Hypersensitivity and Auto

Immune Disorders

Rozina Somani
April 18,2014
Objectives
By the end of the session learners will be able to
 Discuss immunological disorders
 Discuss the concept of hypersensitivity
 Discuss the diagnostic , Medical and surgical
management for patients with immunological disorders
Functions Of The Immune System
 Defense against infections
 Recognition of self , non-self and altered-
self .
 Eliminate non-self, altered-self invaders .
Autoimmune disorder
An autoimmune disorder is a condition that
occurs when the immune system attacks and
destroys its own healthy body tissue.
Autoimmune diseases arise from an
inappropriate immune response of the body
against substances and tissues normally
present in the body autoimmunity.
Immune Response
 Immune Response Antigens are large
molecules (usually proteins) on the
surface of cells, viruses, fungi, bacteria,
and some non-living substances such as
toxins, chemicals, drugs, and foreign
particles. The immune system recognizes
antigens and produces antibodies that
destroy substances containing antigens.
Structure Of Immune System
continued…..

 Secondary lymphoid tissue include Blood ,

Lymph ,Pharyngeal and Gut associated
lymphoid tissues.
 Secondary lymphoid tissue trap antigens and
make it available for mature lymphocytes .
 In secondary lymphoid tissues T & B cells
further mature to become Memory and killer
T-Cells and Plasma cells.
Lymphocytes

 Lymphocytes are chief cell of immune

system .
 Posses diversity ,specificity ,memory , self
and non-self recognition .
 20-40 % of cells in blood are lymphocytes
 Circulate in blood and have capability of
migrating to tissue .
T-Lymphocytes

 There are different subsets of T-Cells

T-Helper (TH ) ,T-Suppressor (T S),
T- Cytotoxic (TC) and T-Delayed Hypersensitivity (TD).
 (TH ) & (T S) cells exercise are immunoregularity role
over the whole specific immune system .
 Cellular interaction between (TH ) and B-Cell is
essential for optimal humoral response to most Antigen
.
B-Lymphocytes

 Antigen independent B-Cell maturation .

 Plasma cell are end cells with a life span
of 2-3 days during which they
continuously synthesized and secrete
Antibodies .
 Antigenic stimulation through antigenic
receptors on B-Cells surface
(immunoglobulins).
MAJOR FUNCTIONS OF CELLS
PARTICIPATING IN IMMUNE RESPONSES
 B cells - recognize antigens and
produce antibodies
 Plasma cells - produce antibodies
 TH cells - help in immune response,
produce cytokines
 Treg cells - inhibit immune respons
produce cytokines
 Tc cell - kill target cells
 Natural Killer cells -Able to to kill virally
infected and transformed cells
 Dendritic cells- present antigens to Th cells
IMMUNOGLOBULINS
(Antibodies )
 Antibodies are glycoprotein's synthesized
and secreted by plasma cells in response
to antigenic stimulation of B-Cells
 There are five serum immunoglobulin
IgG,IgA,IgM,IgD and IgE .
IgG

 Constitute about 75% of total serum

immunogloblins.
 Bacteriolytic, viricidal, and precipitating
antibody.
 In an immune response it appears late
and persists for longer duration
 Half-life is 18 to 23 days.
 Carries the major burden of neutralizing
bacterial toxins.
IgM

 Accounts for 5 to 10 % of total

immunoglobulins.
 Half-life is 5-days
 Can’t cross the placental barrier .
 The first one to appear in response to an antigen
and also the first one to disappear from the
serum .
 The first immunoglobulin ,synthesized by the
neonates .
IgA

 2 subclasses: IgA1 and 2.

 It is present in 2 forms:
 Serum IgA: monomeric, forms 15-20%
of serum Igs.
 Secretory IgA: predominant in secretions
e.g. saliva,tears, colostrum, bronchial,
genitourinary and intestinal secretions, has
a protective role against invading
pathogens.
IgD

 Less than 1% of total serum Igs.

 Monomeric.
 Present on B-cell membrane and acts as a B-
cell receptor.
 Exact function not known.
IgE

 Present in trace amounts in normal serum.

