Concept on Immune Response and Inflammation

Prepared by: Kirk Odrey O. Jimenez, R.N.

INFLAMMATORY
RESPONSE
THE INFLAMMATORY RESPONSE
 “In-flame”-to set fire (red, hot, pain)
 Second line of defense
 Serves to bring defense and healing mechanisms to the
site of injury (trauma, infection)
 A complex response to sub-lethal injury to a tissue
 Sequential reaction to cell injury
 It is a physiologic protective response
DEFENSE MECHANISM
AGAINST INJURY AND
INFECTION
A systemic view
BARRIER DEFENSE
Skin
 Primary organ of protection
 16% of body weight

 Normal flora

 Layers of lipid; fatty acids

 Chemical barrier-controlling the

entrance and exit of substances

BARRIER DEFENSE
Mucous membrane
 Moist lining in the passages that
contains mucus-secreting cells
that is open directly or indirectly
to external environment
 Line areas not covered by skin

 Prevents binding of pathogens or

toxins
CHEMICAL DEFENSE
Gastric Acid
 Secreted by the stomach
 Ph renders some organism
incapable of infecting the
rest of the body
CHEMICAL DEFENSE
Lysozyme
 most ubiquitous antimicrobial
factor in the body)
 An enzyme that breaks down
the cell wall of many bacteria
 Found in: mucus, saliva, sweat,
tears
CELLULAR
DEFENSE
Mononuclear Phagocyte System (MPS)
 A widespread system of phagocytic cells (devouring cells)
scattered throughout various body tissues. Some of the
phagocytic cells are fixed in a variety of tissues such as
lymphoid tissue, liver (Kupffer’s cells), spleen, bone marrow,
lungs (alveolar macrophage), peripheral blood (monocyte),
loose connective tissue (histiocyte) and blood vessels. Other
cells making up the reticuloendothelial network are not
stationary and are given the name wandering macrophages.
Mononuclear Phagocyte System
 The role of these cells
is to ingest foreign
particular matter and
damaged host tissues.
Mononuclear Phagocyte System
 Composed of:
 Thymus-sternum
 Lymphatic tissue
 Leukocytes
 Lymphocytes
 Numerous chemical mediators
 Mononuclear Phagocyte System
Bone Marrow

Myelocytic cells Lyphocytic cells

•Lymphocytic cells
•Neutrophils Natural Killer cells B cells T Cells
•Eosinophils
• Basophils Plasma
Antibodies •Cytotoxic T
•Monnocytes/macrophages Cells
cells
•Helper T
cells
•Suppression
T cells
Mononuclear Phagocyte System
 Blood monocytes
 migrate to various tissues
 mature to macrophages (inside the tissue)
 Tissue macrophages scattered in connective
tissues or clustered in organs.
CHEMICAL
MEDIATORS OF
INFLAMMATION
Histamine
 First chemical mediator in the inflammatory
response
 A vasoamine that causes
 Dilation of local blood vessels
 Increase permeability
 Contraction of smooth muscles (causes fluid to move from
blood vessels into tissue—hyperemia)
 Hyperemia-presence of increased amount of blood in a body part
Bradykinin
 Plasma protein formed when injury release clotting
factors (Factor XII converts to Factor XIIa)
 Causes:

 Increase vascular permeability

 Vasodilation
 Smooth muscle contraction
Prostaglandins
 Ubiquitous (present anywhere at once) lipid-soluble
molecules derived from arachidonic acid
 Causes:

