Inflammation (dr.ahsan)patho.docx
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Inflammation is the body's protective response to injury or infection. It involves vascular changes like vasodilation and increased permeability that allow fluid proteins and immune cells to move from blood vessels into injured tissues. Acute inflammation occurs immediately after injury and lasts a few days at most. It is characterized by neutrophil accumulation and involves vascular changes and fluid exudation that cause swelling. Neutrophils migrate to injury sites through a process involving rolling, adhesion and chemotaxis in response to chemical signals, and then phagocytose and destroy pathogens through enzymatic lysis before undergoing apoptosis.
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INFLAMMATORY RESPONSES
This document provides an overview of inflammatory responses. It defines inflammation as the protective response by host cells to eliminate the initial cause of cell injury and restore homeostasis. The document then describes the types of inflammation as acute or chronic, and the key cellular and vascular changes involved in each. It also discusses the various mediators of inflammation, systemic effects like fever and acute phase reactions, and common anti-inflammatory pharmacology treatments.
Lect 4-inflammation-2-
1. The document defines and classifies inflammation as either acute or chronic based on duration and predominant cell types.
2. Acute inflammation is short-term, involving increased vascular permeability and neutrophil infiltration, while chronic inflammation lasts weeks to years with lymphocytes and macrophages predominant.
3. Chronic inflammation can lead to tissue damage through macrophage release of reactive oxygen species and is associated with conditions like cancer, fibrosis and impaired tissue function.
Definition, types & vascular events of inflammation
The document defines inflammation and its causes. It describes acute inflammation and the associated vascular events that occur, including transient vasoconstriction followed by vasodilatation and increased blood flow. This causes alterations in vascular permeability, initially allowing a plasma transudate to form and later an inflammatory exudate due to direct endothelial cell damage or the effects of chemical mediators. These vascular events underlie the five cardinal signs of inflammation.
Dr prashanth jain;basic pathology
Cellular adaptations and injury can occur through various mechanisms:
(1) When cells are exposed to stressors, they may undergo reversible changes like atrophy, hypertrophy, hyperplasia, metaplasia, or dysplasia to adapt. (2) If the stressors are severe or persistent, irreversible cell injury and death through necrosis or apoptosis can result. (3) Cellular injury can be caused by free radicals, hypoxia, physical trauma, chemicals, radiation, or biological agents and can lead to tissue dysfunction or infection if necrosis occurs.
Inflammation
This document defines inflammation and describes its historical understanding and cardinal signs. Inflammation is defined as the host response to local injury and is fundamentally a vascular phenomenon. The four cardinal signs described by Celsus in the 1st century AD are redness, heat, swelling, and pain. Rudolf Virchow later added a fifth sign of loss of function. The document outlines the stimuli that can cause inflammation including physical, chemical, biological, and immunological factors. It describes the key cells involved in acute and chronic inflammation such as neutrophils, macrophages, lymphocytes, and plasma cells. It distinguishes between acute inflammation which has a rapid onset and involves neutrophils and chronic inflammation which has a slower onset and involves lymphocytes and macrophages.
ACUTE INFLAMMATION
Inflammation is a complex reaction to injurious stimuli that consists of vascular responses, migration of leukocytes, and systemic responses. It involves vasodilation, increased vascular permeability, leukocyte adhesion and transmigration, release of inflammatory mediators, and activation of the complement system. The goal of inflammation is to destroy, dilute or wall off injurious agents. Prolonged inflammation can lead to chronic conditions like arthritis and atherosclerosis.
Shock
Shock is a life-threatening condition defined by a reduction in effective circulating blood volume and inadequate tissue perfusion. It can be caused by hypovolaemia, cardiac dysfunction, infection, trauma or other conditions. The main characteristics of shock are hypotension, hypoperfusion of tissues, and cellular injury if not resolved. Prolonged shock can lead to multi-organ failure and death.
Acute inflammation(pathology)
This document discusses acute inflammation. It describes the steps of the inflammatory response, including recognition of the injurious agent, recruitment and activation of leukocytes, removal of the agent, regulation of the response, and resolution. It details the vascular changes that occur, including vasodilation, increased permeability, and endothelial cell contraction. It also discusses the cellular events of leukocyte recruitment, activation, and phagocytosis. It outlines stimuli for acute inflammation and mechanisms of termination of the inflammatory response.
