The Immune System

Immunity: the body’s specific protective response to invading foreign agent or

organism

Immunopathology: the study of diseases that result from dysfunction of the

immune system

Innate Immunity – Non- specific response – primary defense mechanism against

invading organisms
Mechanical mechanisms:
1. Skin and Mucous Membranes
2. Tears and Saliva and Urine Tract such as intact skin, chemical barriers,
and acidic gastric secretions or enzymes in tears and saliva
Chemical mediators - histamine, bradykinin, complement, and prostaglandins;
interferons
 Cells – WBCs – most important cellular component Inflammatory response
- Phagocytic Cells
- Neutrophils – first cells to enter infected area
- Macrophage - larger, responsible late stages of infection,
cleanup dead neutrophils and other cellular debris;
• Monocytes + macrophage = Mononuclear phagocytic
system
• dust cells = lungs; Kupffer cells = liver; microglia =
CNS
- Cells of Inflammation
- Basophils motile WBC Release chemicals that produce
- Mast Cells non-motile an inflammation response
- Eosinophils – initiate inflammation

Adaptive Immunity – Specific immunity - second line of defense; specific against

a foreign antigen
- exhibits specificity and memory
Result of prior exposure to an antigen
Active or passive

Antigens – stimulate adaptive immunity response, influence production of B cells

2 groups
1 Foreign antigens – introduced from outside of the body; bacteria, viruses,
chemicals released by microorganism;
pollen, animal hairs, foods, drugs – overreaction of the immune system
2 Self- antigens – produced by person’s body that stimulate immune response
- autoimmune disease – self-antigens stimulate unwanted destruction of
normal tissue
2 parts
1 Humoral Immunity – humors = body fluids
2. Cell-mediated – blood cells alone responsible for immunity

2 types of Lymphocytes
1 B cells – Produce antibodies or immunoglobulins; stimulate production of
plasma cells (site of antibody production); Antibody-mediated Immunity
2 T cells – T lymphocytes; responsible for cell-mediated immunity; stimulates
immune response;assists B cells to produce antibodies

Stem cells

Pre T cells Pre B cells

Thymus Red Bone Marrow

T cells B cells

Role of Antibodies
• Agglutination of antigens
• Opsonization
• Promote release of vasoactive substances; activationof complement system
and phagocytosis
• Act in concert with other components of the immune system
• Types of immunoglobulins: IgA, IgD, IgE,IgG, and
IgM

Complement system:
 Opsonization - enhancing phagocytosis of antigens
 Chemotaxis - attracting macrophages and neutrophils
 Lysis - rupturing membranes of foreign cells
 Clumping of antigen-bearing agents
 Altering the molecular structure of viruses

Immunoglobulins:
Comparison of Different Types of hypersensitivity
 type-III
type-I type-II type-IV
characteristics (immune
(anaphylactic) (cytotoxic) (delayed type)
complex)

antibody IgE IgG, IgM IgG, IgM None

antigen exogenous cell surface soluble tissues & organs

response time 15-30 minutes minutes-hours 3-8 hours 48-72 hours

erythema and
erythema and
appearance weal & flare lysis and necrosis edema,
induration
necrosis

basophils and antibody and complement monocytes and

histology
eosinophil complement and neutrophils lymphocytes

transferred with antibody antibody antibody T-cells

erythroblastosis
SLE, farmer's
lung disease tuberculin test,
allergic asthma,
examples fetalis, poison ivy,
hay fever
Goodpasture's granuloma
nephritis

• IgG (75% of total Immunoglobulin)

▪ Appears in serum and tissues
▪ Assumes a major role in blood-borne and tissue infections
▪ Activates the complement system
▪ Enhances phagocytosis
▪ Crosses the placenta
• IgA (15% of total Immunoglobulin)
▪ Appears in body fluids (saliva, tears, mucous mem to protect body suface)
▪ Protects against respiratory, GIT, and GUT infections
▪ Prevents absorption of antigen from food
▪ Found in colostrums for protection

IgM (10% of total Immunoglobulins)

