Nursing Management of Clients with Stressors of Immune Function NUR133 Lecture # 7 K. Burger, MSEd,...

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