HIV, Anaphylaxis, and Immunity(1)

Immunity CHAPTER 17 THE IMMUNE SYSTEM PROTECTION AGAINST DISEASE BY NEUTRALIZING, ELIMINATING, OR DESTROYING ORGANISMS, AND BODY TISSUE RECOVERY IMMUNOCOMPETENT REDUCTION IN IMMUNITY TEMPORARY PERMANENT BODY DEFENSES PHYSICAL BARRIERS NORMAL FLORA CHEMICAL BARRIERS SELF VS. NON-SELF NON-SELF: PATHOGENS, CANCER CELLS, INFECTED CELLS, CELLS FROM OTHERS SELF-TOLERANCE: AFFECTED BY PROTEINS ON THE PLASMA MEMBRANE HUMAN LEUKOCYTE ANTIGENS ORGANIZATION OF THE IMMUNE SYSTEM NERVOUS SYSTEM, ENDOCRINE SYSTEM, AND GASTROINTESTINAL SYSTEM BONE MARROW- THE SOURCE OF ALL BLOOD CELLS STEM CELLS: UNDIFFERENTIATED EXPOSURE TO SPECIFIC GROWTH FACTORS DIRECTS DIFFERENTIATION ERYTHROCYTES, LEUKOCYTES, PLATELETS FUNCTIONS OF LEUKOCYTES (NORMAL VALUE 5,000 TO 10,000) RECOGNITION DESTRUCTION ANTIBODY PRODUCTION COMPLEMENT ACTIVATION CYTOKINE PRODUCTION INFLAMMATION OCCURS WITH ILLNESS OR INJURY NATURAL IMMUNITY/INNATE IMMUNITY BARRIERS OR ATTACKING FORCES IMMEDIATE PROTECTION, SHORT-TERM, NON-SPECIFIC, DOES NOT PROVIDE ADDITIONAL PROTECTION WITH REPEATED EXPOSRE NON-TRANSFERABLE INFLAMMATION CAUSES VISIBLE RESPONSES CELL TYPES INVOLVED WITH INFLAMMATION NEUTROPHILS MACROPHAGES BASOPHILS EOSINOPHILS MAST CELLS INFLAMMATION PHAGOCYTOSIS NEUTROPHILS AND MACROPHAGES 7 STAGES: EXPOSURE AND INVASION ATTRACTION ADHERENCE RECOGNITION CELLULAR INGESTION PHAGOSOME FORMATION DEGRADATION SEQUENCE OF INFLAMMATION CARDINAL MANIFESTATIONS STAGES STAGE 1: VASCULAR STAGE 2: CELLULAR EXUDATE STAGE 3: REPAIR AND REPLACEMENT IMMUNITY ADAPTIVE, LONG TERM RESISTANCE, SPECIFIC ANTIBODY MEDIATED IMMUNITY (HUMORAL IMMUNITY) B-CELLS ANTIGEN ANTIBODY INTERACTIONS EXPOSURE RECOGNITION SENSITIZATION ANTIBODY PRODUCTION/RELEASE ANTIBODY CLASSIFICATION ACQUIRING HUMORAL IMMUNITY ACTIVE: NATURAL OR ARTIFICIAL PASSIVE IMMUNITY ADAPTIVE, LONG TERM RESISTANCE, SPECIFIC CELL MEDIATED IMMUNITY REGULATE FUNCTIONS OF ANTIBODY MEDIATED IMMUNITY BY PRODUCING AND RELEASING CYTOKINES. CELL TYPES T- LYMPHOCYTES (T-CELLS) NATURAL KILLER CELLS CYTOKINES PROTECTION PROVIDED BY CELL MEDIATED IMMUNITY MANAGEMENT OF PATIENTS WITH HIV AND AIDS CHAPTER 19 EPIDEMIOLOGY 1.2 MILLION IN THE U.S. ARE INFECTED 1 IN 5 ARE UNAWARE 50,000 NEW CASES EACH YEAR PATHOPHYSIOLOGY RETROVIRUS- INSERTS ITS RNA INTO HOST RNA, RESULTING IN REPLICATION WHEN CONVERTING TO DNA CONTAINS “DOCKING PROTEINS” THAT HELP IT CONNECT WITH BODY CELLS TARGETS CD4 RECEPTORS (T-CELLS) PROCESS OF INFECTION ACUTE INFECTION