the immune system the body’s protective response to invading foreign organisms

The Immune System

The body’s protective response to invading foreign organisms

Immune System: Functions

Protects from pathogens and foreign moleculesParasitesBacteriaViruses

Removes dead/damaged cells Attempts to recognize and remove abnormal

cells

Immune System: Pathologies

Incorrect responsesAutoimmune disease

Overactive responsesAllergies

Lack of response Immunodeficiency disease (AIDS)

Body Defenses: Two Lines

First line of defense Physical and chemical barriers:

Skin, epithelial linings, and cilia Acids, mucous, and lysozymes

Second line of defense Innate, non-specific, immediate response Acquired; attack a specific pathogen (antigen)

3 processes needed for immunity:

Inflammation

Cell-mediated Immunity

Antibody-mediated/Humoral

Immunity

Figure 24-2a

Lymphatic System: Anatomy

Key Cells of the Immune System

Leukocytes (white blood cells)

Cells of the Immune System

Figure 24-4

Cells

Leukocytes: 5 major categories. Neutrophils: Phagocytic cells that wander throughout

the connective tissue destroying bacterias. Eosinophils: Phagocytic cells that destroy allergens,

antigen & anti-body complexes, & some inflammatory chemicals.

Surround larger parasites & attack them with enzymes to weaken or destroy them.

Defend against allergies & parasitic worm infections.

Basophils: Helper cells that secrete vasodilators & anticoagulants in order to speed other leukocytes to the infected zone.

Cells

Lymphocytes: A variety of cells active in the immune response.

Natural Killer Cells (NK Cells): Attack any cell with an unusual plasma membrane, such as cells that are infected by a virus or have become cancerous.

Cytolysis: Perforin protein is injected into the cell to cause it to “explode”.

Granzymes: Cause the cell to self-destruct. Found in the spleen, red bone marrow, & lymph nodes.

Monocytes: Wandering cells that eventually turn into macrophages.

Inflammation (natural immunity)

Inflammation: One of the body’s most common responses to tissue damage. Occurs in roughly the same way in any tissue.

Four Cardinal signs of Inflammation: RednessSwellingHeatPain

Major cells of inflammation:

Neutrophils:1st line defense against invaders in blood and

ECF.Destroy invaders by phagocytosisAbsolute neutrophil count is used to

determine a person’s risk for infection

Major cells of inflammation:

MacrophagesPreform phagocytosis, repair injured tissueStimulate CMI + AMILong life span and plenty of energy to

degrade many foreign proteins.

Phagocytes

•Cells under attack release histamine.•Purpose is to engulf and destroy invaders

Cells

Major cells of inflammation:

BasophilsCause the manifestation of inflammationContain chemicals that act on b. vessels

Heparin inhibits blood clotting Histamine constricts small veins & respiratory

smooth muscle

Major cells of inflammation:

EosinophilsAct against infestations of parasitic larvae

Can inhibit and induce inflammation

Number increases during allergic reaction

Immune System

Specific Immune Defenses: Cells

specifically geared toward fighting certain invaders, and remembering previous foreign invaders so that they can be rapidly eliminated in the future.

Immune System Two Divisions of the Immune System:

1. Humoral Immunity aka Antibody-Mediated Immunity:

Driven by B cells.

2. Cell-mediated immunity:

Driven by T cells.

What is specific immunity?

Specific response Memory for future

reinvasion Antibody-based

B cells primary actors Cell-mediated

T cells only

Antigens

Antigen: Typically large molecules, often proteins.

Antigen Processing

Major Histocompatability Complex (MHC): “Self-antigens” that are unique to all of your body cells except red blood cells.Help T-cells recognize which cells are foreign. MHC-1s: Cells that posses MHC and are

labeled “you” by the T-cells.

Antibodies Also known as immunoglobulins Some act as labels to identify

antigens for phagocytes Some work as antitoxins

i.e. block toxins for e.g. those causing diphtheria and tetanus

Some attach to bacteria making them less active easier for phagocytes to engulf

Some cause agglutination (clumping together) of bacteria

Humoral Immunity

Humoral Immunity aka Antibody-Mediated Immunity

B cells (B-lymphocytes) produce antibodies to engage in a complex purging process.

Immunoglobulins (Igs) Antibodies made up of glycoproteins called

globulins.

Antigen-Binding Site Tips of each chain are called variable regions &

are areas where the antibody attaches to the antigen.

B -Lymphocytes

Receptors recognize an antigen on the surface of the invader, the B-cell divides rapidly.

