ADULT ALLERGIC/HYPERSENSITIVITY DISORDERS 2014 PHYSIOLOGIC OVERVIEW: ANTIBODIES react with allergens by____________.

COATING antigens surfaces NEUTRALIZING antigens if with toxins PRECIPITATING antigens out of solution if they are dissolved Phagocytes of blood and tissues can dispose of them if inappropriate or exaggerated ALLERGY or HYPERSENSITIVITY LOCK AND KEY ANTIGEN (key) . foreign_____? ANTIBODY (lock) formed by plasma cells and lymphocytes FUNCTION OF IG (GAMDE) Found in lymph nodes, tonsils, appendix, Peyers patches, blood, lymph _____________________? involved in allergic disorders and some parasitic infections LYMPHOCYTES B LYMPHOCYTES PROGRAMMED to produce ONE specific antibody T LYMPHOCYTES ASSIST B cellls in producing antibodies Secrete substances that direct the flow of cell activity, destroy target cells, and stimulate macrophages T CELL DOES NOT BIND FREE ANTIGENS

ANTIGENS CPA (complete protein antigens) e.g. animal danders, pollens, horse serum; stimulate a complete humoral response LMW (low-molecular weight substances ) e.g. medications ; haptens/ incomplete antigens CHEMICAL MEDIATORS types: PRIMARY: preformed & found in mast cells or SECONDARY: inactive precursors; formed/released basophils in response to primary mediators PRIMARY MEDIATORS 1. HISTAMINE : 2. EOSINOPHIL CHEMOTACTIC FACTOR Of ANAPHYLAXIS 3. PLATELET-ACTIVATING FACTOR 4. PROSTAGLANDINS HISTAMINE: released by mast cells Effects within 15 min after antigen contact H1 RECEPTOR: bronchiolar & vascular smooth muscle cells H2 RECEPTOR: gastric parietal cells EFFECTS: erythema, localized edema (wheals, pruritus); bronchial spasm, wheezing; DILATION of small venules, CONSTRICTION of bigger vessels; INC secretion of gastric & mucosal cells-> diarrhea

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EOSINOPHIL CHEMOTACTIC FACTOR OF ANAPHYLAXIS AFFECTS movement of eosinophils to site of allergens Preformed in MAST CELLS RELEASED from disrupted mast cells PLATELET-ACTIVATING FACTOR INITIATES platelet aggregation and WBC INFILTRATION at sites of immediate hypersensitivity rx BRONCHIAL CONSTRICTION INCREASES vascular permeability PROSTAGLANDINS Smooth muscle contration Vasodilation Increased capillary permeability FEVER, PAIN SECONDARY MEDIATORS 1. LEUKOTRIENES 2. BRADYKININ 3. SEROTONIN LEUKOTRIENES: derived from ARACHIDONIC ACID ACTIVATED by mast cell degranulation, or SRS-A(slow reacting substances of anaphylaxis INITIATES inflammatory response Smooth muscle contraction Bronchial constriction INCREASES mucus secretions in airways Wheal-and-flare reactions of the skin MORE POTENT THAN HISTAMINE in causing bronchospasm BRADYKININ DERIVED from precursor KININOGEN INCREASES vascular permeability edema DILATES blood vessels BP ? Bronchial spasm STIMULATES nerve cell fibers ? SEROTONIN Preformed in platelets POTENT VASOCONSTRICTOR CONTRACTION OF bronchial muscle ***HYPERSENSITIVITY and AUTOIMMUNITY*** increased/excessive/aberrant immune reactions to the presence of an antigen tissue injury, disease, and destruction FOLLOWS RE-EXPOSURE after sensitization, or build up of antibodies in a predisposed person Does it usually occur with first exposure to allergen ???

