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Trisha Economidis, MS, ARNP Spring, 2012 WAR DECLARED….. We are at war with our environment Troops are prepared to fight from every sector of the body to keep us safe (and healthy) Regiments on the ready include: Antibodies Immunoglobulins White Blood cells Immune Response Teams: Humoral and Cell-Mediated Immunity And others……. Immune System Review: Public Enemy Number ONE Antigen – a protein that stimulates an immune reaction, causing production of antibodies. Viruses Bacteria Fungi Parasites Etc….. Immune System Review Antibody – a globulin (PRO) produced by B cells as a defense mechanism against foreign materials. Combines in a lock and key style with antigens First Line of Defense: Primary Defenses Prevent organisms from entering the body Skin Respiratory Tree Tears/Saliva Gi Tract – acidic environment, peristalsis Bile - antimicrobial GU tract – mucous membranes Secondary Defenses Phagocytosis White blood cells TO THE RESCUE! Secondary Defense #2 Complement Cascade Set of proteins called complement that trigger release of chemicals that attack the cell membranes of pathogens causing them to rupture Secondary Defense #3: Inflammation Begins when histamine and other chemicals are released directly from damaged cells or from basophils in response to complement Histamine/chemical release Dilation and increased Permeability of blood vessels flow of phagocytes, antimicrobials, O2, & nutrients to area of damage Secondary Defense #4 Fever Increases metabolism Inhibits pathogen multiplication Triggers specific immune responses Tertiary Defenses: Specific Immunity Body recognizes and destroys pathogens encountered before Lymphocytes – WBCs that mature to either T cells or B cells 2 Types of Specific Immunity 1. Humoral Immunity– B (lymphs) cells stimulated to become plasma cells and produce antibodies (immunoglobulins) to the antigens. Antibodies bind to and destroy antigens. Specific Immunity No. 2: Cell-Mediated Immunity: Acts to destroy body cells that have become infected. T Cells are responsible for cell-mediated immunity: Cytotoxic (Killer) T cells Helper T cells Memory T cells Suppressor T cells WBC’s – Name, Rank & Serial Number Reported in the WBC Differential with a CBC Basophils 0.5-1% - Release histamine and heparin granules Eosinophils 1-3% - Destroy helminths, mediate allergic reactions Monocytes – 3-8% - Phagocytize directly Lymphocytes (20-35%) – T lymphs – recognize, attack and destroy antigens; B lymphs – produce immunoglobulins to attack and destroy antigens Neutrophils – 55-70%. First to arrive – Phagocytize! Bands – Immature neutrophils (normally 3-5% of total WBCs) Segmented (Segs) – Mature neutrophils –( normally 50-65T of total WBCs) Shift to the Left?????? In an acute infection more lymphocytes are produced A “shift to the left” occurs when there are more bands (immature or baby neutrophils) in circulation than there are segs (mature or grownup neutrophils) “Shift to the left” Higher number of bands than segs (usually when bands reach 6%) in circulation called bandemia. Indicates body is responding to an acute infection, usually bacterial, or to Stress (i.e. women in childbirth) Immunoglobulins (Ig) – the Special Agents of Humoral Immunity IgM – Goes after “first time offenders” IgG – most common one. (AKA: Gamma Globulin) – Active against bacteria and viruses IgE – primarily responsible for allergic response and parasitic infections IgA – secreted by mucous membranes around body openings. Provides more protection for points of entry. IgD – found of surface of B cells. Trap potential pathogens What are the “weapons” of the Immunoglobulin Agents??? Phagocytosis Neutralization Agglutination Activation of complement and inflammation Two Types of Immunity Innate (Native) Adaptive (Acquired) Present at birth Body can make it or receive it First line of defense Specific response Non-specific response Results from adaptive Neutrophils first on the site response to invasion by an antigen (antibody formation) Can be passive or active Can be naturally produced or artificially acquired Cannot be developed or transferred Adaptive Immunity Assessment of the Immune system Chief complaint – subjective data Review biographic data: age, gender, race, ethnic background, family history Comprehensive health history Physical Assessment Immune System Diagnostics Allergy testing (will discuss with allergies) Cd4-T cell counts (Helper T’s) – reflection of immune status (normal: 500-1600 cells/mm3) Viral Load testing – measures the presence of HIV viral genetic material in the patient’s blood rather than the body’s response to the virus ELISA/Western Blot Antibody testing ANA antinuclear antibody Immune System Diagnostics Rheumatoid Factor Serum Complement ESR (erythrocyte sedimentation rate) HLA testing – Human Leukocyte Antigen Health Promotion and the Immune System – Boosting your Immunity Diet – Balanced diet Exercise – Regular, moderate work-outs Stress relief Get enough sleep Use sun exposure protection Quit smoking or Don’t Start Avoid Excess alcohol Immunizations up-to-date Pharmacologic Management of Immune Disorders Antibiotics (anti-infectives) Use: treatment/prophylaxis of bacterial infections Cautions: Can depress bone marrow; Superinfections Cephalosporins Penicillins Fluoroquinolones Macrolides Sulfonamides Tetracyclines Pharmacological Interventions Antivirals – Destroy viruses either directly or by inhibiting the ability to replicate acyclovir (Zovirax); HSV-1, HSV-2, VZV osetamivir (Tamiflu), zanamivir (Relenza); Influenza Types A & B Pharmacological Interventions Antifungals Kill or stop growth of fungal infections of skin, mucus membranes, & systemic Topical Clotrimazole, ketoconazole, miconazole, nystatin Systemic Amphotericin B, fluconazole, ketoconazole Pharmacological Interventions Anti-inflammatory Corticosteroids Used for anti-inflammatory and immunosuppressive properties Topical, inhaled, intranasal, opthalmic, IV, PO, IM Long, intermediate, and short-acting Pharmacological Interventions Antihistamines Relief of symptoms associated with allergies, rhinitis, urticaria 1st generation-sedating Chlor-trimeton (chlorpheninamine) Dramamine (dimenthydrinate) Benadryl (dephenhydramine) Atarax, Vistaril (hydroxyzine) 2nd generation-non-sedating Allegra (fexofenadine) Claritin (loratadine) Zyrtec (cetirizine) Pharmacological Interventions Adrenergic sympathomimetic - Epinephrine Inhibits release of hypersensitivity mediators Inhibits reaction from mast cells Produces bronchodilation, vasoconstriction Epinephrine (Adrenalin) 0.3mg-0.5 mg subcutaneously or IM (Adults) Pharmacological Interventions Immunotherapy SC injections weekly/biweekly of allergen extracts Goals of Therapy Stimulate IgG levels for allergen binding Decrease IgE levels ALWAYS EXPECT ADVERSE REACTIONS!!! Pharmacological Interventions Biologic Response Modifers (BRMs) Broad class of drugs that alter the body’s response to diseases such as cancer and autoimmune, inflammatory and infections diseases Immune Modulators – either enhance or reduce immune responses (some can do both) Interferons Monoclonal antibodies Interleukins Disease-modifying antirheumatoid arthritis drugs Pharmacological Interventions Immunosuppressant Drugs – Decrease or prevent an immune response cyclosporine (Sandimmune, Neoral, Gengraf) Used to prevent organ rejection in liver, kidney, and heart transplants; treatment of RA and psoriasis. Off-label use in rejection prevention of pancreas, bone marrow, heart/lung transplants. muromonab-CD3 (Orthoclone OKT3) Only one indicated to treat acute organ rejection in kidney, liver and heart transplant Pharmacological Interventions Antimalarial (What’s this doing HERE?) Plaquenil (hydroxychloroquine) – used to decrease joint and muscle pain in early or mild Rheumatoid Arthritis or Lupus (SLE) Gold Therapy – Rarely used in the U.S. because of toxicities, but may see in patients from other countries. Antigout – Acute: colchicine and an NSAID Chronic: allopurinol (Zyloprim), probenecid (Benemid) Organ Donation/Transplant: One Boy’s Story http://www.youtube.com/watch?v=yA8671CyM7w 7 year old, Nicholas Green Nursing Management of Clients with Organ Transplants Transplant success tied to matching tissue antigens, HLA (Human Leukocyte Antigens) Autograft Allograft Xenograft Histocompatibility – ability of cells and tissues to survive transplantation without immunologic interference by the recipient Host-versus-Graft Transplant Rejection Complex process