Nursing Management of Clients with Stressors of Immune Function
Download
Report
Transcript 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
Eosinophils
Basophils
Lymphocytes: B-lymphocytes/ T-lymphocytes
Monocytes
Immune Response
COMPONENTS
OTHER
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 System
Acquired 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 of
Adaptive 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
Type II
Type III
Type IV
Type V
Immediate: atopic reaction
rhinitis/ anaphylaxis
Cytotoxic: transfusion reaction
Mediated: Immune complex
Rheumatoid arthritis
Delayed: Poison ivy, PPD
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)
Hypersensitivity
Assessment
History: family hx, exposures, symptoms
Physical: headache, rhinorrhea, tearing eyes
Labs: elevated eosinophils
elevated ESR
Skin testing: scratch / intradermal
Food challenge
Hypersensitivity
Nursing 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
Hypersensitivity
Interventions
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 Immunodeficiency
AIDS
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 Immunodeficiency
AIDS
Classifications
A – HIV positive
B - Infected with HIV
C – AIDs
Progression
Months – Years
Dependent on:
Means of acquisition
Personal factors
Acquired Immunodeficiency
HIV / AIDS
Assessment
History
Physical exam
Testing
ELISA
Western Blot
Viral load
CBC with differential
CD4 / CD8 count
Additional Resource
Testing 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 / AIDs
Clinical Manifestations (cont)
Endocrine complications
Aids Dementia Complex
Wasting Syndrome
Skin Changes
HIV / AIDS
Nursing 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 Interventions
Drug 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