Alterations in Immunity Lecture Notes PDF

ALTERATIONS IN IMMUNITY PATHOPHYSIOLOGY – NURS 3203  TYPES OF ALTERATIONS IN IMMUNE FUNCTION HYPERSENSITIVITY EXAGGERATED IMMUNE RESPONSE TO A FOREIGN SUBSTANCE AUTOIMMUNE MISTAKES SELF AS NONSELF IMMUNODEFICIENCY INADEQUATE IMMUNE REACTION ...

ALTERATIONS IN IMMUNITY PATHOPHYSIOLOGY – NURS 3203  TYPES OF ALTERATIONS IN IMMUNE FUNCTION HYPERSENSITIVITY EXAGGERATED IMMUNE RESPONSE TO A FOREIGN SUBSTANCE AUTOIMMUNE MISTAKES SELF AS NONSELF IMMUNODEFICIENCY INADEQUATE IMMUNE REACTION  HYPERSENSITIVITY INFLATED RESPONSE TO ANTIGEN LEADS TO INFLAMMATION, WHICH DESTROYS HEALTHY TISSUE CAN BE IMMEDIATE OR DELAYED FOUR TYPES: TYPE I: IGE MEDIATED TYPE II: CYTOTOXIC HYPERSENSITIVITY REACTION TYPE III: IMMUNE COMPLEX–MEDIATED TYPE IV: DELAYED HYPERSENSITIVITY REACTION  TYPES OF HYPERSENSITIVITY TYPE I, IGE MEDIATED PRODUCES AN IMMEDIATE RESPONSE. LOCAL OR SYSTEMIC. ALLERGEN ACTIVATES T-HELPER CELLS THAT STIMULATE B CELLS TO PRODUCE IGE. IGE COATS MAST CELLS AND BASOPHILS, SENSITIZING THEM TO THE ALLERGEN. AT NEXT EXPOSURE, THE ANTIGEN BINDS WITH THE SURFACE IGE, RELEASING MEDIATORS AND TRIGGERING THE COMPLEMENT SYSTEM.  TYPES OF HYPERSENSITIVITY TYPE I, IGE MEDIATED REPEATED EXPOSURE TO THE ALLERGEN IS NECESSARY TO CAUSE THIS RESPONSE. EXAMPLES: HAY FEVER, FOOD ALLERGIES, ASTHMA AND ANAPHYLAXIS TREATMENT INCLUDES EPINEPHRINE, ANTIHISTAMINES, CORTICOSTEROIDS, AND DESENSITIZING INJECTIONS.  TYPES OF HYPERSENSITIVITY TYPE II, CYTOTOXIC HYPERSENSITIVITY REACTION IGG OR IGM TYPE ANTIBODIES BIND TO ANTIGEN ON INDIVIDUAL’S OWN CELLS. ANTIGEN MAY BE INTRINSIC OR EXTRINSIC. RECOGNITION OF THESE CELLS BY MACROPHAGES TRIGGERS ANTIBODY PRODUCTION. LYSIS OF CELLS OCCURS BECAUSE OF THE ACTIVATION OF THE COMPLEMENT AND BY PHAGOCYTOSIS. USUALLY IMMEDIATE RESPONSES.  TYPES OF HYPERSENSITIVITY TYPE II, CYTOTOXIC HYPERSENSITIVITY REACTION EXAMPLES: BLOOD TRANSFUSION REACTION AND ERYTHROBLASTOSIS FETALIS TREATMENT INCLUDES ENSURING BLOOD COMPATIBILITY (TRANSFUSION) AND ADMINISTERING MEDICATION TO PREVENT MATERNAL ANTIBODY DEVELOPMENT (RHO[D]).  TYPES OF HYPERSENSITIVITY TYPE III, IMMUNE COMPLEX–MEDIATED HYPERSENSITIVITY REACTION CIRCULATING ANTIGEN–ANTIBODY COMPLEXES ACCUMULATE AND ARE DEPOSITED IN THE TISSUE. TRIGGERS THE COMPLEMENT SYSTEM, CAUSING INFLAMMATION. EXAMPLE: AUTOIMMUNE CONDITIONS (E.G., SYSTEMIC LUPUS ERYTHEMATOSUS) TREATMENT IS DISEASE SPECIFIC.  TYPES OF HYPERSENSITIVITY TYPE IV, DELAYED HYPERSENSITIVITY REACTION CELL-MEDIATED RATHER THAN ANTIBODY-MEDIATED INVOLVING THE T CELLS. ANTIGEN PRESENTATION RESULTS IN CYTOKINE RELEASE, LEADING TO INFLAMMATION. CAUSES SEVERE TISSUE INJURY AND FIBROSIS EXAMPLES: TUBERCULIN SKIN TESTING, TRANSPLANT REACTIONS, AND CONTACT DERMATITIS TREATMENT IS DISEASE SPECIFIC.  AUTOIMMUNE DISORDERS IMMUNE SYSTEM LOSES THE ABILITY TO RECOGNIZE SELF. DEFENSES ARE DIRECTED AGAINST HOST. CAN AFFECT ANY TISSUE. THE MECHANISM THAT TRIGGERS THIS RESPONSE IS NOT CLEAR.  