NURSING CARE OF CLIENTS WITH IMMUNOLOGIC DISORDERS
IMMUNE SYSTEM
 The Immune system is composed of an
integrated collection of various cell types,
each with designated functional role in
defending against infection and invasion by
other microorganism
 Major components of the Immune system:
1. Bone marrow
2. WBC’s- produced by the bone
marrow
3. Lymphoid tissues including the
thymus gland, spleen, lymph nodes,
tonsils & adenoids, similar tissues in
the GIT (Appendix), respiratory and
reproductive systems
Bone marrow
 WBC’s are produced in the bone marrow
 lymphocytes are generated from stem cells
(are undifferentiated cells that are able to
repair and replace damaged tissues and
organ)
 descendants of stem cells became
lymphocytes
o B-lymphocytes (10-20%) mature in
the bone marrow and enters to
circulation
o T-lymphocytes (60-70%) move from
the bone marrow to the thymus,
where they mature into several
kinds of cells with different
functions
Lymphoid tissues
 Spleen-composed of red & white pulps; acts
like a filter
 Red pulp is the site where old and injured
RBC’s are destroyed
 White pulp contains concentrations of
lymphocytes
 Lymph nodes are distributed throughout
the body
o connected by lymph channels &
capillaries which remove foreign
material from the lymph system before
it enters the blood stream
o also serve as centers for immune cell
proliferation
IMMUNITY-the body’s specific protective
response to an invading foreign agent or
organism
2 types of Immunity
1. Natural (Innate)-a non-specific immunity
that is present with birth
i. -cells involved in this response
(macrophages, dendritic ells,
natural killer (NK) cells
2. Acquired (Adaptive)-specific immunity that
develops after birth
 Inflammatory response is the major
function of the natural immune system. It is
facilitated by physical and chemical barriers
that are part of the human organism
 Physical surface barrier- intact skin, mucous
membranes & cilia of the respiratory tract
 Chemical barrier-mucus, acidic gastric
secretions, enzyme in tears and saliva, and
substances in sebaceous and sweat
secretions
Acquired Immune response
2 mechanisms
1. the cell-mediated response, involving T-cell
activation
2. effector mechanism, involving B-cell
maturation and production of antibodies
*2 types of acquired immunity
1. active-acquired immunity=the immunologic
defense are developed by the person’s own
body; typically last many years or even a
lifetime
2. Passive-acquired immunity=temporary
immunity transmitted from a source outside
the body that has developed.
Example: immunity from previous disease
or immunization
*Both types of acquired immunity involve
humoral and cellular immunologic response
Response to invasion
 The phagocytic immune response
 The humoral or antibody immune
response
 The cellular immune response
 NURSING CARE OF CLIENTS WITH IMMUNOLOGIC DISORDERS
PHAGOCYTIC IMMUNE RESPONSE
 1st line of defense
 involves the WBC (granulocytes and
macrophages) which have the ability to
ingest foreign particles
 phagocytes also remove the body’s own
dying or dead cells
 necrotic cells release substances that trigger
an inflammatory response
 Apoptosis-programmed cell death
HUMORAL IMMUNE RESPONSE
 2nd protective response
 Sometimes called Antibody response
 Begins with the B-lymphocytes which can
transform into plasma cells that
manufacture antibodies
 These antibodies are specific proteins that
are transported in the blood stream to
disable invaders
CELLULAR IMMUNE RESPONSE
 3rd mechanism of defense
 also involves the T-lymphocytes which can
turn into special cytotoxic ( or Killer) T-cells
that can attack the pathogens
ANTIBODIES-are large proteins called
IMMUNOGLOBULINS
 Called immunoglobulins because they are
found in the globulin fraction of the plasma
proteins
 5 different types of immunoglobulins
1. IgA= 15% of total
immunoglobulins
 appears in body fluids (blood,
saliva, tears, breast milk,
pulmonary, GI, prostatic and vaginal
secretions)
 protects against respiratory, GI, GU
infections
 prevents absorption of antigens
from food
 passes to neonate in breast milk for
protection
2. IgD= 0.2%
 appears in small amount in
serum
 possibly influences B-
lymphocytes differentiation
 acts as an antigen receptor of B-