LATENCY OPPORTUNISTIC INFECTIONS AND CANCERS STAGES OF HIV INFECTION STAGE I LAB CONFIRMATION WITH T-CELL >500, NO CLINICAL EVIDENCE STAGE II LAB CONFIRMATION WITH T-CELL 200-499, NO CLINICAL EVIDENCE STAGE III AIDS; LAB CONFIRMATION WITH T-CELL <200, OR DOCUMENTED SIGNS AND SYMPTOMS STAGE UNKNOWN LAB CONFIRMATION WITH UNKNOWN T-CELL COUNT, NO CLINICAL EVIDENCE HIV TRANSMISSION BODY FLUIDS SKIN AND MUCOSA BREAKS MOTHER TO INFANT BLOOD AND BLOOD PRODUCTS HEALTH CARE PROVIDERS STANDARD PRECAUTIONS POST-EXPOSURE PROPHYLAXIS HIV PREVENTION AND EDUCATION SEXUAL PRACTICE MONOGAMY CONDOM USE GERONTOLOGICAL CONSIDERATIONS SAFE DRUG USE NEEDLE EXCHANGE NEEDLE CLEANING REPRODUCTION PATIENT ASSESSMENT HISTORY PHYSICAL ASSESSMENT OPPORTUNISTIC INFECTIONS MALIGNANCY DIAGNOSTIC TESTING ELA OR ELISA WESTERN BLOT VIRAL LOAD TESTING NEGATIVE TESTING IMPLICATIONS MAY TAKE UP TO 6 MONTHS FROM EXPOSURE CLINICAL MANIFESTATIONS OF HIV OPPORTUNISTIC INFECTIONS FUNGAL INFECTIONS PNEUMOCYSTIS PNEUMONIA CANDIDA TOXOPLASMOSIS ENCEPHALITIS MYCOBACTERIUM TUBERCULOSIS MALIGNANCIES KAPOSI’S SARCOMA BURKITT’S LYMPHOMA ENDOCRINE LIPODYSTROPHY GONADAL DYSFUNCTION ADRENAL DYSFUNCTION OTHER AIDS WASTING SYNDROME SKIN CHANGES KIDNEY PROBLEMS SKIN CHANGES HIV TREATMENT PREVENTION OF INFECTION IS #1 PRIORITY CD4 COUNT REMAINS THE STRONGEST DETERMINANT OF TREATMENT RESPONSE, DISEASE PROGRESSION, AND SURVIVAL GOALS OF TREATMENT: PREVENT TRANSMISSION REDUCE MORBIDITY RESTORE IMMUNOLOGIC FUNCTIONSUPPRESS VIRAL LOAD OFTEN REQUIRES MORE THAN ONE MEDICATION FOR TREATMENT MOST COMMON IS AZT SUPPORTIVE CARE ENHANCING OXYGENATION MANAGING PAIN ENHANCING NUTRITION MINIMIZING DIARRHEA RESTORING SKIN INTEGRITY MINIMIZING CONFUSION/PROVIDING SELF-MANAGEMENT EDUCATION PSYCHOSOCIAL PREPARATION AND MANAGEMENT Immune Hypersensitivities CHAPTER 20 Hypersensitivity HYPERSENSITIVITY: PROLONGED, EXCESSIVE, OR WRONG TIME RESPONSE TO AN ANTIGEN USUALLY DOES NOT OCCUR IN FIRST EXPOSURE TO AN ANTIGEN VASOACTIVE AMINE: HISTAMINE- CAUSES CAPILLARY LEAKING, NASAL SECRETIONS, AND ITCHING. TYPES: (A)TYPE I: RAPID HYPERSENSITIVITY (C)TYPE II: CYTOTOXIC HYPERSENSITIVITY (I)TYPE III: COMPLEX HYPERSENSITIVITY (D)TYPE IV: DELAYED HYPERSENSITIVITY TYPE I HYPERSENSITIVITY IMMEDIATE OR RAPID RESPONSE INCREASE IN IgE ALLERGEN CONTACT INGESTION INJECTION CONTACT INHALED ALLERGIC RHINITIS LATEX ALLERGY CAN BE RELATED TO FREQUENT EXPOSURE OR CERTAIN FOOD ALLERGIES ALLERGY TESTING TREATMENT AVOIDANCE MEDICATIONS DESENSITIZATION