Immune

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  • Immune

    1. 1. Immune Functioning
    2. 2. Major structures for immune functioning  Lymph nodes – small organs throughout the body designed to receive fluids from peripheral tissue sites. Clusters found in many areas  Spleen – the largest lymphoid organ. Supports humoral immune response to blood-borne pathogens. Also assists in filtering for damaged RBCs
    3. 3. Major structures  Thymus - contributed to the maintenance and functioning of T-cells  Bone Marrow – generates pluripotent stem cells for cell generation including RBCs, WBCs, antibody production  Blood – houses RBCs, WBCs and platelets
    4. 4. “Shift to the left” is the release of immature neutrophills to fight infection
    5. 5. WBC Functioning  Granulocytes – neutrophils, eosinophils and basophils  Nongranulocytes – lymphocytes and monocytes
    6. 6. Cellular WBC response as seen on a CBC differential  Neutrophils – one of the most plentiful along with lymphocytes  55-70% of differential smear  Most (90%) remain in the bone marrow for storage  Neutrophils in circulation also adhere to endothelial lining of small blood vessels  1st on the scene for inflammatory response (usually within 6-12 hrs)
    7. 7. Cellular WBC response also trauma  Elevated with acute and surgery inflammatory reaction or acute infection  Survive for only 24-48 hrs  “segs” refer to mature cells  “bands” refer to immature
    8. 8. mature immature
    9. 9. Lymphocyte activity  Total lymphocytes accounts for 20-40% of differential smear  T-lymphocytes (mature in thymus)  B-lymphocytes (mature in bone marrow)  T Cytotoxic (CD8)  T Helper (CD4)  NK cells
    10. 10. Lymphocytes  T-lymphocytes primarily involved in cell-mediated immunity, serve as NK cells and T4 helper cells  B-lymphocytes primarily and humoral immunity  The lymphocytes circulating in the blood are primarily responsible for fighting chronic bacterial and acute viral infections i.e. long standing i.e. rhino virus pneumonia or celleulitis
    11. 11. Cellular WBC response  Monocytes – triggered by chemotactic factors becoming a macrophage in lung, connective or lymphoid tissue to remove foreign substances by phagocytosis  Arrives on site within 3-7 days  4-8% of diff smear  Elevated in long-standing infections  Produces interferon, the body’s own immunostimulant
    12. 12. Cellular immune response  Eosinophils – very small percentage seen in the WBC count (1-4% of diff smear)  Elevated in parasitic infections and IgE-mediated allergic responses  Do not respond to bacterial infections
    13. 13. Cellular immune response  Eosinophils – house heparin, histamine and serotonin in the cytoplasm  Eos infiltrate the tissue affected by allergy to further the inflammatory reaction
    14. 14. Cellular immune response  Basophils – only 1-2 % of differential smear  Also supports IgE-mediated allergic responses
    15. 15. Cells identified in the WBC differential
    16. 16. leukocytosis=too WBC differential many white blood cells  Total WBCs (leukocytes) 5000-11000/mm3  Neutrophils 50-70%  Lymphocytes 20-40%  Monocytes 4-8%  Eosinophils 0-4%  Basophils 0-2%
    17. 17. Human Immunity  Direct (active) immunity  Indirect (inactive) immunity through intrauterine sources or other naturally and synthetically- generated immunoglobulins (antibodies) see chapter 12 for active vs passive
    18. 18. Active Immunity  Humoral immunity (IgG, IgA, IgM) available in the blood  Mucosal immunity (secretory IgA) available in the mucus of the GI, respi and urogenital tracts  Cell-mediated immunity (T-lymphocytes)  Type I hypersensitivity reactions (IgE response in mast cells found in respiratory and GI tracts) passive immunity is lost; active immunity last longer
    19. 19. Primary and Secondary Antibody Response
