NURSING CARE OF CLIENTS WITH IMMUNOLOGIC DISORDERS

IMMUNE SYSTEM IMMUNITY-the body’s specific protective

response to an invading foreign agent or
 The Immune system is composed of an
organism
integrated collection of various cell types,
each with designated functional role in 2 types of Immunity
defending against infection and invasion by
other microorganism 1. Natural (Innate)-a non-specific immunity
that is present with birth
 Major components of the Immune system: i. -cells involved in this response
(macrophages, dendritic ells,
1. Bone marrow
natural killer (NK) cells
2. WBC’s- produced by the bone
2. Acquired (Adaptive)-specific immunity that
marrow
3. Lymphoid tissues including the develops after birth
thymus gland, spleen, lymph nodes,
tonsils & adenoids, similar tissues in  Inflammatory response is the major
the GIT (Appendix), respiratory and function of the natural immune system. It is
reproductive systems facilitated by physical and chemical barriers
that are part of the human organism
 Physical surface barrier- intact skin, mucous
Bone marrow membranes & cilia of the respiratory tract
 WBC’s are produced in the bone marrow  Chemical barrier-mucus, acidic gastric
 lymphocytes are generated from stem cells secretions, enzyme in tears and saliva, and
(are undifferentiated cells that are able to substances in sebaceous and sweat
repair and replace damaged tissues and secretions
organ)
 descendants of stem cells became
lymphocytes Acquired Immune response
o B-lymphocytes (10-20%) mature in
2 mechanisms
the bone marrow and enters to
circulation 1. the cell-mediated response, involving T-cell
o T-lymphocytes (60-70%) move from activation
the bone marrow to the thymus, 2. effector mechanism, involving B-cell
where they mature into several maturation and production of antibodies
kinds of cells with different
*2 types of acquired immunity
functions
1. active-acquired immunity=the immunologic
defense are developed by the person’s own
Lymphoid tissues body; typically last many years or even a
lifetime
 Spleen-composed of red & white pulps; acts 2. Passive-acquired immunity=temporary
like a filter immunity transmitted from a source outside
 Red pulp is the site where old and injured the body that has developed.
RBC’s are destroyed
 White pulp contains concentrations of Example: immunity from previous disease
lymphocytes or immunization
 Lymph nodes are distributed throughout *Both types of acquired immunity involve
the body humoral and cellular immunologic response
o connected by lymph channels &
capillaries which remove foreign
material from the lymph system before Response to invasion
it enters the blood stream
o also serve as centers for immune cell  The phagocytic immune response
proliferation  The humoral or antibody immune
response
 The cellular immune response
 NURSING CARE OF CLIENTS WITH IMMUNOLOGIC DISORDERS

PHAGOCYTIC IMMUNE RESPONSE 2. IgD= 0.2%

 1st line of defense  appears in small amount in
 involves the WBC (granulocytes and serum
macrophages) which have the ability to  possibly influences B-
ingest foreign particles lymphocytes differentiation
 phagocytes also remove the body’s own  acts as an antigen receptor of B-
dying or dead cells cells
 necrotic cells release substances that trigger
an inflammatory response 3. IgE= 0.04%
 Apoptosis-programmed cell death
 causes an allergic response
 appears in serum
 takes part in allergic &
HUMORAL IMMUNE RESPONSE hypersensitivity reaction
 combats parasitic infection
 2nd protective response
 Sometimes called Antibody response
 Begins with the B-lymphocytes which can 4. IgG =75%
transform into plasma cells that  appears in serum & tissues
manufacture antibodies (interstitial fluid)
 These antibodies are specific proteins that  assumes a major role in blood-
are transported in the blood stream to borne and tissue infection
disable invaders  activates the complement
system
 enhances phagocytosis
 crosses the placenta
CELLULAR IMMUNE RESPONSE
 3rd mechanism of defense 5. IgM =10%
 also involves the T-lymphocytes which can  appears in intravascular serum
turn into special cytotoxic ( or Killer) T-cells  act as the 1st immunoglobulin
that can attack the pathogens produced in response to
bacterial and viral infection
 activates the complement
ANTIBODIES-are large proteins called system
IMMUNOGLOBULINS
 Called immunoglobulins because they are CELLULAR IMMUNE RESPONSE
found in the globulin fraction of the plasma
proteins  The B-lymphocytes are responsible for
humoral immunity and the T-lymphocytes
 5 different types of immunoglobulins are primarily responsible for cellular
immunity
1. IgA= 15% of total  Complement system-circulating plasma
immunoglobulins proteins made in the liver and activated
 appears in body fluids (blood, when an antibody connects with its antigen
saliva, tears, breast milk,
pulmonary, GI, prostatic and vaginal 3 major functions
secretions) 1. defending the body against bacterial infection
 protects against respiratory, GI, GU
infections 2. bridging natural & acquired immunity
 prevents absorption of antigens 3. disposing of immune complexes and the by-
from food products associated with inflammation
 passes to neonate in breast milk for
protection
 NURSING CARE OF CLIENTS WITH IMMUNOLOGIC DISORDERS