Recommended
INFLAMMATORY RESPONSES
This document provides an overview of inflammatory responses. It defines inflammation as the protective response by host cells to eliminate the initial cause of cell injury and restore homeostasis. The document then describes the types of inflammation as acute or chronic, and the key cellular and vascular changes involved in each. It also discusses the various mediators of inflammation, systemic effects like fever and acute phase reactions, and common anti-inflammatory pharmacology treatments.
Lect 4-inflammation-2-
1. The document defines and classifies inflammation as either acute or chronic based on duration and predominant cell types.
2. Acute inflammation is short-term, involving increased vascular permeability and neutrophil infiltration, while chronic inflammation lasts weeks to years with lymphocytes and macrophages predominant.
3. Chronic inflammation can lead to tissue damage through macrophage release of reactive oxygen species and is associated with conditions like cancer, fibrosis and impaired tissue function.
Definition, types & vascular events of inflammation
The document defines inflammation and its causes. It describes acute inflammation and the associated vascular events that occur, including transient vasoconstriction followed by vasodilatation and increased blood flow. This causes alterations in vascular permeability, initially allowing a plasma transudate to form and later an inflammatory exudate due to direct endothelial cell damage or the effects of chemical mediators. These vascular events underlie the five cardinal signs of inflammation.
Dr prashanth jain;basic pathology
Cellular adaptations and injury can occur through various mechanisms:
(1) When cells are exposed to stressors, they may undergo reversible changes like atrophy, hypertrophy, hyperplasia, metaplasia, or dysplasia to adapt. (2) If the stressors are severe or persistent, irreversible cell injury and death through necrosis or apoptosis can result. (3) Cellular injury can be caused by free radicals, hypoxia, physical trauma, chemicals, radiation, or biological agents and can lead to tissue dysfunction or infection if necrosis occurs.
Inflammation
This document defines inflammation and describes its historical understanding and cardinal signs. Inflammation is defined as the host response to local injury and is fundamentally a vascular phenomenon. The four cardinal signs described by Celsus in the 1st century AD are redness, heat, swelling, and pain. Rudolf Virchow later added a fifth sign of loss of function. The document outlines the stimuli that can cause inflammation including physical, chemical, biological, and immunological factors. It describes the key cells involved in acute and chronic inflammation such as neutrophils, macrophages, lymphocytes, and plasma cells. It distinguishes between acute inflammation which has a rapid onset and involves neutrophils and chronic inflammation which has a slower onset and involves lymphocytes and macrophages.
ACUTE INFLAMMATION
Inflammation is a complex reaction to injurious stimuli that consists of vascular responses, migration of leukocytes, and systemic responses. It involves vasodilation, increased vascular permeability, leukocyte adhesion and transmigration, release of inflammatory mediators, and activation of the complement system. The goal of inflammation is to destroy, dilute or wall off injurious agents. Prolonged inflammation can lead to chronic conditions like arthritis and atherosclerosis.
Shock
Shock is a life-threatening condition defined by a reduction in effective circulating blood volume and inadequate tissue perfusion. It can be caused by hypovolaemia, cardiac dysfunction, infection, trauma or other conditions. The main characteristics of shock are hypotension, hypoperfusion of tissues, and cellular injury if not resolved. Prolonged shock can lead to multi-organ failure and death.
Acute inflammation(pathology)
This document discusses acute inflammation. It describes the steps of the inflammatory response, including recognition of the injurious agent, recruitment and activation of leukocytes, removal of the agent, regulation of the response, and resolution. It details the vascular changes that occur, including vasodilation, increased permeability, and endothelial cell contraction. It also discusses the cellular events of leukocyte recruitment, activation, and phagocytosis. It outlines stimuli for acute inflammation and mechanisms of termination of the inflammatory response.
Inflammation
This document provides an overview of inflammation. It defines inflammation and divides it into acute and chronic types. The components of inflammation include vascular reactions and cellular reactions. Acute inflammation is characterized by neutrophil accumulation and lasts for a short period, while chronic inflammation involves lymphocytes and macrophages and lasts longer. The document further describes the stimuli, vascular changes, and cellular events involved in acute inflammation, including leukocyte margination, rolling, adhesion, transmigration, and phagocytosis. It also discusses the chemical mediators and outcomes of acute inflammation.
