2.

Autoimmunity
or Autoantibodies
Inappropriate reaction by the immune system in
which antibodies form against self antigens,
mistaken as foreign.
E.g.
– Tissue injury ( may help the body rid itself of damaged
or necrotic self component)
Etiology:
– Altered antigens
– Cross reactive antibodies
– Viral factors
– Hormonal factors
– Genetic factors
Pathophysiology: 3 ways of auto immune response
cause disease

The action of antibodies on cell surfaces: by

direct antibody-mediated cellular cytotoxicity---
interference with receptors --- or complement
activation.
The circulation and deposition of small immune
complexes : soluble antigen-antibody complexes
– invade and deposit in the capillaries, the
synovium of joints--- it causes tissue damage via
activation of the complement system.
Activation of sensitized T lymphocytes: by the
release of lymphokines.
– Intervention:
Anti-inflammatory agents – symptomatic
relief.
 Assessment and
Management of Patients With
Allergic Disorders
 Allergic Reactions
Allergy
– An inappropriate, often harmful response of
the immune system to normally harmless
substances
– Hypersensitive reaction to an allergen initiated
by immunological mechanisms that is usually
mediated by IgE antibodies
Allergen: the substance that causes the allergic
response
Atopy: allergic reactions characterized by IgE
antibody action and a genetic predisposition
 Immunoglobulins and Allergic
Response
Antibodies (IgE, IgD, IgG, IgM, and IgA) react
with specific effector cells and molecules, and
function to protect the body
IgE antibodies are involved in allergic disorders
IgE molecules bind to an allergen and trigger
mast cells or basophils
These cells then release chemical mediators such
as histamine, serotonin, kinins, SRS-A, and
neutrophil factor
These chemical substances cause the reactions
seen in allergic response
Immunoglobulins and Allergic Response
(cont.)
Allergen triggers the B cell to make IgE antibody, which
attaches to the mast cell; when that allergen reappears, it binds
to the IgE and triggers the mast cell to release its chemicals
 Hypersensitivity
A reflection of excessive or aberrant
immune response
Sensitization: initiates the buildup of
antibodies
Predisposing Factors
Host defenses
Nature of the allergen
Concentration of the allergen
Route of allergen entrance into the
body
Exposure to the allergen
Types of hypersensitivity reactions
– Anaphylactic: type I
– Cytotoxic: type II
– Immune complex: type III
– Delayed type: type IV
Type I—Anaphylactic Reaction
– Type I.Anaphylactic shock
Most severe form of type I hypersensitivity
Clinical Manifestations:
– Itching
– Edema
– Sneezing ( wheezing, dyspnea, cyanosis,
circulatory shock)
– ASAP emergency treatment
Prevention:
– History: drugs ( antibiotics- penicilllins); Foods
( seafoods); Insect venoms; Biologicals
( vaccines, hormones, enzymes, antisera); blood
products; allergen extracts; diagnostic agents
( dye)
Type II—Cytotoxic Reaction
– Type II Cytolytic or Cytotoxic
Hypersensitivity
The antigen-antibody complex and complement
attach to a cell – circulating blood cell  cell lysis.
Blood transfusion - blood incompatibility  cell lysis
( transfusion reaction – of donor RBC)
Note: Blood transfusion > 100ml. incompatible –
renal damage, circulatory shock, and death.STOP
Transfusion ASAP.
Clinical Manifestations:
– Headache and backpain
– Chest pain- similar to angina
– N& V
– Tachycardia and hypotension
– Hematuria
Type III—Immune Complex Reaction
Type III Immune Complex Hypersensitivity
– From the formation or deposition of
antigen-antibody complexes in tissues
– Molecular size – larger – rapidly cleared
by phagocytic cells.--- smaller persists
longer in circulation  spleen and liver
 Inflammation - acute or chronic
disease of the organ system
E.g. serum sickness, urticaria,
arthritis, arteritis,
glomerulonephritis.
Type IV—Delayed or Cellular
Reaction
Type IV Cell Mediated Delayed
Hypersensitivity
– Sensitized T cells respond to antigens by releasing
lymphokines, which direct phagocytic cell activity.
– E.g.
Delayed hypersensitivity – chronic infection ( TB)

Graft versus host disease or transplant rejection

- Contact Dermatitis (48-72)
- Granuloma formation- 10-28 days, (leprosy)
 Management of Patients With
Allergic Disorders
History and manifestations; comprehensive allergy
history;

