Hypersensitivity Reactions
•Download as PPTX, PDF•
2 likes•126 views
This document discusses hypersensitivity reactions of types III and IV. Type III reactions are immune complex-mediated, where immune complexes form in circulation and deposit in tissues, activating the classical complement pathway and causing damage. They can cause conditions like serum sickness, arthritis, and glomerulonephritis. Type IV reactions are cell-mediated, initiated by sensitized T lymphocytes, and involve delayed-type hypersensitivity to intracellular pathogens mediated by CD4 T cells or cytotoxic CD8 T cell responses. Treatment involves symptom relief with antihistamines or corticosteroids, exposure prevention, and sometimes desensitization or immunoregulation.
Report
Share
Report
Share
Recommended
Immune response to hiv infection
This slide contains detailed information of the immunological response happens during the HIV infection in human
Immunopathology lecture 2+3 ,final
The document discusses different types of immune disorders:
1. Hypersensitivity reactions (allergies) are caused by an exaggerated immune response upon re-exposure to an antigen and are classified into four types.
2. Autoimmune diseases occur when the immune system attacks the body's own tissues.
3. Immunodeficiency diseases result from inadequate immune response.
4. Amyloidosis involves abnormal protein buildup in tissues.
TYPE IV HYPERSENSITIVITY
Type 4 hypersensitivity, detailed description of type 4 hypersensitivity mechanism, CD8 cells role, and CD4 cells activity
Immunology of tuberculosis
The document discusses the immunology of tuberculosis. It covers the stages of pathogenesis of M. tuberculosis infection, the host immune response including innate and acquired immunity, and the pro-inflammatory and anti-inflammatory mediators involved in tuberculosis. The key points are:
1) M. tuberculosis is an intracellular pathogen that infects the lungs and can spread to other organs. The host immune response involves phagocytosis by alveolar macrophages and recruitment of other immune cells.
2) Both the innate and acquired immune responses are involved in the host defense against M. tuberculosis. Important components include neutrophils, NK cells, TLR signaling, and the cell-mediated immune response involving CD4 and CD8 T cells.
Immunopathology 5
This document summarizes secondary immunodeficiency states and acquired immunodeficiency syndrome (AIDS). It describes AIDS as being caused by the human immunodeficiency virus (HIV) which leads to immunosuppression and opportunistic infections. The virus is transmitted through unprotected sex, blood transfusions, from mother to child, and sharing of infected needles. HIV infects immune cells like CD4+ T cells and macrophages. This results in loss of CD4+ T cells and ultimately immune system failure putting individuals at risk for infections and cancers.
Diseases Of The Immune System (2)
There are two main categories of diseases that affect the immune system: autoimmune diseases and immunodeficiency diseases. Autoimmune diseases occur when the immune system loses self-tolerance and attacks the body's own tissues, examples include systemic lupus erythematosus, rheumatoid arthritis, and scleroderma. Immunodeficiency diseases weaken the immune system, leaving the body vulnerable to infection; examples are severe combined immunodeficiency, DiGeorge syndrome, agammaglobulinemia, and acquired immunodeficiency syndrome (AIDS) caused by the human immunodeficiency virus (HIV).
Immunopathology 1
This document summarizes different types of immunity and hypersensitivity reactions. It describes two broad categories of immunity: innate immunity which provides a first line of defense, and adaptive immunity which develops after exposure and recognizes specific antigens. It then discusses four types of hypersensitivity reactions (Type I-IV) mediated by different immune mechanisms in response to various antigens, providing examples of diseases associated with each type.
Role of cytokines in type iv hypersensitivity
Type IV hypersensitivity, also known as delayed type hypersensitivity, involves CD4+ T cells that recognize antigens presented by macrophages and secrete cytokines like IL-2 and interferon gamma. This stimulates proliferation of more Th1 cells and activation of macrophages and CD8+ T cells. Activated macrophages produce hydrolytic enzymes and CD8+ T cells destroy target cells. Examples of type IV hypersensitivity diseases include contact dermatitis, temporal arteritis, and symptoms of tuberculosis.
Recommended
Immune response to hiv infection
This slide contains detailed information of the immunological response happens during the HIV infection in human
Immunopathology lecture 2+3 ,final
The document discusses different types of immune disorders:
1. Hypersensitivity reactions (allergies) are caused by an exaggerated immune response upon re-exposure to an antigen and are classified into four types.
2. Autoimmune diseases occur when the immune system attacks the body's own tissues.
3. Immunodeficiency diseases result from inadequate immune response.
4. Amyloidosis involves abnormal protein buildup in tissues.
TYPE IV HYPERSENSITIVITY
Type 4 hypersensitivity, detailed description of type 4 hypersensitivity mechanism, CD8 cells role, and CD4 cells activity
Immunology of tuberculosis
The document discusses the immunology of tuberculosis. It covers the stages of pathogenesis of M. tuberculosis infection, the host immune response including innate and acquired immunity, and the pro-inflammatory and anti-inflammatory mediators involved in tuberculosis. The key points are:
1) M. tuberculosis is an intracellular pathogen that infects the lungs and can spread to other organs. The host immune response involves phagocytosis by alveolar macrophages and recruitment of other immune cells.
2) Both the innate and acquired immune responses are involved in the host defense against M. tuberculosis. Important components include neutrophils, NK cells, TLR signaling, and the cell-mediated immune response involving CD4 and CD8 T cells.
Immunopathology 5
This document summarizes secondary immunodeficiency states and acquired immunodeficiency syndrome (AIDS). It describes AIDS as being caused by the human immunodeficiency virus (HIV) which leads to immunosuppression and opportunistic infections. The virus is transmitted through unprotected sex, blood transfusions, from mother to child, and sharing of infected needles. HIV infects immune cells like CD4+ T cells and macrophages. This results in loss of CD4+ T cells and ultimately immune system failure putting individuals at risk for infections and cancers.