Beneficial effects of inflammation
The document discusses the local and systemic effects of acute inflammation. Locally, the fluid exudate released during inflammation can have beneficial effects like allowing antibodies to enter tissues and neutralize microorganisms or toxins. It also describes how fibrin formation from exuded fibrinogen can trap microbes and stimulate their phagocytosis, while drainage of exudate to lymph nodes can stimulate the immune response there.
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)
Morphology of-acute-inflammation
1. The document describes the different morphological patterns of acute inflammation including serous, fibrinous, suppurative, hemorrhagic, catarrhal, membranous, and necrotizing inflammation.
2. It also discusses the systemic effects of acute inflammation known as the acute phase response, including fever, increased acute phase proteins, and changes in white blood cells.
3. The fates of acute inflammation are described as resolution, healing, suppuration, or progression to chronic inflammation.
Inflammation
Inflammation is the body's response to infection, injury, or irritation. The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function. Acute inflammation occurs rapidly and is short-lived, while chronic inflammation persists over a longer period of time. Mediators of inflammation such as histamine, prostaglandins, and cytokines are released from platelets, neutrophils, monocytes, and mast cells to regulate the inflammatory response. Defective or excessive inflammation can lead to increased susceptibility to infection or disease.
Acute inflammation
The document summarizes inflammation and the key cellular processes involved. It describes how acute inflammation is characterized by fluid rich in proteins and PMNs, occurring over minutes to days. Chronic inflammation involves lymphocytes and macrophages over weeks to years. The classic signs of acute inflammation are described as heat, redness, swelling, pain, and loss of function. The vascular changes in acute inflammation include transient vasoconstriction, vasodilation, increased permeability and extravasation of PMNs. Leukocyte adhesion and transmigration are also summarized.
7 shock
Hemodynamic derangements and shock can be classified in several ways. Shock is defined as inadequate tissue perfusion resulting in cellular oxygen debt. There are four main types of shock based on hemodynamic parameters: hemorrhagic, cardiogenic, distributive, and obstructive. Etiologically, shock can be caused by hemorrhage, cardiac issues like myocardial infarction, sepsis/systemic inflammatory response syndrome, or anaphylaxis due to peripheral vasodilation. If not treated, shock can progress to organ dysfunction and failure due to hypoxic injury. Management involves identifying the cause, restoring intravascular volume and blood pressure, and treating the underlying condition.
Inflammation (Acute and Chronic) Prof Mulazim Hussain Bukhari
This document discusses acute inflammation. It defines inflammation, outlines the causes and molecular events of inflammation including vasodilation, vascular leakage, and leukocyte recruitment. It describes the cardinal signs of inflammation and summarizes the mechanisms of increased vascular permeability and leukocyte extravasation through selectin-mediated rolling, integrin-mediated adhesion, and transmigration across endothelial cells.
Infamattion in dentistry (dept of public health dentistry )
1. The document discusses inflammation and its chemical mediators. It defines inflammation and outlines its classification into acute and chronic types.
2. Acute inflammation is described in detail, including its vascular and cellular events like increased permeability and leukocyte migration.
3. The document then covers the various chemical mediators involved in inflammation, such as histamine, prostaglandins, cytokines, and complement proteins.
4. Chronic inflammation is introduced as prolonged inflammation where tissue damage and repair occur simultaneously. Its causes and features are briefly outlined.
inflammation
This document provides information about inflammation and repair. It begins by noting the importance but also potential harm of inflammation. It then lists goals of general pathology education related to inflammation. The document outlines inflammation processes including acute inflammation, chronic inflammation, and wound healing. It recommends several reference texts and provides a detailed lecture outline on topics such as classification of inflammation, the signs of inflammation, and generalities of the inflammatory response.
Inflammation
Acute inflammation is characterized by two major components: vascular changes and cellular events. The vascular changes include vasodilation, increased vascular permeability, and slowing of blood flow. This allows plasma proteins and leukocytes to leave the bloodstream and enter the injured tissues. The cellular events involve the migration of phagocytes such as neutrophils from the bloodstream into the injured tissues by the processes of margination, pavementing, emigration, and chemotaxis. The phagocytes then recognize, attach to, engulf, and destroy pathogens and cellular debris through phagocytosis, resolving the inflammatory response.