cells
3. IgE= 0.04%
 causes an allergic response
 appears in serum
 takes part in allergic &
hypersensitivity reaction
 combats parasitic infection
4. IgG =75%
 appears in serum & tissues
(interstitial fluid)
 assumes a major role in blood-
borne and tissue infection
 activates the complement
system
 enhances phagocytosis
 crosses the placenta
5. IgM =10%
 appears in intravascular serum
 act as the 1st immunoglobulin
produced in response to
bacterial and viral infection
 activates the complement
system
CELLULAR IMMUNE RESPONSE
 The B-lymphocytes are responsible for
humoral immunity and the T-lymphocytes
are primarily responsible for cellular
immunity
 Complement system-circulating plasma
proteins made in the liver and activated
when an antibody connects with its antigen
3 major functions
1. defending the body against bacterial infection
2. bridging natural & acquired immunity
3. disposing of immune complexes and the by-
products associated with inflammation
 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,
frequency, urgency, and frequent infections
 emotional lability-mood swings, irritability,
euphoria
 associated signs- poorly articulated speech
& dysphagia
Diagnostics:
 some may undergo periodic testing & close
observation because of the difficulty in
diagnosing MS
 in 1/3 of patients, EEG shows non-specific
abnormalities
 lumbar puncture reveals CSF with increased
gamma globulin fraction of IgG but normal
TCHON levels
 electrophoresis in CSF gamma globulin,
oligoclonal bands of Ig can be detected
 CT scans-reveal lesions within the brain’s
white matter
 MRI used to evaluate disease progression
since this is the most sensitive method of
detecting lesions
RX: to shorten exacerbation to relieve
neurologic deficits to help patient maintain as
normal a lifestyle as possible
Drug therapy:
 Methylprednisolone=to reduce CNS
inflammation
 Dexamethasone, Prednisone,
Betamethasone & Prednisolone for acute
exacerbations
 Glatiramer acetate=to reduce the frequency
of attacks; for relapsing MS
 Interferon beta 1a or Interferon beta 1b in
reducing disability progression & in
decreasing the frequency of exacerbations
Multiple Sclerosis
In conjunction with corticosteroids:
 Fluoxetine to combat depression
 Baclofen or Dantrolene to relieve
spasticity
 Oxybutynin to relieve urine retention &
minimize frequency & urgency
Management during acute exacerbations
 bed rest
 physical therapy & massages
 measures to prevent fatigue
 meticulous skin care to prevent pressure
ulcers
 bowel and bladder training (prn)
 antibiotic treatment of bladder infection
 counselling
GUILLAIN-BARRE SYNDROME
 An acute rapidly progressive and potentially
fatal form of polyneuritis
 A rare neurologic disorder in which the
immune system attacks healthy nerve cells
in the peripheral nervous system
 This leads to weakness, numbness, and
tingling and can eventually cause paralysis.
 CAUSE: unknown
-cell-mediated immunologic attack on
peripheral nerves in response to a virus
*PRECIPITATING FACTORS: mild febrile or viral
illness, surgery, rabies or swine influenza
vaccination, Hodgkin’s disease or some other
cancers, SLE
GBS PATHOPHYSIOLOGY
This syndrome causes inflammation and
degenerative changes in the posterior (sensory)
and anterior (motor) nerve roots
S/S:
 Symmetrical muscle weakness, in the legs
first (ascending type) & then extending to
the arms & facial nerves within 24-72 hours
 Facial diplegia with ophthalmoplegia (ocular
paralysis)
 Dysphagia, Dysarthria (slurred speech)
 Hypotonia, Areflexia
DIAGNOSTICS
 Protein levels in CSF-increased, several days
after onset of S/S, and peak in 4-6 weeks
 WBC in CSF-normal
 CBC-leukocytosis in immature forms
 Electromyography –shows repeated firing of
the same motor unit instead of widespread
sectional stimulation
TREATMENT:
 needs hospitalization
 monitor respiratory status regularly
(because of the ascending pathology of the
disease; may cause respiratory failure
 mechanical ventilation
 plasmapheresis-which temporarily reduced
circulating antibodies
 high dose immune globulins and steroids
 NURSING CARE OF CLIENTS WITH IMMUNOLOGIC DISORDERS
MANAGEMENT:
 Watch for ascending motor loss (sensation
is not loss)
 Monitor VS and LOC