 Increase amount of circulating complexes

Immunologic Disorders (Ig-AG) and the presence of vasoactive
amines will lead to increased vascular
Hypersensitivity reaction permeability therefore tissue damage
 The joints & the kidneys are susceptible to
HYPERSENSITIVITY-an allergic reaction
this injury
provoked by re-exposure to a specific type of
 Associated with SLE, rheumatoid arthritis,
antigen referred as allergen
nephritis, bacterial endocarditis, serum
sickness, intradermal injection and post-
4 types of hypersensitivity reaction
streptococcal glomerulonephritis
1. Type I Anaphylactic hypersensitivity
4. TYPE IV DELAYED TYPE HYPERSENSITIVITY
 most severe form
 AKA Cellular hypersensitivity
 Anaphylaxis is the most severe immune-
 Occurs 24-72 hours after exposure to an
mediated reaction
allergen
 an immediate reaction beginning within
 Mediated by sensitized T cells &
minutes of exposure to an antigen;
macrophages
mediated by IgE antibodies
 ID injection of tuberculin or PPD
 the primary chemical mediators are
 Sensitized cells react with the antigen near
responsible for the S/S of Type I HPS
or at the site of injection.
(because of their effect on lungs, skin &
 Lymphokines are released and attract,
GIT)
activate and retain macrophages at the
 S/S edema in many tissues including the
site.
larynx, accompanied by hypotension,
 These macrophages release lysozymes
bronchospasm, CV collapse in severe
causing tissue damage. Edema and fibrin
cases
are responsible for the (
 Example contact dermatitis, type 1 DM,
2. Type II Cytotoxic Hypersensitivity
graft, multiple sclerosis, poison ivy
 the result of a cross-reacting antibody
involves the binding of either IgG or IgM
antibody to the cell-bound antigen
 the result of an antigen-antibody IMMUNOLOGIC DISORDERS
binding is activation of the complement
cascade & MULTIPLE SCLEROSIS
 destruction of the cell to which the a chronic disability in young adults resulting
antigen is bound.
from progressive demyelination of the brain
 associated with several disorders:
and spinal cord
o Myasthenia gravis-the body
mistakenly generates  Characterized by remissions and
antibodies against normal nerve exacerbations
ending receptors  Prognosis varies
o Goodpasture syndrome-it
 Causes: Unknown
generates antibodies against
-may be caused by an autoimmune
lung & renal tissue, producing
response to a slow-acting or latent viral
lung damage & renal failure
o associated with RBC destruction infection or by environment or genetic
such as Hemolytic disease of factors
the newborn, drug-induced Pathophysiology:
immune hemolytic anemia,
incompatibility reactions in BT  axon demyelination and nerve fiber loss
o Rheumatic fever occur in patches throughout the CNS
o Erythroblastosis fetalis including widely disseminated & varied
neurologic dysfunction
3. TYPE III IMMUNE COMPLEX
HYPERSENSITIVITY Signs and symptoms:
 Involves immune complexes that are
 vision disturbance as optic neuritis,
formed when antigens bind to antibodies
diplopia, ophthalmoplegia & blurred vision
(antibody-mediated)
 These complexes are cleared from the  sensory impairment-paresthesia
circulation by phagocytic action. If these  muscle dysfunction-weakness, paralysis
complexes are deposited in tissues or ranging from monoplegia to quadriplegia,
vascular endothelium, it contributes to spasticity, hyperreflexia, intention tremor &
injury gait ataxia
 NURSING CARE OF CLIENTS WITH IMMUNOLOGIC DISORDERS

 urinary disturbances-incontinence,  meticulous skin care to prevent pressure

frequency, urgency, and frequent infections ulcers
 emotional lability-mood swings, irritability,  bowel and bladder training (prn)
euphoria  antibiotic treatment of bladder infection
 associated signs- poorly articulated speech  counselling
& dysphagia