 Monomeric.
 Associated with atopic diseases, e.g. bronchial
asthma.
 Homocytotropic, and plays a role in type I
hypersensitivity.
 May be important in immunity to helminthic
parasites.
Hypersensitivity Reactions

 When an immunological sensitized

individual comes in contact with same
antigen second time it leads to secondary
boosting of immune system .
 Secondary response may be excessive
leading to tissue damage .
 Such reaction is called hypersensitivity or
Allergy .
 Classification of Hypersensitivity

 Type I – Anaphylactic ,Atopic hypersensitivity.

 Type II –Antibody dependent cytotoxic
hypersensitivity.
 Type III – Immune complex mediated
hypersensitivity.
 Type IV –Cell mediated (Delayed type)
hypersensitivity.
 .
Types of hypersensitivity reactions
Type I: Anaphylactic hypersensitivity:

 It is an immediate reaction beginning within minutes of

exposure to an antigen.

 It is mediated by I.e. antibodies.

 It requires previous exposure to specific antigen.

 It usually affects on skin, lungs and gastrointestinal

tract.

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Anaphylactic (type I)
Hypersensitivity

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Anaphylactic (type I) Hypersensitivity

 Examples:
◦ Asthma
◦ Allergic rhinitis
◦ Systemic anaphylaxis.
◦ Atopic dermatitis

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 Types of hypersensitivity reactions
Type II: cytotoxic hypersensitivity

 It occurs when the system mistakenly identifies a

normal constituent of the body as foreign.

 This reaction may be a result of cross-reacting

antibody, possibly leading to cell and tissue
damage

 It involves activation of complement by IgG or

IgM antibody binding to an antigenic cell.

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Cytotoxic (type II) Hypersensitivity

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Cytotoxic (type II) Hypersensitivity
Examples:
 Myasthenia gravis

 Blood Transfusion reaction

 Hemolytic anemia of new born

 Thrombocytopenia

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Types of hypersensitivity reactions
Type III: Immune complex hypersensitivity
 It involves in the formation of immune
complexes when antigen binds to antibodies.

 These type III complexes deposit in tissues

or vascular endothelium and leads to injury
with the help of vasoactive amines and the
increase number of circulating complexes.

 The joints and kidneys are particularly

susceptible.

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Immune complex (type III) hypersensitivity

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 Immune complex (type III)
hypersensitivity
Examples:
 Systemic lupus erythematosus

 Rheumatoid arthritis

 Serum sickness

 Nephritis

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Types of hypersensitivity reactions
Type IV: Cell mediated hypersensitivity

 Also known as cellular hypersensitivity

 It occurs 24-72 hrs after exposure to an allergen

 The reaction is mediated by sensitized T cells and

macrophages.

 The reaction results in tissue damage by releasing

lymphokines, macrophages and lysozymes.

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Cell mediated (type IV) HYPERSENSITIVITY

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 Cell Mediated (type IV)
HYPERSENSITIVITY
Examples:

 Contact dermatitis

 Tuberculin test.

 Organ transplantation (graft- versus -host

disease)

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Immunological
disorders
 Allergic Rhinitis

It is also called as Hay Fever

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 ALLERGIC RHINITIS
Definition:
“It is an inflammation of the nasal mucosa by an
allergen”.

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 Types of allergic rhinitis:
Perennial Seasonal
 Year-round with  Early spring, early
allergic triggers fall, early summer
 Sneezing, itching,  Intense symptoms
watery discharge from triggered by air-borne
nose and eyes pollens, house dust
and animal feather.

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Pathophysiology: ALLERGIC RHINITIS
Inhalation of an antigen (sensitization)

Re-exposure

Nasal mucosa reacts (histamine is mediator)

Slowing of ciliary action, edema formation and

leukocyte infiltration

Tissue edema and increase capillary permeability

(vasodilatation).

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Clinical manifestations: ALLERGIC RHINITIS
• Nasal congestion

• Clear to greenish rhinorrhea

• Intermittent sneezing and nasal itching

• Headache

• Pain over Para nasal sinuses

• Epistaxis

• Fatigue, loss of sleep and poor coordination.

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 Allergic rhinitis
Diagnostic tests:
• Nasal smears (nasal eosinophilia)

• Total serum IgE

Medical management:
• Oral anti histamines (blocks the action of histamine)

• Adrenergic nasal decongestant

• Mast cell stabilizers.

• Analgesics and antipyretics.