AUTOIMMUNE DISORDERS KNOWN CHARACTERISTICS GENETICS PLAYS A ROLE. MORE PREVALENT IN FEMALES. ONSET IS FREQUENTLY ASSOCIATED WITH AN ABNORMAL STRESSOR, PHYSICAL OR PSYCHOLOGICAL. ARE FREQUENTLY PROGRESSIVE RELAPSING-REMITTING DISORDERS CHARACTERIZED BY PERIODS OF EXACERBATION AND REMISSION.  SYSTEMIC LUPUS ERYTHEMATOSUS CHRONIC INFLAMMATORY AUTOIMMUNE CONDITION. MAY AFFECT CONNECTIVE TISSUE OF ANY BODY ORGAN. REMISSION AND EXACERBATIONS—STRESSORS TEND TO TRIGGER. DISEASE PROGRESSION VARIES FROM MILD TO SEVERE. MORE COMMON IN WOMEN, ASIANS, AND AFRICAN AMERICANS. CAUSE IS UNCLEAR, BUT IT’S THOUGHT THAT B CELLS ARE ACTIVATED TO PRODUCE AUTOANTIBODIES AND AUTOANTIGENS THAT COMBINE TO FORM IMMUNE COMPLEXES, WHICH ATTACK THE BODY’S OWN TISSUES.  SYSTEMIC LUPUS ERYTHEMATOSUS DIAGNOSTIC CRITERIA (FOUR OR MORE OR MORE OF THE FOLLOWING) SEROSITIS IMMUNOLOGICAL PHENOMENA ORAL ULCERS ANTINUCLEAR ANTIBODY ARTHRITIS NEUROLOGICAL DISORDERS (SEIZURES/PSYCHOSIS) PHOTOSENSITIVITY MALAR RASH (BUTTERFLY RASH OVER BLOOD DISORDERS CHEEKS) (DECREASED COUNT) DISCOID RASH (PATCHY REDNESS RENAL INVOLVEMENT THAT CAN CAUSE SCARRING) Copyright Medical News Today at https:// www.medicalnewstoday.com/articles/323653  SYSTEMIC LUPUS ERYTHEMATOSUS TREATMENT NO CURE—ONLY SYMPTOM MANAGEMENT STRESS MANAGEMENT AND HEALTH PROMOTION BEHAVIORS PHARMACOLOGICAL NSAIDS, ANTIMALARIALS, CORTICOSTEROIDS, IMMUNOSUPPRESSANTS, AND DMARDS PLASMAPHERESIS PROGNOSIS IMPROVES WITH EARLY DIAGNOSIS AND TREATMENT.  IMMUNODEFICIENCY DIMINISHED OR ABSENT IMMUNE RESPONSE RENDERS THE PERSON SUSCEPTIBLE TO DISEASE NORMALLY PREVENTED OPPORTUNISTIC INFECTIONS MAY BE ACUTE OR CHRONIC CLASSIFICATIONS PRIMARY SECONDARY  AIDS HIV PARASITIC RETROVIRUS THAT INFECTS CD4 AND MACROPHAGES UPON ENTRY TWO PRIMARY TYPES TYPE 1 IS THE MOST COMMON STRAIN. TYPE 2 IS MORE COMMON IN WEST AFRICA; PROGRESSES TO DISEASE MORE SLOWLY. TRANSMISSION BLOOD AND BODILY FLUIDS  AIDS PROGRESSION LATENT (ASYMPTOMATIC) PHASE. VIRUS IS REPRODUCING, USUALLY FOR SEVERAL YEARS. INFECTIONS BEGIN AS THE VIRAL NUMBER RISES, DESTROYING THE CD4 CELLS (T-LYMPHOCYTES) PROGRESSION TAKES THREE FORMS. IMMUNODEFICIENCY AUTOIMMUNITY NEUROLOGICAL DYSFUNCTION  AIDS PROGRESSION HIV  AIDS WHEN CD4+ COUNT IS 500 CELLS/ΜL DEFINING ILLNESSES CATEGORY 2: 200–499 PRESENT CATEGORY 3: < 200  AIDS TREATMENT NO CURE COMBINATION THERAPY WORKS BEST HIGHLY ACTIVE ANTIRETROVIRAL THERAPY (HAART) MAY HAVE TO CHANGE REGIMEN DUE TO VIRAL ADAPTATION OTHER MEDICINES AND VACCINES WILL BE USED TO PREVENT OPPORTUNISTIC INFECTIONS AS NEEDED VACCINATIONS TRANSMISSION PREVENTION  INDIVIDUALS AT RISK FOR IMMUNE DYSFUNCTION VERY YOUNG AND VERY OLD CHRONIC DISEASES, ESPECIALLY POOR NUTRITION DIABETES MELLITUS IMPAIRED SKIN INTEGRITY CORTICOSTEROID THERAPY CHEMOTHERAPY CIRCULATORY ISSUES ALTERATIONS IN NORMAL SMOKING FLORA DUE TO ANTIBIOTIC ALCOHOL CONSUMPTION THERAPY IMMUNODEFICIENCY STATES  IMMUNE-BUILDING STRATEGIES INCREASING FLUID INTAKE EATING A WELL-BALANCED DIET INCREASING ANTIOXIDANTS AND PROTEIN INTAKE GETTING ADEQUATE SLEEP AVOIDING CAFFEINE AND REFINED SUGAR SPENDING TIME OUTDOORS REDUCING STRESS