Diagnostics: GUILLAIN-BARRE SYNDROME

 some may undergo periodic testing & close  An acute rapidly progressive and potentially
observation because of the difficulty in fatal form of polyneuritis
diagnosing MS  A rare neurologic disorder in which the
 in 1/3 of patients, EEG shows non-specific immune system attacks healthy nerve cells
abnormalities in the peripheral nervous system
 lumbar puncture reveals CSF with increased  This leads to weakness, numbness, and
gamma globulin fraction of IgG but normal tingling and can eventually cause paralysis.
TCHON levels  CAUSE: unknown
 electrophoresis in CSF gamma globulin, -cell-mediated immunologic attack on
oligoclonal bands of Ig can be detected peripheral nerves in response to a virus
 CT scans-reveal lesions within the brain’s *PRECIPITATING FACTORS: mild febrile or viral
white matter illness, surgery, rabies or swine influenza
 MRI used to evaluate disease progression vaccination, Hodgkin’s disease or some other
since this is the most sensitive method of cancers, SLE
detecting lesions

RX: to shorten exacerbation to relieve GBS PATHOPHYSIOLOGY

neurologic deficits to help patient maintain as
This syndrome causes inflammation and
normal a lifestyle as possible
degenerative changes in the posterior (sensory)
and anterior (motor) nerve roots

Drug therapy:
S/S:
 Methylprednisolone=to reduce CNS
inflammation  Symmetrical muscle weakness, in the legs
 Dexamethasone, Prednisone, first (ascending type) & then extending to
Betamethasone & Prednisolone for acute the arms & facial nerves within 24-72 hours
exacerbations  Facial diplegia with ophthalmoplegia (ocular
 Glatiramer acetate=to reduce the frequency paralysis)
of attacks; for relapsing MS  Dysphagia, Dysarthria (slurred speech)
 Interferon beta 1a or Interferon beta 1b in  Hypotonia, Areflexia
reducing disability progression & in DIAGNOSTICS
decreasing the frequency of exacerbations
 Protein levels in CSF-increased, several days
after onset of S/S, and peak in 4-6 weeks
 WBC in CSF-normal
Multiple Sclerosis
 CBC-leukocytosis in immature forms
In conjunction with corticosteroids:  Electromyography –shows repeated firing of
the same motor unit instead of widespread
 Fluoxetine to combat depression
 Baclofen or Dantrolene to relieve sectional stimulation
spasticity TREATMENT:
 Oxybutynin to relieve urine retention &
minimize frequency & urgency  needs hospitalization
 monitor respiratory status regularly
(because of the ascending pathology of the
Management during acute exacerbations
disease; may cause respiratory failure
 bed rest  mechanical ventilation
 physical therapy & massages  plasmapheresis-which temporarily reduced
 measures to prevent fatigue circulating antibodies
 high dose immune globulins and steroids
 NURSING CARE OF CLIENTS WITH IMMUNOLOGIC DISORDERS

