simultaneous active inflammation, tissue destruction, and attempts at repair. Chronic inflammation can arise from persistent infections, immune-mediated diseases, or prolonged exposure to toxic substances. Key cells involved include macrophages, lymphocytes, and plasma cells. Chronic inflammation is characterized by infiltration of mononuclear cells, tissue destruction, and attempts at repair through fibrosis. Granulomatous inflammation features microscopic granulomas composed of activated macrophages surrounded by lymphocytes. Tuberculosis is provided as an example of a disease involving granulomatous inflammation.
11,12
Acute inflammation is the body's initial protective response to harmful stimuli or damaged tissue. It is characterized by vascular changes such as increased blood flow and vascular permeability, as well as the recruitment of immune cells like neutrophils to the site of injury. A variety of chemical mediators are involved in regulating the inflammatory response, including histamine, prostaglandins, cytokines, free radicals, and components of the complement system. Acute inflammation can resolve with repair of the damaged tissue, result in fibrosis or scarring if damage is extensive, or progress to a chronic inflammatory state.
Difference between acute and chronic inflammation
Acute inflammation is the early response of the body to short-term adverse stimuli and is not specific, involving dendritic cells, Kupffer cells, histiocytes, resistant macrophages, and mast cells in response to physical or chemical damage or pathogen invasion. Chronic inflammation is the prolonged inflammatory response lasting months or years, is specific involving acquired immunity, and responds to prolonged irritation by microorganisms through fibrosis and angiogenesis involving macrophages, neutrophils and lymphocytes.
Inflammation
This document summarizes the key aspects of inflammation. It defines inflammation as the body's protective response to injury. The classic signs of inflammation are described as heat, redness, swelling, pain, and loss of function. The mechanisms of inflammation are explained, including vasodilation, exudation, edema, and emigration of cells. Different chemical mediators that contribute to inflammation are also outlined.
MID2163 TOPIC 3
Inflammation is the body's response to injury or infection and is characterized by redness, swelling, heat, pain, and loss of function. It involves increased blood flow, exudation of fluid, and emigration of leukocytes. The goals are to remove harmful stimuli, limit tissue damage, and initiate repair. Acute inflammation is short-lived and has beneficial effects like fighting infection, but can also cause harmful tissue swelling and pain.
Inflammation
This document summarizes the key aspects of inflammation. It begins by defining inflammation and describing the cardinal signs. It then discusses the etiological factors, types of inflammation (acute vs chronic), and the haemodynamic and cellular events in acute inflammation. Specifically, it outlines the vascular changes, increased permeability, exudation of leukocytes, and process of phagocytosis. It also discusses the chemical mediators of inflammation like histamine, kinins, cytokines, prostaglandins, and the resolution of inflammation. Finally, it concludes that inflammation is an important immune response but better understanding its pathways could aid in treating diseases.
Chronic inflammation
Chronic inflammation is defined as prolonged inflammation and tissue destruction occurring simultaneously. It can result from acute inflammation persisting, recurrent acute attacks, or starting de novo from low pathogenicity organisms. Features include mononuclear cell infiltration, tissue destruction, and proliferative changes like granulation tissue formation and fibrosis. Examples given are tuberculosis, leprosy, and actinomycosis. Granulomas are characteristic of chronic granulomatous inflammation and are composed of epithelioid cells, giant cells, lymphocytes, and may show caseation necrosis.
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Acute inflammation is the immediate response to tissue injury and involves vasodilation, increased vascular permeability leading to edema, and leukocyte emigration. The key events in acute inflammation are vascular changes, leukocyte migration into tissues, and the release of chemical mediators. Chronic inflammation is a prolonged inflammatory response involving lymphocytes, macrophages and plasma cells that can lead to tissue destruction and attempts at repair through fibrosis. [/SUMMARY]
Inflammation
Inflammation is the body's immediate response to damage to its tissues and cells by pathogens, noxious stimuli such as chemicals, or physical injury. Acute inflammation is a short-term response that usually results in healing: leukocytes infiltrate the damaged region, removing the stimulus and repairing the tissue. Chronic inflammation, by contrast, is a prolonged, dysregulated and maladaptive response that involves active inflammation, tissue destruction and attempts at tissue repair. Such persistent inflammation is associated with many chronic human conditions and diseases, including allergy, atherosclerosis, cancer, arthritis and autoimmune diseases.
