Seminar on Anaphylaxis 7-6-12

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    SEMINAR ON ANAPHYLAXIS

    BY

    LIDIYAMOL.P.V

    1ST YEAR M.SC NURSINGGOVT. CON , THRISSUR

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    HISTORY OF IMMUNOLOGY:-

    Immunology is a science that examines the

    structure and function of the immune system.

    The earliest known reference to immunity was

    during the plague of Athens in 430 BC.

    . Thucydides noted that people who had

    recovered from a previous bout of the disease

    could nurse the sick without contracting the

    illness a second time.

    http://en.wikipedia.org/wiki/Immunologyhttp://en.wikipedia.org/wiki/Plague_of_Athenshttp://en.wikipedia.org/wiki/Thucydideshttp://en.wikipedia.org/wiki/Thucydideshttp://en.wikipedia.org/wiki/Plague_of_Athenshttp://en.wikipedia.org/wiki/Immunology
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    HISTORY OF IMMUNOLOGY:-

    CONTD

    Immunology made a great advance towards

    the end of the 19th century, through rapid

    developments, in the study ofhumoral

    immunity and cellular immunity. Particularly

    important was the work ofPaul Ehrlich, who

    proposed the side-chain theory to explain the

    specificity of the antigen-antibody reaction

    http://en.wikipedia.org/wiki/Humoral_immunityhttp://en.wikipedia.org/wiki/Humoral_immunityhttp://en.wikipedia.org/wiki/Cell-mediated_immunityhttp://en.wikipedia.org/wiki/Paul_Ehrlichhttp://en.wikipedia.org/wiki/Side-chain_theoryhttp://en.wikipedia.org/wiki/Side-chain_theoryhttp://en.wikipedia.org/wiki/Side-chain_theoryhttp://en.wikipedia.org/wiki/Side-chain_theoryhttp://en.wikipedia.org/wiki/Paul_Ehrlichhttp://en.wikipedia.org/wiki/Cell-mediated_immunityhttp://en.wikipedia.org/wiki/Humoral_immunityhttp://en.wikipedia.org/wiki/Humoral_immunityhttp://en.wikipedia.org/wiki/Humoral_immunity
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    FACTORS THAT DETERMINE AN

    ALLERGIC RESPONSE:-

    Responsiveness of the host to the allergen:

    Amount of allergen:

    Nature of the allergen: Route of entrance of the allergen

    Timing of exposure to the allergen

    Site of the allergen immune mediatorreaction

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    FACTORS THAT DETERMINE AN

    ALLERGIC RESPONSE:- CONTD

    Hosts threshold of reactivity

    The hosts immune system can be

    changed by factors such as stress, fatigue, or

    infection, all of which can decrease the

    responsiveness of immune system to potential

    allergens.

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    CLASSIFICATION OF HYPERSENSITIVITY

    REACTIONS:-

    IMMEDIATE HYPERSENSITIVITY (B-CELL ORANTIBODY MEDIATED)

    Anaphylaxis

    Atopy Antibody mediated cell damage

    Arthus phenomenon

    Serum sickness

    DELAYED HYPERSENSITIVITY (T- CELL MEDIATED) Infection (tuberculin)

    Contact dermatitis

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    Coombs and Gell (1963) classification

    of hypersensitivity reactions

    Type I (anaphylactic, IgE or reagin dependent):

    Antibodies (cytotropic IgE antibodies ) are

    fixed on the surface of tissue cells ( mast cells

    and basophils ) in sensitised individuals. The

    antigen combines with the cell fixed antibody

    leading to release of vasoactive amines which

    produces clinical reactions.

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    Coombs and Gell (1963) classification

    of hypersensitivity reactions

    Type II (cytotoxic or cell stimulating):

    This type of reaction is initiated by IgE (OR

    rarely IgM) antibodies that reacts with the

    cell surface or tissue antigen. Cell or

    tissuedamage occurs in the presence of

    complement or mononuclear cells. Type II

    reactions are intermediate betweenhypersensitivity and auto immunity.