involving both antibody-mediated and cell mediated responses Hyperacute Rejection – Begins immediately and can’t be stopped once it begins Acute rejection – occurs 1-3 mo post-transplant. Most common rejection and is treatable. Chronic rejection – occurs from 4 mos to yrs posttransplant. No cure. Once organ cannot function, another transplant is only course. Treatment of Transplant rejection Maintenance therapy – Ongoing immune suppressants Ex. cyclosporin, Imuran & a corticosteroid (prednisone) Rescue therapy – treats acute rejection. Ex: ALG , murononab-CD3. Most effective during first course of treatment What is an allergy? Allergy is an exaggerated immune response to an antigen (foreign or allergen) to which the patient has been previously exposed. Also called hypersensitivity Allergy Terminology Allergen – an antigen that causes an allergic sensitization Mast cell – a tissue cell that contains granules filled with chemical mediators such as histamine and heparin. Play a major role in allergies as well as immune system function. Atopic – relating to a hereditary predisposition toward developing certain allergic reactions Why does an allergic reaction occur? 1. First time exposure to an allergen, our body responds by making “antigen-specific” IgE 2. The antigen-specific IgE binds to the surface of mast cells and basophils (both have granules containing chemical mediators including histamine that will be released when stimulated) 3. Once the IgE is formed, we are sensitized to that allergen Hypersensitivity (allergic) Reactions Type I reaction – occurs when the already sensitized person (see previous slide) is reexposed to the allergen (IgE mediated) Histamine and other chemicals are released from the cells Inflammatory response occurs from other proteins released from the cells that draw more WBC’s to the area Anaphylaxis – Serious Type I Reaction Immediate life-threatening systemic reaction Can occur in seconds to minutes Not common Life-threatening and can be fatal What can cause it: allergy shots, insect bites/stings, foods (peanuts, eggs, shellfish, etc.) medications, blood products, contrast media, exercise, skin testing. Anaphylaxis – What does it look like? Respiratory – bronchospasm, laryngeal edema, wheezing, cough Cardiovascular – hypotension, tachycardia, palpitations, syncope Skin – urticaria, angioedema, pruitus, erythema GI – N/V/D/, abdominal pain Emergency Care 1. 2. 3. Recognize symptoms A, B, Cs Administer drugs -Epinephrine 1:1000 0.3-0.5 mL SQ or Epi-pen 0.3 mL IM (adults), 0.15 mL IM (children) -Oxygen -Antihistamines -Bronchodilators History of Anaphylaxis? Obtain Medical Alert Bracelet Carry Epi-pen Did I inherit my allergies? Yes, and no…. The tendency to produce IgE to certain antigen exposure is based on genetic inheritance. Allergic tendencies are inherited (atopy); specific allergies are NOT inherited Other Hypersensitivity Reactions Type II: Cytotoxic – involve IgG. Body makes antibodies that attack self cells resulting in death of the cell. Ex. Hemolytic anemias, hemolytic transfusion reactions (person gets wrong blood type in a transfusion) Hypersensitivity Reactions, cont. Type III: Immune Complex Reactions – too many circulating antigens form large antigen-antibody complexes that lodge in small blood vessel walls; triggering inflammation and tissue damage. Type IV: Delayed Hypersensitivity Reactions – Sensitized T cells react to antigens by triggering macrophages to destroy the antigen. Type V: Stimulatory Reactions - autoantibodies constantly stimulate reaction from normal cells resulting in a “turned on” state continuously Allergy Testing Method-Apply to arms or back Cutaneous scratch or prick Intradermal (the most accurate) **Patch (for contact dermatitis) Response Produces localized response (wheal & flare) Diagnostic for allergies to specific antigen Positive reaction within minutes Lasts 8-12 hours RAST Testing (Radioallergosorbent) RAST testing Shows the blood level of IgE (antibody) directed against a specific antigen Advantages-can be used in people with extensive eczema or dermatitis who cannot undergo skin testing. Disadvantages-Results must be interpreted in the light of your symptoms and history: A positive response to an allergen indicates only a