Antigens are presented to the B-cells by macrophages

B -Lymphocytes

Type Number of ag binding sites

Site of action Functions

IgG 2 •Blood

•Tissue fluid

•CAN CROSS PLACENTA

•Increase macrophage activity

•Antitoxins

•Agglutination

IgM 10 •Blood

•Tissue fluid

Agglutination

IgA 2 or 4 •Secretions (saliva, tears, small intestine, vaginal, prostate, nasal, breast milk)

•Stop bacteria adhering to host cells

•Prevents bacteria forming colonies on mucous membranes

IgE 2 Tissues •Activate mast cells

HISTAMINE

•Worm response

When help arrives . . .

The T-helper cell receptor “docks” with the B cell’s MHComplex

B cells proliferate . . . Antigen & T-helper cell

Proliferation of cell line

Naïve cell

B cells differentiate into . . .

Antibody producing cells [attack mode]Memory cells [remembers & future

protection]Antigen & T-helper cell

memory

antibodies

AMI in summary

An invaders attacks…Antigen is phagocytized by the B cell

Broken into non-infective pieces & attached to MHC which is placed on the cell membrane surface here it is recognized by the helper T cell…

Cell Mediated Immunity

Cellular Immunity:

Lymphocytes directly attack & destroy foreign cells & infected host cells.

T-Cells or T-lymphocytes activated by a specific antigen.

Cellular Immunity

Types of T-Cells involved in Cell-mediated Response: Cytotoxic T-Cells: Responsible for actual

attacking of the foreign body or infected cell. Helper T-Cells: Stimulate other helper T-

cells, cytotoxic T-cells, and B cells. Suppressor T-Cells: Help regulate the attack

& prevent tissue destruction. Memory T-Cells: Remain as an immune

response and stimulate faster responses if the same antigen invades again.

Figure 24-16

T Lymphocytes: Cell-MediatedRoles of T lymphocytes and NK cells in cell-

mediated immunity

What happens in a cell-mediated response? The key events:

Surveillance and recognitionAttackMemory

Types of Immunity Active Immunity: You encountered the

pathogen yourself and developed your own antibodies to it.

Passive Immunity: You received antibodies directly introduced into the body.

Naturally Acquired: Antibodies are received through natural means.

Artificially Aquired: Antibodies are received through artificial (scientific) methods.

Vaccination

A preparation containing antigenic

material: Whole live microorganism Dead microorganism Attenuated (harmless) microorganism Toxoid (harmless form of toxin) Preparation of harmless ags

Disorders of the Immune System

Hypersensitivity Disorders Allergy Anaphylaxis Transfusion reactions, transplant rejection

Immunodeficiency Disorders HIV/AIDS

Autoimmune Systemic lupus erythematosus, rheumatoid arthritis etc.

Hypersensitivity

Excessive reaction to an antigen (allergen) to which most people do not react Includes

Allergies Transplant reaction Transfusion

Hypersensitivity Disorders

Reaction may be Local (gastrointestinal, skin, resp, conjuctaval) or systemic (anaphylactic)

Q: What factors affect the severity of a hypersensitivity reaction?

Host response Exposure amount Nature of the allergen Route of allergen entry Repeated Exposure (

Hypersensitivity Assessment

Subjective InformationPruritus, nausea and uneasiness

History of present illnessOnset, frequency and duration of symptomsNature and progression of s/sPossible exposures of known allergens/common allergensChronic, seasonal or single episode Aggravating & alleviating factors

Hypersensitivity Assessment

Physical Assessment Respiratory

S/Sx caused by Bronchoconstriction—SOB, difficulty breathing, wheezing, & coughing

Sneezing, excessive nasal secretions, inflamed nasal membranes

Cardiovascular S/Sx caused by Vasodilation—Flushing, Hypotension, Edema Shock followed by cardiovascular collapse and respiratory arrest

GI Nauses, vomiting, diarrhea

Skin Rash, areas of raised inflammation (urticaria/hives)

Hypersensitivity Studies & Medical Management Studies—CBC, Total serum IgE levels, skin

testing

Medical Management Immediate intervention Symptom management & long term control Environmental control

Hypersensitivity—Medications Oxygen—if respiratory assistance needed Bronchodilators

Emergency bronchodilator—Epinephrine 1:1,000 SQ–Anaphylactic reactions (may need to following with IV Epi)

Antihistamines—symptom management & long term control First Generation—Prototype Diphenhydramine Second Generation—Prototype Fexofenadine

Leukotriene inhibitors—Inhibits the release of leukotrienes from mast cells & basophils)

Prototype—montelukast (Singulair) Steroids—symptom management & long term control

Systemic—Prototype Prednisone

Allergies

When the immune system responds to harmless substances

Allergens – antigenic substances Allergens include house dust, animal skin,

pollen, house dust mite and its faeces

Immunoglobulins and Allergic Response

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

Allergic Responses

First exposureSensitizationActivation, clone B cells, form antibodies and

memory cells Re-exposure

Many antibodies, activated T cells, intensified response, inflammation

Allergies

Histamine causes blood vessels to widen and become leaky.

