NURS 304: ADULT NURSING LECTURER: Ms. Mackey Assessment of Immune Function Immune System + Antibody “An antibody is protein substance developed bythe body in cesponse ta and interacting witha specie antigen + Antigen — A substance that induces the production of antibody + Immunoglobulins — Antibodies (protein molecules eA, E, G, M, D) The Immune System + Immunity: the body’s specific protective response to invading foreign agent or organism + Immunopathology + Immune disorders Autoimmunity - normal protected immune response Hypersensitivity ~ exaggerated response to antigen — Gammopathies over production of immunoglobulins Immune deficiencies: primary and secondary Central and Peripheral Lymphoid OrgansDevelopment of Cells of the Immune System Physiology === Pathophysioloay = ee ee es Cellular Immune Response ‘© B lymphocytes: humoral immunity + Produce antibodies or immunoglobulins ‘¢ Tlymphocytes: cellar immunity + Attack invaders directly, secrete cytokines, and stimulate immune system responses + Helper cells + OytotoxicT cells + Memory cells + Suppressor T cells (suppress immune response) Immune Function © Natural immunity: nonspecific response to any foreign invader + White blood cal ation: releate cell mediators such as histamine, bradykinin, and prostaglandins, and engulf (phagocytic) foreign substances “Inflammatory response «Physical barrier, such as intact skin, chemical barriers, and acidic gastric secretions or enaymes in tare and saliva ‘© Acquired immunity: specific against a foreign antigen + Result of prior exposure to an antigen + Adive or passive Variables That Effect Immune System Function + Age and gender + Nutetion + Presence of conditions or disorders: cancer/neoplasm, chronicilinss, autoimmune disorders, surgery/trauma Allergies History of infection or immunization Genetic factors Ltestyle ‘Medications and transfusions PyschoneuroimmunologicfactarsTests to Evaluate Immune Function © WBC count and differential © Bone marrow biopsy ‘¢ Humoral and cellular immunity tests Phagocytic cell function test © Complement component tests © Hypersensitivity tests «© Specific antigen-antibody tests © HIV infection tests Immunoglobulins and Allergic Response © Antibodies (IgE, lgD, IgG, IgM, and IgA) react with other cells and molecules, to protect the body © Ig€ antibodies are involved in allergic disorders © IgE molecules bind to an allergen and trigger mast cells or basophils, ‘© These cells then release chemical mediators such as histamine, serotonin, kinins, and neutrophil + chemical substances cause the reactions seen in allergic response Allergic Reactions Allergy “An inappropriate often harmful response of the immune system to normally harmless substances + Hypersenstive reaction to an allergen initiated by Immunological mechanisms which i usually mediated by ig€ antibodies © Allergen: the substance that causes the allergic response ‘© Atopy: refersto the allergic reactions characterized by Igé antibody action and a genetic predisposition Hypersensitivity © A reflection of excessive immune response « Sensitization: initiates the buildup of antibodies © Types of hypersensitivity reactions: + Anaphylactic: Type, eg. asthma, allergic rhinitis + Oytotexic: Type, e.g. myasthenia gravis, Rh Immune complex: Type Il, e.g. SLE, rheumatoid arthritis, + Delayed-type: Type lV, occurs 1-3/7 after exposure to antigen, eg. contact dermatitis,Management of Patients with Allergic Disorders + History and manifestations; comprehensive allergy history + Diagnostic tests = €BC—eosinophil count Total serum IgE ~Skintests Prevention and Treatment of Anaphylaxis ‘# Screen and prevent! ‘© Treat respiratory problems, oxygen, intubation, and cardiopulmonary resuscitation as needed © Epinephrine 1:1,0005Q ‘© Auto injection system: epiPen ‘* May follow with IV epinephrine IV fluids Medication + Oxygen, if respiratory need + Epinephrine used for anaphylactic reactions + Antihistamines (benadryl, zrytec, claratine) + Corticosteroids (prednasone) Other Allergic Disorders + Contact dermatitis + Atopic dermatitis + Drug reactions (dermatitis medicamentosa) + Urticaria + Food allergy + Serum sickness + Latex allergyManagement of Patients With Immunodeficiency Primary Immunodeficiency + Usually seen in infants and young children + Manifestations: vary according to type, severe or recurrent infections, failure to thrive or poor growth, positive family history + Potential complications: recurrent, severe, potentially fatal infections; related blood dyscrasias or malignancies + Treatment: varies by type, treatment of infection, immunoglobulin Rx, stem cell or bone ‘marrow transplant Immunodeficiency Disorders © Primary: genetic + Inborn errars af immune function + May effect phagocytic function, 8 cells and/orT cells, orthe complement system + Eg DiGeorge Syndrome, IpA deficiency, Wiscot Aldrich Syndrome (thrombocytopenia), phagocytic disorders Secondary + Acquired + Related to underlying disorders, diseases, toxic substances, or medications + HIV/AIDS, autoimmune disorders «SLE, Nursing Management + Monitor for signs and symptoms of infections + Monitor lab values + Promote good nutrition + Address anxiety, stress, and coping + Strategies to reduce risk of infection Handwashing and strict aseptic technique ~ Patient protection and hygiene measures: skin care, promote normal bowel and bladder function, pulmonary hygienePatient Teaching HIV/AIDS Infection + Signs and symptoms of infection + Medication + Human immunodeficiency virus is a member + Prevention of infection of the retrovirus family that causes AIDS. — Hand washing — Characterized by long incubation period — Avoid crowds and persons with infections ~ Carries genetic material in form of RNA — Hygiene and cleaning, c atiene and dean + HIV infection is pandemic + Lifestyle modifications to reduce risk + Follow-up care Transmission of HIV High-Risk Behaviors + Transmitted by body fluids containing HIV orinfected CD4 lymphocytes Sharing infected nection eauipment = Blood, seminal fluid, vaginal secretions, * Having sexual relations with infect amniotic fluid, and breast milk individuals Most prenatal infections occur during delivery + Casual contact does not cause transmission + Breaks in skin or mucosa increase riskPrevention Standard Precautions * Standard precautions ‘* Standard precautions infection control practices + Safer sex practices and safer behaviors used to prevent transmission of diseases that can Abstinence be acquired by contact with blood, body fluids, non- — Reduce the number of sexual partners to one intact skin. — Always use latex condoms; if allergicto latex, ‘¢ Hand hygiene use nor-latex condoms «Personal Protective Equipment (PPE) + Donot share drug injection equipment ‘© Respiratory hygiene + Blood screening and treatment of blood ‘Proper disposal of soiled material products ‘Environmental control © Disposal of sharps Physiology Stages of HIV Disease Pathophysiology + Primary infection + HIV asymptomatic + HIV symptomatic + AIDSPrimary Infection + AKA acute HIV infection /acute HIV syndrome + Period from infection to development of HIV antibodies + Symptoms: noneto flu-like syndrome + Period of rapid viral replication and dissemination through the body = CD4+ (500 ~1500 cells/mm") + Viral set point: amount of virus in body HIV Asymptomatic + More than 500 CD4+T lymphpocytes/mm? + Chronic asymptomatic state begins + Body has sufficient immune response to defend against pathogens + Individual is relatively well Acute HiV infection 7 orm aettewy HIV Symptomatic ¢ 200-499 cD4+ lymphpocytes/mm? © CD4T cells gradually fall ‘© The patient develops symptoms or conditions related to the HIV infection © Conditions are classified as category B conditions + Oral candidiasis + Cervical dysplasia + Herpes zoster (shingles) + Fever, diartheax 2/12AIDS + Less than 200 CD4+ lymphocytes/mm? + As levels drop below 100 cell/mm? the immune system is significantly