 Vasodilation and increase permeability

 Pain (increase sensitivity of nerve endings)
 Fever (reset the thermostat in hypothalamus)
 Increase platelet aggregation to help in clotting
Plasma proteases
 Kinins activated complement proteins and clotting
factors
Leukotrienes
 Formed from arachidonic acid
 Important mediator in bronchial asthma and
immediate hypersensitivity reaction
 May cause vasodilation and increased capillary
permeability
Complement system
 The byproduct of antibody antigen combination
that triggers inflammatory response
 Primary mediator of the humoral immune system
response
 Helps body produce inflammation and helps
localize infectious agents
WHAT the complement system does?
 Enhance phagocytosis (coats microbes to make
them more vulnerable to phagocytosis)
 Enhance chemotaxis
 Cause cell lysis
Physiology of Inflammation
IMMUNE RESPONSE
Immunity
 Normal adaptive response designed to protect the
body against potentially harmful foreign
substances, infections, and other sources of nonself
antigens
FUNCTIONS
 Third line of defense
 Specific defense mechanism
 Resists invasion by microorganisms
 Combats infection
Developmental Aspects of the Lymphatic System
and Body Defenses
 Except for thymus and spleen, the lymphoid organs
are poorly developed before birth
 A newborn has no functioning lymphocytes at
birth; only passive immunity from the mother
 If lymphatics are removed or lost, severe edema
results, but vessels grow back in time
4 R’s of the Immune Response
 Responds
 Remembers
 Recognizes
 Regulates 
PROPERTIES OF THE IMMUNE SYSTEM
 Specificity (respond)
 Immune system mounts a response that interacts with a specific
antigen
 When foreign antigen comes-series of cellular changes occurs-
formation of specific antibody or sensitized lymphocyte that
attaches to a specific antigen
PROPERTIES OF THE IMMUNE SYSTEM
 Recognition (Remember)
 Memory
 Immune system has unique ability to remember the ANTIGEN
 First time exposure to antigen-primary immune response
 Subsequent exposure to the same antigen –secondary immune
response
PROPERTIES OF THE IMMUNE SYSTEM
 Self –recognition (Recognize)
 Distinguish difference between the body’s own proteins and
foreign proteins
 Failure-leads to tissue destruction
 Only reacts if they recognize as invader
PROPERTIES OF THE IMMUNE SYSTEM
 Self-regulation (regulate)
 Immune system-- regulates its action
 Self-regulation allows the immune system to monitor itself by:
 “turning on” when antigen invades
 “turning off” when invader has been eradicated
 Regulation prevents the destruction of healthy or host tissues
 Inability to regulate results to chronic inflammation and damage
to host tissues
TYPES OF IMMUNITY
 Naturally Acquired Immunity
 -exists in person without prior contact with antigen
 -innate or Genetic immunity: Immunity or organism is born
with
 Active-has encounter the antigen and was able to

develop antibodies
 Passive-Breastfeeding
TYPES OF IMMUNITY
 Artificially Acquired Immunity
 Acquired through artificial means
 Active immunity- e.g tetanus toxoid; live attenuated vaccine –
OPV, BCG
 Passive immunity-the body doesn’t need to make antibodies
because the antibodies are readily made outside the body
 -anti serum, snake anti venum serum