Inflammation part 1 by
- Inflammation is the body's protective response to injury or infection that involves increased blood flow, immune cell activity, and release of chemical mediators. It has both acute and chronic forms.
- The cardinal signs of inflammation are redness, heat, swelling, pain, and loss of function. It involves vascular changes like increased permeability and leukocyte emigration from blood vessels.
- Leukocytes like neutrophils, macrophages, and lymphocytes are involved. Chemical mediators regulate the inflammatory response. Acute inflammation typically resolves in a few days while chronic inflammation persists long-term.
1. inflammation introduction-dr. sinhasan- mdzah
Inflammation is the body's response to injury or infection and is characterized by redness, swelling, heat, pain, and loss of function. It is a protective process that helps destroy and remove harmful substances from the body and prevents minor infections from becoming overwhelming. The inflammatory response involves vascular changes like increased blood flow, exudation of fluid and proteins from blood vessels, and emigration of white blood cells. It can be either acute, resolving on its own, or chronic, persisting long-term and potentially causing tissue damage. Historically, the five cardinal signs of inflammation were identified and chemical mediators were found to play a key role. Stimuli that can cause inflammation include infections, trauma, toxins, and immune reactions
Cardiovascular System
This document discusses several cardiovascular conditions:
1. Rheumatic heart disease results from rheumatic fever caused by streptococcal infections and causes valvular damage over time.
2. Atherosclerosis is caused by lipid accumulation in artery walls and leads to complications like heart attacks and strokes.
3. Hypertension, if uncontrolled, can cause hyaline or hyperplastic arteriolosclerosis and end-organ damage.
4. Ischemic heart disease, including angina and myocardial infarction, occurs when atherosclerosis limits blood flow to the heart.
Inflammation Lect
1. Inflammation is the body's response to infection, irritation, or injury, characterized by redness, swelling, heat, and pain. It involves the immune system and blood vessels.
2. Acute inflammation is a short-term response to recent injury or infection, marked by increased blood flow, blood vessel permeability, and migration of white blood cells. Chronic inflammation is a long-term response involving lymphocytes, macrophages, and fibrosis.
3. Inflammation can resolve, lead to abscess or fibrosis, and is mediated by chemical signals like histamine, bradykinin, prostaglandins, and cytokines. Different cell types and patterns characterize specific inflammatory diseases.
Inflammation
Definition of inflammation, Causes, Signs of inflammation, Types of inflammation, Triple response, Phagocytosis, Transudate or Exudate, Difference between transudate and exudate, Granuloma and Granulomatous inflammation
Acute inflammation / dental implant courses by Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Acute inflammation
PREPARED BY: MUHAMMAD ARIFF B. MAHDZUB
BACHELOR MEDICINE AND SURGERY (MBBS)
UNIVERSITY COLLEGE SHAHPUTRA, KUANTAN
Inflammation
Inflammation is the body's response to injury or infection that helps eliminate the injurious agent and initiate healing. It is classified as either acute or chronic. Acute inflammation occurs rapidly, lasting minutes to days, characterized by increased blood flow, vascular permeability, and white blood cell migration. The cardinal signs are redness, heat, swelling, pain, and loss of function. Chemical mediators released from plasma and cells initiate and sustain acute inflammation and its effects. Outcomes include resolution, fibrosis, abscess, or progression to chronic inflammation.
Inflammation Part 2
The document summarizes key aspects of acute and chronic inflammation. Acute inflammation is triggered by various stimuli and involves increased blood flow, vascular permeability, and leukocyte migration. It aims to eliminate injurious agents. Chronic inflammation arises from persistent infections, toxins, or autoimmunity and is characterized by mononuclear cell infiltration and attempts at repair through fibrosis. Nutrition can impact inflammation through deficiencies, essential fatty acids, antioxidants, and factors related to over-nutrition like obesity.
Shock and its management
Shock and its management is summarized as follows:
1. Shock is a life-threatening condition characterized by inadequate tissue perfusion due to reduced circulating blood volume or cardiac output.
2. Shock is classified as hypovolemic, cardiogenic, septic, traumatic, neurogenic, or hypoadrenal based on etiology.
3. The pathophysiology involves reduced circulating volume, impaired tissue oxygenation, and release of inflammatory mediators, progressing from compensated to decompensated to irreversible stages if left untreated.
shock.ppt3333333333333333333333333333333
Shock results from the failure of the cardiovascular system to provide sufficient blood circulation.
