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Hypersensitivity and Autoimmunity (Type I: Rapid Hypersensitivity…

- - - - :star: Examples:
        Positive protein derivative (PPD) for TB
        Contact dematitis
        Poison Ivy skin rashes
        loal response to insect stings
        tissue transplant rejections
        sarcoidosis
        
        :black_flag: Dx Studies
        Patch testing : involves applying test chemicals that contain the allergens. The patch remains in place for 48 hours. If redness, swelling, or blisters are present, the patient is given a list of items containing that chemical to be avoided.
        
        Nursing Management:
        
        Advise the patient to avoid the offending antigen
        
        Monitor the reaction site and sites distal to the reaction for circulation adequacy
        
        Medications:
        Corticosteroids
        (diphenhydramine is of minimal benefit for type IV reactions because histamine is not the main mediator)
- - - - Pt. Preparation
        
        Glucocorticoids & antihistamines are discontinued for up to 4 wks. before test
        
        Sprays to reduce mucous membranes are permitted unless they contain antihistamines
        
        some recommend NSAIDs & Aspirin be withheld
        
        Procedure
        
        Inside of the forearm or back: clean w/ soap & water & remove surface oils w/ alcohol
        
        Small drops of sera containing diff. known allergens are place on the skin --> pricked w/ a bifurcated skin testing needle
        
        Control drops are applied (NS negative)
        
        histamine drops are (+) controls
        :warning: ensure emergency equipment -- manual resuscitation bag, O2, suction equipment, IV infusion set, & drugs for anaphylaxis (epinephrine & diphenhydramine)
        
        Follow Up Care
        
        wash solution from skin & give topical steroids & oral antihistamines
        
        Repeat open application testing (ROAT)
        -Intradermal Testing
        
        Oral food challenges
        
        Avoidance Therapy
        
        urge pt to avoid direct or close contact w/ agents
        
        Teach pt that many airborne allergens can be reduced by air -conditioning & air-cleaning units
        
        Remove cloth drapes, upholstered furniture & carpeting reduces airborne allergens
        
        Cover mattresses & pillows w/ plastic or ultra fine mesh cover
        
        Launder bed linens weekly in hot water & detergent
        
        Keep pets out of bedroom
        
        Frequent bathing of pets, or keeping them outside DEC allergen exposure
        
        Drug Therapy
        
        Some drugs reduce the response, & other drugs prevent the response.
        - Decongestants
        
        Work by causing vasoconstriction in the inflamed tissue, thereby reducing the edema.
        
        Often contain ephedrine, phenylephrine, or pseudo ephedrine
        
        Secretions are reduced w/ vasoconstrictors + anticholinergics (scopolamine or atropine)
        
        SE: dry mouth, INC BP, & sleep difficulties
        • Antihistamines
        
        Block histamine from binding to the receptor, preventing vasodilation & capillary leak
        
        Cause sedations – diphenhydramine (Benadryl, Allerdryl), chlorpheniramine (Allergy, Aller-Chlor, Chlor-Trimeton)
        
        Less sedating – desloratadine (Clarinex), cetirizine (Zyrtec), & fexofenadine (Allegra)
        • Corticosteroids
        
        DEC inflammatory & immune responses in many ways, one is by preventing the synthesis of mediators.
        
        Nasal sprays – prevent symptoms of rhinitis
        
        Systemic – severe side effects, short term
        • Mast cell stabilizing
        
        crosmolyn sodium (Nasalcrom) – prevent mast cell membranes from opening when an allergen binds to IgE.
        
        Not useful during an acute episode
        • Leukotriene modifiers
        
        Treat allergic rhinitis
        
        Zileuton (Zyflo) – prevents leukotriene synthesis
        
        Zafirlukast (Accolate) – blocks the leukotriene receptor
        
        Desensitization Therapy
        
        "allergy shots" needed when allergens are identified & cannot be avoided easily
        
        subQ injections of small amounts of allergens
        
        dilute of allergen is compounded (1:100,000 or 1:1,000,000)
        
        an increasing dose is given weekly until the pt is receiving a 0.5mL dose
        
        Injections are given weekly for the 1st yr, every other week for the 2nd yr, & every 3-4 wks for the 3rd yr
        
        recommended for 5 yrs
        
        appears to reduce allergic responses by competition
  - - - Pathophysiology
        Involves all blood vessels and bronchiolar smooth muscle causing widespread blood vessel dilation, decreased cardiac output, and bronchoconsriction
        :warning: when symptoms occur in a pt who has not been previously exposed to the allergen, known as anaphylactoid
        
