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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 Eosinophils Basophils Lymphocytes: B-lymphocytes/ T-lymphocytes Monocytes
Immune Response
COMPONENTSOTHER
Bone marrow / stem cells Lymph nodes Spleen Thymus Tonsils/adenoids Appendix GALT
Immune Response
Innate
Non-specific First line of defense Immediate Inflammatory
process
Adaptive
Specific Sustained Antibody mediated
or Cell mediated
Adaptive Immune SystemAcquired Immunity
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
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
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
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
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)
HypersensitivityAssessment
History: family hx, exposures, symptoms Physical: headache, rhinorrhea, tearing eyes Labs: elevated eosinophils
elevated ESR Skin testing: scratch / intradermal Food challenge
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
HypersensitivityInterventions
Avoidance therapy Desensitization therapy Drug therapy
Decongestants Antihistamines Corticosteroids Mast Cell Stabilizers Leukotriene Antagonists
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, Corticosteroids
to stabilize
Immunodeficiency
Absence or inadequate production of immune bodies
Primary ( congenital ) Secondary ( acquired) Induced ( related to external stressors )
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
Acquired ImmunodeficiencyAIDS
Classifications A – HIV positive B - Infected with HIV C – AIDs
Progression Months – Years Dependent on:
Means of acquisition Personal factors
Acquired ImmunodeficiencyHIV / AIDS
Assessment
History Physical exam Testing
ELISA Western Blot Viral load CBC with differential CD4 / CD8 count
Additional ResourceTesting Guidelines
NYS DEPARTMENT OF HEALTH
HIV / AIDS Web Resource
http://www.health.state.ny.us/diseases/aids/index.htm
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
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
HIV / AIDsClinical Manifestations (cont)
Endocrine complications Aids Dementia Complex Wasting Syndrome Skin Changes
HIV / AIDSNursing Diagnoses
Risk for infection Impaired skin integrity Diarrhea Imbalanced nutrition Acute/ Chronic pain Impaired gas exchange Disturbed thought processes Social isolation
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
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