    20. 20. Class and Function of Immunoglobulins (Antibodies)  IgG – 75%  IgA – 15%  IgM – 10%  IgE - <1%  IgD - <1%
    21. 21. Class and Function of Immunoglobulins (Antibodies)  IgG – present in circulation and tissue, first Ig produced in secondary response, crosses placenta  IgA – present in circulation of mucous secretions; prevents adherence on mucosal surface deficiency leads to a lot of skin infections and mucous membrane infections. secreted through breast milk
    22. 22. Class and Function of Immunoglobulins  IgM – present in circulation; first Ig of primary immune response. Large and cannot move to tissues  IgE – present in mast cells, mediates hypersensitivity reactions  IgD – lymphocytes
    23. 23. Active, Acquired Immunity  A result of invasion by a foreign substance OR through inoculation of a less virulent antigen  Subsequent reinvasion generates a greater response
    24. 24. Types of Acquired, Specific Immunity  Active (Natural) – contact with antigen through clinical infection  Active (Artificial) – immunization with live or killed antigen  Passive (Natural) – transplacental transfer of antibodies (lost at 3-6months)  Passive (Artificial) – injection of serum from immune globulin
    25. 25. Human Hypersensitivity Reactions  Type I – immediate or anaphylactic  Type II – cytolytic or cytotoxic  Type III – immune complex  Type IV – cell-mediated, delayed 1&2 are immediate 3 is associated with chronic disease 4 is delayed
    26. 26. Human Hypersensitivity Reactions  Type I – Immediate/anaplylactic  IgE initiated  Mast cell degranulation → histamine and leukotriene release  Reaction includes anaphylaxis, atopic diseases such as allergies and asthma, skin reactions asthma is a type of allergic disease under sub category atopia
    27. 27. Causes of Anaphylaxis  Drugs  Foods  Insect sting  Allergy  Latex allergy
    28. 28. Causes of Anaphylaxis  Drugs – PCN, sulfonamides, insulins, ASA, TCN, tetracycline cephalosporins, (antibiotic) chemotherapeutic agents, NSAIDs  Insects – wasps, bees, hornets, ants
    29. 29. Causes of Anaphylaxis  Foods – eggs, nuts, shellfish, fish, chocolate, strawberries  Animal Sera – tetanus, rabies, diptheria, snake venom antitoxins  Therapeutic Treatments – blood products, Iodine-based media
    30. 30. S & S of Anaphylaxis  Hives, wheal-and-flare reaction, itching  Angioedema  Dyspnea, wheezing fainting  Syncope, ↓ BP, flushing  N & V, diarrhea, abd pain  Onset generally 5-30 mins after antigen  See Fig. 14-11 on p. 226
    31. 31. Treatment for Anaphylactic Shock  Epinephrine (SC, IM or IV) 0.5ml 1:10,000 IV for severe  Remove antigen  02 non rebreather mask best source with out intabation  Maintain vascular volume by ↑ legs, fluid resuscitation with NS or LR  Vasopressive agents such as dopamine (Intropin)
    32. 32. Latex Allergy (Type I)  Common in the U.S. population  Incidence higher among HCWs  An allergy to the natural latex proteins and occurs within minutes of exposure
    33. 33. Latex Allergy (Type I)  Apparent relationship with allergy to certain medications including bananas, avocado, apricot, papaya, kiwi  S & S include dermatitis, itching, urticaria, sneezing/coughing, wheezing, vascular collapse
    34. 34. Latex Allergy
    35. 35. Other Type I Hypersensitivities  Atopic conditions – a broad category used to describe many conditions that are IgE stimulated. Includes hay fever, asthma, and all conditions cited hereafter  To repeat, allergic rhinitis fits here
    36. 36. Atopic Conditions (cont.)  Atopic dermatitis – often complaints of itchy skin. May be dry. Lesions may develop. Treatment includes ↓exposure and the response. Cool compresses, lubricants, avoid scratching
    37. 37. Eczema – a form of atopic dermatitis Tx: topical corticosteroids avoid triggers Gel sticks better than creams or lotions
    38. 38. Other Type I Hypersensitivities  Urticaria – (hives) a systemic response because of an allergen  Histamine → localized vasodilation, transudation, and flaring