potential allergic reaction that may not be the cause of your symptoms. Twice as expensive as skin testing. Results are not immediately available. Immunodeficiency Disorders Therapy-induced immunodeficiency disorders Drug induced: Cytotoxic Drugs Corticosteroids Cyclosporin Radiation Induced Immunodeficiency Therapy Induced Immunosuppression Treatment Improve the immune function – possibly give biologic response modifiers Protect from infection Good hand washing Limit number of people entering room Careful and regular assessments Low bacterial diet No fresh flowers or potted plants Congenital (Primary Immune Deficiencies Defect in one or more immune components Present at birth Classified by type of immune function that is impaired System Lupus Erythematosus (SLE) Chronic, multi-system, autoimmune disease Affects more women than men Affects more African American women than European American women SLE thought to be a combination of environmental and genetic factors Lupus: Signs and Symptoms Skin: Butterfly rash Raynaud’s Phenomenon Lupus: Signs/ Symptoms Musculoskeletal System Muscle and joint pain very common with exacerbations and remissions Arthritis – affects primarily distal joints: hands, wrists, fingers, toes, ankles, knees, etc. May have tendon involvement and rupture Knees and hips can have treatment related osteonecrosis from steroid therapy Lupus: Signs/Symptoms Cardiac System Pericarditis - most common cardiac manifestation Myocarditis Anemia Leukopenia Thrombocytopenia Lupus: Signs/Symptoms Respiratory System Pleuritis – Inflammation of the pleura Pleural Effusions – Fluid build-up between pleura and chest cavity Pneumonia Lupus: Signs/Symptoms Gastrointestinal/Hepatic Systems Can affect any area of the GI system as well as pancreas, spleen, or liver Ex: oral ulcers, peptic ulcers, abdominal pain/N/V/D, pancreatitis, hepatomegaly, GERD, ulcerative colitis Lupus: Signs/Symptoms Renal System Lupus Nephritis – leading cause of death among patients diagnosed with SLE (Lupus) s/s to monitor for: fluid retention (edema, wgt gain), hematuria, proteinuria, changes in urine output, hypertension Lupus: Signs/Symptoms Neurologic System Neuropathies Psychoses, depression Seizures, migraine headaches CNS vasculitis Peripheral neuropathies CNS Vasculitis Lupus: Signs/Symptoms Constitutional Symptoms Fatigue Weight changes/loss or gain Fever Arthralgias Lupus: S/S Psychosocial Issues Altered body image/poor self-concept Chronic fatigue/weakness may prevent being as socially active as previously Fear and anxiety may occur due to the unpredictability of flares or the progression of the disease, necessity of life style changes, etc. Lupus: Diagnosis Lab tests: Antinuclear antibody ESR (sed rate) Serum complement Various antibody titers CBC – looking for pancytopenia Specific testing for body system involvement Urinalysis/24 hr urine Diagnostic Imaging: CXR, Hand x-rays, CT OR MRI Lupus: Treatment Pharmacologic Management NSAIDS Antimalarials (Plaquenil) Corticosteroid Therapy Immunosuppressive ages (methotrexate or Imuran) Lupus: Treatment Non-pharmacologic Management Avoid direct exposure to sunlight Use sunscreen with SPF of 30 or higher Some physicians recommend avoiding use of oral contraceptives Careful skin and hair care with mild soaps/shampoos Lupus: Important Patient Education Importance of skin care Monitor body temp and other warning signs of a flare: increased fatigue, pain, abdominal discomfort, rash, headache, dizziness Reproductive impact Avoid exposure to infection Need to follow treatment plan, including follow-up appointments and prompt reporting of a flare Preventive health care Medic Alert bracelet Rheumatoid Arthritis (RA) Chronic, progressive, systemic, inflammatory, autoimmune disease that affects joints and other tissues or organ systems. Most prevalent in European Americans Affects 0.5% to 1% of the population worldwide; women more frequently than men RA Pathophysiology Cause: believed to be genetic and environmental Autoantibodies (rheumatoid factors) attack healthy tissue, especially synovial membranes, causing inflammation. Immune processes activated Activation of the inflammatory and immune response damages the synovial membrane. RA Signs/Symptoms Onset may be acute and severe (usually precipitated by a stressor such as surgery or an infection) Or onset may be insidious Joints primarily affected are hands, wrists, knees and feet Joint involvement usually bilateral and symmetric. Disease symptoms described as early or late and joint (articular) or systemic (extra-articular) RA Signs/Symptoms Early Disease Manifestations: Joint stiffness, swelling, pain Systemic: Low-grade fever Fatigue Weakness Anorexia Paresthesias RA Signs/Symptoms Late Disease Manifestations Joint deformities (swan neck and ulnar deviation) Moderate to severe pain and morning stiffness Swan neck deformity Ulnar deviation RA Signs/Symptoms Late Disease Manifestations – Systemic Osteoporosis Anemia Weight loss Subcutaneous nodules Peripheral neropathy Vasculitis Pericarditis Sjogren’s syndrome Renal disease RA Diagnosis Based on patient’s hx, physical assessment, and diagnostic tests Lab tests: Rheumatoid factor ESR and C-reactive protein CBC Synovial fluid exam X-rays of affected joints RA Treatment Surgical Management: A synovectomy to remove inflamed synovium may be necessary for knee or elbow Total joint arthroplasty may be necessary for joint deformity and destruction Arthrodesis (joint fusion) to stabilize joints such as cervical vertebrae, wrists, and ankles. RA Treatment Pharmacological Management: NSAIDS Antimalarials Corticosteroids, oral or intra-articular for temporary relief Disease-Modifying Antirheumatic Drugs (DMARDS) to reduce disease activity: methotrexate, Imuran, Cytoxan or BMR’s: Humira, Enbrel, Remicade RA Treatment Non-pharmacological treatment Balanced program of rest and exercise – energy conservation Physical and Occupational therapy Heat and cold Assistive devices and splints Balanced nutrition Scleroderma (Systemic Sclerosis) Autoimmune disorder of connective tissue Characterized by hardening(sclero) and thickening of the skin (derma), blood vessels, synovium, skeletal muscles, and internal organs Approximately 300,000 people in the US have Scleroderma Affects women more than men by 3:1 Affects more African Americans than Caucasians Scleroderma - Pathophysiology Early stages very similar to SLE – often misdiagnosed Can be limited or diffuse May have CREST syndrome: Calcinosis Raynaud’s phenomenon Esophageal dysmotility Sclerodactyly Telangiectasia Scleroderma Signs/Symptoms Musculoskeletal - Joint pain GI: Dysphagia and reflux, esophagitis, diarrhea or constipation, abdominal cramping and malabsorption Skin: Bilateral, symmetric swelling of hands and sometimes feet. After edematous phase, the skin becomes hard and thick. Facial changes – skin tightening leads to loss of skin lines, appearance of disappearing lips Scleroderma Signs/Symptoms Facial skin symptoms: Tightening of the skin Disappearing lips Decreased mobility of eyelids Evolving process Body image and psychosocial issues Scleroderma Signs and Symptoms Cardiovascular: Raynaud’s Syndrome, Myocardial fibrosis, Pericarditis and dysrhythmias Pulmonary: Lung fibrosis, pulmonary hypertension, exertional dyspnea Renal – proteinuria, hematuria, hypertension, and renal failure Scleroderma Diagnosis ANA: of at least 1:40 Lab tests/results similar to SLE: ESR – elevated; CBC- may show anemia, RF – elevated in about 30% Barium swallow – may show esophageal dysmotility X-ray of hands & wrists – muscle atrophy, osteopenia No single diagnostic test – overlap with other autoimmune diseases so diagnosis may initially be difficult Scleroderma Treatment Corticosteroids & immunosuppressants – tried to slow the progression Identify early organ involvement and treat aggressively Skin protection and careful ongoing assessments Gastric secretion blockers for esophagitis/reflux. Avoid spicy foods, caffeine, alcohol NSAIDS for joint pain Be aware that the side effects from many of the pharmacological treatments can worsen symptoms of the disease http://www.youtube.com/watch?v=Lf8NihhvGhg Gout Metabolic d/o characterized by an acute inflammatory arthritis triggered by crystallization of urate within the joints. May be caused by an inborn error of metabolism or as the result of another disease process or factor; i.e. crash diets, renal insufficiency Affects approximately 3 million Americans each year, and over twice that man have been affected