Diseases Of The Immune System (2)
There are two main categories of diseases that affect the immune system: autoimmune diseases and immunodeficiency diseases. Autoimmune diseases occur when the immune system loses self-tolerance and attacks the body's own tissues, examples include systemic lupus erythematosus, rheumatoid arthritis, and scleroderma. Immunodeficiency diseases weaken the immune system, leaving the body vulnerable to infection; examples are severe combined immunodeficiency, DiGeorge syndrome, agammaglobulinemia, and acquired immunodeficiency syndrome (AIDS) caused by the human immunodeficiency virus (HIV).
Immunopathology 1
This document summarizes different types of immunity and hypersensitivity reactions. It describes two broad categories of immunity: innate immunity which provides a first line of defense, and adaptive immunity which develops after exposure and recognizes specific antigens. It then discusses four types of hypersensitivity reactions (Type I-IV) mediated by different immune mechanisms in response to various antigens, providing examples of diseases associated with each type.
Role of cytokines in type iv hypersensitivity
Type IV hypersensitivity, also known as delayed type hypersensitivity, involves CD4+ T cells that recognize antigens presented by macrophages and secrete cytokines like IL-2 and interferon gamma. This stimulates proliferation of more Th1 cells and activation of macrophages and CD8+ T cells. Activated macrophages produce hydrolytic enzymes and CD8+ T cells destroy target cells. Examples of type IV hypersensitivity diseases include contact dermatitis, temporal arteritis, and symptoms of tuberculosis.
Pathology - immune system
The document summarizes key aspects of the immune system and immune response. It discusses three lines of defense - physical and chemical barriers as the first line, nonspecific immune cells and responses as the second line, and specific immune responses mediated by lymphocytes and antibodies as the third line. It describes the cells involved in innate and adaptive immunity, including phagocytes, lymphocytes, and antigen presenting cells. It also outlines the functions of the immune system in recognition of antigens, mounting effector responses, regulation, and generation of immunological memory.
2. hypersensitivity rn dr. sinhasan, mdzah
This document summarizes the different types of hypersensitivity reactions. It describes type I immediate hypersensitivity which involves IgE antibodies, mast cell degranulation, and the release of inflammatory mediators. Type II hypersensitivity involves cell-bound antibodies leading to cell destruction. Type III hypersensitivity is caused by immune complex deposition which activates the complement system and causes inflammation. Type IV hypersensitivity is T-cell mediated and involves delayed hypersensitivity reactions like contact dermatitis and transplant rejection.
Imm 17 type iv hs
Type IV hypersensitivity, also known as delayed-type hypersensitivity, is a T cell-mediated immune response that occurs when antigen-specific CD4+ T cells mount an inflammatory response upon reexposure to an antigen hours or days after initial sensitization. There are three main variants of type IV hypersensitivity reactions: contact hypersensitivity, tuberculin-type hypersensitivity, and granulomatous hypersensitivity. Contact hypersensitivity involves skin inflammation at the site of contact with haptens or contact allergens and can be tested via patch testing. Tuberculin-type hypersensitivity is demonstrated by the Mantoux tuberculin skin test and involves induration of the skin after intradermal exposure to bacterial
Immunity against prtozoan diaseases
The document summarizes immunity against various protozoan diseases. It discusses that immunity against protozoa depends on the location of the parasite, with humoral immunity most effective for bloodstream parasites and cell-mediated responses for intracellular parasites. Effector cells like macrophages, neutrophils, and eosinophils can kill protozoa and worms. Immunity against specific protozoa involves both innate and acquired responses, including antibodies, B cells, plasma cells, memory cells, macrophages, NK cells, cytokines and effector T cells playing roles in protection.
Type iv hypersensitivity reaction
Type-IV hypersensitivity reactions are cell-mediated immune responses caused by cytokines from CD4+ T cells or cytotoxic CD8+ T cells. They involve the proliferation and differentiation of antigen-responsive T cells into subsets like TH1 dominated by macrophages or TH17 dominated by neutrophils. Examples include tuberculosis reactions, contact dermatitis, and autoimmune diseases like rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, psoriasis, and type 1 diabetes.
Diseases of the Immune System
Primary immunodeficiencies are caused by genetic defects that impair the immune system's ability to fight infections. They can be classified as humoral, affecting antibody production; cellular, affecting T cells and cell-mediated immunity; or combined. Common primary immunodeficiencies include X-linked agammaglobulinemia, isolated IgA deficiency, common variable immunodeficiency, hyper IgM syndrome, and severe combined immunodeficiency. Secondary immunodeficiencies are acquired, having underlying causes like infections, malnutrition, aging, or drugs. Acquired immunodeficiency syndrome (AIDS) is caused by the human immunodeficiency virus (HIV).
Chronic inflammation
This document discusses chronic inflammation. It defines chronic inflammation as a prolonged inflammatory response lasting weeks or months where inflammation, tissue injury, and repair occur simultaneously. Chronic inflammation can be caused by persistent infections, hypersensitivity reactions, prolonged toxic exposures, or recurrent acute inflammation. It is characterized by mononuclear cell infiltration, tissue destruction or necrosis, and attempts at healing. Macrophages and lymphocytes are the major cell types involved. Macrophages play key roles through phagocytosis, tissue repair, and secreting inflammatory mediators. Chronic inflammation can also involve plasma cells, mast cells, and eosinophils and their mediators. Granulomatous inflammation is a specific type of chronic inflammation forming granulomas made of epithelio
Hypersensitivity
This document defines types of hypersensitivity reactions and allergies. It describes four main types of reactions: Type 1 IgE-mediated reactions like anaphylaxis occur rapidly via histamine release. Type 2 cytotoxic reactions damage cells via IgG/IgM antibodies. Type 3 immune complex reactions involve antigen-antibody complexes activating complement and attracting inflammatory cells. Type 4 delayed hypersensitivity reactions occur via T cell activation and cytokine release over hours to days.