 Assess respiratory function, watch for
increased PaCO2 such as confusion and
tachypnea
 Auscultate breath sounds
 Turn to sides
 Encourage coughing & deep breathing
 Emergency airway
 Meticulous skin care
 Passive ROM exercises (use Hubbard tank to
prevent contracture)
 Evaluate gag reflex; administer NGT
 Prevent hypotension with slow position
changes
 I & O q8h (urine retention)
 Relieve constipation
 Refer to PT
RHEUMATOID ARTHRITIS
 A chronic systemic inflammatory disease
that primarily attacks peripheral joints, and
surrounding muscles, tendons, ligaments &
blood vessels
 Potentially crippling, requires life-long
treatment
 Prognosis worsens with development of
nodules, vasculitis & increase titers of
Rheumatoid factor
 Causes: unknown (autoimmune basis)
 Pathophysiology:
o Cartilage damage resulting from
inflammation triggers further
immune response, including
complement activation
o Complements attracts
polymorphonuclear leukocytes and
stimulates the release of
inflammatory mediators which
exacerbates joint destruction
Signs and symptoms:
 fatigue, malaise, anorexia
 persistent low grade fever
 weight loss
 lymphadenopathy
 vague articular symptoms
 joint pain, tenderness, warmth, swelling
occur bilaterally and symmetrically
 morning stiffness
 paresthesia in the hands and feet
 stiff, weak or painful muscles
RA DIAGNOSTICS
 X-ray=bone demineralization and soft tissue
swelling
 (+) RF test occurs in 75%-80%
 Synovial fluid analysis usually shows
increased volume and turbidity but
decreased viscosity and complement
 Serum globulins are increased
 ESR also increased
 CBC=moderate anemia and slight
leukocytosis
Treatment:
 Salicylates-ASA
 NSAIDs=Indomethacin, Ketorolac, Ibuprofen
 Anti-malarials=Chloroquine,
Hydroxychloroquine
 Gold sodium thiomalate= anti-rheumatic
and antineoplastic
 Penicillamine
 Corticosteroids
 Immunosuppressives= Methotrexate,
Cyclophosphamide, Azathiopine
SUPPORTIVE MEASURES
-8-10 hours of sleep, adequate nutrition,
frequent rest periods, splinting to rest inflamed
joints, ROM exercises, heat application (relaxes
muscles & relieves pain) via moist heat (hot
soaks, paraffin baths & whirlpool), ice packs
during acute episodes
Surgery:
 Synovectomy
 Joint reconstruction or total joint
arthroplasty
 Monitor the duration not the intensity of
morning stiffness (because duration reflects
the severity of the disease), encourage hot
baths at HS or in the morning to reduce the
need for pain medication
 Weight reduction coz obesity adds stress to
the joints
The Patient with a Tissue Transplant
2 types of transplantation
 Transplantation of avascular tissues-
routine with little need for tissue matching,
immunosuppression
 Transplantation of organs-increasingly
common; success is tied to obtaining an
organ with tissue antigens as close to those
of recipient as possible
 NURSING CARE OF CLIENTS WITH IMMUNOLOGIC DISORDERS
HLA type Human Leukocyte antigen
 a kind of genetic test used to identify
certain individual variations in a person’s
immune system
o aka HLA typing
o HLA
 HLA matching
 to know how closely the transplant
recipient matches their donor
Types of HLA
 HLA-A 59 HLA-A CHONs
 HLA-B 118
 HLA-DR 124
 A (+) HLA test means HLA-B 27 is present,
suggesting a greater risk for developing
certain auto-immune disorders
 AUTOGRAFT –transplant of patient’s own
tissue
 ALLOGRAFT – between members of the
same species that have different genotypes
and HLA
- may come from living donors,
cadavers, those who meet criteria
for brain death
* XENOGRAFT- from animal to human
Histocompatibility: ability of cells & tissues to
survive transplantation without immunologic
 Interference by recipient
 determined by tissue typing
*TYPES OF REJECTION:
1. Hyperacute tissue rejection=2-3 days after
transplant
2. Acute tissue rejection=most common,
treatable
3. Chronic tissue rejection=4 months to a year
after transplant
4. Graft-virus-host disease GVHD=potentially
fatal
DIAGNOSTICS:
 blood type of donor & recipient
 crossmatching
 HLA testing of donor & recipient
 Mixed Lymphocyte Culture (MLC) assay test
 Panel reactive antibodies
 UTZ/MRI
 Tissue biopsies of transplanted organ
MEDICATIONS: Maintenance therapy
 Antilymphocyte therapy & use of