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FOUR TYPES TYPE I: IMMEDIATE HYPERSENSITIVITY/ ANAPHYLACTIC TYPE II: CYTOTOXIC AND CYTOLYTIC REACTIONS TYPE III: IMMUNE COMPLEX HYPERSENSITIVITY RESPONSES TYPE IV: DELAYED HYPERSENSITIVITY RESPONSE

TYPE I: IMMEDIATE/ANAPHYLACTIC: the most severe rx GENERALIZED, IMMEDIATE, AND SEVERE RESPONSES TO A SPECIFIC ALLERGEN thru inhalation, ingestion, injection, or skin contact E.G. PENICILLIN, FOREIGN SERUM, STINGING INSECT VENOM, CONTRAST MEDIA DYES, ALLERGEN EXTRACTS, HOUSE DUST MITES, ANIMAL DANDERS, FOOD CHEMICALS TYPE I: CD4+ helper T cells & MAST CELLS/BASOPHILS During sensitization, the IgE antibodies bind to receptors on the surface of tissue mast cells & blood basophils("sensitized) Later exposure to the same allergen cross-links the bound IgE on sensitized cells, degranulation & secretion of pharmacologically active mediators i.e., histamine, leukotriene (LTC4 and LTD4), and prostaglandin that act on the surrounding tissues vasodilation and smooth-muscle contraction 2 TYPES OF ANAPHYLAXIS SYSTEMIC LOCAL SYSTEMIC ANAPHYLAXIS - when an offending allergen enters the circulation, it reacts in widespread areas of the body with IgE attached to basophils & to mast cells (located immediately outside the small blood vessels) > release of chemical mediators like HISTAMINE, BRADYKININ, SRA-S **targets skin, lungs, mucous membranes, vasculature hives, bronchiolar constriction, hypopharynx or laryngeal edema, hypotension, vascular collapse ****A MEDICAL EMERGENCY AND IF UNTREATED, MAY RESULT TO HYPOXIA, HYPOTENSION, SHOCK, AND DEATH LOCAL ANAPHYLAXIS localized type 1 response to a specific antigen IgE mediated; urticaria, allergic rhinitis and asthma CAUSES environmental allergens like drugs, plant and animal products, air pollutants **thru inhalation, ingestion, injection, or direct touch DISTINCTIVE FEATURE overproduction of atopic( people with a familial tendency to develop these reactions) reagin-type(IgE type) antibodies to normally harmless antigen in the environment believed to be INHERITED URTICARIA, ALLERGIC RHINITIS, BRONCHIAL ASTHMA, ATOPIC DERMATITIS, ANGIONEUROTIC EDEMA ATOPY : Ig-E mediated diseases with a genetic component
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URTICARIA/ATOPIC DERMATITIS wheal or flare responses, hives, vesicles; a cutaneous reaction common causes: drugs (pcn, asa, codeine), foods(strawberry, shellfish, tomato, cheese, chocolate), insect bite and stings, inhaled allergens and intestinal parasites **if deeper tissues, angioedema ***DIAGNOSTIC TESTS: SKIN TESTS scratch; intradermal/intracutaneous IgE concentration in serum normal-<1mcg/ml NURSING PROBLEMS allergic response respiratory dysfunction cardiovascular alterations fear and altered comfort INTERVENTION: allergic response epinephrine sc or iv if stinging insect, scrape stinger away with knife blade or any sharp instrument if IV drug stop administering and apply tourniquet above site ****call DR. STAT If stable, reduced allergen exp sleep with bedroom windows closed use high filter air conditioning ride in cars (closed windows) avoid trips to rural areas during summer and strong wind wear masks in areas of high exposure clean areas with animal danders/ no pets with furs/ feathers Control house dust concentration ..encase pillows and mattresses with plastic/ air-tight coverings ..eliminate rugs and dust-collecting items in bedrooms ..air conditioning units with high filtering capacity, constant air flow and cool environment Management hyposensitization or desensitization drug therapy antihistaminics sympathomimetics topical corticosteroids histamine inhibitors RESPIRATORY DYSFUNCTION **respiratory distress epinephrine respiratory support ransport to hospital facility
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CARDIOVASCULAR ALTERATIONS fluid shifting hypotension, shock, and circulatory collapse FEAR COMFORT ALTERATION Avoid cause symptomatic relief emotional support sedatives/tranquilizers TYPE II: CYTOTOXIC & CYTOLYTIC REACTIONS/HYPERSENSITIVITY THE SYSTEM mistakenly identifies a normal constituent of the body as FOREIGN RESULT OF a cross-reacting antibody cell & tissue damage TYPE II: CYTOTOXIC AND CYTOLYTIC REACTIONS ABO INCOMPATIBILITY Rh INCOMPATIBILITY HLA INCOMPABILITY MYASTHENIA GRAVIS TYPE III: IMMUNE COMPLEX HYPERSENSITIVITY kidneys and joints are susceptible disseminated/systemic lupus erythematosus Rheumatoid arthritis GlomerulonephritiS --occur when antigen and antibody combine to form complement-activating soluble complexes in and around small blood vessels (MICROPRECIPITATES) IgG When there is ANTIBODY EXCESS, large complexes are formed which precipitate out and are phagocytized..NO HARM. When there is ANTIGEN EXCESS, small complexes (locally toxic to tissue and remain soluble) are formed pass through the vascular endothelium; adhere to the membranes of the vascular wall Complement activation attracts granulocytes which participate in inflammatory response.