Patho inflammation
This document discusses inflammation and healing. It defines inflammation as the local response of living tissues to injury. The causes of inflammation can be exogenous, such as physical or chemical agents, or endogenous like circulation disorders or metabolic products. The classic signs of inflammation are redness, swelling, heat, and pain. Acute inflammation involves rapid onset and short duration, while chronic inflammation has insidious onset and longer duration. Acute inflammation is characterized by increased blood flow, vascular permeability, and leukocyte infiltration. Chronic inflammation features infiltration by mononuclear cells like macrophages and lymphocytes, along with simultaneous tissue destruction and healing.
Acute and chronic inflammation(1)
Acute inflammation is an immediate protective response to injury that involves vasodilation, increased vascular permeability, and leukocyte migration. It is characterized by redness, warmth, swelling and pain. If the injury persists, acute inflammation can progress to chronic inflammation, a prolonged response involving lymphocytes, macrophages and plasma cells that can lead to tissue destruction and attempts at repair through fibrosis. The key events and mediators of acute inflammation include histamine release, complement activation, kinin system activation, leukotriene and prostaglandin production, and cytokine signaling.
Acute inflammation
The document discusses acute inflammation. It defines inflammation and lists its causes. Acute inflammation is characterized by rapid onset and short duration. It involves vascular events like vasodilation, increased permeability and cellular events like recruitment and migration of leukocytes to the site of injury via adhesion molecules. Leukocytes recognize and remove microbes via phagocytosis and intracellular killing to resolve the inflammatory response.
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Chronic inflammation is characterized by prolonged inflammation, simultaneous tissue injury and healing, and infiltration by mononuclear cells. It occurs in persistent infections, prolonged exposure to toxic agents, and autoimmune conditions. The macrophage plays a prominent role in chronic inflammation through recruitment, proliferation, differentiation, and release of inflammatory mediators and proteins. Granulomatous inflammation forms aggregations of activated macrophages that appear in response to bacteria, parasites, fungi, dusts, and foreign materials. Chronic inflammation involves ongoing tissue damage, repair through angiogenesis and fibrosis, and macrophage-driven processes.
Inflammation
1. The cellular events of inflammation involve the adhesion of leukocytes to endothelial cells, their migration through blood vessels into tissues, and chemotaxis towards inflammatory stimuli.
2. Phagocytosis is the process by which phagocytes engulf pathogens or debris through opsonization, engulfment, degranulation, and degradation. Phagocytes release reactive oxygen species and enzymes to kill pathogens intracellularly.
3. The resolution of acute inflammation involves demolition of exudates by macrophages, with complete healing and return to normal tissue, or formation of granulation tissue and fibrosis if resolution is delayed. Prolonged inflammation can result in suppuration and abscess formation.
Inflammation
This document provides an overview of inflammation, including its definition, history, types (acute and chronic), classical signs, vascular and cellular events, chemical mediators, and outcomes. Inflammation is defined as a protective response to injury or infection that involves increased blood flow, blood vessel permeability, and the migration of white blood cells. The classical signs of inflammation are heat, redness, swelling, pain, and loss of function. Key events in acute inflammation include increased vascular permeability, chemotaxis of white blood cells, phagocytosis of pathogens, and the release of chemical mediators like histamine and cytokines. Chronic inflammation is long-lasting inflammation that involves ongoing tissue damage and repair. Systemic inflammatory response syndrome (SIRS)
Acute and chronic inflammation 1 robbins
This document summarizes acute inflammation and the key chemical mediators involved. It describes how injury causes vasodilation, increased vascular permeability, and leukocyte emigration through the actions of histamine, bradykinin, prostaglandins, leukotrienes, cytokines, and other mediators. These chemical mediators cause effects like vasodilation, increased vascular permeability, chemotaxis, fever, pain, and tissue damage during acute inflammatory responses.
Chronic inflammation
Chronic inflammation is prolonged inflammation that can last weeks to years. It involves ongoing tissue destruction and attempts at repair through fibrosis. It can follow acute inflammation or result from persistent infections like tuberculosis. Common features include mononuclear cell infiltration of macrophages, lymphocytes and plasma cells, as well as proliferative changes like angiogenesis and fibrosis. Chronic inflammation can be non-specific or granulomatous, characterized by granulomas which form to contain hard to eliminate agents and involve epithelioid cells, giant cells, and caseous necrosis. Examples include chronic cholecystitis and pyelonephritis.
Inflammation med
Prepared by MD,PhD, Associate Professor, Marta R. Gerasymchuk
Department of Pathophysiology, Ivano-Frankivsk National
Medical University
Acute and chronic inflammation
Acute inflammation is an immediate response to injury that involves increased blood flow, vascular permeability, and recruitment of leukocytes. This response aims to remove injurious stimuli and initiate tissue repair. It can resolve with complete healing or progress to chronic inflammation. Chronic inflammation is a prolonged response involving lymphocytes, macrophages and mediators that drives simultaneous tissue injury and repair through fibrosis. It underlies conditions like infection, autoimmunity and foreign body reactions. Systemic effects include fever, leukocytosis and acute phase responses.