        Teaching
        
        Teach pt with a history of allergic reaction to avoid allergen whenever possible
        
        Teach to wear a medical alert bracelet and to alert health personnel about specific allergies
        
        Advise to carry an emergency anaphylaxis kit
        
        Emergency anaphylaxis kit
        
        injectable epinephrine (sometimes called "bee sting kit"
        
        Epinephrine injector (EpiPen) 0.3mg/2ml
        
        Practice assembly of injection device
        
        Keep the device with you at all times; carry at least 2
        
        When needed, inject the drug into the top of the thigh, slightly to the outside, making sure the needle is straight
        
        Use when ANY symptom of anaphylaxis is present and call 911
        
        After use, get to the nearest hospital for monitoring for 4-6 hr
        
        Protect the device from light and keep at room temp
        
        Store in refrigerator
        
        Keep safety cap in place until ready to use the device
        
        Check for expiration date, drug clarity, security of cap
        
        Assessment
        
        Subtle initial symptoms (severe abdominal cramping and diarrhea)
        
        Feeling of uneasiness, apprehension, weakness, and impending doom
        
        Anxious & frightened
        
        Generalized itching and uticaria (hives)
        
        Erythema and sometimes angioedema of the eyes, lips, or tongue
        
        Intensely itchy skin wheals or hives; may form large red blotches
        
        Histamine causes bronchoconstriction, mucosal edema, and excess mucus production
        
        Respiratory s/s: congestion, rhinorrhea, dyspnea, respiratory distress with wheezing
        
        On auscultation: crackles, wheezing, and reduced breath sounds
        
        Laryngeal edema, "lump in the throat", hoarseness, and stridor
        
        Stridor and anxiety increase as the aiway begins to close
        
        Increasing bronchoconstriction leads to reduced chest excursion and impaired air movement
        
        Respiratory failure
        
        Hypoxemia
        
        Hypotension with rapid, weak, irregular pulse
        
        Nursing Interventions
        
        Assess respiratory status, airway, and oxygen saturation
        
        Call the rapid response team
        
        Ensure that intubation and tracheostomy equipment is ready
        
        Apply oxygen using high-flow, non-rebreather mask at 90% to 100%
        
        Immediately discontinue the IV rug of a pt having an anaphylactic reaction to that drug. DO NOT discontinue the IV, but change the tubing and hang normal saline
        
        If the pt does not have an IV, start one immediately and start NS
        
        Be prepared to administer epinephrine IV or IM
        
        Keep HOB elevated about 10 degrees if hypotension is present; if BP is normal, elevate to 45 degrees or higher
        
        Raise the feet and the legs
        
        Stay with the patient
        
        Reassure the patient that the appropriate interventions are being instituted
        
        Drug Therapy
        :red_flag:Sympathomimetics (1st Line Drugs)
        
        epinephrine
        
        isoprotereol
        
        ephedrine sulfate
        :red_flag: Antihistamines (2nd Line Drugs)
        
        diphenhydramine
        :red_flag: Corticosteroids (2nd Line Drugs)
        
        hydrocortisone sodium succinate (IV/IM)
        
        dexamethasone (IV/IM)
        
        methlyprednisolone (IV/IM)
        
        prednisone (po)
        :red_flag:Vasopressors (Support Drugs)
        
        norepinephrine
        
        dopamine
        
        Side Effects
        Sumpathomimetics: pallor, twitching, nervousness, muscle twitching,sweating, anxiety, insomina, hypertension, headache, hyperglycemia
        diphenhydramine: drowsiness, confusion, insomina, headache, vertigo, photosensitivity, diplopia, nausea, vomiting, dry mouth
        Corticosteroids: fluid and sodium retention, HTN, cushingoid state, gastric distress, adrenal suppression, psychosis, osteoporosis, susceptibility to infection
        norepinephrine: headache, tachycardia, fibrillation, decreased urine output, HTN, metabolic acidosis
        dopamine: dysrhthmias, tachycardia, HTN, dyspnea, N&V, azotemia, headache
- - - - The self-reactive B-cells become activated and start creating IgM and with the help with CD4 T-helper cells, it create IgG antibodies which attach themselves to antigens to host cells. There are 2 types of antigens that are involved with hypersensitivity, Intrinsic which is normally made by the host cell, and extrinsic which are made from a medications (penicillin) or an infection that gets attached to the host cell.
        