SYSTEMIC LUPUS ERYTHEMATOSUS chronic multisystem autoimmune disorder more in women (childbearing years), than men unknown GENETICS; HORMONAL, ENVIRONMENTAL TRIGGERS B and T cells contribute to the immune response B cells : promote onset and flare ups FACTORS FOR SLE GENETIC HORMONAL: ONSET during childbearing years ENVIRONMENTAL/CHEMICAL: sunlight, thermal burns, meds (hydralazine, procainamide, INH, chlorpromazine)
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Pathology **failure of the regulatory system inability to slow/ halt production of inappropriate antibodies produces B lymphocyte-stimulating factors which lead to production of AUTOANTIBODIES w/c combine with other elements of the immune system to activate immune complexes and combine with immune system constituents, to form COMPLEMENT DEPOSITED IN ORGANS INFLAMMATION and TISSUE NECROSIS Clinical manifestations SKIN butterfly-rash of the malar region of the face, with erythema, edema; discoid(scarred, ringshaped) lesions in the shoulders, arms, upper back; discoid lesions (erythematous, scaly plaques) on face, scalp, external ear, neck; alopecia ARTHRITIS/synovitis bilateral, symmetric (hands, wrists, joints) but no joint destruction/nonerosion (RA), deformities or tendon rupture CARDITIS pericarditis(most common), pleural effusion, myo-/endocarditis, CAD PULMONARY pleuritis, pleural effusion, lupus pneumonia, pulmo hemorrhage, embolism GI oral ulcers, acute/subacute abd pain, pancreatitis, spontaneous bacterial peritonitis, bowel infarction RENAL nephritis CNS neuropsychiatric (depression, psychosis), TIA/CVA; epilepsy, migraine, GBS, chorea HEMATOLOGIC - hemolytic anemia, leucopenia, thrombocytopenia CONSTITUTIONAL fever, weight gain, fatigue AT RISK? >FEMALES ASIAN, LATINO, AFRICAN-AMERICAN AGES 15-45 RELATED TO SOMEONE WITH SLE DIAGNOSTIC EVALUATION: NO SINGLE LAB TEST CONFIRMS CBC - < platelets, wbc, rbc ANA (+) >ESR URINALYSIS - + rbc, prot 24-hr urine for protein and crea clearance chest x-ray;xray hands and wrist CT SCAN/MRI brain, abdomen, cerebral arteriogram MANAGEMENT: PHARMA & NON-PHARMA NSAIDS ANTIMALARIALS (to decrease disease activity) CORTICOSTEROIDS IMMUNOSUPPRESSIVES/IMMUNOMODIFIERS (to stop autoantibody production) e.g. INTERLEUKINS, INTERFERONS ANTIHYPERTENSIVES DIURETICS