MANAGEMENT: RA DIAGNOSTICS

 Watch for ascending motor loss (sensation  X-ray=bone demineralization and soft tissue
is not loss) swelling
 Monitor VS and LOC  (+) RF test occurs in 75%-80%
 Assess respiratory function, watch for  Synovial fluid analysis usually shows
increased PaCO2 such as confusion and increased volume and turbidity but
tachypnea decreased viscosity and complement
 Auscultate breath sounds  Serum globulins are increased
 Turn to sides  ESR also increased
 Encourage coughing & deep breathing  CBC=moderate anemia and slight
 Emergency airway leukocytosis
 Meticulous skin care
 Passive ROM exercises (use Hubbard tank to
Treatment:
prevent contracture)
 Evaluate gag reflex; administer NGT  Salicylates-ASA
 Prevent hypotension with slow position  NSAIDs=Indomethacin, Ketorolac, Ibuprofen
changes  Anti-malarials=Chloroquine,
 I & O q8h (urine retention) Hydroxychloroquine
 Relieve constipation  Gold sodium thiomalate= anti-rheumatic
 Refer to PT and antineoplastic
 Penicillamine
 Corticosteroids
RHEUMATOID ARTHRITIS  Immunosuppressives= Methotrexate,
Cyclophosphamide, Azathiopine
 A chronic systemic inflammatory disease
SUPPORTIVE MEASURES
that primarily attacks peripheral joints, and
surrounding muscles, tendons, ligaments & -8-10 hours of sleep, adequate nutrition,
blood vessels frequent rest periods, splinting to rest inflamed
 Potentially crippling, requires life-long joints, ROM exercises, heat application (relaxes
treatment muscles & relieves pain) via moist heat (hot
 Prognosis worsens with development of soaks, paraffin baths & whirlpool), ice packs
nodules, vasculitis & increase titers of during acute episodes
Rheumatoid factor
 Causes: unknown (autoimmune basis)
 Pathophysiology: Surgery:
o Cartilage damage resulting from
inflammation triggers further  Synovectomy
immune response, including  Joint reconstruction or total joint
complement activation arthroplasty
o Complements attracts  Monitor the duration not the intensity of
polymorphonuclear leukocytes and morning stiffness (because duration reflects
stimulates the release of the severity of the disease), encourage hot
inflammatory mediators which baths at HS or in the morning to reduce the
exacerbates joint destruction need for pain medication
 Weight reduction coz obesity adds stress to
the joints
Signs and symptoms:

 fatigue, malaise, anorexia The Patient with a Tissue Transplant

 persistent low grade fever
 weight loss 2 types of transplantation
 lymphadenopathy
 Transplantation of avascular tissues-
 vague articular symptoms
routine with little need for tissue matching,
 joint pain, tenderness, warmth, swelling
immunosuppression
occur bilaterally and symmetrically
 Transplantation of organs-increasingly
 morning stiffness
common; success is tied to obtaining an
 paresthesia in the hands and feet
organ with tissue antigens as close to those
 stiff, weak or painful muscles
of recipient as possible
 NURSING CARE OF CLIENTS WITH IMMUNOLOGIC DISORDERS

HLA type Human Leukocyte antigen MEDICATIONS: Maintenance therapy

 a kind of genetic test used to identify  Antilymphocyte therapy & use of

certain individual variations in a person’s monoclonal antibodies
immune system  Immunosuppressive agents
o aka HLA typing  Azathioprine (Imuran)
o HLA  Muromonab-CD3 OKT3
 HLA matching  Polyclonal antilymphocyte antibodies
 to know how closely the transplant
recipient matches their donor
SYSTEMIC LUPUS
Types of HLA ERYTHEMATOSUS (SLE)
 HLA-A 59 HLA-A CHONs  An autoimmune disease in which the body’s
 HLA-B 118 immune system mistakenly attacks healthy
 HLA-DR 124 tissue
 A (+) HLA test means HLA-B 27 is present,  A chronic inflammatory disorder of the
suggesting a greater risk for developing connective tissue
certain auto-immune disorders  Affects multi-organ system as well as skin;
fatal
 More common in women than men
 AUTOGRAFT –transplant of patient’s own especially during child-bearing years
tissue  Occurs worldwide; most prevalent among
 ALLOGRAFT – between members of the Asians and Blacks (Africans, Caribbean,
same species that have different genotypes Chinese
and HLA  Onset: 15-45 y/o
- may come from living donors,  Prognosis: 15 years survival
cadavers, those who meet criteria
for brain death 4 kinds of LUPUS:
* XENOGRAFT- from animal to human  Systemic Lupus Erythematosus (SLE) most
common form
 Cutaneous lupus- a form of lupus that is
Histocompatibility: ability of cells & tissues to limited to the skin
survive transplantation without immunologic  Drug-induced lupus- a lupus-like disease
caused by certain medications
 Interference by recipient
 Neonatal lupus-a rare condition that affects
 determined by tissue typing
infants of women who have lupus; most
*TYPES OF REJECTION: commonly presenting with a rash
resembling discoid lupus erythema with
1. Hyperacute tissue rejection=2-3 days after
systemic abnormality as heart block,
transplant
hepatomegaly and splenomegaly; usually
2. Acute tissue rejection=most common,
benign and self-limited
treatable
 SLE associated with Anti-phospholipid
3. Chronic tissue rejection=4 months to a year
antibody syndrome (thrombotic disease)
after transplant
wherein autoantibodies to phospholipids
4. Graft-virus-host disease GVHD=potentially
are present in the serum; ie: prolonged PTT
fatal
occurs with Hemorrhagic disease
 A (+) test for APA have earned the term
lupus anticoagulant
DIAGNOSTICS:
 Anti-cardiolipin antibody which can cause a
 blood type of donor & recipient false (+) test for syphilis
 crossmatching
 HLA testing of donor & recipient
 Mixed Lymphocyte Culture (MLC) assay test
 Panel reactive antibodies
 UTZ/MRI
 Tissue biopsies of transplanted organ
 NURSING CARE OF CLIENTS WITH IMMUNOLOGIC DISORDERS

