Anaphylaxis

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  • Pathogen – a disease producing agent or invading substance that causes an immune response. Anitgen – any substance capable of producing an immune response. Including toxins released by bacteria. The body has 2 mschanisma to destroy and illiminate these antigens Cellular immunity – results from a direct attack by specialized cells of the immune system Humoral immunity – reults from the attack of antibodies (immunoglobins) IgA, Igd, IgE, IgM. Manufactured by B cells.
  • Primary response – initial response to an antigen Secondary response – If the body is exposed a second time, antibodies specific to the antigen are released. Natural Immunity – present at birht Aquired immunity – developed over time resulting from an exposure Active immunity – aquired following exposeure, results in production of antibodies Induced active immunity – vacination Passive Immunity – administration of immunity Natural passive – placental barrier from mother to child Induced passive – tetanus
  • Sensitization is the initial exposure of a person to an antigen that results in an immune response. Subsequent exposures result in a much stronger secondary response. Hypersensitivity or Allergy Delayed hypersensitivity – result of cellular immunity, days and hours following exposure, skin rash ie poison ivy Immediate hypersenitivity – ex hay fever, drug allergies, asthma,
  • Allergen, a substance capable of inducing allergic reaction ie drugs, food, animals, insects, fungi molds IgE is released following exposure – IgE binds to basophil (special white blood cells) and mast cells (granulocytes), these cells release histamine and heparin , which are stored in granules, into the sourounding tissues. This process is called degranulation or allergic reaction. Histamine caues bronhoconstriction, vasodilation, increased vascular permeability, increased intestinal motility. Angioedema – swelling of hands and face and upper airway from increased vascular permeability. Histamine receptors (H1 and H2) – the goal of histamine response is to limit bodies exposure to antigens. Broncoconstriction reduses antigens entering resiratory track, vascular permiability removes antigens from circulatory system etc.
  • epi – sympathetic agonist, causes increased heart rate inotropic peripheral vasoconstriction reverse bronchospasm reverse capilary permebility .3 to .5 1:1,000 subQ, .3 - .5 mg 1:10,000 IV, peds .01 mg/kg, antihistamines – benadryl non selective H1 H2 blocker 25 – 50 mg IV, zantac ex selective H2 used for ulcers but also effects vascular syst corticosteroids – of little benefit in the intial stages but help suppress the inflammatory response ie solu-medrol vasopressors – dopamine beta agonist – albuterol to reduce bronchospasm and laryngeal edema
  • Anaphylaxis

    1. 1. Allergies andAnaphylaxis
    2. 2. Sections Pathophysiology Assessment Findings in Anaphylaxis Management of Anaphylaxis Assessment Findings in Allergic Reaction Management of Allergic Reactions Patient Education
    3. 3. Allergies and Anaphylaxis Allergic Reaction  An exaggerated response by the immune system to a foreign substance Anaphylaxis  An unusual or exaggerated allergic reaction  A life-threatening emergency
    4. 4. Pathophysiology The Immune System  Pathogens  Toxins  Cellular Immunity  Humoral Immunity  Antibodies (Immunoglobulins) • IgA, IgD, IgE, IgG, IgM
    5. 5. Pathophysiology Immune Response  Exposure to antigen produces primary response with general antibodies.  Immune system develops antigen-specific antibodies and memory.  Future exposures generate a faster secondary response. Natural and Acquired Immunity Induced Active Immunity Active and Passive Immunity
    6. 6. Allergies Sensitization Hypersensitivity  Delayed  Results from cellular immunity and does not involve antibodies.  Commonly results in skin rash.  Results from exposure to certain drugs or chemicals.  Immediate  Exposure quickly results in secondary response.  More severe than delayed hypersensitivity.
    7. 7. Allergies Allergen  Exposure generates secondary response.  Large quantities of IgE are released.  Allergen binds to IgE, causing chemical release. • Release is “allergic reaction.” • Includes histamines, heparin, and other substances that are designed to minimize the body’s exposure to an antigen. • Histamine causes bronchoconstriction, vasodilation, increased gastric motility, and increased vascular permeability. • Angioneurotic edema.
    8. 8. Anaphylaxis Causes
    9. 9. Anaphylaxis Causes  Injections  Most anaphylaxis results from the injected route.  Allergen rapidly distributed throughout the body, resulting in massive histamine release. • Parenteral penicillin injections and insect stings. • Affects cardiovascular, respiratory, gastrointestinal, and integumentary systems. • Significant plasma loss through increased vascular permeability. • Slow-reacting substance of anaphylaxis.
    10. 10. Assessment Findings in Anaphylaxis Focused History & Physical Exam  Focused History  SAMPLE & OPQRST History • Rapid onset, usually 30–60 seconds following exposure. • Speed of reaction is indicative of severity. • Previous allergies and reactions.  Physical Exam  Presence of severe respiratory difficulty is key to differentiating anaphylaxis from allergic reaction.
    11. 11. AssessmentFindings inAnaphylaxis Physical Exam  Facial or laryngeal edema  Abnormal breath sounds  Hives and urticaria  Hyperactive bowel sounds  Vital sign deterioration as the reaction progresses
    12. 12. Management of Anaphylaxis Scene Safety  Consider the possibility of trauma. Protect the Airway.  Use airway adjuncts with care.  Intubate early in severe cases to prevent total occlusion of the airway.  Be prepared to place a surgical airway.
    13. 13. Management of Anaphylaxis Support Breathing  High-flow oxygen or assisted ventilation if indicated. Establish IV Access  Patient may be volume-depleted due to “third spacing” of fluid.  Administer crystalloid solution at appropriate rate.  Place a second IV line if indicated.
    14. 14. Management of Anaphylaxis Administer Medications:  Oxygen  Epinephrine  Antihistamines  Corticosteroids  Vasopressors  Beta-agonists  Other agents Psychological Support
    15. 15. Assessment Findings in Allergic Reaction
    16. 16. Management of Allergic Reactions Scene safety Protect the airway. Support breathing. Establish IV access. Administer medications:  Antihistamines  Epinephrine
    17. 17. Patient Education Prevention of Reactions Recognition of Signs/Symptoms  Patient-initiated treatment  Epinephrine auto-injectors Desensitization
    18. 18. Summary Pathophysiology Assessment Findings in Anaphylaxis Management of Anaphylaxis Assessment Findings in Allergic Reaction Management of Allergic Reactions Patient Education

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