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 Allergic rhinitis
Nursing management:

Assessment
• Examination (Assess symptoms)
• History of patient (Allergy assessment)

Diagnosis
• Ineffective breathing pattern related to allergic
reactions
• Knowledge deficit related to allergy and the
recommended modifications in life style and self-care
practices
• Ineffective individual coping with condition and need
for environmental modification.

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 Allergic rhinitis
Nursing interventions:

1. Patient is instructed to modify the environment

to reduce the severity.

2. Encourage for deep breathing and cough

frequently for adequate gas exchange.

3. Encourage for steam inhalation

4. Promote rest.

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 Atopic dermatitis (eczema)
It is a type I immediate hypersensitivity
Definition:
Inflammation of the skin

Incidences/Causes:
• Familial tendency

• It is highest in infants and children

• 1% population is suffering from this disease

• Aggravated in low humidity and in winter.

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Pathophysiology: Atopic dermatitis
Allergen /Sensitizing antigen

Effect the skin (changes in lipid content, sebaceous gland activity and
sweating)

Skin reduced water-binding capacity in the skin

Higher trans epidermal water loss and decreased water content

Dry skin

Itching, rubbing leads to infection

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Clinical manifestations: Atopic dermatitis

• Red oozing crusting rash (in childhood)

• Dry thick brownish – grey and scaly skin

(later stage)

• Pruritis

• Lesion are mostly found on hand, foot,

back of the knees, neck, face, eyelids and
elbow bands.

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Medical Management:
Atopic dermatitis
• Moisturizers
• Topical and
systemic steroids
• Antibiotics
• Antihistamines
• Perform allergen
test

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Nursing management: Atopic dermatitis
• Assess and maintain hygiene (daily bath)

• Determine dietary and other allergen (cow milk, egg,

Soya, wheat, nut, fish)

• Teach to avoid allergen

• Keep wound area moist

• Teach proper use of medicines

• Avoid scratching (wear cotton fabrics, washing with

mild detergent)

• Prevent from secondary infection

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 Anaphylaxis
Definition:

It is an immediate life threatening systemic reaction that

can occur on exposure to particular substances

It is an immediate (type I hypersensitivity) immunologic

reaction, results from IgE antibody

This reaction affects many tissues and organs.

Death may occur due to respiratory tract spasm and

constriction or collapse.

.
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Causes: Anaphylaxis

• Food ( peanuts, fish, milk, eggs, wheat and chocolate).

• Medications (penicillin, NSAID’s)

• Insects stings (bees, ants)

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Pathophysiology: Anaphylaxis

Interaction of foreign antigen with IgE antibodies

Release of histamine

Activation of platelets, eosinophils and neutrophils

smooth muscle spasm, bronchospasm, mucosal edema

and inflammation.

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Clinical manifestations: Anaphylaxis

Mild Moderate Severe

Peripheral tingling Flushing Broncospasm

Sensation of Itching Laryngeal edema

warmth
Fullness in mouth bronchospasm Severe Dyspnea,
and throat cyanosis
Nasal congestion Edema of larynx Hypotension
Periorbital Dyspnea Cardiac arrest and
swelling coma may follow.
Pruiritis Cough
Sneezing wheezing
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Medical management: Anaphylaxis

1. If cardiac arrest then cardiopulmonary resuscitation

initiated.
2. Antihistamine to prevent recurrence reaction
3. Start intravenous fluids to maintain hemodynamics.
4. Give aminophylline for bronchospasm

Nursing management: Anaphylaxis

1. Assess for signs of anaphylaxis.

2. Restore effective breathing
3. Reduce anxiety by reassuring the patient
4. Provide oxygen, and maintain airway
5. Monitor vital signs.

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 SYSTEMIC LUPUS
ERYTHEMATOSUS (SLE)
Definition:
SLE is a chronic, multisystem inflammatory
disorder associated with the abnormalities of
immune system. Thus, affecting connective tissue,
blood vessels and serous and mucosal membranes.

Inflammatory reaction produces the biochemical

and structural changes.

It is characterized by remission and exacerbation

and often has an insidious onset.

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 SYSTEMIC LUPUS
ERYTHEMATOSUS (SLE)
Incidence:
 SLE occurs most commonly in younger
women b/w the ages of 15-40 years.
(hormonal changes)
 It occurs 10 times more frequently in
women than men.
 Has a familial tendency.

