Nursing Management of Clients with Stressors of Immune Function

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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
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Immune Response
COMPONENTS
OTHER
 Bone marrow / stem cells
 Lymph nodes
 Spleen
 Thymus
 Tonsils/adenoids
 Appendix
 GALT
Immune Response
Innate
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Non-specific
First line of defense
Immediate
Inflammatory
process
Adaptive
Specific
 Sustained
 Antibody mediated
or
 Cell mediated
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Adaptive Immune System
Acquired Immunity
Antibody Mediated
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B-Lymphocytes react to
extracellular antigens
Sensitization occurs
Division into Plasma
and Memory Cell
Antibody response
Immediate
and
Long-term
Cell Mediated
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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
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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
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Type I
Type II
 Type III
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Type IV
 Type V
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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)
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Hypersensitivity
Assessment
History: family hx, exposures, symptoms
 Physical: headache, rhinorrhea, tearing eyes
 Labs: elevated eosinophils
elevated ESR
 Skin testing: scratch / intradermal
 Food challenge
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Hypersensitivity
Nursing Diagnoses

Ineffective health maintenance r/t deficient
knowledge regarding allergies
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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
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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
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Immunodeficiency

Absence or inadequate production of
immune bodies
Primary ( congenital )
 Secondary ( acquired)
 Induced ( related to external stressors )
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Acquired Immunodeficiency
AIDS
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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
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Classifications
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A – HIV positive
B - Infected with HIV
C – AIDs
Progression
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Months – Years
Dependent on:
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Means of acquisition
Personal factors
Acquired Immunodeficiency
HIV / AIDS
Assessment
History
 Physical exam
 Testing
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ELISA
 Western Blot
 Viral load
 CBC with differential
 CD4 / CD8 count
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Additional Resource
Testing Guidelines
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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
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HIV / AIDS
Clinical Manifestations
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Opportunistic Infections
Protozoal - Pneumocystis carinii (PCP)
 Fungal Candida albicans
 Bacterial - Mycobacterium avium (MAC)
Mycobacterium tuberculosis
 Viral Cytomegalovirus (CMV)
Herpes simplex (HSV)
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Malignancies
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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)
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Nucleoside Reverse Transcriptase Inhibitors:
Retrovir AZT
 Non-nucleoside RTI: Viramune
 Protease Inhibitors : Invirase
 Fusion Inhibitors: Fuzeon
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Immune enhancers: BRMs
 Antibiotics: Bactrim, Pentam, Flagyl
 Antituberculars: INH
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