Diagnostic tests
– CBC-eosinophil count

– Total serum IgE

– Skin tests: note precautions

Screening procedures
 Medication
Oxygen, if respiratory assistance needed

Epinephrine for anaphylactic reactions

AntiHistamines

Corticosteroids
Prevention and Treatment of Anaphylaxis
Screen and prevent:

Treat respiratory problems; provide oxygen,

intubation, and cardiopulmonary resuscitation as
needed

Epinephrine: 1:1,000 SQ

Auto injection system: EpiPen

May follow with IV epinephrine

IV fluids
 Other Allergic Disorders
Contact dermatitis
Atopic dermatitis
Drug reactions (dermatitis medicamentosa)
Urticaria and angioneurotic edema
Food allergy
Serum sickness
Latex allergy
The round or disk shaped (discoid) rash of lupus produces
red, raised patches with scales. The pores (hair follicles)
may be plugged. Scarring often occurs in older lesions. The
majority (approximately 90%) of individuals with discoid
lupus have only skin involvement as compared to more
generalized involvement in systemic lupus erythematosis
(SLE).
Systemic Lupus Erythematous (SLE)

a chronic inflammatory disease of

autoimmune origin.
presence of autoantibodies to numerous
nuclear proteins, blood and nerve cells,
and blood proteins.
Inflammation – every organ system.
Lesions: connective tissue of the vascular
system, the kidney, the dermis, the
serous, synovial membranes.
Long and chronic, with exacerbations,
remissions.
 Etiology and Incidence

SLE is associated with a genetic

predisposition to the disease as well
as a family history autoimmune
disorders.

It occurs most commonly in women,

especially among those ages 20-30;
incidence is higher among African
Americans than whites
 PATHOPHYSIOLOGY
(process & manifestation)

 SLE is characterized by the formation of

antibodies (IgE and IgM) against the
body’s nucleic acids, phospholipids, white
blood cells, red blood cells, and
coagulation components.

 Antigen-antibody complexes against host

DNA form and deposit in a variety of
tissues, causing diffuse damage.

 Neutrophils attempt to phagocytize the

antigen-antibody complexes, but are
ineffective.
Lysosomal enzymes are released,
further propagating the tissue
damage.

The glomerular basement membrane

of the kidneys is particularly
susceptible to complex deposition; as
a result, there is a high incidence of
renal failure secondary to SLE.

Deposition of complex also occurs in

the brain, heart lung, GI tract
,spleen and skin.
Clinical Manifestations:
– Joint inflammation ( arthritis)
– Classic butterfly rash over the cheeks and
bridge of the nose.
– Photosensitivity
– renal, cardiac, and CNS dysfunction.
(Raynaud’s Syndrome)
– GI symptoms: n&v, esophagitis, anorexia
Other symptoms:
Wt. loss; fever, malaise; lethargy
Laboratory Findings:
– Presence of LE cells ( autoantibodies)
– Decreased complement levels
– Presence of immune complexes in
serum
– Presence of antibodies to DNA and
antinuclear antibodies.
– Decreased levels of rbc, wbc,
plateletsIncreased gamma globulin
fraction d/t increased antibody
production.
Nursing Diagnoses:
– Impaires physicl mobility d/t arthritis, malaise and
lethargy.
– Alt. in comfort: pain d/t inflammation
– Fluid volume deficit d/t vomiting
– Alt. in nutrition: less than body requirements d/t
anorexia, nausea, esophagitis.
– Potential for infection d/t poor physical condition
– Grieving d.t chronic nature of SLE and advent
exacerbations
– Disturbance in self concept: body image d/t butterfly
rash and alopecia
– Alt. in tissue perfusion: renal, GI and peripheral d/t
vasculitis.
Pharmacologic and Medical Intervention:
– NSAID anti inflammatory agents e.g.
Salicylates ( Aspirin)
– Anti malarial drugs – cutaneous and joint
inflammation.
– Corticosteroids – d/t systemic inflammatory
manifestations of the disease.
– Cytotoxic agents : alkylating agents
( cyclosphamide), and antifolates
( methotrexate)
– Plasmapheresis – remove circulating
autoantibodies and immune complexes from
the blood before organ and tissue damage
occurs.
 Other Interventions
Improve airway clearance
– Use semi-Fowler's or high-Fowler’s
position
– Pulmonary therapy; coughing and deep
breathing; postural drainage;
percussion; and vibration
– Ensure adequate rest
Pain
– Administer medications as prescribed
– Provide skin and perianal care