Acute and chronic inflammation
The document summarizes key aspects of inflammation. It describes inflammation as the body's response to eliminate harmful stimuli like damaged cells and microbes. The response involves vascular changes that increase blood flow and permeability, allowing immune cells and proteins to reach affected tissues. This causes swelling, redness and other classic signs of inflammation. The document outlines the precise roles of different immune cells, chemical mediators, and vascular changes involved in both acute and chronic inflammatory responses. It also discusses how inflammation can be beneficial by fighting infection but also harmful if improperly controlled and linked to various diseases.
Inflammation 7
The document discusses chronic inflammation and its outcomes. Chronic inflammation can result when acute inflammation fails to resolve due to persistence of the injurious agent or interference with the healing process. It is characterized by prolonged inflammation that involves tissue injury and attempted repair occurring simultaneously. Macrophages play a dominant role in chronic inflammation by attempting to eliminate injurious agents and initiate repair, but also cause much of the tissue damage through their activation. Other cells like lymphocytes, plasma cells, eosinophils and mast cells are also involved. Granulomatous inflammation is a distinctive pattern of chronic inflammation seen in certain infectious and non-infectious conditions as an attempt to contain a difficult to eradicate agent.
Chronic granulomatous disease (cgd)
Chronic granulomatous disease (CGD) is an inherited immune disorder where phagocytes cannot kill ingested bacteria and fungi, leading to recurrent infections. It is caused by mutations affecting the NADPH oxidase enzyme complex needed for reactive oxygen species production. Patients experience severe lung, skin, and organ infections from catalase-positive microbes early in life. Diagnosis involves tests assessing reactive oxygen species levels. Treatment requires lifelong antibiotics, antifungals, immunoglobulin therapy, and stem cell transplantation.
Productive inflammation
This document discusses chronic inflammation and its characteristics. It notes that chronic inflammation is defined as a prolonged process where tissue destruction and inflammation occur simultaneously. Key features of chronic inflammation include mononuclear cell infiltration, tissue destruction and necrosis caused by activated macrophages, and proliferative changes like angiogenesis and fibrosis. The outcomes of chronic inflammation depend on the type and location but often result in scarring or sclerosis.
Acute and chronic inflammation
Inflammation is the body's protective response to injury or infection that involves vascular and cellular components. The classic signs of acute inflammation are heat, redness, swelling, pain, and loss of function. This response involves increased blood flow, leakage of fluid into tissues, and migration of white blood cells. Chemical mediators like histamine, kinins, prostaglandins, and cytokines are released that regulate inflammation. Acute inflammation may resolve with repair or progress to chronic inflammation involving lymphocytes and macrophages if the trigger persists. Systemic effects can include fever, loss of appetite, and changes in white blood cell counts.
Chronic inflammation
Chronic inflammation is defined as prolonged inflammation that lasts weeks or months, characterized by ongoing tissue destruction and healing simultaneously. It involves infiltration by mononuclear cells like macrophages, lymphocytes, and plasma cells, as well as tissue destruction and repair through angiogenesis and fibrosis. Chronic inflammation can be caused by bacterial, fungal, parasitic, or miscellaneous agents and is characterized by formation of granulomas consisting of activated macrophages, lymphocytes, and occasional plasma cells. Tuberculosis causes chronic inflammation through formation of tuberculous lesions containing caseous necrosis surrounded by lymphocytes, epithelioid cells, and giant cells.
Inflammation adel-1
This document provides an overview of acute and chronic inflammation. It defines inflammation and outlines the main types, including acute and chronic inflammation. Acute inflammation is defined as a rapid, transient response and its stages are described as transient vasoconstriction, persistent vasodilation, increased permeability, fluid exudate formation, cellular exudate accumulation, and resolution or progression. Chronic inflammation is defined as prolonged inflammation that involves attempts at repair. Its causes include persisting infections or irritants and autoimmune reactions. The document outlines the cells involved in chronic inflammation and types of mixed acute and chronic inflammation.
Inflammatory response
The document describes the cells and proteins involved in the inflammatory response. It details the roles of mast cells, tissue macrophages, dendritic cells, complement proteins, neutrophils, and macrophages. Mast cells detect pathogens and secrete histamine to increase vascular permeability. Tissue macrophages and dendritic cells secrete cytokines to attract more immune cells. Complement proteins assist in pathogen detection and removal. Neutrophils and macrophages migrate to sites of infection and phagocytose pathogens. Macrophages also present antigens to lymphocytes to stimulate an adaptive immune response.