DISEASE OF IMMUNITY
The document discusses diseases of immunity, including hypersensitivity reactions and autoimmune diseases. It describes the innate and adaptive immune system, cells involved like T cells, B cells, cytokines, and histocompatibility molecules. Hypersensitivity reactions are classified and immediate (Type I) hypersensitivity is explained, where re-exposure to an antigen leads to rapid allergic reactions mediated by IgE and mast cells.
Hypersenstivrt 4
Hypersensitivity Type IV is a delayed type hypersensitivity that involves cell-mediated responses without antigen-antibody interactions. T lymphocytes recognize antigens that have been processed and presented by antigen-presenting cells via MHC molecules. Activated CD4+ T cells secrete cytokines that regulate the immune response, while activated CD8+ T cells kill cells displaying endogenous antigens on their MHC Class I molecules through the release of perforins and granzymes. This leads to loss of cell content and cell death.
Immunological Diseases
The document discusses various types of immunological disorders including hypersensitivity reactions. It defines four types of hypersensitivity reactions: type I or immediate hypersensitivity which involves IgE antibodies and is often seen in conditions like asthma and food allergies. Type II involves cytotoxic hypersensitivity where the immune system attacks the body's own cells. Type III involves immune complex hypersensitivity resulting in conditions like lupus. Type IV is cell-mediated hypersensitivity seen in contact dermatitis. Specific conditions discussed in more detail include allergic rhinitis, atopic dermatitis, anaphylaxis, transplantation rejection, and graft-versus-host disease.
Immunopathology 3
Autoimmune diseases result from immune reactions against self-antigens and loss of self-tolerance. They can be organ-specific like type 1 diabetes which targets pancreatic beta cells, or systemic like systemic lupus erythematosus which affects multiple organs. Central and peripheral tolerance mechanisms normally prevent autoimmunity, but their failure allows self-reactive T and B cells to escape and cause tissue damage. Common autoimmune diseases include rheumatoid arthritis, Sjögren's syndrome, systemic sclerosis, and inflammatory myopathies.
Autoimmunity and autoimmune disease
The document summarizes a chapter about autoimmunity and autoimmune diseases from three perspectives:
1) It outlines several key autoimmune diseases, their causes from abnormal immune responses against self-antigens, and their symptoms.
2) It discusses the use of animal models to study the mechanisms and potential treatments of autoimmune diseases.
3) It examines current therapeutic approaches that aim to suppress autoimmune responses through drugs or removal of target organs, and potential alternative strategies like inducing tolerance to self-antigens.
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.
IMMUNOPATHOLOGY
This document discusses different types of hypersensitivity and immunopathology. It covers four main types of hypersensitivity reactions (Type I-IV) that vary in severity from mild to life-threatening. Type I is an immediate reaction mediated by IgE antibodies and mast cells. Type II involves IgG and IgM antibodies against cell surface antigens. Type III reactions are caused by immune complexes circulating in the bloodstream. Type IV is a delayed hypersensitivity mediated by T cells. The document also discusses autoimmune disease, where the immune system attacks the body's own tissues, and immunodeficiencies that increase susceptibility to infection.
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.
Immunity and its applied aspect
The document provides an overview of immunology and the immune system. It discusses key topics such as antigens, antibodies, antigen-antibody reactions, innate immunity, acquired immunity, and hypersensitivity. The immune system is made up of cells and organs that protect the body from pathogens and foreign substances. It responds to antigens through both cellular and humoral responses in order to neutralize or eliminate the antigen.
hypersensitivity reactions type 3 and 4
Hypersensitivity is an exaggerated or misdirected immune response that results in tissue injury. It occurs upon re-exposure to a substance an individual is already sensitized to. Reactions can be immediate or delayed. Gell and Coombs classified hypersensitivity into four types based on time course and immune mechanism involved. Type III is immune complex-mediated hypersensitivity. Immune complexes activate complement and recruit neutrophils, causing tissue damage. Typical manifestations are Arthus reactions and serum sickness. Type IV is cell-mediated delayed hypersensitivity involving activation of sensitized T cells upon re-exposure. Contact hypersensitivity and tuberculin reactions are examples.
Inflammation
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.
Immune system disorders
Allergies, transplant rejection, and autoimmune diseases are caused by immune responses against substances that the immune system mistakenly sees as foreign. Allergies are caused by an immune response against harmless antigens, resulting in symptoms like a runny nose and sneezing. Transplant rejection occurs when the immune system attacks transplanted organs or tissue that are slightly different from the recipient's own. Autoimmune diseases happen when the immune system mistakenly attacks the body's own cells and tissues, as seen in conditions like type 1 diabetes, myasthenia gravis, and systemic lupus erythematosus.
Hypersensitivity dr. agale
This document discusses the four main types of hypersensitivity reactions:
Type 1 involves IgE antibodies and leads to immediate allergic reactions. Type 2 occurs when IgG or IgM antibodies bind to antigens on cell surfaces and trigger phagocytosis or cell damage. Type 3 involves immune complex formation that activates the complement system and causes inflammation. Type 4 is a delayed cell-mediated response involving sensitized T lymphocytes. Examples like tuberculosis and contact dermatitis are given. The tuberculin test for detecting sensitization to TB and mechanisms of transplant rejection are also summarized.
Hypersensitivity reactions
This document discusses the different types of hypersensitivity reactions:
1. Type I reactions are immediate and antibody-mediated, involving IgE. They cause conditions like allergic asthma and anaphylaxis.
2. Type II reactions are cytotoxic and involve IgG/IgM binding to cell surfaces and activating complement. They can lyse cells.
3. Type III reactions involve soluble immune complexes activating complement and causing inflammation. They include serum sickness.
4. Type IV reactions are delayed, cell-mediated responses involving sensitized T cells and cytokines. They cause conditions like contact dermatitis.
More Related Content
What's hot
Pathology - immune system
The document summarizes key aspects of the immune system and immune response. It discusses three lines of defense - physical and chemical barriers as the first line, nonspecific immune cells and responses as the second line, and specific immune responses mediated by lymphocytes and antibodies as the third line. It describes the cells involved in innate and adaptive immunity, including phagocytes, lymphocytes, and antigen presenting cells. It also outlines the functions of the immune system in recognition of antigens, mounting effector responses, regulation, and generation of immunological memory.