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GOALS OF TREATMENT P/V progressive loss of organ function REDUCE exacerbation MINIMIZE diseases-related disabilities P/C complications from therapy PHARMACOLOGIC THERAPY CORTICOSTEROIDS ANTIMALARIAL DRUGS: hydroxychloroquine (Plaquenil) ? NSAIDS ? IMMUNOSUPPRESIVE AGENTS (alkylating , purine analogues) MEDICAL MANAGEMENT: NON-PHARMA NON-PHARMA**to avoid exacerbation, to reduce s/s o AVOID direct exposure to sunlight o BEHAVIOR MODIFICATION o JOINT PROTECTION o ENERGY PRESERVATION REFERRALS COMPLICATIONS RENAL FAILURE PERMANENT NEURO DAMAGE INFECTION DEATH NURSING DIAGNOSES ACUTE AND CHRONIC PAIN r/2 inflammation of joints and surrounding structures POWERLESSNESS r/2 unpredictable course of disease RISK for IMPAIRED SKIN AND ORAL MM INTEGRITY r/2 skin/oral lesions FATIGUE r/2 chronic inflammatory process BODY IMAGE DISTURBANCE KNOWLEDGE DEFICIENCY REDUCE PAIN administer meds as ordered hot/cold app, relaxation techniques, non-strenuous exercises INCREASING CONTROL OVER DISEASE PROCESS AVOID FACTORS THAT exacerbate disease: ***exposure to sunlight and ultraviolet rays(Sunscreen with SPF 15 or greater; Avoid prolonged sun exposure; Wear protective, lightweight clothing; AVOID exposure to drugs and chemicals**hairspray, hair dyes, med/supplements unless prescribed teach self-administration of drugs/ordered ENCOURAGE good nutrition, sleep habits, exercise, rest, and relaxation ENCOURAGE exp of feelings, counseling, referrals

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MAINTAIN SKIN & MM INTEGRITY Fashion enhancers Good oral hygiene AVOID hot/spicy foods Inspect mount for ulcers REDUCING FATIGUE ADVISE : fatigue level will fluctuate with disease activity MODIFY sked with several rest periods TEACH relaxation techniques PRESERVE URINARY ELIMINATION I and O, renal function tests, dialysis CLIENT EDUCATION and HEALTH MAINTENANCE CLOSE FOLLOW-UP REPRODUCTION AVOID pregnancy during time of severe disease activity, immunomodulators may have teratogenic effects, some drugs may cause sterility FAMILY SUPPORT EVALUATION/EXPECTED OUTCOMES Verbalization/compliance Reports mouth ulcers, healing, no interference with appetite; rest- 3x/day with adequate energy to carry out activities; pain reduction Urine output adequate TYPE IV: DELAYED-TYPE HYPERSENSITIVITY. CELLULAR HYPERSENSITIVITY OCCURS 24-72 h after exposure to allergen MEDIATED BY sensitized T cells and macrophages rather than antibodies TYPE IV: DELAYED HYPERSENSITIVITY RESPONSE The combination of an antigen with a sensitized T lymphocyte. creates tissue-damaging reactions causing delayed hypersensitivity either by RELEASING LYMPHOKINES or by DIRECT T-LYMPHOCYTE-MEDIATED CELL DESTRUCTION E.G. TUBERCULIN SKIN TEST;CONTACT DERMATITIS, TRANSPLANT GRAFT REJECTION exposure to haptens e.g. dye, nickel, poisonous plants,cosmetics, soaps, paints, starch, fabric conditioner DX: patch test

Problems & intervention altered comfort rash, pruritus knowledge deficit Intervention: topical corticosteroid creams; wet dressings

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RENAL TRANSPLANT REJECTION ACUTE HYPERACUTE CHRONIC I. ACUTE INTERMEDIATE REJECTION most common; cell-mediated response usually occurs after the first week and within four months II. HYPERACUTE REJECTION w/in 1st 48 hrs post- transplantation Once clamps of BV are released, the kidney is filled with blood & becomes PINK. However, in a short time, it becomes SOFT, BLUE, MOTTLED .ischemia, destruction Cause: reaction of circulating antibodies (humoral) of the recipient with the antigens present in the donor kidney. III. CHRONIC (late) REJECTION months or years (usually 2 yrs and final failure follows in 5 years) post- transplantation progressive deterioration of renal functioN humoral; irreversiblE effects: oliguria to anuria due to tubular necrosis, fever, kidney enlargement with tenderness, proteinuria, and hypertension INTERVENTION: PREVENTION and S/S histocompatibility matching tests immunosuppression :** a. azathioprine b. prednisone c. cyclophosphamide d. antilymphocytic globulin e. Cyclosporine S/S fever, swelling over graft site, tenderness, irritability, restlessness

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