To maintain circulatory homeostasis the following mechanisms must be present –
1. a functioning of heart to circulate blood .
A sufficient amount of blood volume .
The capability of the vascular system , accommodating blood flow to the capillaries and returning to the right side of the heart.
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Inflammation
This document provides an overview of inflammation. It defines inflammation and divides it into acute and chronic types. The components of inflammation include vascular reactions and cellular reactions. Acute inflammation is characterized by neutrophil accumulation and lasts for a short period, while chronic inflammation involves lymphocytes and macrophages and lasts longer. The document further describes the stimuli, vascular changes, and cellular events involved in acute inflammation, including leukocyte margination, rolling, adhesion, transmigration, and phagocytosis. It also discusses the chemical mediators and outcomes of acute inflammation.
Beneficial effects of inflammation
The document discusses the local and systemic effects of acute inflammation. Locally, the fluid exudate released during inflammation can have beneficial effects like allowing antibodies to enter tissues and neutralize microorganisms or toxins. It also describes how fibrin formation from exuded fibrinogen can trap microbes and stimulate their phagocytosis, while drainage of exudate to lymph nodes can stimulate the immune response there.
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)
Morphology of-acute-inflammation
1. The document describes the different morphological patterns of acute inflammation including serous, fibrinous, suppurative, hemorrhagic, catarrhal, membranous, and necrotizing inflammation.
2. It also discusses the systemic effects of acute inflammation known as the acute phase response, including fever, increased acute phase proteins, and changes in white blood cells.
3. The fates of acute inflammation are described as resolution, healing, suppuration, or progression to chronic inflammation.
Inflammation
Inflammation is the body's response to infection, injury, or irritation. The cardinal signs of inflammation are redness, swelling, heat, pain, and loss of function. Acute inflammation occurs rapidly and is short-lived, while chronic inflammation persists over a longer period of time. Mediators of inflammation such as histamine, prostaglandins, and cytokines are released from platelets, neutrophils, monocytes, and mast cells to regulate the inflammatory response. Defective or excessive inflammation can lead to increased susceptibility to infection or disease.
Acute inflammation
The document summarizes inflammation and the key cellular processes involved. It describes how acute inflammation is characterized by fluid rich in proteins and PMNs, occurring over minutes to days. Chronic inflammation involves lymphocytes and macrophages over weeks to years. The classic signs of acute inflammation are described as heat, redness, swelling, pain, and loss of function. The vascular changes in acute inflammation include transient vasoconstriction, vasodilation, increased permeability and extravasation of PMNs. Leukocyte adhesion and transmigration are also summarized.
7 shock
Hemodynamic derangements and shock can be classified in several ways. Shock is defined as inadequate tissue perfusion resulting in cellular oxygen debt. There are four main types of shock based on hemodynamic parameters: hemorrhagic, cardiogenic, distributive, and obstructive. Etiologically, shock can be caused by hemorrhage, cardiac issues like myocardial infarction, sepsis/systemic inflammatory response syndrome, or anaphylaxis due to peripheral vasodilation. If not treated, shock can progress to organ dysfunction and failure due to hypoxic injury. Management involves identifying the cause, restoring intravascular volume and blood pressure, and treating the underlying condition.
Inflammation (Acute and Chronic) Prof Mulazim Hussain Bukhari
This document discusses acute inflammation. It defines inflammation, outlines the causes and molecular events of inflammation including vasodilation, vascular leakage, and leukocyte recruitment. It describes the cardinal signs of inflammation and summarizes the mechanisms of increased vascular permeability and leukocyte extravasation through selectin-mediated rolling, integrin-mediated adhesion, and transmigration across endothelial cells.
Infamattion in dentistry (dept of public health dentistry )
1. The document discusses inflammation and its chemical mediators. It defines inflammation and outlines its classification into acute and chronic types.
2. Acute inflammation is described in detail, including its vascular and cellular events like increased permeability and leukocyte migration.
3. The document then covers the various chemical mediators involved in inflammation, such as histamine, prostaglandins, cytokines, and complement proteins.