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 SYSTEMIC LUPUS
ERYTHEMATOSUS (SLE)
Causes:
 Unknown
 Autoimmune activity and hyperactivity of immune
system.
 Inherited defects in the regulation of immune activity
 Environmental stimuli (viral, bacterial infections,
sunlight or UV light etc.).
 Physical and emotional stress
 Drug induced SLE is associated with the adverse
reaction of some drugs, i.e. procainamide, hydralazine,
phenytoin

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SYSTEMIC LUPUS ERYTHEMATOSUS
(SLE)
Pathophysiology:
It is a immune-complex (type III ) hypersensitivity reaction.

Causative factor stimulate production of auto reactive B- lymphocytes

These B cells produce ANA (antinuclear antibodies).

ANA will attack the DNA within the cell nuclei, cell membranes of
RBC’s, WBCs and platelets.

Formation of immune complexes in serum and organ tissues.

Complexes can cause vasculitis, inflammation of connective tissues.

Decrease oxygen in organ and tissues

Organ and tissue damage.

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SYSTEMIC LUPUS
ERYTHEMATOSUS (SLE)
Clinical manifestations:
 Whole-body symptoms (fatigue, weight loss, fever,
mental disturbance, lymphadenopathy).
 Specific organ symptoms
◦ Skin changes
 Skin lesions consisting of butterfly shaped
rash across the bridge of nose and cheeks).
 Circular patches of raised, scaly skin (discoid
lesions), which are more inflammatory and
have a tendency to scar.
 Painless mouth ulcer
◦ Joint pain and stiffness
 Few joints are affected at any time, especially
the hands). 54
Clinical manifestations: SLE
butterfly rash

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 Clinical manifestations: SLE
 Kidneys (common in SLE)
Leading causes of death in client with SLE renal failure
from the kidney involvement.
 Nephritis
se glomerular filtration rate and proteinuria
Increase serum Cr levels
 Pulmonary and cardiovascular (due to
pleuritis and pericarditis)
 Chest pain
 Shortness of breath

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Clinical manifestations: SLE
 Nervous system
◦ Difficulty in understanding and thinking clearly
◦ Weakness and numbness
◦ Depression, seizures and psychosis

 Blood
◦ Leucopenia
◦ Anemia
◦ Thrombocytopenia

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Diagnostic tests: SLE….
 History & physical examination.
 CBC (anemia, leucopenia)
 Blood test (serum creatinine)
 Urine analysis (protein urea)

Medical management:
The goal of treatment is preventing progressive loss
of organ function, reducing likelihood acute disease
and minimizing disease related disabilities.
 Corticosteroids (e.g. prednisone)
 Immunosuppressive agents (cyclophosphamide and
azathioprine)
 NSAID’s (e.g. aspirin, ibuprofen)

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Nursing management: SLE

Assessment:
 History and physical examination
 Drug history
Goal:
 Maintenance of skin integrity
 Prevention of additional infection
 Promotion of a healthy life style and reduction of
stress.
 Relief of discomfort.

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Nursing diagnosis:
 Fatigue related to chronic inflammatory process
and to decreased oxygenation of tissues as result of
anemia.
 Pain related to inflammation of joints, muscles and
serosal membranes.
 Body image disturbance r/t presence of butterfly
rash.
 Fluid volume excess r/t decreasing in renal function
 Altered thought process r/t inflammation of cells in
cerebral cortex
 High risk for infection r/t inflammatory destruction
of leukocytes and corticosteroids suppression of
immune function

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SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
Implementation:
 A detailed record of patients fatigue to help patient plan a
schedule for activity and adequate rest.
 Nurse can assess pain level by using NPR scale (Numerical
Pain Rating) from the scale of 0-10 before administering pain
medications to monitor effectiveness.
 Detect early signs of fluid retention through daily weights and
compare I/O.
 Protect patient from nosocomial infection as patient is on
corticosteroids.
 avoid exposure to sunlight
 Monitor patient’s level of orientation and provide psychological
care.
 Take safety precaution for seizures.
 Communicate with the patient about the impact of disease that
can promote acceptance and increase compliance to treatment.