 -“short term”
HUMORAL RESPONSE
Humoral Immune Response
Antibodies (Immunoglobulins)
(Igs)
 Soluble proteins secreted
by B cells (plasma cells)
 Carried in blood plasma
 Capable of binding
specifically to an antigen
Antibodies (Immunoglobulins)
(Igs)
 Five major immunoglobulin classes
 IgM – can fix complement
 IgA – found mainly in mucus
 IgD – important in activation of B cell
 IgG – can cross the placental barrier
 IgE – involved in allergies
CELLULAR MEDIATED
IMMUNE RESPONSE
Cellular (Cell-Mediated) Immune
Response
Suppressor T cells
 Release chemicals to suppress the activity of T and B
cells
 Stop the immune response to prevent uncontrolled
activity
 A few members of each clone are memory cells
Disorders Associated with the Immune
System
Hypersensitivity
Disorders of Immunity: Allergies
(Hypersensitivity)
 Abnormal, vigorous immune responses
 Types of allergies
 Immediate hypersensitivity
 Triggered by release of histamine from IgE binding to
mast cells
 Reactions begin within seconds of contact with allergen
 Anaphylactic shock – dangerous, systemic response
Disorders of Immunity: Allergies
(Hypersensitivity)
 Types of allergies (continued)
 Delayed hypersensitivity
 Triggered by the release of lymphokines from activated
helper T cells
 Symptoms usually appear 1–3 days after contact with
antigen
Hypersensitivities
 Four types based on type of antibodies and kinds of
reactions
 Reactions occur on second and later exposure to
antigen
 Response causes host damage
TYPE I - ANAPHYLAXIS
Type I - Anaphylaxis
 Allergic reaction
 Antigen is called allergen
 Antibody is IgE
 Cells are mast cells and basophils
 IgE antibody is produced and attaches by Fc end to
mast cells and basophils
 Effects may be local or systemic
 Second and later exposures result in antigen binding to
IgE on cells
 Cells release active compounds
 Histamine, leukotrienes, prostaglandins
 Mediators cause vasodilation, edema, erythema, mucus
production, smooth muscle contraction
 Wheals, hives, runny nose, watery eyes, gastrointestinal
disturbances are result
 Allergies of upper respiratory tract result from inhaled
allergens
 Mold, animal dander, pollens, mites
 Asthma is a response of the lower respiratory tract
( contraction of bronchi)
 Food allergies may result from
 Eggs, peanuts, tree nuts, milk, soy, fish, wheat, and peas, or foods
known to have high contents of protein or iodine.
Allergic Rhinitis
Allergic Rhinitis
 Most common form of allergy
 Seasonal-Hay Fever
 Perennial
 Sneezing, nasal itching, runny nose, itchy red eyes
 Usually self limiting, may lead to sinusitis, nasal
polyps, asthma, and chronic bronchitis
Allergic Rhinitis S/Sx
Allergic Rhinitis
 TX with removal of offending agent
 Antihistamines/Decongestants
 Corticosteroids
 Inhalation/Nasal spays
 Rhinophototheraphy
 Nursing Management
 Education
 Allergen Avoidance
 Monitor of symptoms
Allergic Rhinitis
 Immunotherapy/Allergy
Shots
 Tolerance reached/antigen
increased until patient no
longer exhibits symptoms
Atopic Dermatitis-Eczema
Atopic Dermatitis-Eczema
Inflammatory skin response
 Often seen in patients with
allergic rhinitis/allergic
asthma
 Pruritus, edema, extremely
dry skin, blisters crusts,
scales
 Increased risk for infection
with open lesions
Atopic Dermatitis-Eczema
 TX symptomatically
 Relief of dryness
 Corticosteroids for anti-inflammatory effect
 Nursing Management
 Assessment and documentation
 Medication administration
 Avoidance of stimuli
 Soaps- cosmetics-chemicals-fabrics
 Education
 Medications and symptom relief
Anaphylaxis
 Anaphylaxis
 Severe systemic hypersensitivity reaction
 Widespread histamine release
 Bronchial narrowing:
 Strider
 Wheezing
 Respiratory arrest
 Hypotension, tachycardia, cardiac arrest
 Sources of Anaphylaxis
 Foods, such as shellfish, nuts, peanuts, eggs and fruits
 Medicines, such as antibiotics, aspirin, over-the-
counter pain relievers, allergy shots and contrast dye
for radiological procedures
 Latex or rubber found in surgical gloves, medical
supplies and many products in your home
 Insect stings, especially from bees, wasps, hornets,
yellow jackets, sawflies and fire ants
 Anaphylaxis
 Immediate treatment guided by symptoms
 Oxygen –Maintain O2 Levels
 Epinephrine- Open/Relax Air ways
 Antihistamines -↓Histamine production
 Corticosteroids-↓Inflammatory process
 Vasopressors-↑Blood Pressure
 Mechanical ventilation-If all else has failed to maintain
life, until source of reaction is diminished or gone.
 Anaphylaxis
 Nursing care
 Early recognition
 Monitoring of VS
 Maintaining airway
 Emotional support
 Education
 Wearing of medical alert ID
 Use of Epi-Pen
Epi-Pen
 The EpiPen Auto-injector is a pre-filled syringe,
ready for use. It can be carried in a pocket, bag or
purse. A tiny, concealed spring-activated needle
penetrates the skin when the syringe is activated.
Urticaria (Hives)
 Urticaria (Hives)
 Release of histamine  Treatment
 In response to  Epinephrine
medications, food, cold,
 Corticosteroids
heat, pressure and stress
 Antihistamines
 Raised, pruritic,
 Histamine H blockers
nontender, erythematous 2

wheals on skin  Gastric Acid

Urticaria (Hives)
 Nursing Management
 Monitoring of symptoms
 Symptomatic relief/Cool soaks
 Medication administration
 Air way management in severe cases
 Education
 Medications and side effects
 Causative agent avoidance
Urticaria
Angioedema
 Angioedema
 Form of urticaria
 Affects submucosal/subcutaneous tissue rather than
skin
 The swellings happen especially in the lips and
other parts of the mouth and throat, the
eyelids, the genitals, and the hand and feet.
 Painless, dermal erythematous/subcutaneous
eruptions, skin/mucous membrane edema
Angioedema

