the immune system
DESCRIPTION
The Immune System. The body’s protective response to invading foreign organisms. Immune System: Functions. Protects from pathogens and foreign molecules Parasites Bacteria Viruses Removes dead/damaged cells Attempts to recognize and remove abnormal cells. Immune System: Pathologies. - PowerPoint PPT PresentationTRANSCRIPT
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The Immune System
The body’s protective response to invading foreign organisms
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Immune System: Functions
Protects from pathogens and foreign moleculesParasitesBacteriaViruses
Removes dead/damaged cells Attempts to recognize and remove abnormal
cells
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Immune System: Pathologies
Incorrect responsesAutoimmune disease
Overactive responsesAllergies
Lack of response Immunodeficiency disease (AIDS)
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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)
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3 processes needed for immunity:
Inflammation
Cell-mediated Immunity
Antibody-mediated/Humoral
Immunity
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Figure 24-2a
Lymphatic System: Anatomy
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Key Cells of the Immune System
Leukocytes (white blood cells)
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Cells of the Immune System
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Figure 24-4
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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.
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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.
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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
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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
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Major cells of inflammation:
MacrophagesPreform phagocytosis, repair injured tissueStimulate CMI + AMILong life span and plenty of energy to
degrade many foreign proteins.
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Phagocytes
•Cells under attack release histamine.•Purpose is to engulf and destroy invaders
Cells
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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
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Major cells of inflammation:
EosinophilsAct against infestations of parasitic larvae
Can inhibit and induce inflammation
Number increases during allergic reaction
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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.
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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.
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What is specific immunity?
Specific response Memory for future
reinvasion Antibody-based
B cells primary actors Cell-mediated
T cells only
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Antigens
Antigen: Typically large molecules, often proteins.
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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.
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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
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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.
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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
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B -Lymphocytes
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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
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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
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B cells differentiate into . . .
Antibody producing cells [attack mode]Memory cells [remembers & future
protection]Antigen & T-helper cell
memory
antibodies
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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…
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Cell Mediated Immunity
Cellular Immunity:
Lymphocytes directly attack & destroy foreign cells & infected host cells.
T-Cells or T-lymphocytes activated by a specific antigen.
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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.
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Figure 24-16
T Lymphocytes: Cell-MediatedRoles of T lymphocytes and NK cells in cell-
mediated immunity
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What happens in a cell-mediated response? The key events:
Surveillance and recognitionAttackMemory
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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.
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Vaccination
A preparation containing antigenic
material: Whole live microorganism Dead microorganism Attenuated (harmless) microorganism Toxoid (harmless form of toxin) Preparation of harmless ags
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Disorders of the Immune System
Hypersensitivity Disorders Allergy Anaphylaxis Transfusion reactions, transplant rejection
Immunodeficiency Disorders HIV/AIDS
Autoimmune Systemic lupus erythematosus, rheumatoid arthritis etc.
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Hypersensitivity
Excessive reaction to an antigen (allergen) to which most people do not react Includes
Allergies Transplant reaction Transfusion
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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 (
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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
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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)
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Hypersensitivity Studies & Medical Management Studies—CBC, Total serum IgE levels, skin
testing
Medical Management Immediate intervention Symptom management & long term control Environmental control
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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
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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
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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
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Allergic Responses
First exposureSensitizationActivation, clone B cells, form antibodies and
memory cells Re-exposure
Many antibodies, activated T cells, intensified response, inflammation
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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
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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
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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
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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
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Anaphylaxis
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Decision tree for patient with anaphylactic reaction
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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
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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
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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)
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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
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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
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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
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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
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Autoimmune Diseases