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Porth - Immunity
Porth - Essentials of Pathophysiology - Immunity
| Question | Answer |
|---|---|
| Passive immunity is transferred from | -Maternal IgG- crosses the placenta -IgA in colostrum -Inoculation of Immune serum or gammaglobulin (pool of antibodies) |
| Passive Immunity | Short term specific protection induced through transfer of protective antibodies against an antigen for specific disease |
| Active Immunity | Specific protection induced following exposure to antigens. Body’s immune response to an antigen. |
| Antigens | substances foreign to the host that can stimulate an immune response .Eg: Microbe, transplanted organ |
| Antigenic determinants or epitopes | -antigens degraded into smaller chemical units |
| Haptens-carrier complexes | Low molecular weight compounds that are unable to stimulate an adequate immune response by themselves |
| Hapten-carrier complexes | Haptens combine with larger carrier proteins to form that act as antigens |
| Types of antigens | Bacteria Fungi Viruses Protozoa Parasites Nonmicrobial agents like transplanted organs |
| Central lymphoid organs | Production and maturation of immune cell Bone marrow –B Cells Thymus- T cells & Plasma cells |
| Peripheral lymphoid tissues | Lymph Nodes, Spleen, tonsils, Appendix, Peyer patches & mucosal lymphoid tissues lining respiratory, GI and reproductive tracts. trap and process antigen |
| Immune Response | The collective, coordinated response of the cells and molecules of the immune system against antigens |
| Components of immune system | Immune cells. Phagocytic leukocytes : Neutrophils , Macrophages (monocytes) Antigen presenting cells (Dendritic cells) Lymphocytes (T- Lymphocytes, B- Lymphocytes, Natural killer cells) Compliment system Cytokines |
| Immune Cells - Phagocytic leukocytes | Neutrophils , Macrophages (monocytes) |
| Antigen presenting cells | Dendritic cells |
| Lymphocytes | T- Lymphocytes, B- Lymphocytes, Natural killer cells |
| Complement System | In circulation as precursors Function to : (1)enhance inflammatory response (2)increase phagocytosis activated in the proper sequence C1..C3..C9) Classical, lectin and alternate pathways merge at C3. |
| Complement System Activation Phase | cleavage of C3 producing C3b opsonins and C3a inflammatory factors |
| Complement System Amplification Phase | Inflammation by inflammatory factors cause |
| Complement System Membrane Attack Response Phase | Formation of a membrane attack complex that leads to the lytic destruction of many kinds of cells |
| Cytokines | soluble proteins secreted by cells of immune system . synthesized for a brief period , not stored, Generates responses by binding to receptors on target cells |
| Pleotropism | Same cytokine mediates different functions (causes side effects) |
| Redundancy | Different cytokines mediates same or overlapping functions (nullify antagonists because other cytokines compensates) |
| Chemokines | Cytokines that stimulate the migration and activation of immune and inflammatory cells |
| Colony stimulating factors | Cytokines that stimulates the bone marrow pluripotent stem cells to produce different types of cells |
| Innate, or nonspecific immunity | First line of rapid immune response. The natural resistance with which a person is born |
| Adaptive, or specific immunity | the second line of defense unique against each foreign agent, responding less rapid, but more effective through lymphocytes and antibodies |
| How does Innate Immunity? | Pathogen recognition recognizes patterns of classes of microbes Pathogen binding to membrane receptors Cell activation , phagocytosis & Intracellular killing |
| Innate Immunity - Pathogen-associated molecular patterns (PAMPS) | Patterns present on the pathogens which are essential for its functioning and infectivity |
| Innate Immunity - Pattern recognition receptors (PRRS) | Host sensors that recognizes patterns on pathogens (PAMPS) and binds it to the leukocyte membranes |
| Innate Immunity - Toll-like receptors (TLRS) | Membrane spanning proteins with horse shoe shaped external PAMPs and internal signaling domain for activating leukocytes |
| Adaptive Immunity - Humoral immunity | Antigen -antibody reactions mediated by B cells |