          
Systemic Anaphylaxis
Systemic Anaphylaxis
 Injected allergens may cause systemic reactions,
including shock
 Mediators cause contraction of smooth muscles of
bronchi, intestinal tract and bladder, and
vasodilation
 Bee stings, penicillin, foods, vaccines, drugs
 Diagnosis and Prevention
 Skin tests may determine specific allergens
 Desensitization involves injections of minute amounts
of allergen
 Stimulate IgG antibodies
 Not always successful
Anaphylaxsis Shock
 Allergic hypersensitivity reaction
 Stimulates mast cells to release histamine & other chemical
mediators into circulation.
 Causes widespread vasodilation & makes the capillaries more
permeable ( leakage) with the shift of fluids ( from vascular into
interstitial space with pooling) resulting in hypotension and
possible vascular collapse!
 No loss of blood volume; just vasodilation
 Also get bronchoconstriction ( no air)
Anaphylactic shock
Causes:

 Foods ( nuts, shellfish, egg whites, chocolate,

strawberries, etc.)
 Insect bites/stings

 Snake venom

 Drugs: antibiotics, vaccines, iodine based-dyes, narcotics,

local anesthetics, blood transfusions, subt: latex,
pollen,molds, food additives
 Manifestations of anaphylactic shock
 Cutaneous: generalized itching, flushing, sensation of
warmth, uticaria (hives), angioedema ( swelling of
eye- lids, lips, and tongue)
 Neuro: restlessness, anxiety, dec. LOC, apprehension
 Resp: SOB, wheezing, laryngeal stridor, rales, cyanosis
 CV: hypotension and tachycardia
 GI: nausea/vomiting & diarrhea
Immediate Treatment
 Maintain airway and
give oxygen @ 100%
 Epinepherine (Epi) 0.2-
0.5 mg of a 1:1000
solution given sub-
cutaneously
 May be repeated q 10-15
min
 Antihistamines like
Benadryl (to control
uticaria)
 Steroids
 Medications given till the
s/s of anaphylaxis
reverses and VS are stable
TYPE II – CYTOTOXIC
REACTIONS
Type II – Cytotoxic Reactions
 Antibody is IgG or IgM
 Cells are often RBCs
 Complement is activated to cause lysis
 Transfusion reactions
 Hemolytic disease of newborns
ABO Blood Group System

Table 19.2
 Rh type
 Named for blood types in Rhesus monkeys
 Antibody is produced following sensitization
 Hemolytic Disease of Newborn
 Mother is Rh negative (lacks D antigen)
 Baby is Rh positive ( has D antigen)
 At or near birth, baby’s cells enter mother’s circulation and
stimulate production of anti -D
 Mother’s IgG antibodies cross placenta and react with baby’s
cells (usually second child)
 Lysis of RBCs causes elevation in bilirubin
 May require exchange transfusion
 Prevented by injection of anti-RH serum
TYPE III – IMMUNE
COMPLEX
Type III – Immune Complex
 insoluble combination of antibody and antigen
 Excess of antigen or antibody results in insoluble
complexes of antigen-antibody
 Immune complexes deposits its self on tissues making the
immune system thinks that the tissue contains the antigen
 Glomerulonephritis – damage to kidney function as complexes
lodge in glomeruli
TYPE IV – CELL
MEDIATED
Type IV – Cell Mediated
 TD cell related; no antibody
 T cells activated and cause inflammation reaction
 Contact dermatitis – haptens combine with skin proteins
and stimulate response
 Poison ivy, allergies to metals, jewelry, latex
 Used in diagnosis of TB and fungal infections (skin tests)
 Reaction takes more than 24 hours to develop
Contact Dermatitis
Contact Dermatitis
 Chemical comes in contact with skin
 On second exposure, T cells secrete