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    Coombs and Gell (1963) classification

    of hypersensitivity reactions

    Type III ([mmune complex or toxic complex

    disease)

    Here the damage is caused by antigen

    antibody complexes. These may precipitate in

    and around small blood vessels, causing

    damage to cells secondarily, or on

    membranes, interfering with their function

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    Coombs and Gell (1963) classification

    of hypersensitivity reactions

    Type IV (ddelayed or cell mediated )

    This is a cell mediated response. The

    antigen activates specifically sensitised CD4

    AND CD8 T cells, leading to the secretion of

    lymphokines, with fluid and phagocyte

    accumulation.

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    DEFINITION

    Type I Reactions:-

    These occur in two forms : the acute,potentially fatal, systemic form called

    anaphylaxis and the chronic or recurrent, non-

    fatal, typically localised form called atopy.

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    DEFINITION:-

    . Anaphylaxis is defined as "a

    serious allergic reaction that is rapid in onset

    and may cause death". It typically results in a

    number of symptoms including an itchy rash,

    throat swelling, and low blood pressure.

    Common causes include insect bites, foods,

    and medications.

    http://en.wikipedia.org/wiki/Allergic_reactionhttp://en.wikipedia.org/wiki/Blood_pressurehttp://en.wikipedia.org/wiki/Blood_pressurehttp://en.wikipedia.org/wiki/Allergic_reaction
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    DEFINITION

    . Anaphylaxis is an acute, potentially fatal,

    multiorgan system reaction caused by the

    release of chemical mediators from mast cells

    and basophils. The classic form involves priorsensitization to an allergen with later re-

    exposure, producing symptoms via an

    immunologic mechanism.

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    DEFINITION

    Anaphylaxis is a clinical response to an

    immediate (type I hypersensitivity)

    immunological reaction between a specific

    antigen and antibody. The reaction result fromIgE antibody.

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    ETIOLOGY

    Food

    Medication

    Venom Risk factors

    People with atopic diseases such

    as asthma, eczema, or allergic rhinitis are athigh risk of anaphylaxis from food, latex,

    and radiocontrast

    http://en.wikipedia.org/wiki/Atopichttp://en.wikipedia.org/wiki/Asthmahttp://en.wikipedia.org/wiki/Eczemahttp://en.wikipedia.org/wiki/Allergic_rhinitishttp://en.wikipedia.org/wiki/Latexhttp://en.wikipedia.org/wiki/Radiocontrasthttp://en.wikipedia.org/wiki/Radiocontrasthttp://en.wikipedia.org/wiki/Latexhttp://en.wikipedia.org/wiki/Allergic_rhinitishttp://en.wikipedia.org/wiki/Eczemahttp://en.wikipedia.org/wiki/Asthmahttp://en.wikipedia.org/wiki/Atopic
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    immune system

    LAYERED DEFENSE:-

    physical barriers prevent pathogens such

    as bacteria and viruses from entering the

    organism. If a pathogen breaches these

    barriers, the innate immune system provides

    an immediate, but non-specific response

    http://en.wikipedia.org/wiki/Bacteriahttp://en.wikipedia.org/wiki/Virushttp://en.wikipedia.org/wiki/Innate_immune_systemhttp://en.wikipedia.org/wiki/Innate_immune_systemhttp://en.wikipedia.org/wiki/Virushttp://en.wikipedia.org/wiki/Bacteria
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    immune system

    If pathogens successfully evade the innate

    response, vertebrates possess a second layer

    of protection, the adaptive immune system,

    which is activated by the innate response.

    http://en.wikipedia.org/wiki/Adaptive_immune_systemhttp://en.wikipedia.org/wiki/Adaptive_immune_system
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    IMMUNE SYSTEM

    SURFACE BARRIERS

    Mechanical, chemical, and biological

    barriers.