Fluid and white blood cells leave capillaries. The area of leakage becomes hot, red and

inflamed

Hypersensitivity—Latex Allergies Latex products in health care—Gloves, tourniquets,

electrode pads, tape, urinary catheters, B/P cuffs, stethoscopes, IV tubing & syringes, O2 masks, etc.

Type I anaphylactic hypersensitivity reaction from rubber latex proteinsExposure—skin, mucous membranes, inhalation or

bloodReaction—ranges from erythema, urticaria, rhinitis,

conjuctivitis to asthma & full blown anaphylactic shock

Latex Allergy

Risk factors for latex allergies Long term exposure Hx of hay fever, asthma & allergies to certain foods

Fruits/vegetables—avocado, guava, kiwi, bananas, tomatoes, peaches, grapes, apricots, potatoes

Nuts—water chestnuts, hazelnuts, peanuts NIOSH Recommendations—National Institute of Occupational Safety &

Health Gloves—powder free, non-latex when unlikely to be in

contact with infectious materials, avoid oil-based hand lotions when wearing glove, hand wash w/ soap after removal

Frequent cleaning of areas with latex-containing dust Know s/sx of latex allergy—if symptoms develop avoid direct

contact with latex gloves and products Medical-alert bracelet & Epi pen

Hypersensitivity—Anaphylaxis

Most severe IgE-mediated allergic reaction

Potentially fatal

Symptoms are often severe with a rapid onset Fall in B/P, laryngeal edema, bronchospasms leading to

CV collapse, MI and Resp. failure First sign may be an “uneasiness” or “sense of impending

doom” or nausea followed quickly by respiratory difficulty and a drop in B/P

Signs—wheezing/stridor, severe dyspnea, congestion, tachycardia, hypotension, cyanosis, pallor, N/V, diarrhea

Anaphylaxis

Decision tree for patient with anaphylactic reaction

Hypersensitivity—Anaphylaxis

Patient education Avoidance of allergen S/Sx requiring immediate medical intervention Medication management

Self administration of subcut epinephrine (Epi-pen) Importance of Benadryl in addition to epinephrine Prevention—taking preventive medications as

ordered Medic-alert identification

Hypersensitivity—Transfusion Reactions

Mild to moderate hypersensitivity reactions S/Sx—Low grade fever, possible chills, urticaria,

diarrhea, cough Stop the transfusion, administer NS IV, Benadryl,

Tylenol, diuretic and a possible steroid Restart transfusion after symptoms subside at a

slower rate

Hemolytic reactions S/Sx—Fever, chills/rigors, urticaria, wheezing,

hypotension Stop the transfusion, O2, NS IV, epinephrine

(severe), antihistamines

Hypersensitivity—Transplant Rejection “Graft versus Host Disease” GVHD

Reaction occurs approx 7-10 days after transplant once blood supply to new tissue has developed

Sensitized lymphocytes cause sloughing at the graft site

Long-term immunosuppressive therapy—Corticosteroids (Prednisone), cyclosporin (Sandimmune) & azathioprine (Imuran)

Immunodeficiency Disorders

Primary Genetic May affect phagocytic function, B cells and/or T cells,

or the complement system

Secondary Acquired Contributing causes: Burns, malnutrition, chronic

stress, diabetes

Primary Immunodeficiency's

Usually seen in infants and young children Manifestations: vary according to type; severe or

recurrent infections; failure to thrive or poor growth; and positive family history

Potential complications: recurrent, severe, potentially fatal infections

Treatment: varies by type; treatment of infection; pooled plasma or immunoglobulin; GM-CSF or GCSF; thymus graft, stem cell, or bone marrow transplant

Immunodeficiency—Nursing Management & Patient Teaching

Monitor for S/Sx of infection Monitor lab values Dietary support Management of stress & anxiety Reduce risk of infection—hand washing, hygiene,

avoiding crowds Medication management

Autoimmune Disorders

Development of a cellular and/or humoral response to one’s own tissue

Disorders tend to cluster—many individuals have more than one autoimmune disorder

Genetic predisposition likely Examples—rheumatoid arthritis (RA), systemic lupus

erythematosus, ulcerative colitis, multiple sclerosis (MS), psoriasis, type 1 diabetes, etc

Treatment Symptom management Plasmapheresis/plasma exchange—removal of plasma (immunoglobuin

—IgG, antigen-antibody complexes, & inflammatory mediators) and replacement with NS, LR, FFP or albumin

Immunosuppressive therapy to prevent recovery of IgG production

Autoimmune Diseases