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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.

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the immune system

The Immune System

The body’s protective response to invading foreign organisms

immune system functions
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
Immune System: Pathologies
  • Incorrect responses
    • Autoimmune disease
  • Overactive responses
    • Allergies
  • Lack of response
    • Immunodeficiency disease (AIDS)
body defenses two lines
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
3 processes needed for immunity:

Inflammation

Immunity

Antibody-mediated/Humoral

Cell-mediated Immunity

key cells of the immune system
Key Cells of the Immune System

Leukocytes (white blood cells)

cells
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.
cells1
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(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:
    • Redness
    • Swelling
    • Heat
    • Pain
major cells of inflammation
Major cells of inflammation:
  • Neutrophils:
    • 1st line defense against invaders in blood and ECF.
    • Destroy invaders by phagocytosis
    • Absolute neutrophil count is used to determine a person’s risk for infection
major cells of inflammation1
Major cells of inflammation:
  • Macrophages
    • Preform phagocytosis, repair injured tissue
    • Stimulate CMI + AMI
    • Long life span and plenty of energy to degrade many foreign proteins.
phagocytes

Cells

Phagocytes

Cells under attack release histamine.

Purpose is to engulf and destroy invaders

major cells of inflammation2
Major cells of inflammation:
  • Basophils
    • Cause the manifestation of inflammation
    • Contain chemicals that act on b. vessels
      • Heparin inhibits blood clotting
      • Histamine constricts small veins & respiratory smooth muscle
major cells of inflammation3
Major cells of inflammation:
  • Eosinophils
    • Act against infestations of parasitic larvae
      • Can inhibit and induce inflammation
    • Number increases during allergic reaction
immune system
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 system1
Immune System
  • Two Divisions of the Immune System:
    • Humoral Immunity aka Antibody-Mediated Immunity:
        • Driven by B cells.
    • Cell-mediated immunity:
        • Driven by T cells.
what is specific immunity
What is specific immunity?
  • Specific response
  • Memory for future reinvasion
  • Antibody-based
    • B cells primary actors
  • Cell-mediated
    • T cells only
antigens
Antigens
  • Antigen:
      • Typically large molecules, often proteins.
antigen processing
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
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
  • 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
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
when help arrives
When help arrives . . .

Antigen & T-helper cell

Naïve cell

Proliferation of cell line

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

B cells proliferate . . .

b cells differentiate into
B cells differentiate into . . .

Antigen & T-helper cell

antibodies

memory

  • Antibody producing cells [attack mode]
  • Memory cells [remembers & future protection]
ami in summary
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
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
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.
t lymphocytes cell mediated
T Lymphocytes: Cell-Mediated

Roles of T lymphocytes and NK cells in cell-mediated immunity

Figure 24-16

what happens in a cell mediated response
What happens in a cell-mediated response?
  • The key events:
    • Surveillance and recognition
    • Attack
    • Memory
types of immunity
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
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
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
Hypersensitivity
  • Excessive reaction to an antigen (allergen) to which most people do not react
    • Includes
      • Allergies
      • Transplant reaction
      • Transfusion
hypersensitivity disorders
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
Hypersensitivity Assessment
  • Subjective Information
    • Pruritus, nausea and uneasiness
  • History of present illness
    • Onset, frequency and duration of symptoms
    • Nature and progression of s/s
    • Possible exposures of known allergens/common allergens
    • Chronic, seasonal or single episode
    • Aggravating & alleviating factors
hypersensitivity assessment1
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
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
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
  • Leukotrieneinhibitors—Inhibits the release of leukotrienes from mast cells & basophils)
    • Prototype—montelukast (Singulair)
  • Steroids—symptom management & long term control
    • Systemic—Prototype Prednisone
allergies
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
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
Allergic Responses
  • First exposure
    • Sensitization
    • Activation, clone B cells, form antibodies and memory cells
  • Re-exposure
    • Many antibodies, activated T cells, intensified response, inflammation
allergies1
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
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 proteins
    • Exposure—skin, mucous membranes, inhalation or blood
    • Reaction—ranges from erythema, urticaria, rhinitis, conjuctivitis to asthma & full blown anaphylactic shock
latex allergy
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
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
hypersensitivity anaphylaxis1
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
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
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
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
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
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
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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