Healing and repair
Healing occurs through regeneration or scar formation depending on the cell and injury type. Wound healing follows two main pathways: primary intention for clean surgical wounds where edges are approximated, or secondary intention for wounds with separated edges and more tissue death. The process involves inflammation, granulation tissue formation, re-epithelialization, wound contraction and ECM deposition. Several local and systemic factors can delay healing including infection, poor blood supply, drugs, and nutritional deficiencies.
4. chronic inflammation granulomatous inflammation -dr. sinhasan- mdzah
This document discusses tuberculosis pathogenesis and granuloma formation. It lists the cell types involved in tuberculosis including CD4 T lymphocytes, monocytes, and epitheloid macrophages. It also lists the stages of tuberculosis progression from bacterial entry to central necrosis, giant cell formation, and fibrosis. Finally, it lists several diseases that can cause granulomatous inflammation including tuberculosis, brucellosis, sarcoidosis, and Crohn's disease.
Inflammation
This document provides an overview of inflammation. It defines inflammation and describes the cellular response and mediators involved in acute inflammation. Acute inflammation aims to remove injurious agents, repair tissue damage, and prepare the body for healing. Without inflammation, infections could not be fought off and wounds would never heal. The document outlines the signs of acute (redness, heat, swelling, pain, loss of function) and differences between acute and chronic inflammation. It discusses the cellular events and outcomes of acute inflammation, as well as special types. Chronic inflammation is characterized by mononuclear cell infiltration and tissue destruction or repair over a long period of time.
6 infarction
1) Myocardial infarction, cerebral infarction, pulmonary infarction, and gangrene of limbs are common examples of infarction that result from obstruction of blood flow.
2) Infarctions are typically wedge-shaped areas of ischemic necrosis caused by occlusion of the arterial blood supply or venous drainage of a tissue.
3) The development of an infarction depends on factors like the nature of the blood supply, the rate of occlusion, the tissue's vulnerability to hypoxia, and the oxygen content of the blood. Tissues with dual blood supplies are less likely to infarct.
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5.chronic inflammation dr ashutosh kumar
- 2. CHRONIC INFLAMMATION-DEFENSE AT A PRICE PROLONGED DURATION WKS TO MONTHS ACTIVE INFLAMMATION, TISSUE DESTRUCTION AND REPAIR ALL occurs SIMULTANEOUSLY
- 3. CAUSES PERSISTENT INFECTION Eg:TB,SYPHILIS LOW TOXICITY EVOKE DELAYED HYPERSENSITIVITY REACTION PROLONGED EXPOSURE TO TOXIC AGENTS ENDO-TOXIC LIPIDS IN ATHEROMA EXO-SILICOSIS, AUTOIMMUNE:caused by excessive and inappropriate activation of the immune system Eg. RA,MS,IBD, Br. Asthma
- 4. FEATURES MONONUCLEAR INFILTRATIION- MACROPHAGES,LYMPHOS,PLASMA CELLS TISSUE DESTRUCTION ATTEMPTS AT HEALING: angiogenesis+ fibrosis
- 5. Chronic infl. Acute infl. collection of chronic inflammatory cells (*) alveolar spaces filled with neutrophils destruction of parenchyma Congested blood vessels fibrosis, (arrows)
- 6. CELLS-MACROPHAGES KEY ROLE PART OF MONOCYTE PHAGOCYTE SYSTEM ORIGIN IN BM BLOOD MONOCYTES TISSUE MACROPHAGES TISSUE MACROPHAGES-MICROGLIA,KUPFFER CELLS,ALVEOLAR MACROPHAGES,OSTEOCLASTS
- 8. CELLS-MACROPHAGES AFTER 48 HRS EMIGRATE INTO SITE OF INFLAMMATION ACTIVATION BY CYTOKINES(IFN GAMMA), ENDOTOXINS INCREASE IN SIZE, MORE LYSOSOMAL ENZYMES, INCREASED METABOLIC ACTIVITY WIDE VARIETY OF BIOLOGICALLY ACTIVE SUB
- 11. CELLS-MACROPHAGES IF IRRITANT PERSISTS MACROS ACCUMULATE RECRUITMENT LOCAL PROLIF IMMOBILIZATION
- 12. CELLS-MACROPHAGES PRODUCTS OF MACROPHAGES ELIMINATION OF MICROBES TISSUE INJURY-PROTEASES,NO,AA METABOLITES FIBROSIS
- 13. CELLS-OTHERS LYMPHOCYTES BOTH IN IMMUNE AND NON IMMUNE TWO WAY INTERACTION WITH MACRO PLASMA CELLS FROM ACTIVATED B-LYMPHOS tertiary lymphoid organs: long standing R.A. EOSINOPHILS IMMUNE,PARASITIC d/t MBP EOTAXIN
- 15. GRANULOMATOUS INFLAMMATION It is a cellular attempt to contain an offending agent that is difficult to eradicate. A granuloma is a focus of chronic inflammation consisting of a microscopic aggregation of macrophages that are transformed into epithelium-like cells, surrounded by a collar of mononuclear leukocytes, principally lymphocytes and occasionally plasma cells.