2. hypersensitivity rn dr. sinhasan, mdzah
This document summarizes the different types of hypersensitivity reactions. It describes type I immediate hypersensitivity which involves IgE antibodies, mast cell degranulation, and the release of inflammatory mediators. Type II hypersensitivity involves cell-bound antibodies leading to cell destruction. Type III hypersensitivity is caused by immune complex deposition which activates the complement system and causes inflammation. Type IV hypersensitivity is T-cell mediated and involves delayed hypersensitivity reactions like contact dermatitis and transplant rejection.
Imm 17 type iv hs
Type IV hypersensitivity, also known as delayed-type hypersensitivity, is a T cell-mediated immune response that occurs when antigen-specific CD4+ T cells mount an inflammatory response upon reexposure to an antigen hours or days after initial sensitization. There are three main variants of type IV hypersensitivity reactions: contact hypersensitivity, tuberculin-type hypersensitivity, and granulomatous hypersensitivity. Contact hypersensitivity involves skin inflammation at the site of contact with haptens or contact allergens and can be tested via patch testing. Tuberculin-type hypersensitivity is demonstrated by the Mantoux tuberculin skin test and involves induration of the skin after intradermal exposure to bacterial
Immunity against prtozoan diaseases
The document summarizes immunity against various protozoan diseases. It discusses that immunity against protozoa depends on the location of the parasite, with humoral immunity most effective for bloodstream parasites and cell-mediated responses for intracellular parasites. Effector cells like macrophages, neutrophils, and eosinophils can kill protozoa and worms. Immunity against specific protozoa involves both innate and acquired responses, including antibodies, B cells, plasma cells, memory cells, macrophages, NK cells, cytokines and effector T cells playing roles in protection.
Type iv hypersensitivity reaction
Type-IV hypersensitivity reactions are cell-mediated immune responses caused by cytokines from CD4+ T cells or cytotoxic CD8+ T cells. They involve the proliferation and differentiation of antigen-responsive T cells into subsets like TH1 dominated by macrophages or TH17 dominated by neutrophils. Examples include tuberculosis reactions, contact dermatitis, and autoimmune diseases like rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, psoriasis, and type 1 diabetes.
Diseases of the Immune System
Primary immunodeficiencies are caused by genetic defects that impair the immune system's ability to fight infections. They can be classified as humoral, affecting antibody production; cellular, affecting T cells and cell-mediated immunity; or combined. Common primary immunodeficiencies include X-linked agammaglobulinemia, isolated IgA deficiency, common variable immunodeficiency, hyper IgM syndrome, and severe combined immunodeficiency. Secondary immunodeficiencies are acquired, having underlying causes like infections, malnutrition, aging, or drugs. Acquired immunodeficiency syndrome (AIDS) is caused by the human immunodeficiency virus (HIV).
Chronic inflammation
This document discusses chronic inflammation. It defines chronic inflammation as a prolonged inflammatory response lasting weeks or months where inflammation, tissue injury, and repair occur simultaneously. Chronic inflammation can be caused by persistent infections, hypersensitivity reactions, prolonged toxic exposures, or recurrent acute inflammation. It is characterized by mononuclear cell infiltration, tissue destruction or necrosis, and attempts at healing. Macrophages and lymphocytes are the major cell types involved. Macrophages play key roles through phagocytosis, tissue repair, and secreting inflammatory mediators. Chronic inflammation can also involve plasma cells, mast cells, and eosinophils and their mediators. Granulomatous inflammation is a specific type of chronic inflammation forming granulomas made of epithelio
Hypersensitivity
This document defines types of hypersensitivity reactions and allergies. It describes four main types of reactions: Type 1 IgE-mediated reactions like anaphylaxis occur rapidly via histamine release. Type 2 cytotoxic reactions damage cells via IgG/IgM antibodies. Type 3 immune complex reactions involve antigen-antibody complexes activating complement and attracting inflammatory cells. Type 4 delayed hypersensitivity reactions occur via T cell activation and cytokine release over hours to days.
DISEASE OF IMMUNITY
The document discusses diseases of immunity, including hypersensitivity reactions and autoimmune diseases. It describes the innate and adaptive immune system, cells involved like T cells, B cells, cytokines, and histocompatibility molecules. Hypersensitivity reactions are classified and immediate (Type I) hypersensitivity is explained, where re-exposure to an antigen leads to rapid allergic reactions mediated by IgE and mast cells.
Hypersenstivrt 4
Hypersensitivity Type IV is a delayed type hypersensitivity that involves cell-mediated responses without antigen-antibody interactions. T lymphocytes recognize antigens that have been processed and presented by antigen-presenting cells via MHC molecules. Activated CD4+ T cells secrete cytokines that regulate the immune response, while activated CD8+ T cells kill cells displaying endogenous antigens on their MHC Class I molecules through the release of perforins and granzymes. This leads to loss of cell content and cell death.
Immunological Diseases
The document discusses various types of immunological disorders including hypersensitivity reactions. It defines four types of hypersensitivity reactions: type I or immediate hypersensitivity which involves IgE antibodies and is often seen in conditions like asthma and food allergies. Type II involves cytotoxic hypersensitivity where the immune system attacks the body's own cells. Type III involves immune complex hypersensitivity resulting in conditions like lupus. Type IV is cell-mediated hypersensitivity seen in contact dermatitis. Specific conditions discussed in more detail include allergic rhinitis, atopic dermatitis, anaphylaxis, transplantation rejection, and graft-versus-host disease.
Immunopathology 3
Autoimmune diseases result from immune reactions against self-antigens and loss of self-tolerance. They can be organ-specific like type 1 diabetes which targets pancreatic beta cells, or systemic like systemic lupus erythematosus which affects multiple organs. Central and peripheral tolerance mechanisms normally prevent autoimmunity, but their failure allows self-reactive T and B cells to escape and cause tissue damage. Common autoimmune diseases include rheumatoid arthritis, Sjögren's syndrome, systemic sclerosis, and inflammatory myopathies.