▪ Appears mostly in intravascular system
▪ Appears as the 1st immunoglobulin produced in response to bacterial and viral
infections
▪ Activates the complement system
▪ responsible for transfusion reactions, often 1st antibody produced in response to
an antigen

IgD (0.2% of total Immunoglobulins)

▪ Appears in small amount in serum
▪ Possibly influences B-lymphocyte differentiation, but role is unclear

IgE (0.004% of total Immunoglobulins)

▪ Appears in serum
▪ binds to mast cells and basophils and takes part in allergic and some
hypersensitivity reactions
▪ Combats parasitic infections

Variables That Affect Immune System Function

• Age and gender
• Nutrition
• Presence of conditions and disorders: cancer/neoplasm, chronic illness,
autoimmune disorders, surgery/trauma
• Allergies
• History of infection and immunization
• Genetic factors
• Lifestyle

• Immune System Disorders:

Autoimmunity - protective immune response paradoxically turns against or
attacks the body, leading to tissue damage

Hypersensitivity - Body produces inappropriate or exaggerated responses to

specific antigens

Gammopathies - Immunoglobulins are overproduces

Immune deficiencies
Primary Deficiency - results from improper development of immune congenital or
inherited
Secondary Deficiency - results from some interference with an already developed
immune system

Allergy = hypersensitive reaction; response of immune system to normally

harmless substances
Invasion of antigen
 Foreign substance in the body

Immune system will remove it

Chemical Mediators – found in mast cells and also in basophils; released when
stimulated by antigens

Histamine – reached within 15 minutes after antigen contact

vasodilation
contraction of bronchial smooth muscle
increases secretions of gastric and mucosal cells
increases permeability
flare and wheal reaction
chemotaxis

Eosinophils Chemotactic Factor – attracts eosinophils and neutrophils

Prostaglandins – vasodilation
vascular permeability
contractions
recruits eosinophils and basophils

Platelet Activating Factor – bronchoconstriction

increases vascular permeability
production of bradykinins
platelet aggregation

Leukotrines – Slow –reacting Substances of Anaphylaxis

Initiates inflammation response
Smooth muscle contraction
Bronchial constriction
Mucous secretions in the airways
Chemotaxis
Increases vascular permeability

Bradykinins - Increases vascular permeability

Vasodilation
Bronchial muscle contractions

Anaphylaxis = IgE Mediated Hypersensitivity

- an immediate, life-threatening allergic reaction that is caused by a

systemic antigen-antibody immune response to a foreign substance
(antigen) introduce into the body
- “without protection”
- US 20, 000 to 50, 000 people each year
 - severe, whole-body allergic reaction

- caused by Type I, IgE mediated hypersensitivity reaction

Type I hypersensitivity (or immediate hypersensitivity) is an allergic reaction
provoked by reexposure to a specific type of antigen referred to as an allergen
4 types of Hypersensitivty
Mediator
I Anaphylactic Immediate IgE Asthma,
Urticaria,

II Cytolytic/Cytotoxic Complement- IgM, IgG Hemolytic

dependent anemia
III Immune Complex Antigen- IgM, IgG Serum
antibody sickness
complexes
IV Cell-mediated/delayed Lymphokine Sensitized T Contact
release cells dermatitis

Allergens

Exposure may be
by ingestion, inhalation, injection, or direct
contact.
Common causes of anaphylaxis include:
 Food - Peanuts, tree nuts (walnuts,
cashews, etc.), shellfish, fish, milk, and
eggs commonly cause anaphylactic
reactions

 Medication - Anaphylactic reactions to medication will typically occur within an

hour after taking the drug, however reactions may occur several hours later
(This is usually due to a toxic reaction: morphine, x-ray dye, and others)
 Insect stings - The symptoms of anaphylactic reactions to insect stings usually
occur within minutes of the sting.
 Latex - Approximately 10 to 17 percent of those employed in the health care
occupations have this allergy.

Pollens and other inhaled allergens rarely cause anaphylaxis. Some people have
an anaphylactic reaction with no known cause.