    INNATE IMMUNE SYSTEM

    The innate response is usually triggered

    when microbes are identified by pattern

    recognition receptors

    http://en.wikipedia.org/wiki/Pattern_recognition_receptorshttp://en.wikipedia.org/wiki/Pattern_recognition_receptorshttp://en.wikipedia.org/wiki/Pattern_recognition_receptorshttp://en.wikipedia.org/wiki/Pattern_recognition_receptors
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    Humoral and chemical barriers

    Inflammation

    Inflammation is one of the first responses ofthe immune system to infection. The

    symptoms of inflammation are redness,

    swelling, heat, and pain, which are caused by

    increased blood flow into tissue.

    http://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Blood
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    . Complement system

    The complement system is a biochemical

    cascade that attacks the surfaces of foreign

    cells

    Complement is the major humoral component

    of the innate immune response

    http://en.wikipedia.org/wiki/Biochemical_cascadehttp://en.wikipedia.org/wiki/Biochemical_cascadehttp://en.wikipedia.org/wiki/Humoral_immunityhttp://en.wikipedia.org/wiki/Humoral_immunityhttp://en.wikipedia.org/wiki/Biochemical_cascadehttp://en.wikipedia.org/wiki/Biochemical_cascade
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    In humans, this response is activated by

    complement binding to antibodies that have

    attached to these microbes or the binding of

    complement proteins to carbohydrates on thesurfaces ofmicrobes. This

    recognition signal triggers a rapid killing

    response

    http://en.wikipedia.org/wiki/Carbohydratehttp://en.wikipedia.org/wiki/Microbehttp://en.wikipedia.org/wiki/Cell_signalinghttp://en.wikipedia.org/wiki/Cell_signalinghttp://en.wikipedia.org/wiki/Microbehttp://en.wikipedia.org/wiki/Carbohydrate
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    Adaptive immune system

    The adaptive immune response is antigen-

    specific and requires the recognition of

    specific "non-self" antigens during a process

    called antigen presentation. Antigenspecificity allows for the generation of

    responses that are tailored to specific

    pathogens or pathogen-infected cells.

    http://en.wikipedia.org/wiki/Antigen_presentationhttp://en.wikipedia.org/wiki/Antigen_presentation
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    Adaptive immune system

    Lymphocytes

    The cells of the adaptive immune system arespecial types of leukocytes,

    called lymphocytes. B cells and T cells are themajor types of lymphocytes and are derivedfrom hematopoietic stem cells in the bonemarrow. B cells are involved in the humoralimmune response, whereas T cells areinvolved in cell-mediated immune response

    http://en.wikipedia.org/wiki/Lymphocytehttp://en.wikipedia.org/wiki/B_cellhttp://en.wikipedia.org/wiki/T_cellhttp://en.wikipedia.org/wiki/Hematopoietic_stem_cellhttp://en.wikipedia.org/wiki/Bone_marrowhttp://en.wikipedia.org/wiki/Bone_marrowhttp://en.wikipedia.org/wiki/Humoral_immunityhttp://en.wikipedia.org/wiki/Humoral_immunityhttp://en.wikipedia.org/wiki/Cell-mediated_immunityhttp://en.wikipedia.org/wiki/Cell-mediated_immunityhttp://en.wikipedia.org/wiki/Cell-mediated_immunityhttp://en.wikipedia.org/wiki/Cell-mediated_immunityhttp://en.wikipedia.org/wiki/Humoral_immunityhttp://en.wikipedia.org/wiki/Humoral_immunityhttp://en.wikipedia.org/wiki/Humoral_immunityhttp://en.wikipedia.org/wiki/Bone_marrowhttp://en.wikipedia.org/wiki/Bone_marrowhttp://en.wikipedia.org/wiki/Hematopoietic_stem_cellhttp://en.wikipedia.org/wiki/T_cellhttp://en.wikipedia.org/wiki/B_cellhttp://en.wikipedia.org/wiki/Lymphocyte
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    Adaptive immune system

    Killer T cells

    Killer T cell are a sub-group of T cells that kill

    cells that are infected with viruses (and other

    pathogens), or are otherwise damaged or

    dysfunctional.

    http://en.wikipedia.org/wiki/Cytotoxic_T_cellhttp://en.wikipedia.org/wiki/Cytotoxic_T_cell
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    Adaptive immune system

    Helper T cells

    Helper T cells regulate both the innate and

    adaptive immune responses and help determinewhich immune responses the body makes to aparticular pathogen. These cells have no cytotoxicactivity and do not kill infected cells or clear

    pathogens directly. They instead control theimmune response by directing other cells toperform these tasks.

    http://en.wikipedia.org/wiki/T_helper_cellhttp://en.wikipedia.org/wiki/T_helper_cell
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    Adaptive immune system

    T cells

    T cells possess an alternative T cell

    receptor (TCR) as opposed to CD4+ and CD8+

    () T cells and share the characteristics of

    helper T cells, cytotoxic T cells and NK cells.