        Extrinsic antigen:
        One good example is a drug (penicillin), it binds to a reb blood cell and becomes an extrinsic antigen. IgG and sometime IgM antigens, bind themselves to the penicillin molecule on the re blood cell creating an antigen-antibody complex. The antigen-antibody complex is only suppose to happen in an infection cell. the process goes through several mechanisms.
        
        Cytotoxic mechanism 1:
        Known as activation of the complement system which is a group of small proteins that will work in an enzymatic cascade to fight off bacterial or infections using a verity of mechanisms.
        
        One of these proteins is called C1 protein. Other proteins are also available which take part of the process too (C2, C3,C4, C5, C6, C7, C8, C9). C3-C5 proteins get split in half and become chemotactic factors, which attracts certain cells. Some of those cell are neutrophils.
        
        Neutrophils degranulate and dump enzymes (peroxidase, myeloperoxidase, and proteinase 3) on the reb blood cells that is being affected. This causes tissue damage to the now affected cells.
        
        Drug reaction causes autoimmune hemolytic anemia. Thrombocytopenia : and neutropenia can occur as well. All which are blood cell type that are being effected.
        
        1 more item...
        
        Good pasture syndrome is also involved in cytotoxic mechanism 1, where intrinsic antigen also bind to collagen of the basement membrane in the glomeruli and kidney or their alveoli in the lungs.
        
        Mechanism 2:
        are involved C5-C9 proteins, although C9 protein develops a bunch of other small proteins which create a membrane attach complex. This complex attacks the cell and creates a tunnel on the cell membrane and allows fluid to interchange in and out.
        
        During this process, the cell swells and eventually burst called cell lysis. This is where the name cytotoxic come from.
        
        Intrinsic antigen:
        Normally made by the host
- - - - These immune complexes then travel and attach themselves to the walls of the blood vessels and initiate and inflammatory response.
      - Signs and symptoms:
        Fever
        urticarial
        arthralgia's
        proteinuria
        rash
        malaise
        lymphadenopathy
        polyarthritis and nephritis about 7-12 days after receiving the causative agent
        
        Management:
        Antihistamines are given for itching and rash
        aspirin for arthralgia's
        Prednisone is given if manifestation are severe.
- - - - Pathophysiology
        Autoimmune destruction of lacrimal, salivary, and vaginal mucus producing glands >
        Insufficient tears cause inflammation and ulceration of the cornea.
        Insufficient saliva decreases digestion of carbohydrates, promotes tooth decay, and increases incidence of oral and nasal infections.
        Vaginal dryness increases the incidence of infection and may cause pain during sexual intercourse.
      - Collaborative Care
        
        Drugs
        a) Low dose chemotherapy: methotrexate and cyclophosphamide.
        b) Corticosteroids
        c) cyclosporine
        d) hydroxychloroquine
        e) rituximab is being investigated
        
        Other interventions
        a) artificial tears and saliva
        b) teach use of humidifiers
        c) water soluble vaginal lubricants and mosturizers
        d) cyclosporin drops increase production of tears
        e) pilocarpine increases salivation
        f) blocking nasal punctum either temporarily with small plugs or surgically to keep tears in contact with eyes.
      - Clinical Manifestations
        a) Blurred vision, burning and itching of the eyes, thick mattering in the conjunctiva.
        b) difficulty swallowing, taste change.
        c) nose bleeds, upper respiratory infections.
        d) enlarged lymph nodes.
        e) if RA, swollen painful joints and limited joint mobility
        f) labs show antinuclear antibodies, anti-SS-A or anti-SS-B antibodies and elevated IgM rheumatoid factor.
    - - Pathophysiology
        Auto-antibodies are made against glomerular basement membrane and neutrophils
        
        Clinical Manifestations
        a) SOB
        b) hemoptysis
        c) decreased urine output
        d) weight gain
        e) generalized non-dependent edema
        f) hypertension
        g) tachycardia
        h) consolidation in lungs
        i) uremia (most common cause of death)
      - Collaborative Care
        
        Drug therapy
        a) high dose of corticosteroids.
        b) same drugs as Sjögren’s syndrome
        
        Other interventions
        a) plasmapheresis to remove auto-antibodies, may need infusion of IV immunoglobulin (IVIG) to maintain antibody protection against infection.
        b) Dialysis, first hemodyalisis and then either hemodyalisis, or peritoneal dialysis depending on situation.
        c) Kidney transplant, in this situation lung continues to be destroyed.