at some time. Occurs more often in men. More common in women who are post-menopausal or taking diuretics Gout 3 clinical stages 1. Asymptomatic – not detected unless a uric acid level is checked. Acute - Extremely painful joint inflammation, usually in the great toe, called podagra Chronic – After repeated episodes of acute gout, urates are deposited in various other connective tissues: synovial fluids (gouty arthritis); subcutaneous tissue (tophi) and kidneys(can form kidney stones and result in kidney failure) Gout treatment Pharmacological Management Acute Gout: NSAID (Indocin) or ibuprofen; and colchicine. Taken until symptoms subside Chronic gout: Prevention is key. Zyloprim (allopurinol) lowers uric acid levels. Benemid(probenecid) promotes excretion of uric acid. May be given one or the other or a combination. Gout treatment Non-pharmacological Management Dietary restrictions on high-purine meats (red and organ meats) and seafood (shellfish and oily fish with bones) may be recommended No alcohol Avoid aspirin and diuretics Drink enough fluid to maintain daily urine output of 2000 mL or more Lyme Disease Most common tick-borne illness in North America Carried by the infected deer tick (black-legged tick) Occurs most often in children and young adults living in rural areas Risk factors: Spending time in wooded or grassy areas Having exposed skin Not removing ticks promptly or properly Lyme Disease: Pathophysiology After an incubation period of 3-30 days after the bite, the spirochete migrates outward into the skin Forms a characteristic erythema migrans (bull’s eye rash) May spread to other skin sites, organs, or nodes Lyme Disease: Signs/Symptoms Stage I: Skin: Bull’s eye rash Musculoskeletal: pain and stiffness in muscles and joints Constitutional: flu-like symptoms, fever, chills, fatigue, body aches If not treated or treatment is unsuccessful, progresses to Stage II Lyme Disease Signs/Symptoms Stage II: Migratory musculoskeletal pain and swelling; especially in the knees Carditis with dysrhythmias, dyspnea, palpitations CNS disorders: meningitis, Bell’s palsy, numbness or weakness in limbs, impaired muscle movement If not diagnosed and treated can progress to Stage III Lyme Disease Signs/Symptoms Stage III (months to years after the tick bite) Chronic recurrent arthritis Chronic fatigue Cardiac complications Thinking/memory issues Lyme Disease: Treatment Antibiotic therapy: doxycycline, tetracycline, amoxicillin, cefuroxime, erythromycin. May be given for 3-4 weeks Aspirin or another NSAID for relief of arthritic symptoms May need assistive devices (splints/crutches) Prevention is the Key Preventing Lyme Disease When walking in wooded or grassy areas: Wear long pants tucked into socks, long sleeves, hat, gloves, shoes Use insect repellents (10-30% DEET) Check yourself, your children and your pets for ticks Remove a tick with tweezers by pulling straight out. Clean with alcohol other antiseptic. Fibromyalgia Common Rheumatic pain syndrome with widespread musculoskeletal pain, stiffness, and tenderness Women affected 9 times more often than men Genetic and environmental factors are thought to contribute Requires a hx of widespread pain in all 4 quadrants of the body for a minimum duration of 3 months and pain in at least 11 of 18 trigger points Fibromyalgia Signs/Symptoms Fatigue, moderate to severe Sleep disorders Problems with cognitive function (Fibro Fog) Irritable Bowel Syndrome Headaches and migraines Anxiety and depression Environmental sensitivities Fibromyalgia Treatment Pharmacological Management is symptomatic: 3 drugs approved as of 2009 to reduce pain levels and improve sleep: Lyrica, Cymbalta, and Savella Tricyclic antidepressants such as amitryptyline may help with pain and sleep as well SSRI’s - treat depression and anxiety Fibromyalgia Treatment Non-pharmacological Management Physical therapy Regular exercise routine Alternative therapies: Massage, acupuncture, chiropractic, yoga Stress management Therapy to assist with depression/anxiety Chronic Fatigue Syndrome or Chronic Fatigue and Immune Dysfunction Syndrome (CFIDS) Complicated disorder characterized by extreme fatigue unexplained by any underlying medical condition May worsen with activity, but doesn’t improve