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Nursing Management of Clients with Stressors of Immune Function

Nursing Management of Clients with Stressors of Immune Function. NUR133 Lecture # 7 K. Burger, MSEd, MSN, RN, CNE. Immune Response. FUNCTIONS Defense against invading pathogens Removal of “worn-out” cells Immune surveillance. Immune Response. COMPONENTS LEUKOCYTES Neutrophils

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Nursing Management of Clients with Stressors of Immune Function

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  1. Nursing Management of Clients withStressors of Immune Function NUR133 Lecture # 7 K. Burger, MSEd, MSN, RN, CNE

  2. Immune Response FUNCTIONS • Defense against invading pathogens • Removal of “worn-out” cells • Immune surveillance

  3. Immune Response COMPONENTS LEUKOCYTES • Neutrophils • Eosinophils • Basophils • Lymphocytes: B-lymphocytes/ T-lymphocytes • Monocytes

  4. Immune Response COMPONENTS OTHER • Bone marrow / stem cells • Lymph nodes • Spleen • Thymus • Tonsils/adenoids • Appendix • GALT

  5. Innate Non-specific First line of defense Immediate Inflammatory process Adaptive Specific Sustained Antibody mediated or Cell mediated Immune Response

  6. Antibody Mediated B-Lymphocytes react to extracellular antigens Sensitization occurs Division into Plasma and Memory Cell Antibody response Immediate and Long-term Cell Mediated T-Lymphocytes react to intracellular antigens Sensitization occurs Proliferation of T-cell subsets: Cytotoxic Helper Suppressor Adaptive Immune SystemAcquired Immunity

  7. Classifications ofAdaptive Immunity • Adaptive immunity • Natural active – most effective/ longest lasting • Artificial active – vaccination / immunization • Natural passive – maternal/fetus transmission • Artificial passive – injection of antibodies

  8. Immune Function Excess Auto-immune Disease • Failure of body to recognize it’s own HLA • Antibody production against self • SLE, Rheumatoid arthritis, Scleroderma +++ Hypersensitivity / Allergic Response • Excessive response to an antigen • Type I – Type V

  9. Hypersensitivity / Allergic Response • Type I Immediate: atopic reaction rhinitis/ anaphylaxis • Type II Cytotoxic: transfusion reaction • Type III Mediated: Immune complex Rheumatoid arthritis • Type IV Delayed: Poison ivy, PPD • Type V Stimulated: Graves disease

  10. Type I Immediate Hypersensitivity • Triggered by allergens: • Pollen, mold, dust, certain foods or meds etc. • B cells synthesize IgE antibodies to allergen • IgE antibodies attach to mast cells/basophils • Result = retained sensitivity • Localized and/or systemic (anaphylactic)

  11. HypersensitivityAssessment • History: family hx, exposures, symptoms • Physical: headache, rhinorrhea, tearing eyes • Labs: elevated eosinophils elevated ESR • Skin testing: scratch / intradermal • Food challenge

  12. HypersensitivityNursing Diagnoses • Ineffective health maintenance r/t deficient knowledge regarding allergies • Latex allergy r/t hypersensitivity to natural rubber latex • Risk for latex allergy r/t repeated exposure to products containing latex

  13. HypersensitivityInterventions • Avoidance therapy • Desensitization therapy • Drug therapy • Decongestants • Antihistamines • Corticosteroids • Mast Cell Stabilizers • Leukotriene Antagonists

  14. Anaphylaxis Emergency Interventions • Establish and maintain open airway • O2 @ high flow ( 4-6 L/min) • Establish IV access with NS or RL • Epinephrine 1:1000 0.3 – 0.5 ml sc • Benadryl 25-100 mg IV • Suction prn • Elevate HOB ( unless severe hypotension) • Theophylline, Beta agonists, Corticosteroidsto stabilize

  15. Immunodeficiency • Absence or inadequate production of immune bodies • Primary ( congenital ) • Secondary ( acquired) • Induced ( related to external stressors )

  16. Acquired ImmunodeficiencyAIDS Pathophysiology • HIV virus docks with CD4 (helper T-cells) • Enters CD4 cell’s DNA • Creates more virus • Virus buds off original host CD4 to attack more cells • CD4 cell no longer working as immune cell

  17. Acquired ImmunodeficiencyAIDS • Classifications • A – HIV positive • B - Infected with HIV • C – AIDs • Progression • Months – Years • Dependent on: • Means of acquisition • Personal factors

  18. Acquired ImmunodeficiencyHIV / AIDSAssessment • History • Physical exam • Testing • ELISA • Western Blot • Viral load • CBC with differential • CD4 / CD8 count

  19. Additional ResourceTesting Guidelines • NYS DEPARTMENT OF HEALTH HIV / AIDS Web Resource http://www.health.state.ny.us/diseases/aids/index.htm

  20. Stages of HIV Infection • Stage I: 3wks-3mos prior to seroconversion. Mild illness S/S or asymptomatic • Stage II: 1-10 yrs after seroconversion Low rate of replication CD4 normal • Stage III: Persistent lymphadenopathy • Stage IV: Rapid replication of HIV virus Multiple opportunistic infections Very low CD4 counts • Stage V: “Full Blown AIDS” CD4 very low

  21. HIV / AIDS Clinical Manifestations • Opportunistic Infections • Protozoal - Pneumocystis carinii (PCP) • Fungal - Candida albicans • Bacterial - Mycobacterium avium (MAC) Mycobacterium tuberculosis • Viral - Cytomegalovirus (CMV) Herpes simplex (HSV) • Malignancies • Kaposi’s Sarcoma

  22. HIV / AIDsClinical Manifestations (cont) • Endocrine complications • Aids Dementia Complex • Wasting Syndrome • Skin Changes

  23. HIV / AIDSNursing Diagnoses • Risk for infection • Impaired skin integrity • Diarrhea • Imbalanced nutrition • Acute/ Chronic pain • Impaired gas exchange • Disturbed thought processes • Social isolation

  24. AIDS/ HIV Interventions • Prevention and early detection of infection • Maintenance of adequate respiratory function • Pain management • Maintenance of skin integrity • Promotion of nutrition and IBW maintenance • Maintenance of self-esteem • Maintenance of orientation

  25. AIDS / HIV InterventionsDrug Therapy • Anti-retroviral agents in “cocktail” HAART ( Highly active anti-retroviral therapy) • Nucleoside Reverse Transcriptase Inhibitors: Retrovir AZT • Non-nucleoside RTI: Viramune • Protease Inhibitors : Invirase • Fusion Inhibitors: Fuzeon • Immune enhancers: BRMs • Antibiotics: Bactrim, Pentam, Flagyl • Antituberculars: INH

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