| Adaptive Immunity - Cell-mediated immunity | Phagocytic cells that attack the specific antigens mediated by T-Cells |
| Adaptive Immunity - Specificity | Recognize and attacks specific microbes (antigens) |
| Adaptive Immunity - Memory | Develops after exposure to the specific antigen. (“remember” the pathogen ,quickly producing a heightened immune response on subsequent encounters ) |
| Adaptive Immunity - Diversity | Can remember and attack billions of diverse antigenic molecules |
| Adaptive Immunity - Self – Nonself | Recognition |
| How does adaptive immunity antigen presentation work | Macrophages and dendritic cells (process and present antigen peptides to CD4+ helper T lymphocytes) |
| How does adaptive immunity Activation of B & T receptors work | On antigen recognition and stimulation by cytokines, B& T lymphocytes multiply and clone into different groups of memory and effector cells |
| Adaptive Immunity - Effector Cells | destroy the antigens |
| Adaptive Immunity - Memory Cells | retain the potential to kill later |
| humoral immunity - primary response | Occurs during the first encounter with an antigen 1-2 weeks of lag: seroconversion period Recovery from many infections occurs due to antibody level. |
| humoral immunity - secondary response | occurs on subsequent exposures to the same antigen mediated by memory cells The memory cells recognize the antigen and respond more efficiently to produce the specific antibody Example: Administration of tetanus booster |
| IgG (gamma globulin) | most abundant |
| IgA | secretory Ig.Body Secretions (tears, saliva etc) |
| IgM | natural antibodies, activates complement |
| IgD | differentiation and maturation of B cells |
| IgE | binds to mast cells and Basophils, hypersensitivity And parasitic reactions |
| Antigen- antibody reaction can result in | Precipitation of antigen antibody complexes Agglutination or clumping of cells Neutralization of bacterial toxins and viruses Lysis and destruction of pathogens Adherence of antigen to immune cells Facilitation of phagocytosis Compliment activation |
| Cell mediated immunity | T cells are produced in the bone marrow and matures in the Thymus and then migrate to lymphoid tissues . On encounter with antigen, they differentiate into memory cells and mature T cells |
| Three main subpopulations of mature T cells | CD4+(helper) Cells, CD8+ (cytotoxic T cells), and Regulatory cells: inhibiting the proliferation self-reactive lymphocytes. |
| antigen presenting cells (APC) activates the CD4+ helper cells. Activated T helper cells | -release cytokines that aid inflammatory process - activates Cytotoxic T cells |
| Cytotoxic T lymphocytes | kills target cells in many ways |
| Cell Mediated Immunity - Functions through T lymphocytes and macrophages | The activation of other T cells and B cells The control of intracellular viral infections The rejection of foreign tissue grafts Delayed hypersensitivity reactions |
| The Elderly Immune System - | Declining ability to adapt to environmental stresses Decline in immune responsiveness Decrease in the size of the thymus gland Biological clock in T cells Altered responses of the immune cells to antigen stimulation |
| Immunizations | Purpose is to protect against infectious diseases. Most effective method is to create a highly immune population. Universal vaccine is the goal. Vaccines carry risk – but risks of disease are much greater. |
| Immunizations and Purpose is to protect against infectious diseases. Most effective method is to create a highly immune population. Universal vaccine is the goal. Vaccines carry risk – but risks of disease are much greater. Immunocompromised children | at special risk from live vaccines |
| Results of Alterations of the Immune System | Immunodeficiency states Allergic or hypersensitivity reactions Transplantation rejection Autoimmune disorders |
| Hypersensitivity Disorders | Excessive or inappropriate activation of the immune system |
| Hypersensitivity Disorders - Types | Type I, Ig-E–mediated disorders Type II, antibody-mediated disorders Type III, complement-mediated immune disorders Type IV, T-cell–mediated disorders |
| Hypersensitivity Disorders - Type I: Ig-E mediated disorders | Allergic reactions caused by Helper T cells and mast cells Intensity of reaction related to the allergen’s portal of entry |