chemicals
 Poison ivy, poison oak, latex rubber

 Reddened, pruritic, fragile vesicles

Contact Dermatitis
Contact Dermatitis
Contact Dermatitis
 Treatment
 Antihistamines, topical drying agents,
corticosteroids
 Tepid baking soda baths or Aveeno baths
 Wash with brown soap (fels-naptha)
 Avoid scratching skin
Children may need to wear protective hand
covers
AUTO-IMMUNITY AND
RHEUMATOID DISORDERS
Disorders of Immunity: Autoimmune
Diseases
 The immune system does not distinguish between
self and noneself
 The body produces antibodies and sensitized T
lymphocytes that attack its own tissues
Disorders of Immunity: Autoimmune Diseases
 Examples of autoimmune diseases
 Multiple sclerosis – white matter of brain and spinal cord

are destroyed
 Myasthenia gravis – impairs communication between nerves

and skeletal muscles

 Juvenile diabetes – destroys pancreatic beta cells that

produce insulin
 Rheumatoid arthritis – destroys joints
Disorders of Immunity: Autoimmune Diseases
 Examples of autoimmune diseases (continued)
 Systemic lupus erythematosus (SLE) – affects kidney,
heart, lung and skin
 Glomerulonephritis – impairment of renal function
 Auto - immunity
 Immune response to self components
 Loss of tolerance
 Type I – antibodies to antigens similar to self antigens
(Hepatitis C)
 Type II – antibodies to cell surface antigens (Graves
disease – thyroid; myasthenia gravis – muscles)
 Type III – immune complexes – Lupus erythematosus –
DNA; rheumatoid arthritis – IgG/IGM/Complement)
Auto - immunity
 Type IV – cell mediated
 Multiple sclerosis - T cells and macrophages attack myelin sheath
of nerves
 genetic susceptibility and possible infectious agent
 Hashimoto’s thyroiditis – thyroid gland
 Insulin-dependent diabetes mellitis - pancreas
Self Tolerance Breakdown
 Inefficient lymphocyte programming
 Appearance of self-proteins in the circulation that
have not been exposed to the immune system
 Eggs
 Sperm
 Eye lens
Self Tolerance Breakdown
 Cross-reaction of antibodies produced against
foreign antigens with self-antigens
 Rheumatic fever
Auto-immune disorders examples
Auto-immune disorders examples
Pernicious Anemia
Pernicious Anemia
 Antibodies against gastric parietal cells and intrinsic factor
 Vitamin B12 deficiency
 Weakness, loss of appetite, swollen gums, pallor, irritability,
confusion, peripheral neuropathy
 RBC production decreased
 Also caused by gastric or small bowel resections
 Corticosteroids
 Lifelong vitamin B12 IM
Idiopathic Autoimmune
Hemolytic Anemia
Idiopathic Autoimmune Hemolytic Anemia
 Autoantibodies attach to RBCs causing lysis or agglutination
 S/Sx
 Mild fatigue, pallor, hypotension, dyspnea, palpitations, jaundice
 Tx and Nursing Management
 Immunosuppressive medications, corticosteroids, folic acid,
oxygen, blood transfusions, erythrocytapheresis (removal of
abnormal RBC), splenectomy
Hashimoto’s Thyroiditis
Hashimoto’s Thyroiditis
 Autoantibodies attacts the thyroid gland causing
over stimulation
 Then autoantibodies destroy the thyroid, causing
hypothyroidism
Hashimoto’s Thyroiditis
 Hashimoto’s Thyroiditis
 TX and Nursing management
 Lifelong thyroxine
 Soft Diet with enlarged thyroid gland
 Overall need good nutrition and fluid intake
 Avoidance of foods high in Iodine
 High fiber diet
 Adequate rest
 Prevention of venous stasis
 Antiembolism stockings
Rheumatoid Arthritis
 Definition

 Rheumatoid Arthritis is a chronic systemic disease

characterized by recurrent inflammation of the
diarthrodial joints and other structures. It attacks
the lining of your joints (synovium) causing
swelling that can result in aching and ankylosis of
a joint and eventually deformity. It is severely
disabling. The severity of the joint may fluctuate
over time, but progressive development of various
degrees of joint destruction, deformity and
disability are the most common outcomes.
 Diagnostic Procedures