4. Chronic inflammation is introduced as prolonged inflammation where tissue damage and repair occur simultaneously. Its causes and features are briefly outlined.
inflammation
This document provides information about inflammation and repair. It begins by noting the importance but also potential harm of inflammation. It then lists goals of general pathology education related to inflammation. The document outlines inflammation processes including acute inflammation, chronic inflammation, and wound healing. It recommends several reference texts and provides a detailed lecture outline on topics such as classification of inflammation, the signs of inflammation, and generalities of the inflammatory response.
Inflammation
Acute inflammation is characterized by two major components: vascular changes and cellular events. The vascular changes include vasodilation, increased vascular permeability, and slowing of blood flow. This allows plasma proteins and leukocytes to leave the bloodstream and enter the injured tissues. The cellular events involve the migration of phagocytes such as neutrophils from the bloodstream into the injured tissues by the processes of margination, pavementing, emigration, and chemotaxis. The phagocytes then recognize, attach to, engulf, and destroy pathogens and cellular debris through phagocytosis, resolving the inflammatory response.
Inflammation part 1 by
- Inflammation is the body's protective response to injury or infection that involves increased blood flow, immune cell activity, and release of chemical mediators. It has both acute and chronic forms.
- The cardinal signs of inflammation are redness, heat, swelling, pain, and loss of function. It involves vascular changes like increased permeability and leukocyte emigration from blood vessels.
- Leukocytes like neutrophils, macrophages, and lymphocytes are involved. Chemical mediators regulate the inflammatory response. Acute inflammation typically resolves in a few days while chronic inflammation persists long-term.
1. inflammation introduction-dr. sinhasan- mdzah
Inflammation is the body's response to injury or infection and is characterized by redness, swelling, heat, pain, and loss of function. It is a protective process that helps destroy and remove harmful substances from the body and prevents minor infections from becoming overwhelming. The inflammatory response involves vascular changes like increased blood flow, exudation of fluid and proteins from blood vessels, and emigration of white blood cells. It can be either acute, resolving on its own, or chronic, persisting long-term and potentially causing tissue damage. Historically, the five cardinal signs of inflammation were identified and chemical mediators were found to play a key role. Stimuli that can cause inflammation include infections, trauma, toxins, and immune reactions
Cardiovascular System
This document discusses several cardiovascular conditions:
1. Rheumatic heart disease results from rheumatic fever caused by streptococcal infections and causes valvular damage over time.
2. Atherosclerosis is caused by lipid accumulation in artery walls and leads to complications like heart attacks and strokes.
3. Hypertension, if uncontrolled, can cause hyaline or hyperplastic arteriolosclerosis and end-organ damage.
4. Ischemic heart disease, including angina and myocardial infarction, occurs when atherosclerosis limits blood flow to the heart.
Inflammation Lect
1. Inflammation is the body's response to infection, irritation, or injury, characterized by redness, swelling, heat, and pain. It involves the immune system and blood vessels.
2. Acute inflammation is a short-term response to recent injury or infection, marked by increased blood flow, blood vessel permeability, and migration of white blood cells. Chronic inflammation is a long-term response involving lymphocytes, macrophages, and fibrosis.
3. Inflammation can resolve, lead to abscess or fibrosis, and is mediated by chemical signals like histamine, bradykinin, prostaglandins, and cytokines. Different cell types and patterns characterize specific inflammatory diseases.
Inflammation
Definition of inflammation, Causes, Signs of inflammation, Types of inflammation, Triple response, Phagocytosis, Transudate or Exudate, Difference between transudate and exudate, Granuloma and Granulomatous inflammation
Acute inflammation / dental implant courses by Indian dental academy
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Acute inflammation
PREPARED BY: MUHAMMAD ARIFF B. MAHDZUB
BACHELOR MEDICINE AND SURGERY (MBBS)
UNIVERSITY COLLEGE SHAHPUTRA, KUANTAN
Inflammation
Inflammation is the body's response to injury or infection that helps eliminate the injurious agent and initiate healing. It is classified as either acute or chronic. Acute inflammation occurs rapidly, lasting minutes to days, characterized by increased blood flow, vascular permeability, and white blood cell migration. The cardinal signs are redness, heat, swelling, pain, and loss of function. Chemical mediators released from plasma and cells initiate and sustain acute inflammation and its effects. Outcomes include resolution, fibrosis, abscess, or progression to chronic inflammation.