| Atopic disorders (Mild Allergic reactions) | Childhood allergies, Hereditary predisposition,. A local reaction of IgE antibodies to environmental agents, Ex: hives, allergic rhinitis ,atopic dermatitis, food allergies, asthma Drug: Antihistamines |
| Histamine Initial Phase | Mast cell sensitization |
| Histamine | mast cell degranulation releasing Histamine |
| Histamine Receptors - H1 receptors - On capillary endothelium | Vasodilation (Skin of the face and upper body; Extensive can cause hypotension) Increased capillary permeability (Edema) |
| Histamine Receptors - H1 receptors - On Bronchial walls | Bronchoconstriction- Breathing difficulty |
| Histamine Receptors - H1 receptors - On CNS | Role in cognition, memory, and sleep/waking cycles |
| Histamine Receptors - H1 receptors - Other | Itching, pain, secretion of mucus |
| Histamine Receptors - H2 receptors | Secretion of gastric acid |
| Type II (Cytotoxic)Hypersensitivity Reactions | Mediated by IgG or IgM antibodies directed against target antigens on the surface of cells or other tissue components (Endogenous antigens & Exogenous antigens) |
| Type II (Cytotoxic)Hypersensitivity Reactions - Results In | -Compliment and antibody mediated cell destruction Mismatched blood transfusion reactions,Rh disease Drug reactions -Compliment & antibody mediated inflammation Glomerulonephritis -Antibody mediated cellular dysfunction Grave’s disease (Hyperthyroid |
| Type III Immune Complex Allergic Disorders | -Mediated by the formation of insoluble antigen–antibody complexes in the circulation that damage the vessel lining & tissues -Immune complexes elicit inflammatory response activating complement & responsible for vasculitis in certain autoimmune diseases |
| Type III Immune Complex Allergic Disorders - Systemic immune complex disorders | Serum sickness: Occurs 7 days after injection of an antigen (horse serum for Tetanus) |
| Type III Immune Complex Allergic Disorders - Localized immune complex reactions | Arthus reaction : Localized tissue necrosis associated with vasculitis caused by immune complexes |
| Type IV Hypersensitivity reactions | Cell-mediated immune response (Mediated by sensitized T lymphocytes) |
| Type IV Hypersensitivity reactions - Direct cell-mediated cytotoxicity | Direct kill of infected cells Ex: Hepatitis |
| Type IV Hypersensitivity reactions - Delayed-type hypersensitivity | -Occurs in response to Soluble protein antigens -Mediated by memory cells and Takes 12 to 72 hours to develop (time to secrete cytokines). Example: Tuberculin test |
| Type IV Hypersensitivity reactions - Allergic contact dermatitis | Occurs 12-24 hrs after re-exposure to allergen & last days to weeks. Characterized by erythematous, papular or vesicular weeping lesions w/ severe pruritus. Location provides a clue about the offending antigen. Patch test useful in confirming the antigen |
| Type IV Hypersensitivity reactions - Hypersensitivity Pneumonitis | -Caused by inhaled antigens Ex: Farmers lung. Complication: Chronic lung disease -Sensitized pulmonary T cells & release inflammatory mediators & response leads to labored breathing, dry cough, chills & fever, headache, malaise |
| Type IV Hypersensitivity reactions - Hypersensitivity Pneumonitis - Treatment | -Subsides w/ hours of removing offender Treatment: removal of offending antigen, and corticosteroids |
| Latex Allergy | -8-12% of healthcare workers have latex sensitivity. -Exposure for patients include dentist office and operating rooms |
| Latex Allergy - Routes of exposure | -Cutaneous & Mucous membrane (Contact & Inhalation) -Internal tissue: Intravascular routes (Catheters) |
| Latex Allergy - Irritant dermatitis | Not an allergic response.(only irritation) |
| Latex Allergy - Ig-E mediated type I hypersensitivity | Allergy to latex proteins. characterized by Urticaria, asthma, anaphylaxis |
| Latex Allergy - Delayed Type IV hypersensitivity(DTH) | -Allergy to additives during manufacturing process -Contact dermatitis that occurs 48-96 hours after |
| Latex Allergy - Treatment | Creating a latex free environment |
| Major histocompatibility complex (MHC) | -Set of molecules displayed on cell surfaces (Lymphocyte recognition and Antigen presentation) -Control the immune response through recognition of self and nonself |