Autoimmunity and autoimmune disease
The document summarizes a chapter about autoimmunity and autoimmune diseases from three perspectives:
1) It outlines several key autoimmune diseases, their causes from abnormal immune responses against self-antigens, and their symptoms.
2) It discusses the use of animal models to study the mechanisms and potential treatments of autoimmune diseases.
3) It examines current therapeutic approaches that aim to suppress autoimmune responses through drugs or removal of target organs, and potential alternative strategies like inducing tolerance to self-antigens.
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.
IMMUNOPATHOLOGY
This document discusses different types of hypersensitivity and immunopathology. It covers four main types of hypersensitivity reactions (Type I-IV) that vary in severity from mild to life-threatening. Type I is an immediate reaction mediated by IgE antibodies and mast cells. Type II involves IgG and IgM antibodies against cell surface antigens. Type III reactions are caused by immune complexes circulating in the bloodstream. Type IV is a delayed hypersensitivity mediated by T cells. The document also discusses autoimmune disease, where the immune system attacks the body's own tissues, and immunodeficiencies that increase susceptibility to infection.
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.
Immunity and its applied aspect
The document provides an overview of immunology and the immune system. It discusses key topics such as antigens, antibodies, antigen-antibody reactions, innate immunity, acquired immunity, and hypersensitivity. The immune system is made up of cells and organs that protect the body from pathogens and foreign substances. It responds to antigens through both cellular and humoral responses in order to neutralize or eliminate the antigen.
hypersensitivity reactions type 3 and 4
Hypersensitivity is an exaggerated or misdirected immune response that results in tissue injury. It occurs upon re-exposure to a substance an individual is already sensitized to. Reactions can be immediate or delayed. Gell and Coombs classified hypersensitivity into four types based on time course and immune mechanism involved. Type III is immune complex-mediated hypersensitivity. Immune complexes activate complement and recruit neutrophils, causing tissue damage. Typical manifestations are Arthus reactions and serum sickness. Type IV is cell-mediated delayed hypersensitivity involving activation of sensitized T cells upon re-exposure. Contact hypersensitivity and tuberculin reactions are examples.
Inflammation
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.
Immune system disorders
Allergies, transplant rejection, and autoimmune diseases are caused by immune responses against substances that the immune system mistakenly sees as foreign. Allergies are caused by an immune response against harmless antigens, resulting in symptoms like a runny nose and sneezing. Transplant rejection occurs when the immune system attacks transplanted organs or tissue that are slightly different from the recipient's own. Autoimmune diseases happen when the immune system mistakenly attacks the body's own cells and tissues, as seen in conditions like type 1 diabetes, myasthenia gravis, and systemic lupus erythematosus.
What's hot (20)
Similar to Hypersensitivity Reactions
Hypersensitivity dr. agale
This document discusses the four main types of hypersensitivity reactions:
Type 1 involves IgE antibodies and leads to immediate allergic reactions. Type 2 occurs when IgG or IgM antibodies bind to antigens on cell surfaces and trigger phagocytosis or cell damage. Type 3 involves immune complex formation that activates the complement system and causes inflammation. Type 4 is a delayed cell-mediated response involving sensitized T lymphocytes. Examples like tuberculosis and contact dermatitis are given. The tuberculin test for detecting sensitization to TB and mechanisms of transplant rejection are also summarized.
Hypersensitivity reactions
This document discusses the different types of hypersensitivity reactions:
1. Type I reactions are immediate and antibody-mediated, involving IgE. They cause conditions like allergic asthma and anaphylaxis.
2. Type II reactions are cytotoxic and involve IgG/IgM binding to cell surfaces and activating complement. They can lyse cells.
3. Type III reactions involve soluble immune complexes activating complement and causing inflammation. They include serum sickness.
4. Type IV reactions are delayed, cell-mediated responses involving sensitized T cells and cytokines. They cause conditions like contact dermatitis.
lecture 9-GRANULOMATOUS INFLAMMATION .ppt
concise lecture with tables and pictures about chronic inflammation, its mediators, mechanism and sequele. Granulomatous inflammation with different types of granulomas along with histopathology pictures and description.
Hypersensitivities
hypersensitivity Undesirable reactions produced by the normal immune system. Hypersensitivity is an exaggerated immune response that results in tissue damage and is manifested in the individual on a second or subsequent contact with an antigen. Hypersensitivity reactions can be classified as either immediate or delayed. Obviously immediate reactions appear faster than delayed ones, but the main difference between them is the nature of the immune response to the antigen.
Hypersensitivity
Hypersensitivity reactions are immune-mediated responses triggered by exposure to usually harmless antigens known as allergens. Common types of hypersensitivity include hay fever, asthma, eczema, bee stings, and food allergies. Allergic responses are caused by IgE antibodies binding to mast cells and basophils, which leads to the release of inflammatory mediators upon re-exposure to the allergen, causing symptoms. Genetic factors influence a person's predisposition to developing allergies. Different types of hypersensitivity reactions involve the activation of various immune cells through antibody-mediated or cell-mediated mechanisms, resulting in tissue inflammation or damage.
Cell-mediated immunity (CMI)
This document discusses cell-mediated immunity (CMI), which is mediated by T lymphocytes and is responsible for detecting and destroying intracellular pathogens like viruses or infected cells, graft rejection, and destroying tumor cells. CMI results in a delayed-type hypersensitivity reaction. Upon first exposure to an antigen, naive T-cells are sensitized and proliferate. Secondary exposures result in a faster and more effective response from memory T-cells. Lymphokines released by activated T-cells mediate immune responses. A positive tuberculin skin test indicates past tuberculosis infection. CMI differs from humoral immunity in its mechanisms, antigens recognized, and hypersensitivity responses.