Inflammation Part 2
The document summarizes key aspects of acute and chronic inflammation. Acute inflammation is triggered by various stimuli and involves increased blood flow, vascular permeability, and leukocyte migration. It aims to eliminate injurious agents. Chronic inflammation arises from persistent infections, toxins, or autoimmunity and is characterized by mononuclear cell infiltration and attempts at repair through fibrosis. Nutrition can impact inflammation through deficiencies, essential fatty acids, antioxidants, and factors related to over-nutrition like obesity.
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Inflammation (Acute and Chronic) Prof Mulazim Hussain Bukhari
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Shock results from the failure of the cardiovascular system to provide sufficient blood circulation.
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A sufficient amount of blood volume .
The capability of the vascular system , accommodating blood flow to the capillaries and returning to the right side of the heart.
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SPECIALLY FOR B.PHARMACY STUDENTS.YOU WILL GET COMPLETE INFORMATION REGARDING SHOCK,ITS EFFECT,ITS TYPES AND MECHENISM AND PATHOLOGY OF SHOCK
شوک در جراحی.pptx
Surgical shock can occur from circulatory failure leading to hypotension and cellular hypoxia. The main types are hypovolemic, distributive, cardiogenic, and obstructive shock. Hypovolemic shock results from reduced intravascular volume and is divided into hemorrhagic and nonhemorrhagic forms. Septic shock is the most common distributive shock caused by sepsis, which involves infection and organ dysfunction. Management of sepsis involves source control, antibiotics, fluids, and vasopressors like norepinephrine. Neurogenic shock results from spinal cord injury and features vasodilation. Anaphylactic shock is a severe allergic reaction treated with epinephrine, steroids, and anti
Inflammation acute + chronic
Inflammation is the body's protective response to injury or infection that involves increased blood flow, swelling, heat, pain, and loss of function. The document outlines the general considerations of inflammation including its definition, causes, and cardinal signs. It then discusses the major events of acute inflammation including vascular changes, exudation of fluid, and recruitment and activation of leukocytes. Finally, it classifies inflammation into acute and chronic types and further classifies acute inflammation based on the type of exudate produced (serous, fibrinous, suppurative, hemorrhagic).
Shock. Etiology, Pathogenesis, Intensive therapy
This document discusses the etiology, pathogenesis, and intensive treatment of shock. It begins with the history and terminology of shock and then discusses the fundamentals of circulatory physiology. It classifies shock into four main types - hypovolemic, cardiogenic, obstructive, and distributive - and describes the pathogenesis and clinical presentation of each. The document outlines the general principles of shock treatment, including fluid resuscitation with crystalloids and colloids, vasopressor support, and blood transfusion as needed. It provides algorithms for infusion-transfusion therapy based on the estimated volume of blood loss.
Inflammation
This document provides an overview of inflammation. It begins by defining inflammation as the protective response to eliminate the initial cause of cell injury. It then discusses the history of inflammation research and identifies common causative agents. The classic signs of inflammation - heat, redness, swelling, pain, and loss of function - are presented. Both acute and chronic inflammation are described, including their features, cellular events, and mediators. Acute inflammation involves vascular changes and leukocyte emigration, recruitment, and activation. Chronic inflammation is prolonged and involves mononuclear cell infiltration, tissue destruction, and proliferative changes. Specific and non-specific forms of chronic inflammation are also distinguished.
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.