| Categories of transplanted tissue - Allogeneic | The donor and recipient are related or unrelated but share similar HLA types |
| Categories of transplanted tissue - Syngeneic | The donor and recipient are identical twins |
| Categories of transplanted tissue - Autologous | The donor and recipient are the same person |
| Patterns of Transplant Rejection - Hyper acute reaction | -Occurs almost immediately after transplantation -Produced by existing recipient antibodies to graft antigens initiating a type III, Arthus-type hypersensitivity reaction |
| Patterns of Transplant Rejection - Acute rejection | -Occurs within first few months after transplantation with signs of organ failure; may occur months or years after immunosuppression has been terminated -T lymphocytes respond to antigens in the graft tissue |
| Patterns of Transplant Rejection - Chronic (host-versus-graft rejection) | -Occurs over a prolonged period -Manifests with dense intimal fibrosis of blood vessels of the transplanted organ. The actual mechanism is unclear but may include release of cytokines that stimulate fibrosis |
| Basic Requirements for Graft-versus-Host Disease | -The transplant must have a functional cellular immune component. -The recipient tissue must bear antigens foreign to the donor tissue. -The recipient immunity must be compromised to the point that it cannot destroy the transplanted cells. |
| Chemokines | cytokines that stimulate the migration and activation of immune and inflammatory cells |
| Colony Stimulating Factors | cytokines that stimulate the bone marrow pluripotent to produce different types of cells |
| Opsonin | any molecule that targets an antigen for immune response |
| Cytokines | cell signaling protein molecules and used for intercellular communication |
| Autoimmune Disease - Mechanisms Postulated to Explain the Tolerant State - Self-tolerance | Ability to differentiate between self and nonself antigens |
| Autoimmune Disease - Mechanisms Postulated to Explain the Tolerant State - Central tolerance | The elimination of self-reactive T cells and B cells in the central lymphoid organs (i.e., the thymus for T cells and the bone marrow for B cells) |
| Autoimmune Disease - Mechanisms Postulated to Explain the Tolerant State - Peripheral tolerance | Derives from the deletion or inactivation of autoreactive T cells or B cells that escaped elimination in the central lymphoid organs |
| Autoimmune Disease - Mechanisms Postulated to Explain the Tolerant State - Anergy | State of unresponsiveness to an antigen |
| Mechanisms of Autoimmune Disease - Heredity and gender | Predisposing HLA types |
| Mechanisms of Autoimmune Disease - Environmental factors | =Trigger events =Infectious and chemical agents |
| Mechanisms of Autoimmune Disease - Failure of self-tolerance - Disorders in MHC | MHC–antigen complex/receptor interactions |
| Mechanisms of Autoimmune Disease - Failure of self-tolerance - Molecular mimicry | Mirobes share an immunologic epitopes with the host causing a mistaken identity |
| Mechanisms of Autoimmune Disease - Failure of self-tolerance - Super-antigens | cause inappropriate activation of T cells |
| Diagnosis and treatment - Criteria for determining an autoimmune disorder | =Evidence of an autoimmune reaction =Determination that the immunologic findings are not secondary to another condition =Lack of other identified causes for the disorder |
| Diagnosis and treatment - Diagnosis of autoimmune disease is based on | Clinical findings, Serologic testing for autoantibodies |
| Diagnosis and treatment - Autoimmune disease treatment | =Treat the underlying cause =Alter the progress of the disease with corticosteriods and immunosuppressants =Plasmapheresis- removing autoreactive cells |
| Immunosuppressants | Inhibit immune response |
| Immunosuppressants - Uses | =Prevention of organ rejection =Treatment of autoimmune diseases |
| Immunosuppressants - Toxicity | =Increased risk of infection =Increased risk of neoplasms |
| Classification of Immunodeficiency States - Primary | congenital or inherited |