monoclonal antibodies
 Immunosuppressive agents
 Azathioprine (Imuran)
 Muromonab-CD3 OKT3
 Polyclonal antilymphocyte antibodies
SYSTEMIC LUPUS
ERYTHEMATOSUS (SLE)
 An autoimmune disease in which the body’s
immune system mistakenly attacks healthy
tissue
 A chronic inflammatory disorder of the
connective tissue
 Affects multi-organ system as well as skin;
fatal
 More common in women than men
especially during child-bearing years
 Occurs worldwide; most prevalent among
Asians and Blacks (Africans, Caribbean,
Chinese
 Onset: 15-45 y/o
 Prognosis: 15 years survival
4 kinds of LUPUS:
 Systemic Lupus Erythematosus (SLE) most
common form
 Cutaneous lupus- a form of lupus that is
limited to the skin
 Drug-induced lupus- a lupus-like disease
caused by certain medications
 Neonatal lupus-a rare condition that affects
infants of women who have lupus; most
commonly presenting with a rash
resembling discoid lupus erythema with
systemic abnormality as heart block,
hepatomegaly and splenomegaly; usually
benign and self-limited
 SLE associated with Anti-phospholipid
antibody syndrome (thrombotic disease)
wherein autoantibodies to phospholipids
are present in the serum; ie: prolonged PTT
occurs with Hemorrhagic disease
 A (+) test for APA have earned the term
lupus anticoagulant
 Anti-cardiolipin antibody which can cause a
false (+) test for syphilis
 NURSING CARE OF CLIENTS WITH IMMUNOLOGIC DISORDERS
Systemic Lupus Erythematosus (SLE) most
common form
Causes: interrelated immunologic,
environmental, hormonal and genetic
Risk factors:
 genetic predisposition female gender
 stress
 smoking
 streptococcal or viral infections
 sunlight
 immunization
 Vitamin D deficiency
 abnormal estrogen metabolism
 pregnancy
 medications-(Procainamide,
hydralazine, Anti-convulsant) less
common ( Penicillin, Sulfa drug,
Hormonal contraceptives)
SLE PATHOLOGY
 Autoimmunity is the prime mechanism
associated with SLE. The body produces
antibodies against the component of its
own cells resulting to immune complex
disease.
 LUPUS is a Latin word for wolf. The disease
was so named in the 13th century as the
rash thought to resemble a wolf bite.
 It is called a great imitator because it
mimics other illnesses
Types of lesions in SLE:
1. Chronic cutaneous (discoid) lupus-thick,
red, scaly patches on the skin
2. Subacute cutaneous lupus-same with
chronic but with distinct edges
3. Acute cutaneous lupus- manifest as a rash
called malar rash or butterfly rash; occurs in
30-60% of SLE cases
SLE Signs and symptoms:
 Facial erythema (butterfly rash)
 Non-erosive arthritis
 Photosensitivity
 Discoid rah (itchy, scaly or flaky, round or
oval rash common on the face, scalp, neck
& chest after sun exposure)
 Oral or nasopharyngeal ulcers
 Pleuritis
 Pericarditis
 Seizures
 Patchy alopecia
 Psychoses
Systemic S/S
 Aching, malaise, fatigue
 Low grade, spiking fever, chills
 Anorexia, weight loss, lymph node
enlargement
 Abdominal pain, nausea, vomiting
 Diarrhea or constipation
 Irregular menses or amenorrhea
Diagnostics:
 Anti-nuclear antibody, anti-DNA, lupus
erythematosus cell tests
 CBC with diff count=anemia, decreased
WBC, decreased platelet count, increased
ESR
 Serum
electrophoresis=hypergammaglobulinemia
(an excess of gamma globulin in the blood)
 Urine studies- RBC, WBC, casts sediments,
protein loss (>3.5g/24h)
 Blood studies-decreased serum
complement C3 & C4 indicate acute phase
of the disease
 CXR-Pleurisy; Lupus Pneumonitis (lung
inflammation)
Management:
 ASA and other NSAIDs may control arthritic
symptoms
 Corticosteroid creams such as
Flurandrenolide for skin lesions
 Anti-malarial drug such as
Hydroxychloroquine for refractory skin
lesions
 Corticosteroids –treatment of choice
 Immunosuppressants (Methotrexate)
****there is no cure for SLE
Nursing management:
 watch for S/S of joint pain or stiffness,
weakness, fever, fatigue, chills
 Observe for DOB, chest pain, edema of
arms and legs
 Note size and type of lesion
 Check urine for blood
 Inspect scalp for hair loss, skin & mucous
membrane for petechiae
 Provide a balanced diet: if with renal
involvement=low salt low protein diet
 Apply hot packs to relieve joint pains &
stiffness, regular exercise
 Monitor VS, I & O, weight and lab findings