 Blood Test
 Imaging

 Synovial Membrane Biopsy

 Synovial Fluid Aspiration and Analysis

Clinical Manifestations

 Clinical manifestations of Rheumatoid Arthritis

vary not only from one client to another but also
in an individual client over the course of the
disease. The American Rheumatism Association
classified Rheumatoid Arthritis as follows:
 Clinical Manifestations

CRITERION DESCRIPTION

1 Morning stiffness in and around joints lasting at least one hour before maximal improvement

Soft tissue swelling ( arthritis) of three or more joint areas ( including the right and left proximal PIP, MCP, wrist, elbow,
2 knee, ankle, and MTP joints

3 Swelling of at least one wrist

4 Simultaneously symmetric swelling in joints listed in criterion 2

5 Subcutaneous rheumatoid nodules

6 Presence of rheumatoid factor

7 Radiographic erosions and/or periarticular osteopenia in hand and/or wrist joints

 Etiology

 The causes of rheumatoid arthritis are unknown. Infectious

agents such as viruses, bacteria, and fungi have long been
suspected. The cause of rheumatoid arthritis is a very active area
of worldwide research. Some scientists believe that the tendency
to develop rheumatoid arthritis may be genetically inherited. It is
suspected that certain infections or factors in the environment
might trigger the immune system to attack the body’s own tissue,
resulting to inflammations of the various organs of the body such
as the lungs or eyes.
 Pathophysiology

Presence of genetic factor

Antigenic Stimulus to
that increases the person’s
any joint of the body
susceptibility to RA

Immune Responses

Macrophages and monocytes migrate

T-Cell and B-Cell
Proliferation to the site of antigenic stimulus (joint)

T Cells produces enzyme that

enhances inflammatory
response
B Cells produce Rheumatoid
Factor
 Pathophysiology

 Tumor
 RF and macrophages bind Necrosis
with the antigen forming Factor- alpha
immune complexes produced by
monocytes
cause joint
 Inflammation of the synovial degradation
membrane: and synovial
tissue
 Localized and Systemic Response
damage
to inflammation begins to
manifest
 Formation of rheumatoid
 Fibrosis and synovial  Pannus formation and
nodules
tissue hypertrophy and invasion of a part of the
hyperplasia joint cavity
Pathophysiology
 Nursing Interventions for Pt. with RA

1. Administer analgesics and other medications as ordered

2. Teach client to take medication as ordered and observe for aspirin
toxicity (tinnitus, bleeding) and other adverse effects of medications
3. Apply heat and cold as ordered; heat paraffin from 125 to 129 oC
4. Promote rest and position to ease joint pains
5. Provide for ROM exercises up to the point of pain, recognizing that some discomfort is
always present
 Nursing Interventions for Pt. with RA
1. Emphasize the need to remain active but incorporate rest periods to avoid fatigue
2. Encourage the clients to verbalize feeling
3. Help set realistic goals focusing on strengths
4. Encourage the use of supportive devices to help client to conserve energy and maintain
independence
5. Provide care for the client following joint replacement
6. Encourage diet rich in nutrient-dense food such as fruits, vegetables, whole grains and
legumes to improve and maintain nutritional status and compensate for nutrient interactions of
corticosteroids and other treatment medication
 Medical Intervention

 Analgesic/ antipyretic agents (aspirin)

 NSAIDs

 Antirheumatic Agents

 Immunosuppressive Agents

 Anti-Malarial Agents

 Anti- neoplastic agents

 Corticosteroids
Surgical Intervention

Arthroplasty
 -an operative procedure of
orthopedic surgery performed,
in which the arthritic or
dysfunctional joint surface is
replaced with something better
or by remodeling or realigning
the joint by osteotomy or some
other procedure.
Systemic lupus erythematosus
(SLE)
Systemic lupus erythematosus (SLE)
 Chronic, multisystem autoimmune disease
 The body produces autoantibodies that attack parts of the body
and lead to inflammation and tissue and organ damage.
 Lupus – Latin term for wolf that was coined to describe skin
lesions resembling wolf bites.
 Called the “great imitator” because easily confused with other
disorders.
 Recurs with flare-ups, then remissions.
 Creates both physical and psychosocial challenges.
 Immune complexes deposited in basement membranes of
capillaries:
 Kidneys
 Heart

 Skin

 Brain

 Joints

* Specific symptoms of SLE depend on which cells or organs are involved

 Systemic lupus erythematosus (SLE)
 SLE is a multiorgan, multisystem autoimmune disease.
 People of both sexes, all ages, and all ethnic groups are susceptible.
 Prevalence of SLE in the United States is 15–50 per 100,000.
 SLE predominantly occurs in women, with a gender ratio of 9:1.
 Onset is usually after puberty, typically in the 20s and 30s.
It is more common in African Americans than in whites.