with rest No single test to confirm a diagnosis Risk factors: Age (40’s and 50’s), female, overweight and inactive, stress Chronic Fatigue Syndrome Signs/Symptoms Fatigue Loss of memory or concentration Sore throat Enlarged lymph nodes in neck or axilla Unexplained muscle pain Multiple joint pain Headache of a new type, pattern or severity Unrefreshing sleep Extreme exhaustion lasting more than 24 hrs after physical or mental exercise Chronic Fatigue Syndrome Treatment Pharmacological Management is symptom focused Antidepressants NSAIDS may help with body aches and pain Non-pharmacological Management: Gentle exercise program Psychological counseling Lifestyle changes: reduce stress, improve sleep habits, pacing Alternative medicine: acupuncture, massage, yoga, or tai chi Support groups may be helpful Spring 2012 Can be transmitted to others within few days of becoming infected Large enough amount of virus must enter body of a susceptible host Factors that determine whether infection occurs after exposure Duration of contact Frequency of contact Volume of fluid Virulence & concentration of organism Host immune status Transmission Sexual Transmission Most common mode Blood and Blood Products Sharing of needles Transfusions Occupational exposures Perinatal Transmission Can occur during pregnancy, at delivery or breastfeeding Modes of Transmission Discovered 1983 A ribonucleic virus (RNA) Called Retroviruses because they replicate backwards Can’t replicate unless in living cell Pathophysiology HIV infects cells with CD4 receptors on surface Lymphocytes, monocytes/macrophages, etc. Targets CD4 T-cells as have more CD4 receptors Viral genetic material enters cell Viral RNA produces viral DNA with help of reverse transcriptase (enzyme made by HIV) Strand of DNA copies itself Viral DNA enters cell nucleus & becomes permanent part of cell’s genetic structure THEN HIV-RNA to HIV-DNA Genetic material replicated during cellular division so All new cells infected and cell’s genetic codes direct cells to make HIV Long strands of HIV-RNA cut to length with assist of enzyme protease Rapid Many errors and mutations HIV Replication Immune Response to HIV B-cells make antibody specific to HIV They reduce viral load in blood Activated T-cells mount cellular response to viruses in lymph nodes CD4 T-cells attracted to lymph nodes where HIV concentrated Once CD4 cells infected virus replicates and spreads throughout body Lymph nodes are reservoir for HIV Protect viruses from contact with drugs Support viral replication HIV damages lymph system and virus spills into blood CD4 T-Lymphocytes Normally have 800-1200/microliter blood >500 for healthy immune system Immune problems 200-499 Severe problems <200 Immune suppression leads to opportunistic infections Normal life span ~ 100 days HIV infected CD4 cells dies after 2 days HIV destroys 1 billion CD4 T-cells every day Bone marrow and Thymus normally produce enough CD4 cells for years but… Eventually HIV destroys more than body can reproduce Decline in CD4 T-lymphocytes (T-helper cells) impairs immune function. Destruction of CD4 T-cells Budding Leaves small holes in cell membrane Cell contents leak out and cell dies Fusion Infected cells clump with other cells into mass that destroys all cells Binding Antibodies against HIV bind to surface of infected cells, activate complement system which destroys infected cells HIV infection of Monocytes HIV infects monocytes by: Attaching to CD4+ receptors on monocytes or… Phagocytic ingestion of monocytes Infected monocytes go to body tissues and differentiate into macrophages HIV replicates in infected macrophages No budding occurs so…. Cell remains intact and becomes HIV factory Clinical Manifestations- Acute Infection Acute Retroviral Syndrome Flu like symptoms Fever Swollen lymph nodes Sore throat Headache malaise Nausea Muscle and joint pain Diarrhea Rash 1-3 weeks after infection Last 1-2 weeks (or months) High level of HIV in blood, CD4+ T cell count down but quickly returns to normal Clinical Manifestations Early Chronic HIV Infection HIV infection to diagnosis AIDS ~ 10 years Asymptomatic …but can have Fatique, headaches, low fever, night sweats, lymphadenopathy Not aware of infection Can transmit to others CD4 count >500 