    The conditions that produce responses from

    T cells are not fully understood

    http://en.wikipedia.org/wiki/Gamma/delta_T_cellshttp://en.wikipedia.org/wiki/Gamma/delta_T_cellshttp://en.wikipedia.org/wiki/T_cell_receptorhttp://en.wikipedia.org/wiki/T_cell_receptorhttp://en.wikipedia.org/wiki/T_cell_receptorhttp://en.wikipedia.org/wiki/T_cell_receptorhttp://en.wikipedia.org/wiki/Gamma/delta_T_cellshttp://en.wikipedia.org/wiki/Gamma/delta_T_cellshttp://en.wikipedia.org/wiki/Gamma/delta_T_cells
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    Adaptive immune system

    B lymphocytes and antibodies

    A B cell identifies pathogens when antibodies onits surface bind to a specific foreign antigen. This

    antigen/antibody complex is taken up by the Bcell and processed by proteolysis into peptides.The B cell then displays these antigenic peptideson its surface MHC class II molecules. This

    combination of MHC and antigen attracts amatching helper T cell, whichreleases lymphokines and activates the B cell.

    http://en.wikipedia.org/wiki/B_cellhttp://en.wikipedia.org/wiki/Proteolysishttp://en.wikipedia.org/wiki/Lymphokinehttp://en.wikipedia.org/wiki/Lymphokinehttp://en.wikipedia.org/wiki/Proteolysishttp://en.wikipedia.org/wiki/B_cell
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    Adaptive immune system

    Immunological memory

    When B cells and T cells are activated and

    begin to replicate, some of their offspring

    become long-lived memory cells. Throughout

    the lifetime of an animal, these memory cells

    remember each specific pathogen

    encountered and can mount a strongresponse if the pathogen is detected again.

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    PATHOPHYSIOLOGY:-

    Type I hypersensitivity are mediated by the IgE

    class of immunoglobulin. In genetically, pre

    disposed people, initial exposure to an

    allergen prompts B lymphocytes to produceIgE antibodies, which sensitize the person to

    the allergen. This initial contact with the

    allergen is known as the sensitizing dose

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    PATHOPHYSIOLOGY

    Once the person is fully sensitized, subsequentexposure ( termed the shocking dose orchallenging dose) results in the allergencombined with the specific IgE antibodies thatare bound to receptor sites on tissue mast cellsand blood basophils. This antigen antibodyreaction results in a rapid release of potent vaso

    active mediators such as histamines, kinins,chemo tactic factors, and active products ofarachidonic acid metabolism

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    PATHOPHYSIOLOGY

    Anaphylaxis is caused by the interaction of aforeign antigen with specific IgE antibodies foundon the surface membrane of mast cells andperipheral blood basophils. The subsequentrelease of histamine and other bioactivemediators cause activation of platelets,eosinophils, and neutrophils and coagulation

    cascade. Smooth muscle spasm, bronchospasm,mucosal eddema, and inflammation, andincreased capillary permeability

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    CLINICAL FEATURES Localised reactions:-

    Hives angioedema

    Systemic anaphylaxis:-

    Apprehension

    Edema of the hands, face, or other parts of the body Dyspnoea

    Respiratory collapse

    Vascular collapse with shock Rapid, regular pulse Falling blood pressure

    Cyanosis

    Death

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    DIAGNOSTIC MEASURES

    The health history including an environmental

    assessment,

    Skin testing and radio allergo sorbent test

    (RAST) may be helpful

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    MEDICAL MANAGEMENT

    Management depends on the severity of the

    reaction. Initially, respiratory and

    cardiovascular functions are evaluated

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    TREATMENT

    Simple BLS (O2, position, etc)

    Anti Histamines

    Benadryl (IV 25-50 mg, PO 50 mg adult, 25 mg ped)

    Corticosteroids

    Decadron, Solu-medrol, etc

    Treat Hypotension

    IV fluids

    Dopamine 5-20 mcg/min

    Epi Drip 2-10 mcg/min

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    TREATMENT

    Broncheodiators

    Albuterol MDI or Neb

    Observe for a minimum 8-12 hours

    Benadryl for 24 hours.

