The immune system
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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

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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

  • Incorrect responses

    • Autoimmune disease

  • Overactive responses

    • Allergies

  • 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:




Cell-mediated Immunity

Lymphatic System: Anatomy

Figure 24-2a

Key Cells of the Immune System

Leukocytes (white blood cells)

Cells of the Immune System

Figure 24-4


  • 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.


  • 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:

    • Redness

    • Swelling

    • Heat

    • Pain

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 inflammation:

  • Macrophages

    • Preform phagocytosis, repair injured tissue

    • Stimulate CMI + AMI

    • Long life span and plenty of energy to degrade many foreign proteins.



Cells under attack release histamine.

Purpose is to engulf and destroy invaders

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 inflammation:

  • Eosinophils

    • Act 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:

    • Humoral Immunity aka Antibody-Mediated Immunity:

      • Driven by B cells.

  • 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


  • 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.


  • 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

    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 . . .

    Antigen & T-helper cell



    • Antibody producing cells [attack mode]

    • Memory cells [remembers & future protection]

    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.

    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?

    • The key events:

      • Surveillance and recognition

      • Attack

      • Memory

    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.


    A preparation containing antigenic


    • 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 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 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


    • 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


    • 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 exposure

      • Sensitization

      • Activation, clone B cells, form antibodies and memory cells

    • Re-exposure

      • Many antibodies, activated T cells, intensified response, inflammation


    • 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 proteins

      • Exposure—skin, mucous membranes, inhalation or blood

      • Reaction—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


    • 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


    Decision tree for patient with anaphylactic reaction


    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

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