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- 1. Inflammation The reaction of livingtissuesto all forms ofinjury. Advantages: - Protective response - Inactivate toxins - Achieve healing&repair Disadvantages: - Encephalitis(swellingof brain) cause death Types of inflammation: 1- Acute inflammation(AI) 2- Chronicinflammation(CI ACUTE INFLAMMATION (AI) Immediate & early response to injury. 1st line of defense againstinjury. Characteristics of(AI): - Relativelyshortduration - Fewminutesup tofewdays - Inflammatoryexudateformation - Predominantlyneutrophil leukocyteaccumulation. Causesof (AI): 1- Trauma 2- Chemical injury 3- Heat 4- Cold 5- Radiation 6- Injurydue to MO(microorganisms) 7- Injurydue to immunological mechanism Changesin (AI): Vascular changes - changesin vascularcaliber:
- 2. Initial vasoconstriction(small BV i.e terminal arterioles (ta)) Persistentvasodilation(persistfordurationof Inflammatoryprocess) - Alteration in local Blood flow: 1st Inc..inbloodvelocitydue todilationof (ta). Thisphase is forshort durationandfollowedby slowingof bloodstream(stasis) forINc.. vascularpermeability. Fluidislostfromblood& viscosityInc..thatslowsdownbloodflow. - Increased vascularpermeability& fluid exudation: Permeabilityof capillaries&venulesisfunctionof pores(intercellularjunctions)b/w vascularendothelial cells. In AIpermeabilityInc..due toactive contraction actinfilamentsinendothelial cells. As a resultwideningof poresoccurwhichallowspassage of large amountof fluid&high molecularwt.proteinsiscalledexudation. Thisexudationof fluidproducestissue swelling,calledinflammatoryedema. Featureshelpin inflammationinitiation: i- plasmaproteins ii- WBCs Patternof vascular permeability: Immediatetransientresponse: In response tomildinjury(permeabilitybegins1-2minsafterinjury&persistsfor20 mins.) Mediate by mediators, o Histamine o Bradykinins o Leukotrienes(cause endothelial cellscontractionresultwideningof Inter-endothelialgaps&leakage of plasmaproteins(exudate formation) ---------------
- 3. delayed- prolonged response: Sunburns,bacterial toxins Immediate-prolongedresponse: Due to necrosisof endothelial cells. - Fluidremove from vessel: Have 2 types, Exudate (highproteinconcentration) Transudate Exudate: It isinflammatoryextravascularfluidthathashighproteinconc.Much cellulardebris whichleaksfromvesselsintointerstitial space due toincreasedvascularpermeability e.gBacterial peritonitis&Tuberculosisperitonitis Fluidexudationmechanism: Factors whichregulate thistransport, Forceswhichholdfluidinsidevessels, Plasmaoncoticpressure (pushesfluidinward) (POP) Vascularhydrostaticpressure (pushesfluidoutward) (VHP) Forceswhichexertfromoutside tovessels, Interstitial oncoticpressure (IOP) Interstitial hydrostaticpressure (IHP) Transudate: (Whenvascularhydrostaticpressure Inc..notdue toinflammation.) It isan ultra-filtrate of bloodplasmawithlow proteincontentresultformincreasedvascular hydrostaticpressure.Here endotheliumpermeabilityisnormal. e.g, RENALFAILURE:
- 4. proteinnotabsorb& remove so,proteinDec..& theirfluidstartto Inc..in organscause edema. LIVER FAILURE: ProteinconcentrationDec..&waterinbloodmove fromvessel toperitoneal & cause fluidinorgans. Leukocytesrole inAI: Neutrophils(15u) &monocytes(20u) (abilitytoengulf bacteria) reachtoinjurysite tocombat infection. How neutrophilsgotoinflammationsite: Steps: 1- Margination: In thisneutrophilsattachto intergriniscalledmargination. [intergrin=some kindsof receptors(hooks) formonendothelial layer] 2- Rolling: The neutrophilsstartrollingonthe intergrin& selectrin&theystucktolumen. 3- Emigration: Stepwise pseudopodsformbyneutrophilspush&the neutrophilsrelease bythe helpof pseudopods. 4- Chemotaxis: It ismovementof WBCsunderthe influence of differentchemicalsonthe site of injury. At site of inflammationdifferentchemicalsproduces,i.e Bacterial products Complementcomponents C5a& C3a Arachidonicacidmetabolites i.e leukotriene B4 TNF & plateletactivatingfactor
- 5. Thus neutrophilssensethese &reachestosite of injury. 5- Phagocytosis: ProcessbywhichMO & otherforeignparticlesare engulfed&destroyedby neutrophils¯ophages. Opsonins:recognition&attachmentof mostof MOs isfacilitatedbycoating themserumproteinscalledopsoninswhichinturnbindtospecif receptorson leukocytes. e.gC3b&IgG. Phagosome:the bacteria+ opsoninswhithneutrophil membrane ispushedinto neutrophil iscalledphagosome. 6- Killing(Lysis): Neutrophil ownenzyme now begantokill bacteria&afterprocessneutrophil auto-phagocytes(apoptosis/self-death) &cell deletedfrombody.