impaired + Development of category C conditions ~ Candidiasis of esophagus, lungs = Cerveal cancer — Kaposi's sarcoma —Peumoneystis pneumonia — Wasting syndrome Clinical Manifestations of HIV/AIDS © Respiratory 4, Pneumacysticcarini pneumonia (PCP): ‘Most common infection + Initial symptoms may be nonspecific and may include nonproductive cough, fever cls, dyspnea, and chest pain + Ifuntreated, progresses to pulmonary impairment and respiratory failure Treatment: pentamidine, TMP-SMZ (bactrim) 2. Mycobacterium avium complex (MAC)- respiratory infection 3. Tuberculosis Diagnostic Tests ‘¢ Enzyme immunoassay (ELISA) ~ test to identify HIV antibodies ‘© Western Blot detects HIV antibodies & confirms EIA «Viral Load— Measures HIV RNA in plasma ‘© CD4 / CDB - monitors the function of immune systems ‘and tracts the progression of the disease + Measures the rata between the CDS on helperT cells ané the C08 on suppressor and cytotoxic cals ‘© Orasure (saliva) © OraQuick Clinical Manifestations © Gastrointestinal 1L Oral candidiasis * iy progres roptages sad stomach 2. Diarrhea related to HIV infection or enteric pathogens 3. Wasting syndromeClinical Manifestations + Kaposi's sarcoma = Cutaneous lesions, but may involve multiple organ systems ~ Lesions cause discomfort, disfigurement, Ulceration, and potential for infection + B-cell lymphomas ‘Treatment + Treatment and protocols are continually veling + mirtroviral agents Nucleoside reverse transriptase inhibitors (NRTI9 Non-nuceoside reverse transcriptase inhibitors (NNATIS) Protease inhibitors (1 = Fusion inhibitors = Use of combination therapy + Management also focuses upon the treatment of spectic manifestations and conditions related tothe dicence Clinical Manifestations ‘¢ Neurologic 1. HIV encephalopathy + Progressive cognitive, behavioral, nd motor dedine 2. Cryptococcus neoformans — fungal infection that can cause meningitis 3. Depression Terminology Anfietovtal Therapy ‘AnfiRetoVitels Highly Active AntiRetroviral Therapy + Triple Therapy = Thee Antzetovzals +The Cocktail”Basic Facts about ARVs Advantages of ARV Therapy + ARVs are divided into 3. * Always.use 3 ormore Scan. Sy “improvedpotent way. + Regimen should be arglable throughclimcal oy erienced HCW. + Reduced How do ARVs control HIV? ‘* ARVs reduce the ability of the HIV vitusto replicate ‘© This increases the functioning of ‘the immune systeme How NNRTIs Work Use of ARVs The ‘Stage’ of HIV depends upon: + Immunological markers (CD4 count) * Clinical symptoms (Opportunistic infections) It also depends on whether the patient is READY to start Bahamas - Adult ARV Therapy HIV infected adults and adolescents should start ARV therapy when they have: + D4 countless than 250/mm? + *Mormat” or not extreme lab values +r 2me/ai Heb <6.5 g/t + ALT >175 1 [alanine aminotransferase)Goals of AVR Therapy — Decline in viral load from pre-treatment levels by 6- 18 weeks after initiating ARVs Undetectable viral load = ultimate goal Basic Facts about Adherence and ARV therapy ‘# ARV blood concentrations must remain constant; low concentrations allow HIV to mutate ‘© HIV mutations cause drug resistance ‘© ARV medications must be taken every day otherwise they will not work ‘# Things that can lower drug concentrations: + Missing 102 ARV medication dases regularly + Taking ARV metication ate + Taking ARVs with certain foods or ether medications ARVs + Require near perfect adherence + HIV resistance + Side effects + Toxicity Determinants to Effective ARV Therapy 1 Patient is not ready? ~ he/she may be non-adherent 1 Patient doesn't understand the drugs? —he/she may take them incorrectly '# Patient doesn’t expect side effects? ~ he/she may be shocked and get put off ARVs or not report any problems ‘© Patient feels alone and unsupported? —he/she may be frightened, reluctant to take drugs arte report any prablemsNurses Role in Monitoring Verbal Reporting: “+ Nurees ae often the frst point af contact “+ Patients often fel more