The incidence in white females is 3.9 per 100,000 and in white males is 0.4
per 100,000. The prevalence in white females is 130 per 100,000
 Pathogenesis and Etiology
 Homozygous deficiencies of early components of complement
(C1q,r,s; C2; C4) confer strong predisposition to SLE, but such
deficiencies are rare.
 Some gene alleles probably contribute to disease susceptibility
by influencing clearance of apoptotic cells (C1q, MBL) or
immune complexes (FcR 2A and 3A), antigen presentation
(HLA-DR2,3,8), B cell maturation (IL-10), T cell activation
(PTPN22), or chemotaxis (MCP-1).
 Female sex is permissive for SLE;
Pathogenesis and Etiology
 Women exposed to estrogen-containing oral
contraceptives or hormone replacement have an
increased risk of developing SLE (1.2- to 2-fold).
 Exposure to ultraviolet light causes flares of SLE in

approximately 70% of patients.

 Most SLE patients have autoantibodies for 3 years or

more before the first symptoms of disease

Pathogenesis and Etiology
 Epstein-Barr virus (EBV) may be one infectious agent that
can trigger SLE in susceptible individuals.
 Children and adults with SLE are more likely to be infected
by EBV.
 EBV activates and infects B lymphocytes and survives in
those cells for decades; it also contains amino acid sequences
that mimic sequences on human spliceosomes.
  Environmental Factors That May Play a Role in the
Pathogenesis of SLE
Definite   
 UV light   
 EBV
Probable   
 Estrogen and prolactin—in humans, female-to-male ratio is 9:1 between menarche and
menopause, 3:1 in young and old  
   Lupus inducing medications  
Hydralazine,   Procainamide ,   Isoniazid   , Hydantoins   , Chlorpromazine  , 
Methyldopa ,   Penicillamine,    Minocycline ,   Tumor necrosis factor-α inhibitors  , 
Interferon-α,
 Environmental Factors That May Play a Role in the
Pathogenesis of SLE
Possible   
 Dietary factors   
 Alfalfa sprouts and related sprouting foods containing    Canavanine    Pristane and
similar substances   
 Infectious agents other than EBV   
 Bacterial DNA   
 Human retroviruses   
 Endotoxins, bacterial lipopolysaccharides
Signs and Symptoms of SLE
 Systemic lupus erythematosus (SLE)
 Musculoskeletal
 Arthralgia, myalgia, and arthritis are the most common manifestations
 Dermatologic
 Photosensitivity--sun exposure exacerbates both skin and systemic signs
 Malar rash--a flat or raised butterfly-shaped erythematous rash over the
cheeks and nose
 Alopecia may occur in patches or all over the body
Malar rash
Subacute cutaneous lupus lesions
Discoid lupus erythematosus
 Systemic lupus erythematosus (SLE)
 Cardiovascular
 Pericarditis, myocarditis, endocarditis, and accelerated atherosclerosis,
leading to a myocardial infarction
 Vasculitis
 Gastrointestinal
 Peritonitis can cause diffuse abdominal pain
 Anorexia, nausea, and vomiting
 Pancreatitis or ascites may develop
 Systemic lupus erythematosus (SLE)
 Pulmonary
 Complications include pulmonary hemorrhage, embolism,
or hypertension; lupus pneumonitis; pleuritis; or interstitial
lung disease
 Hematologic
 Anemia, leukopenia, thrombocytopenia, and lymphopenia
are common
 Systemic lupus erythematosus (SLE)
 Renal
 50% of clients within one year
 Nephritis is an early manifestation
 Proteinuria, casts, and red cells in the urine
 Neurological
 Mild to severe complications (severe headache, seizures,
peripheral neuropathy, delirium or psychosis)
Diagnostic Tests-SLE
 Serum antinuclear antibody (ANA) test
 Anti-Smith (anti-Sm)
 Anti-double-stranded DNA (anti-dsDNA)
 Antiphospholipid (APL) antibodies
 Syphilis tests (VDRL or RPR)
 In vitro diagnostic immunoassay system
 Detects six autoantibodies simultaneously
TX and Nursing Management
 Decrease inflammation
 Suppress the overactive immune system
 Prevent symptom flares
 Minimize complications related to disease or
treatment
 Medications used to treat SLE
 Nonsteroidal anti-inflammatory drugs (NSAIDs)
 Musculoskeletal problems, pain, stiffness, inflammation, and
fever
 Antimalarial drugs (Plaquenil, Aralen)
 Help with arthritis, rash, mouth ulcers, fatigue, and fever
 Take effect slowly over months
 Corticosteroids (multiple uses)
 Treat rash and arthritis
 Medications for SLE
 Cytotoxic drugs
 Azathioprine (Imuran), cyclophosphamide (Cytoxan),
methotrexate (Rheumatrex, Trexall) and cyclosporine
(Neoral, Sandimmune)
 Suppress the hyperactive immune response associated
with SLE
 Monitor for bone marrow suppression and susceptibility
to infection
Patient Teaching with SLE
 Avoid sun exposure; use sunscreen with UVA and UVB
protection of SPF 15 or more, and wear protective clothing
 Stay alert to symptoms of a flare or infection; contact health
care provider if they occur
 Maintain an active lifestyle
 Get plenty of rest
 Eat a well-balanced diet and take multivitamins
 Special diet if have hypertension, dyslipidemia, or hyperglycemia
Patient teaching (con’t)
 Avoid smoking
 Ask health care provider about alcohol limitations
 Consider joining local support group for assistance
managing/coping with this lifelong disorder
TRANSPLANTATION
 Transplantation
 HLA typing to determine compatibility
 Rejection may also be related to cell damage response
 Grafts
 Autograft – self
 Isograft - identical twin, inbred animals
 Allograft – same species
 Xenograft – different species
 Risk of rejection is relative
Bone Marrow Transplants
 Destroy recipients bone marrow cells
 Replace with a compatible marrow
 Risk of Graft versus host reaction
 Immunocompetent cells in graft react with and destroy
recipient cells
Immunosuppression
 Success of transplants related to ability to block T cell
rejection while preserving B cell function