| Classification of Immunodeficiency States - Secondary | =Due to increased loss or decreased production of immunoglobulins: =Malnutrition =Infection (e.g., AIDS) =Kidney disease =Neoplastic disease (e.g., lymphoma) =Immunosuppressive therapy (e.g., corticosteroids or transplant rejection medications) |
| Humoral Immunodeficiencies - B-Cell and Viruses | =B-cell function and immunoglobulin or antibody production are involved. =Viruses usually handled normally, except for enteroviruses that cause GI infections |
| Humoral Immunodeficiencies | =Defects in humoral immunity increase the risk of recurrent pyogenic infections. =Humoral immunity usually is not as important in defending against intracellular bacteria (mycobacteria), fungi, and protozoa. |
| Primary Humoral Immunodeficiency Disorders - Genetic disorders of | the B lymphocytes |
| Approximately 70% of primary immunodeficiencies are | Primary Humoral Immunodeficiency Disorders |
| Primary Humoral Immunodeficiency Disorders - Immunoglobulin production depends on | =The differentiation of stem cells to mature B lymphocytes =The generation of immunoglobulin-producing plasma cells |
| Primary Humoral Immunodeficiency Disorders - Can interrupt the production of one or all of the immunoglobulins | =X- linked (Bruton) agammaglobilinemia =Common variable immunodeficiency =Selective immunoglobulin A deficiency =Immunoglobulin G subclass deficiency |
| Are Cell Mediated (T cell) immunodeficiency disorder more or less clinically severe than B-Cell disorders | Clinically T-Cell disorders are more severe than B-Cell Disorders |
| Cell Mediated (T cell) immunodeficiency - Treatment | Transplantation of thymic tissue, bone marrow transplantation or stem cell transplantation |
| Cell Mediated (T cell) immunodeficiency - DiGeorge Syndrome | Embryonic development defect occurring before 12th week of gestation. Failure of development of the thymus and parathyroid gland and congenital defects of the head, neck and heart |
| Cell Mediated (T cell) immunodeficiency - X-linked hyper IgM | Boys susceptible to pyogenic infections (severe local inflamations) and autoimmune disorders of blood |
| Cell Mediated (T cell) immunodeficiency - Secondary cell mediated immunodeficiency disorders are described | in conjunction with acute viral infections and malignancies like lymphomas |
| Combined T-Cell and B-Cell Immunodeficiencies - Severe combined immunodeficiency (SCID) | =Affects both B cells and T cells resulting in the loss of both humoral and cell mediated immunity |
| Combined T-Cell and B-Cell Immunodeficiencies - Caused by | =mutation in any gene that influence lymphocyte development =X-linked SCID |
| Combined T-Cell and B-Cell Immunodeficiencies - Combined immunodeficiency disorders (CID) | =Impaired but not absent function of T cells and B cells |
| Combined T-Cell and B-Cell Immunodeficiencies - Combined immunodeficiency disorders (CID) - Ataxia-telangiectasis | cerebellar ataxia, dilated capillaries |
| Combined T-Cell and B-Cell Immunodeficiencies - Combined immunodeficiency disorders (CID) - Wiskott-Aldrich syndrome | eczema, bleeding disorder |
| Disorders of the Complement System - Primary | =Most transmitted as autosomal-recessive traits & can involve 1 or more complement component =Causes autoimmune diseases like SLE & Lupus like syndrome & repeated life threatening infections like meningitis and Pneumonia =Patients should receive vaccine |
| Disorders of the Complement System - Secondary | Can occur in persons with functionally normal complement systems because of rapid activation and turnover or reduced synthesis of complement components |
| Disorders of the Complement System - Primary - Uncontrolled activation | leading to episodic (1-4 days)disfiguring edema involving face, neck, abdomen. Treated with Danazol (synthetic androgen with anabolic potential) |
| Dysfunction of the Phagocytic System | A defect in phagocytic functions or a reduction in the absolute number of available cells disrupt the system |
| Dysfunction of the Phagocytic System - Susceptible to | =Candida species =Filamentous fungi |
| Dysfunction of the Phagocytic System - Primary | =Chronic granulomatous disease (CGD) =Chediak- Higashi syndrome |
| Dysfunction of the Phagocytic System - Secondary | Found in DM, leukemia, malnutrition and viral infections like AIDS. |
Created by:
rjjaramillo
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