1st exposure = no manifestations

Sensitization stage (body produces IgE antibodies)
 IgE attaches to Mast cells and basophils

Reexposure

Immediate response to allergens

Degranulation

Clinical Manifestations

Mild: redness, pruritus, swelling, urticaria

Moderate: slight difficulty of breathing with nasal flaring

More edema

Severe: decreased breath sounds

pulmonary congestion

others: pallor, clammy skin

tachycardia
hypotension
anxiety
restless
decreasing LOC

* without immediate intervention may lead to Anaphylactic shock

death
 Antigen (allergen)

Antibody (IgE) Attach to Mast cells,

Basophils

Histamine, luekotriene,
cytokines, prostaglandins

Peripheral Constriction of extra

vasodilatation vascular smooth muscle
(brochoconstriction,
Increased Capillary laryngo-spasm, cramps)
permeability
Increased SVR

Extravasation of
intravascular fluids

Edema Relative
hypovolemia

Decreased Cardiac
output

Decreased tissue
perfusion

Impaired cellular
metabolism
Diagnosis

Rapid development of symptoms in response to a suspect allergen.

Skin allergy testing

RAST blood tests – radioallergosorbent test – uses principle of

immunoabsorption and determine to what substances a person is allergic.

PFT – Pulmonary function test – confirm diagnosis or to evaluate respiratory

status, asses severity of lung obstruction

Blood assays – measure total amount of IgE normally present in the circulation

Nx Dx:

Ineffective airway clearance rt laryngeal edema and bronchospasm

Assessment

1. Maintain patent airway. Continually monitor respiratory rate and depth and
breathe sounds for respiratory effort and effectiveness of ventilation
(assess need for intubation, tracheotomy, O2 therapy).
2. Immediately assess, and circulation if presentation is severe, and
intervene with cardiopulmonary resuscitation as appropriate
3. If presentation is less severe, assess vital signs, degree of respiratory
distress, and presence of angioedema.
4. Watch out for Hypotension and shock
5. Remove causative agent. Immediate treatment should include application
of tourniquet above site of antigen injection (allergy injection, insect sting) or
skin test site, to slow the absorption of antigen into the system.
6. Epinephrine 0.1 to 0.5 mg (0.01 mg/kg) is injected into opposite arm
subcutaneously (S.C) or I.M. may repeat every 15 to 20 minutes, if necessary,
to cause vasoconstriction, decrease capillary permeability, relax airway
smooth muscle, and inhibit mass cell mediator release.
7. Bronchodilators are given to relax bronchial smooth muscle.
8. Antihistamines, such as diphenhydramine and, possibly H2-histmaine
blockers, such as ranitidine, may be given to block the effects of histamine.
9. Corticosteroids are given to decrease vascular permeability and diminish
the migration of inflammatory cells; may be helpful in preventing late-phase
responses.
10. Rapidly infuse I.V. fluids to fill vasodilated circulatory system and raise
blood pressure.
11. Monitor central venous pressure to ensure adequate fluid volume and to
prevent fluid overload.
12. Insert indwelling catheter and monitor urine output hourly to ensure kidney
perfusion.
 13. Remain responsive to the patient, who may remain alert but not
completely coherent because of hypotension, hypoxemia, and effects of
medication.
14. When the patient is stable and alert, give a concise explanation of
anaphylaxis and the treatment that was given.
15. Keep family and significant others informed of the patient’s condition and
treatment being given.
16. Prevent further exposure to antigens
17. When new allergy identified, the nurse advices the patient to wear or carry
identification that names the specific allergens or antigens
18. Maintain Hypoallergenic diet

Medications

Epinephrine – drug of choice – reverses many distressing symptoms

Antihistamine – prevent/reduce permeability; reversing effects of histamine
- diphenhydramine, promethazine, loratidine
- benadryl – treat minor symptoms allergy
corticosteroids – inhibits prostagandins synthesi
- hydtocortisone, bethametasone
- prednisone
bronchodilator – treatment of bronchial spasm