Systemic Lupus Erythematosus (SLE) most Systemic S/S

common form
 Aching, malaise, fatigue
Causes: interrelated immunologic,  Low grade, spiking fever, chills
environmental, hormonal and genetic  Anorexia, weight loss, lymph node
enlargement
Risk factors:
 Abdominal pain, nausea, vomiting
 genetic predisposition female gender  Diarrhea or constipation
 stress  Irregular menses or amenorrhea
 smoking
 streptococcal or viral infections
 sunlight Diagnostics:
 immunization
 Anti-nuclear antibody, anti-DNA, lupus
 Vitamin D deficiency
erythematosus cell tests
 abnormal estrogen metabolism
 CBC with diff count=anemia, decreased
 pregnancy
WBC, decreased platelet count, increased
 medications-(Procainamide,
ESR
hydralazine, Anti-convulsant) less
 Serum
common ( Penicillin, Sulfa drug,
electrophoresis=hypergammaglobulinemia
Hormonal contraceptives)
(an excess of gamma globulin in the blood)
 Urine studies- RBC, WBC, casts sediments,
SLE PATHOLOGY protein loss (>3.5g/24h)
 Blood studies-decreased serum
 Autoimmunity is the prime mechanism
complement C3 & C4 indicate acute phase
associated with SLE. The body produces
of the disease
antibodies against the component of its
 CXR-Pleurisy; Lupus Pneumonitis (lung
own cells resulting to immune complex
inflammation)
disease.
 LUPUS is a Latin word for wolf. The disease
was so named in the 13th century as the
Management:
rash thought to resemble a wolf bite.
 It is called a great imitator because it  ASA and other NSAIDs may control arthritic
mimics other illnesses symptoms
 Corticosteroid creams such as
Types of lesions in SLE:
Flurandrenolide for skin lesions
1. Chronic cutaneous (discoid) lupus-thick,  Anti-malarial drug such as
red, scaly patches on the skin Hydroxychloroquine for refractory skin
2. Subacute cutaneous lupus-same with lesions
chronic but with distinct edges  Corticosteroids –treatment of choice
3. Acute cutaneous lupus- manifest as a rash  Immunosuppressants (Methotrexate)
called malar rash or butterfly rash; occurs in ****there is no cure for SLE
30-60% of SLE cases

Nursing management:
SLE Signs and symptoms:
 watch for S/S of joint pain or stiffness,
weakness, fever, fatigue, chills
 Facial erythema (butterfly rash)  Observe for DOB, chest pain, edema of
 Non-erosive arthritis arms and legs
 Photosensitivity  Note size and type of lesion
 Discoid rah (itchy, scaly or flaky, round or  Check urine for blood
oval rash common on the face, scalp, neck  Inspect scalp for hair loss, skin & mucous
& chest after sun exposure) membrane for petechiae
 Oral or nasopharyngeal ulcers  Provide a balanced diet: if with renal
 Pleuritis involvement=low salt low protein diet
 Pericarditis  Apply hot packs to relieve joint pains &
 Seizures stiffness, regular exercise
 Patchy alopecia  Monitor VS, I & O, weight and lab findings
 Psychoses