Clinical Manifestations Intermediate Chronic Infection Symptoms become worse Persistent fever Drenching night sweats Diarrhea Severe fatique Localized infections Thrush, shingles, vaginal candidiasis, oral/genital herpes, Kaposi’s Sarcoma, oral hairy leukoplakia CD4 count 200-499 Lymphadenopathy Viral Load rises Clinical Manifestations Late Chronic Infection See Diagnostic Criteria for AIDS CDC HIV positive And CD 4 cell count < 200 cells/mm3 Or an opportunistic infection Decrease absolute # of lymphocytes All factors = increased risk for opportunistic diseases Screening Tests Detect HIV antibodies Not useful first few months of infection because of Window period All infants of HIV infected Moms will test positive up to 18 months as antibodies cross placental barrier. (instead test for HIV antigens or do viral cultures) ELISA (enzyme immunoassay)(EIA) Western Blot (IFA) Diagnostic Studies Tests used to Determine when to start treatment Determine efficacy of treatment Determine if clinical goals are being met Monitor CD4 T-cell lymphocyte counts Viral load (viral burden) counts (the best indication) Tests for resistance to ART Lab Studies to evaluate response to treatment Goals of Care Monitoring disease progression and immune function Initiating and monitoring drug therapy Preventing opportunistic diseases Detecting and treating opportunistic diseases Managing symptoms Preventing or minimizing complications of treatment Initial Visit Gather baseline data Complete H&P Immunization hx Psychosocial hx Dietary evaluation Establish rapport Initiate Education HIV treatment Preventing transmission Improving health Family planning Report to state health department Goals of Drug Therapy Decrease viral replication & delay progression of disease Prevent viral resistance to drugs Decrease HIV RNA levels to < 50 copies/microliter Increase CD4+ T-cells to >200 (800-1200 preferred) Delay development of HIV related symptoms Antiretroviral Drugs Work at various points in HIV replication cycle; decrease chance of drug resistance 3 primary groups of drugs Inhibit ability of HIV to make DNA copy early in replication Inhibits ability of virus to reproduce in late stages of replication Prevents entry of HIV into cell Nucleoside Reverse Transcriptase Inhibitors (NRTI’s) HIV DNA chain left incomplete by blocking chain development Nonnucleoside Reverse Transcriptase Inhibitors (NNRTI’s) Block conversion of HIV RNA to HIV DNA Nucleotide Reverse Transcriptase Inhibitors Drugs that work by inhibiting activity of reverse transcriptase Identify Risk behaviors Blood transfusions (esp. before 1985)/clotting factors Shared needles Sexual practices STD’s Nursing Management For client with unknown status Identify Risk behaviors Blood transfusions (esp. before 1985)/clotting factors Shared needles Sexual practices STD’s Nursing Management For client with unknown status Health History Route of infection, TB, STD’s frequent infections Meds Perception of Health Nutrition Alcohol / drug use Elimination Cognitive Role/relationships Sexuality Nursing Assessment for clients with HIV Infection Patient Education Health Promotion Prevent disease Detect early so early intervention Prevention Develop safer, healthier, less risky behaviors Education about Safe activities vs. Risk reducing activities Abstinence Outercourse Monogomous partners Condoms Plastic wrap/latex dental dams Do not use drugs – if you do don’t share equipment Don’t have intercourse when under the influence of drugs/slcohol Prevent HIV in women Treat HIV infected pregnant women with Zidovudine Decreases rate of transmission Minimal side effects for baby Combination therapy Can decrease risk to <2% Decreasing Risks of Perinatal Transmission Follow Standard Precautions /Transmission based precautions Post exposure prophylaxis (PEP) with combination ART Base on type of exposure Volume of exposure Status of source Decreasing Occupational Risks Nutritional support to maintain lean body mass, levels of vitamins & micronutrients, fluid balance Eat nutrient dense foods Eliminate alcohol, smoking, illicit drugs Adequate rest and exercise Stress reduction Avoid exposure to infections Mental health counseling / support groups Early Intervention Health Promotion to improve immune function