Cell Mediated Immunity.pptx
This document discusses cell-mediated immunity and T-cell mediated diseases. It begins with an overview of the immune system and outlines cell-mediated immunity and the role of T-cells. It describes how T-cells recognize antigens via T-cell receptors and discusses the development and roles of different T-cell types. It then explains how T-cells are involved in hypersensitivity reactions, autoimmune diseases like type 1 diabetes, rheumatoid arthritis, multiple sclerosis, and organ transplant rejection.
Hypersensitivity
This document discusses the classification and mechanisms of hypersensitivity reactions. It describes four main types of hypersensitivity: Type I is an immediate or anaphylactic reaction mediated by IgE antibodies binding to mast cells and basophils. Type II involves antibody-dependent cytotoxic reactions. Type III occurs when antigen-antibody complexes are deposited in tissues, activating the complement system and causing inflammation. Type IV is a cell-mediated or delayed hypersensitivity response. The document provides detailed explanations of the pathophysiology, clinical presentations, diagnosis and treatment of these hypersensitivity reactions.
immunopathology-1-130219045942-phpapp01.pdf
Jdf fjfnfnd kkdjdjjd dksowbdo nf ifngnf kdododbf dkkskskfbbf firibf fkdkskskjc ciirtbiff d ksksbvig rkdifue coekwnnxifbcog wnkcnf sbkcndikfc ivnevi je jdkbsjskwoos fkdkdkkdkd djdjdnjc fjdjdbdjidisnxbxidjdbbciv xj nd kdnndjx xisndn xndjbds sbsindvbfbidn bddjjdjd djxjdnnd jdjdnsisooslc kkskdkdkkdkkd
Acute and Chronic inflammation & Wound Healing
This document discusses acute and chronic inflammation and wound healing. It defines inflammation and describes its purpose. There are two main types: acute and chronic inflammation. Acute inflammation is short-term and involves chemicals like toll-like receptors and arachidonic acid metabolites. Chronic inflammation is long-lasting and characterized by lymphocytes and macrophages. It can lead to outcomes like scarring, amyloidosis, or neoplastic transformation. Wound healing involves regeneration or repair through granulation tissue formation and is affected by factors like infection, nutrition, and vascular disease. Abnormal wound healing can result in dehiscence or scarring.
Immunity
The document provides an overview of the immune system including:
- Definitions of immunity and its functions of destroying pathogens and abnormal cells.
- The two types of immunity - innate (non-specific) and acquired (specific).
- Innate immunity includes anatomical, physiological, chemical, and biological barriers.
- Acquired immunity can be naturally acquired active, artificially acquired active, naturally acquired passive, or artificially acquired passive.
- Immunity also involves B cells, T cells, and humoral versus cellular responses.
- Immunological disorders include hypersensitivity, autoimmune diseases, and immunodeficiencies.
drug hypersensitivity made easy
Drug hypersensitivity is an immune-mediated reaction to a drug that ranges from mild to severe symptoms like rash and anaphylaxis. It differs from expected adverse drug effects or interactions. Diagnosis is clinical with occasional skin testing use, and treatment involves drug discontinuation, supportive care like antihistamines, and sometimes desensitization.
drug hypersensitivity
Drug hypersensitivity is an immune-mediated reaction to a drug that ranges from mild to severe symptoms like rash and anaphylaxis. It differs from expected adverse drug effects or interactions. Diagnosis is clinical with occasional skin testing use, and treatment involves drug discontinuation, supportive care like antihistamines, and sometimes desensitization.
Inflammation overview
1. The document discusses inflammation, describing it as the body's protective response to injury or infection that helps rid the body of damaging stimuli and initiate repair of tissues.
2. It notes the four cardinal signs of inflammation as heat, redness, swelling, and pain, and explains the causes, types, and components of the inflammatory response.
3. The summary outlines the functions of inflammation in destroying pathogens, limiting their spread, and repairing damaged tissues, as well as the roles of plasma proteins, leukocytes, and tissue phagocytes in mounting an inflammatory response.
Immunopathology
There are two main types of immunity: innate and adaptive. Innate immunity provides initial defense through barriers, phagocytes, and proteins. Adaptive immunity has cellular and humoral components, mediated by T and B lymphocytes, which provide stronger, antigen-specific responses. Hypersensitivity reactions are caused by immune responses against harmless antigens, and include four types. Type I is immediate and antibody-mediated. Type II involves antibody and complement attack of cells. Type III occurs when immune complexes deposit in tissues. Type IV is delayed and cell-mediated. Disorders can also result from immune deficiencies or reactions against self.
Type iv hypersensitivity reactions
Type IV hypersensitivity reactions are T cell-mediated responses that cause tissue damage. They occur when T cells respond to antigens in tissues, releasing cytokines that activate macrophages and cause inflammation. This results in conditions like contact dermatitis and delayed-type hypersensitivity reactions. The tissue injury in these diseases is caused by macrophages and neutrophils that are activated by T cells. Treatment focuses on reducing inflammation and inhibiting T cell responses.
The Immune System
The immune system has both innate and acquired responses. The innate response is non-specific and provides immediate protection against infection. The acquired response is antigen-specific and develops over time through exposure to pathogens. It provides long-lasting immunity through immunological memory. The two main cell types of the acquired response are B cells and T cells. B cells produce antibodies while T cells help activate other immune cells. Together they provide a highly targeted defense against pathogens.
Basic Immunology 21 26
This document discusses hypersensitivity reactions and autoimmune diseases. It describes the four types of hypersensitivity reactions according to the Gell and Coombs classification: Type I (immediate), Type II (cytotoxic), Type III (immune complex-mediated), and Type IV (delayed type hypersensitivity). It provides details on the mechanisms and examples of each type. The document then discusses immunological tolerance, including central and peripheral tolerance. It explains how a breakdown in tolerance can lead to autoimmune diseases and provides examples like Graves' disease, myasthenia gravis, hemolytic anemia, and systemic lupus erythematosus.