comfortable rising levee wih + Nursing atvties (e.g vital signs) provides opportunity for informal conversation re: problems/ieeues ‘Assessment: patient experiencing any sie effects? How are they feeling? Any problems? Follow up: Referral af concemms te Dactor, Racognsing Urgent referrals; Good communication Side Effects of NRTIs © AZT (Retrovir): anaemia, headache, neutropenia, fatigue ‘© 3TC (Epivir): nausea, diarrhoea, headache fatigue, skin rash, abdominal pai, increase LFTs © daT (Zerit): headache, nausea, vomiting, diarrhoea, rash, increase LFTs, peripheral neuropathy, pancreatitis © dai (Videx): nausea, vomiting, diarrhoea, abdominal pain, peripheral neuropathy, increase LFTs, pancreatitis Blood Samples Correct cinical decisions depend on meaningful ‘lineal laboratory information i Ngee net FSGS ecSBConed whichimay ior Sppropriate clinical decisions This depends on proper specimen collection Common blood tests: ‘cD4 Count. Viral Load Monitoring Labs (FBC, LETS) Resistance Testing Side Effects of NNRTIs + Efavirenz (Efavirenz): rash, sedative effects, headache, nausea, diarrhoea, vivid dreams, insomnia, increase LFTs, hepatitis, + Nevirapine (Viramune): headache, nausea, rash, diarrhoea, increase LFTs, hepatitis, liver failureSevere Side Effects or Adverse Events. + Some side effects may be severe €€ rash, hepatitis lactic acidosis, pancreatitis, hyperlipidaemia, peripheral neuropathy + ARVs may need to be stopped/or changed + Early identification and prompt, appropriate management is essential Our Role. Asnurses, we have avital role to play in ensuring side effects are identified, managed and treated appropriately and effectively Other toxicities. Regular monitoring of blood levels ieeecantialto dantity ARV toxics cacjree Liver function Kidney funetion Appropriate intervention can are imerventi cholesterol cose How do we do this + Educating patients + Prompt recognition and reporting * Understanding ab tests and results + Eepainng nb tess to patients + Therapeutic intervention + Providing support and counselling for patient and family + Ensuring folow up of patients * Educating the general publicCollaborative Problems/Potential Complications + Opportunistic infections + Impaired breathing or respiratory failure + Wasting syndrome + Fluid and electrolyte imbalance + Adverse reaction to medication Opportunistic Infections * Bacterial —Tuberculosis (TB) —Strep pneumonia + Viral —KaposiSarcoma —Herpes — Influenza (flu) * Toxoplasma gondii encephalitis * Cryptosporidium spp. infection Opportunistic Infections © An opportur fection is an infection caused by pathogens, particularly opportunistic pathogens (bacterial, viral, fungal or protozoan) ‘that usually do not cause disease in a healthy host @Parasi “Pneumocystis carinii Fungal ‘Candida + Cryptococcus Aims & Collaborative Goals + Monitoring of disease progression + Prevent opportunistic infection + Monitoring antiretrovital treatment + Management of signs and symptoms + Prevent complications of treatmentsNursing Management: Assessment ‘© Assess physical and psychosocial status Identify potential risk factors: IV drug abuse, risky sexual practices ‘¢ Immune system function © Nutritional status ‘© Skin integrity ‘© Respiratory & neurologic status ‘Fluid and electrolyte balance ¢ Knowledge level Promoting Usual Bowel Pattern ‘* Assess bowel pattern and factors that may exacerbate diarrhea ‘© avoid foods that act as bowel irritants, such as raw fruits and vegetables, carbonated beverages, spicy foods, and foods of extreme temperatures ‘© Small, frequent meals ‘© Administer medications as prescribed ‘© Assess and promote self-care strategies to control diarthea skin Integrity + Frequent routine assessment of skin and + Reposition at least every 2hours and as needed + Pressure reduction devices + Instruct patient to avoid scratching + Use gentle, nondrying soaps or cleansers + avoid adhesive tape + Perianal skin care Activity Intolerance + Maintain balance