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Rheumatoid arthritis (RA)
Definition:
 Rheumatoid arthritis is a auto immune,
systemic, progressive, inflammatory
connective tissue disorder, affecting mainly
the small, peripheral joints in a pattern of
symmetric distribution.
(smeltzer et al, 2004)

RA affect the synovial tissues of the joint and

articular cartilage which result in
inflammation, joint destruction, deformity and
disability.
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Rheumatoid Arthritis ( RA)
 It could have systemic manifestation
 Rheumatoid nodules
 Vasculitis
 Lung disease
 Blood disorder
 osteoporosis
4/24/2015 64
Rheumatoid arthritis (RA)
Incidence:
women are more affected b/w ages 40-60 years.

Causes: unknown, although there are:

◦ Familial
◦ Genetic factor
◦ virus or microorganisms
◦ Immunologic mechanism (RF antibodies against
IgG).

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 Pathophysiology: RA
Stage I: triggering factor acts on synovium

Inflammatory changes (initially localized)

Tissue thickens with edema and congestion

Stage II: the formation of the layer of inflammatory granulation tissue

(pannus)

Extending from articular surface to the joint interior

Progressive damage of the joint capsule and subchondral bone.

Stage III: granulation tissue invaded with tough fibrous tissue

Converted to scar tissue

Distortion of the affected joint b/c of inhibition of joint movement.

Stage IV: Bone ankylosis (firm bony union) and fixation

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Rheumatoid arthritis (RA)

Clinical manifestations:
 Symmetrical pattern of affected joints
 Joint inflammation often affecting the
wrist and finger joints closest to the
hand
 Joint inflammation sometimes affecting
other joints, including the neck,
shoulders, elbows, hips, knees, ankles,
and feet in later stages.
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 Clinical manifestations: RA

 Tender, warm, swollen joints

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Clinical manifestations: RA

 Nodules over bony prominence.

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Clinical manifestations: RA

 Fatigue, occasional fevers, a general

sense of not feeling well
 Pain and stiffness lasting for more
than 30-60 minutes in the morning
or after a long rest
 Guarded movement or limited ROM
and strength

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Clinical manifestations: RA

 Ulnar drift

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Clinical Manifestations
 Enlarged spleen and lymph nodes
 Depression and early afternoon fatigue.
Rheumatoid arthritis (RA)

Diagnostic Evaluation:
◦ History taking and physical examination
◦ Laboratory findings:
 increased rheumatoid factor
 increased ESR and C-reactive protein
 Synovial fluid analysis

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Diagnostic evaluation:

 Radiology:
 X-ray
 CT scan and MRI
Rheumatoid arthritis (RA)
Medical management:
 NSAID’s (ibuprofen, mefanamic acid,
aspirin)
 Corticosteroids (prednisone, hydrocortisone)
 Immunosuppressive (azathioprine,
methotrexate)
 Biological modifier i.e. TNF- inhibitor.

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Rheumatoid arthritis (RA)
Surgical management:
 Total joint replacement
 Synovectomy

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Other Measures:
 Meditation, yoga
 Acupuncture
 Anti inflammatory herbs: ginger
 Vegetarian diet (low in animal protein and
sugar) and fruits
 hydrotherapy
NURSING MANAGEMENT: RA
Nursing diagnosis:
 Alteration in comfort i.e., pain R/t
inflammation, joint deformity and joint
destruction.
 Impaired physical mobility R/t pain,
stiffness and impaired joint function.
 Fatigue and activity intolerance r/t
systemic inflammation, anemia, and
impaired mobility.
 Self care deficit r/t joint deformity, pain,
immobility.
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NURSING MANAGEMENT: RA
 Provide: local comfort measures:
◦ Application of heat and cold
 Encourage patient to have more rest when the disease
is active and more exercise when it is not.
 Pain medication before exercise and before bed time.
 Encourage patient to exercise for maintaining healthy
and strong muscles, preserving joint mobility, and
maintaining flexibility
 Physical therapy for stretching and ROM exercises.
 Massage over the surrounding muscles.
 Provide early morning assistance.
 Plan patient activities.

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Cont, …
 Teach about the use of splints, that are mostly applied on
wrists and hands, but also on ankles and feet to reduce pain
and swelling.
 Frequent positioning.
 Choose exercises such as stretching, and low-impact aerobics
(swimming, water aerobics). Use caution with any exercise
that puts pressure on the joints, like jogging and heavy weight
lifting.
 Promote nutrition, that is, overall nutritious diet with high
caloric, protein, and calcium is important.
Thank You