 Cyclosporine – blocks interleukin 2

 Other drugs may block IL-2 or both T and B cell
functions
 Monoclonal antibodies are also available
GENERAL INTERVENTIONS FOR
CLIENTS WITH IMMUNE EXCESS,
HYPERSENSITIVITY, AND AUTO
IMMUNITY
ANAPHILAXIX/HYPERSENSIT
IVITY
Interventions
 First assess respiratory function; an airway must be
established.
 CPR may be needed.
 Epinephrine is given as soon as symptoms appear.
 Antihistamines treat angioedema and urticaria.
 Oxygen reduces hypoxemia.
Collaborative Management
 History
 Physical assessment/clinical manifestations
 Laboratory assessment
 Allergy testing including skin testing, scratch
testing, intradermal testing, oral food challenge
 Avoidance therapy, symptomatic therapy, drug
therapy
Drug Therapy
 Decongestant
 Antihistamines
 Corticosteroids
 Mast cell stabilizers
 Leukotriene antagonists
 Complementary and alternative therapy
 Desensitization therapy
AUTOIMMUNE AND RHEUMATOID
DISORDERS
Collaborative Intervention:
 Laboratory and Clinical assessment to determine
the extent of the disease
 Giving of corticosteroids for the control of the
immune system
 The administration of antibiotics to combat the side
effects of the corticosteroids
NURSING MANAGEMENT
Nursing Management
 Health assessment focusing on health history, what
triggers the disease, what alleviates the disease, the
duration of the disease and the usual gravity of the disease
 Assessment on the clients prior knowledge of the disease
and treatment
 Assessment on the support system and other demographics
 Nursing Management
 Provision of a clean, cool, safe environment, void of possible
allergens.
 Health teaching on the cause and nature of allergies and other
immunologic disorders
 Establishing a support system
 Health teaching on things to be avoided and things to be done
during exacerbations of the disease.
 Health teachings on the signs and symptoms and when to refer to a
physician