between activity and rest + Instruction regarding energy conservation techniques + Relaxation measures + Strengthening musclesMaintaining Thought Processes ‘© Assess mental and neurologic status ‘© Use clear, simple lan guage if mental status is altered ‘© Establish and maintain a daily routine * Orientation techniques ‘© Ensure patient safety and protect from injury ‘© Instruct and involve family in communication and care Decreasing Isolation ‘© Promote an atmosphere of acceptance and understanding ‘© Assess social interactions and monitor behaviors ‘© Allow patient to express feelings ‘© Address psychosocial issues « Provide information related to the spread of infection © Educate ancillary personnel, family, and partners Nutrition ‘© Monitor weight, 1&0, dietary intake, and factors that interfere with nutrition © Dietary consult © Control of nausea with antiemetics © Oral hygiene © Treatment of oral discomfort « Dietary supplements © May require enteral feedings or parenteral nutrition Other Interventions + Improving airway clearance — Postion in semi-Fowler’s or high Fowler's — Pulmonary therapy; coughing and deep breathing, postural drainage, percussion, and vibration — Ensure adequate rest + Pain — Medications as prescribed — Skin and perianal carePrevention of Infection + Hand Hygiene — Proper washing of hands + Reverse barrier nursing for patients who's decrease WBC (neutropenia) — Proper use of protective barriers + Monitor blood investigations (WBC) for early intervention, report abnormal readings + Monitoring of v/s Prevention of Infection + Ensure pts. environment is kept clean to prevent transfer of organisms + Educate pt. on importance of hand washing, clean environment to prevent transmission of organisms + Ensuring pt. receives a nutritionally balanced diet for maintenance of immune system + Administration of anti infectives if prescribed Prevention of Infection + Minimize visitors with infections because of pts. Immuné response + Use strict asepsis for all invasive procedures Objectives + By the end of this session you should be able to: Define the term SLE + Identify the etiology of SLE + Explain the pathiphysiology of SLE; + Discuss the signs and symptoms of SLE; and + Discuss the medical and nusring management of SLE.Systemic Lupus Erythematosus (SLE) Incidence * Chronic multisystem inflammatory + SLE affects 2to 8 persons per 100,000 in isease United states — Occurs more frequently in women > Gears more eaverny inom + Most cases occur in women of childbearing years * Associated with abnormalities of immune + Peak incidence occurs between 15 — 40yrs. a + Female to male ratio of 9:1 + Results from interactions among genetic, hormonal environmental and + African, Asian, Hispanic and Native Americans Hanae a three times more likely to develop than whites Etiology SLE: Pathophysiology + Etiology is unknown + There is a disturbed immune regulation that + Most probable causes causes an over production of autoantibodies ~ Genetic influence + This disturbance is caused by a combination of — Hormones factors: ~ Erwironmental factors (ultra violet light) ~ Genetic ~ Certain medications — Hormonal + Hydralazine, procainanmide * Quinine, methyldop isnized, phenytoin — Environmental — MedicationPathophysiology contd. + Abnormal suppressor T cell function ‘causes the increase in autoantibody production + The autoantibodies combine with antigens to form immune complexes + Theimmune complexes are deposited in vascular and tissue surfaces which triggers an inflammatory response + Theinflammatory process leads to tissue damage Clinical Manifestations Clinical Manifestations + Onset may be acute (sudden) or insidious (gradual) + Ranges from a relatively mild disorder to rapidly progressing + Can affect any body system + Most commonly affects the skin/muscles, lining of lungs, heart, nervous tissue, and kidneys + Characterized by exacerbations and remission Clinical Manifestations + Dermatologic — Cutaneous vascular lesions = Discoid LE (chronic rash) = Buttery rash = Oral/nasopharyngeal ulcers — AlopeciaClinical Manifestations + Musculoskeletal = Polyarthralgia with morning stiffness = Arthritis + Swan nackingers + nar deviation * Subluxation with hypertaty of joins A | hy be Clinical Manifestations + Nervous system = Generalized/focal seizures = Peripheral neuropathy = Cognitive dysfunction + Disorientation Memory deficits + Paychiatrie symptoms Clinical Manifestations + Renal — Lupus nephritis “+ Ranging om milé proteinuria to glomeruonephritis + Primary goa in reatment i slowing the progression + Serum creatinine and urinanalysis is done to screen for renal involvement Diagnostic Studies + No specifictest + SLE is diagnosed primarily on criteria relating to patient history, physical examination, and laboratory findingsDiagnostic Tests Collaborative Care + CBC for hematologic problems + Goa + UA for lupus nephritis, — Early diagnosis, + yerays of affected joints ~ Preventing loss of organ fucrtions + Chest xray for pulmonary problems Tne see reed debs + ECG for cardiac problems + Antinuclear antibody test (ANA) SLE: Drug therapy SLE: Drug therapy cont. + NSAIDs + Corticosteroids (prednisone) — Reduce inflammation — Used to stabilize cellsreducing the inflammatory + Antimalarial drugs process — Controls disease by decreasing bodies Block chemical pathways & decrease # of production of antigens circulating lymphocytes + Immunosuppressive and Steroi¢-sparing drugsNursing Management Nursing Management Nursing Diagnoses Planning + Fatigue + Overall goals + Acute pain — Have satisfactory pain relief + Impaired skin integrity — Comply with therapeutic regimen to achieve ‘maximum symptom management — Demonstrate awareness of, and avoid activities ‘that cause disease exacerbation (triggers) — Maintain optimal role function and a positive sei + Ineffective therapeutic regimen management + Body image disturbance image Nursing Management Nursing Management Nursing Implementation Nursing Implementation + Acute intervention + Acute intervention (cont’d) ~ During exacerbation, patient will become — Observe for ‘abruptly, dramatically ill + Fever pattern: — Record severity of symptoms and response to * oi infammation therapy + Unison of tion + Location and degree of discomfort, + FatgabltyNursing Management Nursing Implementation + Acute intervention (cont'd) = Monitor weight and 18.0 ~ Collect 24-hour urine sample — Assess neurological status — Explain nature of disease — Provide support Nursing Management Renee cone tc op, ait § erence sures es he tera or ata) $ Rtancs o exponen atom 5 Grettzuncen ruc aest 1) na prc Nursing Management Nursing Implementation + Ambulatory and home care (Discharge) — Reiterate that adherence to treatment does not necessarily halt progression — Minimize exposure to precipitating factors— fatigue, sun, stress, infection, drugs — Teach energy conservation and relaxation — For joint problems, allthe teaching for RA related to joint protection, ROM, and positioning to prevent contractures Nursing Management + Lupus and pregnancy ~ Infertility can resut from SLE treatment regimen ~ SLE is associated with complications of pregnancy — Pregnancy & post partum can cause exacerbations ofSle — Women with serious SLE should be counseled against pregnancyNursing Management + Psychosocial issues — Counsel patient and family that SLE has good prognosis — Physical effects can lead to isolation, self-esteem, and body image disturbances — Assist patient in developing goals Nursing Management Evaluation + Expected outcomes (cont'd) + Expression of satisfaction with activity level + Pacing of activities to match level of tolerance + Expression of confidence in ability to manage SLE over time and in home environment Nursing Management Evaluation * Expected outcomes + Performance of activities of daily living without pain + Limitation of direct exposure to sun and use of sunscreen + No open skin lesions