METHODS FOR TREATMENT ANAPHYLAXIS RAPID RELEASE OF ANTIGEN THAT RESULTS IN A LIFE-THREATENING RESPONSE MOST COMMONLY CAUSED BY FOOD, MEDICATION, INSECT STINGS, AND LATEX MOST COMMONLY BEGIN WITHIN 2 HOURS OF EXPOSURE CLINICAL MANIFESTATIONS: MULTIPLE ORGAN INVOLVEMENT MILD REACTION: TINGLING, FULLNESS IN MOUTH OR THROAT, NASAL CONGESTION, PERIORBITAL EDEMA, PRURITIS, SNEEZING, EYE TEARING., ANGIOEDEMA MODERATE REACTION: FLUSHING, ANXIETY, ITCHING, BRONCHOSPASM, DYSPNEA, COUGH, WHEEZING. SEVERE REACTION: ABRUPT ONSET- MILDER SYMPTOMS ALONG WITH LARYNGEAL EDEMA, HYPOTENSION, CYANOSIS, DYSPHAGIA, VOMITING, DIARRHEA, SEIZURES, CARDIAC ARREST MANAGEMENT OF ANAPHYLAXIS MEDICAL MANAGEMENT MANAGEMENT OF SYMPTOMS ANTIHISTAMINES CORTICOSTEROIDS IV FLUIDS VASOPRESSORS (EPINEPHRINE) FIRST!! MONITORING AFTER EPINEPHRINE ADMINISTRATION NURSING MANAGEMENT ASSESSMENT TEACHING URITICARIA AND ANGIONEUROTIC EDEMA URTICARIA: HIVES TYPE I IMMEDIATE HYPERSENSITIVITY MAY INVOLVE SKIN AS WELL AS MUCUS MEMBRANES MAY OCCUR EPISODICALLY CHRONIC IF EPISODES OCCUR OVER GREATER THAN 6 WEEKS ANGIONEUROTIC EDEMA: ANGIOEDEMA INVOLVES DEEPER LAYERS OF SKIN WITH MORE DIFFUSE SWELLING ERYTHEMA MAY OR MAY NOT BE PRESENT MAY HAVE RAPID OR SLOW ONSET MAY BE HEREDITARY ANGIOEDEMA: OCCUR SPONTANEOUSLY, NOT ALLERGIC RELATED TYPE II HYPERSENSITIVITY CYTOTOXIC RESPONSE AUTOANTIBODIES AGAINST SELF CELLS IMMUNE HEMOLYTIC ANEMIA TRANSFUSION REACTIONS IMMUNE THROMBOCYTOPENIA PURPURA TREATMENT STOP THE CAUSE OR INFUSION PLASMAPHERESIS CONTROL OF SYMPTOMS COMPLICATIONS HEMOLYTIC CRISIS KIDNEY FAILURE TYPE III HYPERSENSITIVITY IMMUNE COMPLEX REACTION IMMUNE COMPLEXES FORM IN THE BLOOD, ACCUMULATING AND CAUSING INFLAMMATION RELATED TO CHRONIC IMMUNE DISORDERS CONNECTIVE TISSUE DISEASE RHEUMATOID ARTHRITIS GLOMERULONEPHRITIS SERUM SICKNESS TYPE IV HYPERSENSITIVITY DELAYED HYPERSENSITIVITY REACTION RELATED TO T-CELL ACTIVATION: SENSITIZED T-CELLS RESPOND TO ANTIGEN OCCURS HOURS TO DAYS AFTER EXPOSURE EXAMPLES: POSITIVE PROTEIN DERIVATIVE TEST CONTACT DERMATITIS TRANSPLANT REJECTIONS MANAGEMENT REMOVAL OF OFFENDING ALLERGEN BENDARYL NOT EFFECTIVE DESENSITIZATION NOT EFFECTIVE CORTICOSTEROIDS AUTOIMMUNE DISORDERS INAPPROPRIATE IMMUNE RESPONSE DIRECTED AGAINST NORMAL TISSUE AND CELLS COMMON AUTO-IMMUNE DISORDERS TABLE 20.2 PAGE 367 SYSTEMIC LUPUS ERYTHEMATOUS RHEUMATOID ARTHRITIS GOODPASTURE’S SYNDROME DIABETES MELLITUS TYPE I HEMOLYTIC ANEMIA AND THROMBOCYTOPENIA PURPURA CROHN’S DISEASE SJOGREN’S SYNDROME