Seminar sunil
Protozoan parasites cause diseases like malaria, leishmaniasis, and trypanosomiasis. Both the innate and adaptive immune systems play crucial roles in defending against protozoan infections. The innate immune system includes mechanisms like cytokines, complement proteins, macrophages, and neutrophils. The adaptive immune system involves antibody production and T cell responses. Protozoan parasites have evolved ways to evade or subvert the host immune response, such as antigenic variation and inhibiting immune cell function, enabling chronic or recurrent infections. An effective immune response against protozoa involves a balance of pro-inflammatory cytokines, T cell subsets, and effector cells and molecules.
non specific host defenses
Non-specific host defenses provide three lines of protection against invading pathogens:
1. Anatomical barriers like the skin and mucous membranes form the first line of defense.
2. Innate immune responses like inflammation, fever, and phagocytosis from white blood cells are the second line of defense.
3. The third line of defense involves specific immune responses from antibodies and lymphocytes that target pathogens that breach the first two lines. Together, these non-specific defenses provide broad protection against microbes.
Similar to Hypersensitivity Reactions (20)
More from Anantha Chaitanya
Malignant otitis externa
Malignant otitis externa is an aggressive infection of the soft tissues of the external ear that spreads to involve the skull base. It is usually caused by Pseudomonas aeruginosa and predominantly affects diabetics. Key features include otalgia, otorrhea, and cranial nerve palsies. Diagnosis involves biopsy showing microabscesses, positive cultures, and imaging showing bone involvement. Treatment requires prolonged high-dose intravenous and then oral antibiotics, with surgery reserved for complications.
Alkali Burns Eye
Alkali burns are severe chemical injuries caused by strong bases like lime and caustic soda. They damage tissues through saponification of lipids and extraction of water from cells. Clinically, they cause necrosis, edema, and inflammation of the conjunctiva, cornea, and iris. Treatment involves immediate and prolonged irrigation, debridement of dead tissue, topical antibiotics, steroids, and anti-collagenase agents to promote healing and prevent complications like symblepharon and corneal ulceration. More severe cases may require surgical procedures like conjunctival advancement or limbal stem cell transplantation. Despite treatment, prognosis remains guarded due to the extensive tissue damage caused by alkalis.
Pathogenesis of asthma
This document summarizes the pathogenesis of bronchial asthma. It describes the pathology as mucosa activation of eosinophils, T lymphocytes, and mast cells, along with thickening of the basement membrane and subepithelial collagen deposition. It then discusses the key cells involved (mast cells, macrophages, dendritic cells, eosinophils, neutrophils, T lymphocytes), mediators (leukotrienes, histamine, prostaglandins), and effects of inflammation (airway remodeling, hyperresponsiveness, epithelial changes, fibrosis, smooth muscle changes). Overall, it provides an overview of the cellular and molecular mechanisms that drive airway inflammation, remodeling, and hyperresponsiveness in asthma.
Myocardial infarction
Mr. X, a 62-year-old smoker, presented to the hospital with severe chest pain. Myocardial infarction (MI), the death of heart muscle, can be classified as ST-segment elevation MI (STEMI) or non-ST-segment elevation MI (NSTEMI) based on electrocardiogram (ECG) findings. The heart receives its blood supply from the left and right coronary arteries, which are commonly blocked by blood clots. Timely reperfusion through procedures like percutaneous coronary intervention (PCI) within 90 minutes of arrival can reduce heart muscle death, as the first hour after symptoms presents the highest likelihood of preventing cell death. Guidelines recommend fibrinolysis or PCI depending on facility capabilities and
Metabolic syndrome
The document discusses metabolic syndrome, which is characterized by insulin resistance and increased waist circumference. It is associated with dyslipidemia, glucose intolerance, hypertension, and proinflammatory cytokines. Clinical features include increased waist circumference, hypertension, and lipoatrophy. Treatment focuses on lifestyle changes like diet, physical activity, and behavior modification to address obesity, lipid levels, blood pressure, and insulin resistance.
Acid base disorders
This document discusses acid-base disorders and provides information on respiratory acidosis and metabolic alkalosis.
It begins with an overview of acid-base buffer systems in the body and the Henderson-Hasselbalch equation used to diagnose acid-base imbalances. It then discusses respiratory acidosis, defining it as a decreased pH and elevated pCO2. Causes include lung diseases that impair ventilation. It increases H+ excretion and HCO3- reabsorption as compensation.
Metabolic alkalosis is then covered, defined as an increased pH and HCO3- concentration. Causes include vomiting, diuretic use, and mineralocorticoid excess. It decreases ventilation as compensation. Two
Abruptio placenta clinical features
This document provides an overview of abruption placenta, including:
1. Couvelaire uterus, which is a severe form associated with massive bleeding into the uterine muscles.
2. Pathological changes in other organs like the liver, kidneys, and blood.
3. A clinical classification system grading abruption from mild to severe.
4. Clinical features that depend on the degree and speed of placental separation.
5. Ultrasonography and differential diagnosis with conditions like placenta previa.
Complications are more severe for concealed abruption, and can include maternal hemorrhage, shock, and death as well as high rates of fetal death from anoxia.
More from Anantha Chaitanya (7)
Recently uploaded
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
ARTHROLOGY PPT NCISM SYLLABUS AYURVEDA STUDENTS
PPT RELATED TO ARTHROLOGY ACCORDING TO NCISM AYURVEDA
Novas diretrizes da OMS para os cuidados perinatais de mais qualidade
Novas diretrizes da OMS para os cuidados perinatais de mais qualidadeProf. Marcus Renato de Carvalho
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Light House Retreats: Plant Medicine Retreat Europe
Our aim is to organise conscious gatherings and retreats for open and inquisitive minds and souls, with and without the assistance of sacred plants.
Top-Vitamin-Supplement-Brands-in-India List
Swisschem Dermacare provides the Top 10 Vitamin Supplement Brands in India. To know more about us give us call at our official number
Integrating Ayurveda into Parkinson’s Management: A Holistic Approach
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Dehradun #ℂall #gIRLS Oyo Hotel 8107221448 #ℂall #gIRL in Dehradun
Dehradun #ℂall #gIRLS Oyo Hotel 8107221448 #ℂall #gIRL in Dehradun
The Best Ayurvedic Antacid Tablets in India
Treat the symptoms of indigestion, heartburn and stomach reflux with the 10 Best Ayurvedic Antacid Tablets in India.