    39. 39. Type I Hypersensitivities - Urticaria  Papules that tend to develop on face, neck, ant. aspect of arms, and abdomen, back  Many causative agents  Avoidance  Cool compresses, antihistamines
    40. 40. Urticaria
    41. 41. Type I Hypersensitivities  Angioedema – similar to urticaria but involves deeper layers of skin and mucosa  Areas affected are significant and include eyelids, lips, tongue, larynx, hands, feet, GIT, and genitalia
    42. 42. Meds used for Allergies  Antihistamines – H1 receptor binding agents to ↓ sneezing, rhinitis, itching. (Zyrtec, Allegra, Claritin). Non-blood brain barrier crossing.  Benadryl (diphenhydramine) does cross BBB if it crosses BBB causes drowsiness
    43. 43. Meds. cont  Decongestants – relieve nasal congestion to ↓ alpha- adrenergic response at entrance to venous plexus of turbinates. (Sudafed, phenylephrine)  Corticosteroids – topical, nasal (Nasocort, Rhinocort)
    44. 44. Meds. cont.  Inhaled steroids – fundamental treatment for asthma. (Flovent, Advair, Azmacort, Vanceril)  Beta-agonists for bronchospasm (Albuterol, salmeterol)
    45. 45. Meds. cont.  Antipruritic Drugs: may be applied topically such as calamine lotion, camphor and menthol  Mast Cell-Stablizing Drugs: inhibit the release of histamines and leukotrienes (Cromolyn). Used to treat allergic rhinitis and asthma
    46. 46. Meds. cont  Leukotriene inhibitors – Leukotrienes contribute airway edema, smooth ms. contraction and inflammation. (Accolate, Singulair) used for allergic rhinitis and allergies
    47. 47. Type II Hypersensitivity reactions  Cytolytic or Cytotoxic  IgG or IgM mediated  Complement activated and cell destruction occurs  Examples of include hemolytic anemia, Rh disease, autoimmune hyperthyroidism, myasthenia gravis, and blood transfusion reactions
    48. 48. Blood Transfusion Reactions  Occurs as a result of intravascular hemolysis or RBCs and includes; H/ A, back pain, chest pain, N & V, ↑ HR, ↓ BP, hematuria, urticaria  Probably IgM-based reaction  Stop the blood and all the tubings including blood death by kidney  Notify the MD and the lab cloggingdue to failure by dead  Maintain vascular RBC  Fluid resuscitation access with new bag of NS  Save the urine
    49. 49. Type III Hypersensitivity Reactions  Immune Complex reactions  Antigens and antibodies bind and occlude capillaries causing urticaria, arthritis, arteritis, glomerulonephritis  Reactions can be localized or systemic  Systemic Lupus Erythmatosus  Acute glomerulonephritis
    50. 50. SLE
    51. 51. Type IV Hypersensitivity Reactions  Cell-mediated, or Delayed  Requires effective T-cell functioning TB testing  Used with PPD testing - edema and fibrin result in induration. Also responsible for caseous lesions that develop with tubercle bacillus
    52. 52. Type IV Hypersensitivity Reactions  Contact dermatitis – a result of contact with an allergen such as lanolin, adhesive, topical medications or plant toxins. Latex allergy due to contact fits here.  Antibodies are formed with first exposure; hypersensitivity reactions occur with later exposure
    53. 53. Hypersensitivity Reaction Prevention  Good assessment and health history. Attending to all food, medication and environmental allergies  Controlling the environment
    54. 54. Immunodeficiency Disorders  Inadequate protection of the body at the cellular, enzyme or humoral level  Primary – inadequate immune cells with mostly genetic causes. Apparent at birth. Most common hypogammaglobulinemia i.e. bubble boys
    55. 55. Immunodeficiency Disorders  Secondary – obtained through other causes such as medication use and disease; medication use by far the most common cause i.e. steroids, chemo, antibiotics, radiation, spleenectomy

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