    Rebound or persitant S/S

    Repeat epinephrine if Sx persist or increase after 10-15

    minutes

    Repeat antihistamine H2 blocker if Sx persist

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    TREATMENT

    Avoidance therapy, in which the patient is

    thought to reduce exposure to trigerring

    antigens, is the most effective treatment to

    decrease allergic attacks

    Immunotherapy is often useful in reducing

    symptoms in patients who cannot avoid

    antigens such as dust mites or pollen

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    PREVENTION

    EDUCATE

    Teach avoidance measures

    Accidents are never planned

    Stress importance of:

    Immediate treatment

    Emphasize the need for follow-up care

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    NURSING MANAGEMENT

    ASSESSMENT:-

    Health history:-

    Assessment data to be collected as part of thehealth history of a patient with allergy includes:

    History of allergic reactions in the past ( e.g., type,frequency or perceived causes)

    Familial history of allergies

    Recent exposure to sensitizing substances (chemicals,drugs)

    Changes in living, working, or environmental conditions

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    NURSING MANAGEMENT

    Characteristics of present environment (house, clothing,plants, trees or animals)

    Increased stress in recent past ( stress aggrevates asthmaticresponse)

    Types of symptoms experienced: respiratory, dermal,gastrointestinal or general

    Alleviating factors, either prescribed, herbal, or over thecounter

    All patients should be questioned about allergies and

    sensitivities to drugs before any drug therapy is initiated. Ifthere is a positive history, the physician is consulted beforea new drug is given, the patient is monitored closely forallergic responses.

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    Physical examination:-

    Important aspects of the physical examination ofthe patient with allergy include inspection andobservation for :

    Rashes (location, and colour) Mouth breathing (nasal obstruction)

    Flaring nares

    Difficulty hearing (plugged Eustachian tubes)

    Pale, bluish turbinates that are oedematous withclear secretions

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    PHYSICAL EXAMINATION

    Tearing

    Dark areas under the eyes ( venous dilation ofthe skin)

    Scleral or conjunctival infections Increased respiratory rate

    Audible wheezing

    Use of accessory muscles for breathing Anxious depression

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    NURSING DIAGNOSES:-

    Ineffective airway clearance related to excess

    secretion production and bronchoconstriction.

    Decreased cardiac output related to

    inadequate venous return to heart, peripheral

    vasodilation.

    Deficient knowledge related to inadequate

    information about allergy control andtreatments.

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    Airway clearence:-

    Cardiac output:-

    Nurse should be alert for the clinical manifstatios

    of anaphylactic shock. At the first sign ofanaphylaxis, the patient is given epinephrine1:1000 solution 0.3 to 0.5 ml s/c or im

    Risk for allergy response:-

    High risk patients are instructed to wear aidentification bracelet.

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    INTERVENTIONS

    Provide supplemental oxygen and observe. Ifhypoxia continues, prepare to help insert anartificial airway.

    Insert an I.V. line for giving emergency drugs and

    volume expanders. Continually reassure the patient and explain all

    tests and treatments to reduce fear and anxiety.

    If the patient undergoes skin or scratch testing.Keep emergency resuscitation equipment nearbyduring and after the test.

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    INTERVENTIONS

    Continuously assess the patients response to

    treatment.

    Monitor vital signs and cardiopulmonary

    and neurologic function. Observe for complications associated with

    anaphylaxis, such as vascular collapse and acuterespiratory insufficiency or obstruction.

    Closely observe a patient with known allergies foranaphylaxis when giving a drug with highanaphylactic potential.

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    COMPLICATIONS

    The primary complication of type I

    hypersensitivity are anaphylactic shock, which

    can leads to death within minutes without

    emergency treatment.

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