Physiology of Chemical Sensation of smell.pdf
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Hemodialysis: Chapter 4, Dialysate Circuit - Dr.Gawad
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Role of Mukta Pishti in the Management of Hyperthyroidism
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
Efficacy of Avartana Sneha in Ayurveda
Avartana Sneha is a unique method of Preparation of Sneha Kalpana in Ayurveda, mainly it is indicated for the Vataja rogas.
How STIs Influence the Development of Pelvic Inflammatory Disease.pptx
STIs may cause PID. For the both disease, herbal medicine Fuyan Pill can be a solution.
Identification and nursing management of congenital malformations .pptx
Identification and nursing management of congenital malformations .pptxMGM SCHOOL/COLLEGE OF NURSING
Identification and nursing management of congenital malformations Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
It includes regulation of combination products and medical devices. FDA and industry liaisons.
Recently uploaded (20)
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists
Novas diretrizes da OMS para os cuidados perinatais de mais qualidade
Novas diretrizes da OMS para os cuidados perinatais de mais qualidade
Light House Retreats: Plant Medicine Retreat Europe
Light House Retreats: Plant Medicine Retreat Europe
Integrating Ayurveda into Parkinson’s Management: A Holistic Approach
Integrating Ayurveda into Parkinson’s Management: A Holistic Approach
Dehradun #ℂall #gIRLS Oyo Hotel 8107221448 #ℂall #gIRL in Dehradun
Dehradun #ℂall #gIRLS Oyo Hotel 8107221448 #ℂall #gIRL in Dehradun
Vestibulocochlear Nerve by Dr. Rabia Inam Gandapore.pptx
Vestibulocochlear Nerve by Dr. Rabia Inam Gandapore.pptx
Hemodialysis: Chapter 4, Dialysate Circuit - Dr.Gawad
Hemodialysis: Chapter 4, Dialysate Circuit - Dr.Gawad
Role of Mukta Pishti in the Management of Hyperthyroidism
Role of Mukta Pishti in the Management of Hyperthyroidism
How STIs Influence the Development of Pelvic Inflammatory Disease.pptx
How STIs Influence the Development of Pelvic Inflammatory Disease.pptx
Identification and nursing management of congenital malformations .pptx
Identification and nursing management of congenital malformations .pptx
Ear and its clinical correlations By Dr. Rabia Inam Gandapore.pptx
Ear and its clinical correlations By Dr. Rabia Inam Gandapore.pptx
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
REGULATION FOR COMBINATION PRODUCTS AND MEDICAL DEVICES.pptx
Hypersensitivity Reactions
- 1. Hypersensitivity Reactions Dr Anantha Chaitanya J Intern BGS GIMS 1
- 2. Hypersensitivity Reaction III Immune Complex Mediated. Formation of immune complexes in circulation → deposit in various tissues → trigger classical pathway of complement activation. Produce damage as they localize within blood vessel walls or when trapped in filtering structures (e.g. renal glomeruli) 2
- 5. Hypersensitivity Reaction III 5 ANTIGEN CLINICAL MANIFESTATION A] EXOGENOUS: Arthritis GN, Infective endocarditis Glomerulonephritis 1) BACTERIA: Y. enterocolitica Streptococci T. pallidum 2) Viruses: Hepatitis B, CMV Polyarteritis nodosa 3) Parasites: Plasmodium Schistosoma Glomerulonephritis 4) Fungi: Actinomycetes Farmer’s lung B] ENDOGENOUS: SLE1) Nuclear Antigens 2) Immunoglobulins Rheumatoid Arthritis 3) Tumor Antigens Glomerulonephritis
- 6. Hypersensitivity Reaction III 1. SERUM SICKNESS: Systemic inflammatory response to deposited immune complexes at many areas of body. Few days to 2 weeks after injection of foreign serum or drug it results in : Fever, Urticaria, Arthralgia, Eosinophilia, Splenomegaly, and Lymphadenopathy. 2. ARTHUS REACTION: It is named after Dr. Arthus. Inflammation caused by the deposition of immune complexes at a localized site. Clinical Manifestation is : Hypersensitivity Pneumonitis. 6
- 7. Hypersensitivity Reaction IV Cell-mediated hypersensitivity. Initiated by sensitized T lymphocytes. Principal pattern of immunologic response to intracellular microbiologic agents (particularly Mycobacterium tuberculosis) as well as viruses, fungi, protozoa & parasites. 7
- 8. Hypersensitivity Reaction IV 1. Delayed-type hypersensitivity: Mediated by CD4 T cells. 1st exposure to Ag → CD4 T cells + class II MHC → differentiation of naïve CD4 T cells to TH1 cells → release of IL-12, IFN-γ, IL-2, TNFα & lymphotoxin. Tuberculin skin test, contact dermatitis, granulomatous inflammation. 2. T Cell-Mediated Cytotoxicity: Mediated by CD8+ T cells. Sensitized CD8+ T cells kill antigen-bearing target cells. Perforin-granzyme-dependent killing → cause perforation of plasma membrane. Fas-FasL-dependent killing → activation of apoptosis. Graft rejection, virus infections, tumor immunity. 8
- 10. Treatment Symptomatic treatment: Anti-histamines, corticosteroids, vasoconstrictors, smooth muscle relaxants. Exposure prevention: Ideal. Not Practical. Barriers: Clothes, creams, filters. Specific hyposensitization: Test → Identify → Controlled Exposure. Nonspecific desensitization: Obsolete. Immunoregulation. Molecular medicine. 10
- 11. Bibliography Textbook of Microbiology, Ananthnarayan, 9th Edition. IADVL Textbook Of Dermatology, 4th Edition. Pathologic Basis Of Disease, Robbins and Cotran, 9th Edition. 11
- 12. Thank You 12