- 16. GRANULOMATOUS INFLAMMATION- EXAMPLES TB SARCOID SYPHILIS(GUMMA) CAT SCRATCH DISEASE LEPROSY BERYLLIOSIS HISTOPLASMA FOREIGN BODY
- 17. GRANULOMA EPITHELIOID CELLS ACTIVATED/MODIFIED MACROPHAGES INDISTINCT CELL BORDERS PALE PINK CYTOPLASM VESICULAR NUCLEUS-SLIPPER SOLE SHAPED LYMPHOCYTES USUALLY FORM A CUFF AROUND EP CELLS MAY BE ADMIXED WITH PLASMA CELLS
- 18. GRANULOMA GIANT CELLS FUSION OF EPITHELIOID CELLS LANGHANS G.C-NUCLEUS IN PERIPHERY-HORSE SHOE MANNER FOREIGN BODY-HAPHAZARD ARRANGEMENT NO SP SIGNIFICANCE ABOUT UNDERLYING CAUSE FIBROSIS SURROUNDING LYMPHOS BURNT OUT-SCARRING
- 19. GRANULOMA TWO MAIN TYPES BASED ON PATHOGENESIS- FB (SUTURE,TALC) AND IMMUNE (TB) IMMUNE POORLY DEGRADABLE AGENT CELL MEDIATED IMMUNITY
- 20. GRANULOMA CENTRAL NECROSIS IS SEEN IN SOME GRANULOMAS PROTOTYPE-TB CASEOUS NECROSIS GROSSLY-CHEESE LIKE MICRO-EOSINOPHILIC,AMORPHOUS GRANULAR DEBRIS
- 21. Granuloma
- 22. A granuloma: a collection of epithelioid histiocytes
- 25. SYSTEMIC EFFECTS OF INFLAMMATION ACUTE PHASE RESPONSE OR SYSTEMIC INFLAMMATORY RESPONSE(SIRS) DUE TO CYTOKINES-TNF,IL-1
- 26. SYSTEMIC EFFECTS OF INFLAMMATION FEVER IL-1 AND TNF ACT ON HYPOTHALAMUS PRODUCE PGs RESET TEMP AT HIGHER LEVEL HOW USEFUL??????
- 27. OSLER “HUMANITY HAS BUT 3 GREAT ENEMIES-FEVER ,FAMINE AND WAR,OF THESE BY FAR THE GREATEST ,THE MOST TERRIBLE IS FEVER”
- 28. SYSTEMIC EFFECTS OF INFLAMMATION ACUTE PHASE PROTEINS SYN IN LIVER,CIRCULATE IN PLASMA MANY FOLD INCREASE IN INFLAMMATION CRP,FIBRINOGEN,SAA POSSIBLE ROLE AS OPSONINS INCREASED ESR-DUE TO FIBRINOGEN
- 29. SYSTEMIC EFFECTS OF INFLAMMATION LEUCOCYTOSIS INCREASED RELEASE FROM BM INCREASED PROLIFERATION FROM PRECUSORS NEUTROPHILIA-MOST BACTERIA LYMPHOCYTOSIS-VIRAL EOS-PARASITIC,ALLERGIC
- 30. SYSTEMIC EFFECTS OF INFLAMMATION ANOREXIA,SOMNOLENCE,DECREASED APPETITE SEV BACTERIAL INFECTION-SEPTIC SHOCK
- 31. IMPT TOPICS ESSAY CHEMICAL MEDIATORS OF INFLAMMATION CELLULAR EVENTS OF INFLAMMATION SHORT TOPICS ADHESION MOLECULES PHAGOCYTOSIS GRANULOMAS SYSTEMIC EFFECTS OF INFLAMMATION CELLULAR EVENTS OF INFLAMMATION VASCULAR EVENTS OF INFLAMMATION KILLING AND DEGRADATION