1. CHAPTERS 3 & 4 DISORDERS OF THE IMMUNE SYSTEM

2. LYMPHOCYTES Small WBCs that are the effector cells of the immune system 3 types: B lymphocytes mature in the bone marrow T lymphocytes mature in the thymus where they also differentiate into cells with various functions Natural killer cells – in the innate immune system. Fast acting, have an innate capacity to instantly recognize, attack, & kill virus infected cells

3. STAGES OF IMMUNE RESPONSE Recognition Lymph nodes and lymphocytes Use circulation to “patrol” tissues and vessels Once foreign invader discovered, immune process initiated

4. STAGES OF IMMUNE RESPONSE Proliferation T-cells and B-cells divide rapidly T-cells  Killer T-cells B-cells  antibodies

5. STAGES OF IMMUNE RESPONSE Response Humoral – antibodies released into the bloodstream Cell-mediated – direct attack on microbe by killer T-cells

6. STAGES OF IMMUNE RESPONSE Effector Depends on which response reaches antigen first: humoral or cell- mediated Outcome: total destruction vs. complete neutralization of invading microbe

7. B LYMPHOCYTE (ANTIBODY)-MEDIATED IMMUNITY Antibody (humoral) mediated B cell activation B cell clones itself and produces antibodies Some vaccines work in this manner

8. T LYMPHOCYTE (DELAYED)- MEDIATED IMMUNITY Cell-mediated T cells(helper/CD 4 ) activates immune cells T cells (cytotoxic/killer CD 8 ) T cells produce cytokines

9. NON-T AND NON-B LYMPHOCYTES INVOLVED IN IMMUNE RESPONSE Null cells Destroy antigen coated with antibody Natural killer cells Defend against microorganisms and some malignant cells

10. MAJOR HISTOCOMPATIBILITY COMPLEX (MHC) Important part of immunity is how antigens are displayed to immune cells The MCH is a glycoprotein complex on the surface of all cells (except RBCs) It allows for immune cells to recognize the cell as self or nonself AKA as Human Leukocyte antigens (HLA)

11. TYPES OF MHC Two types of MHC MHC I: display antigens synthesized inside a virus infected or cancerous cell MHC II: present on the surface of macrophages and dendritic cells, which capture and display external nonself antigen Critical difference between the two: the immune system attacks the cell with the MHC I display but just reads the MHC II display

12. HYPERSENSITIVITY  A reflection of excessive or aberrant immune response  Sensitization: initiates the buildup of antibodies

13. HYPERSENSITIVITY Types of hypersensitivity reactions B Cell Mediated: Immediate (Anaphylactic): type I Cytotoxic: type II Immune complex: type III T Cell Mediated: Delayed type: type IV

14. TYPE I IMMEDIATE REACTION Occurs within a few minutes after an antigen combines with preformed antibody created by B cells from an earlier exposure Sensitizing exposure: IgE antibodies are secreted by B cells and attach to mast cells The initial exposure produces no symptoms but sets the stage for exposure, the antigen combines with IGE antibody already present on the surface of mast cells Results in vascular dilation, congestion, mucus secretion, and inflammation

15. TYPE I—ANAPHYLACTIC REACTION

16. TYPE II HYPERSENSITIVITY  Normal body constituent identified as foreign  Chemical mediators released  Activation of complement cascade  cell destruction  Diseases: myasthenia gravis, Goodpasture [lung and renal damage], blood transfusion incompatibility

17. TYPE II—CYTOTOXIC REACTION

18. TYPE II HYPERSENSITIVITY

19. TYPE III—IMMUNE COMPLEX REACTION

20. TYPE III HYPERSENSITIVITY  Immune complex hypersensivity  Free antigen and antibody combine to form an immune complex depositing in tissue, which damages it and causes an inflammatory reaction

21. TYPE III

22. TYPE IV IMMUNE REACTION T cell reaction No antibodies are produced and clinical reaction is delayed a few days after antigen contact Example: Mycobacterium tuberculosis; Contact dermatitis (most common Type IV)

23. TYPE IV—DELAYED OR CELLULAR REACTION

24. ALLERGIC DISORDERS & ATOPY Allergy: exaggerated but otherwise normal immune response to foreign antigen regardless of the type of hypersensitivity reaction Allergen: any substance (antigen) causing an allergic reaction Atopy: allergy due to Type I Most allergies are atopic

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26. IMMUNOGLOBULINS AND ALLERGIC RESPONSE  Antibodies (IgE, IgD, IgG, IgM, and IgA) react with specific effector cells and molecules, and function to protect the body  IgE antibodies are involved in allergic disorders  IgE molecules bind to an allergen and trigger mast cells or basophils

27. IMMUNOGLOBULINS AND ALLERGIC RESPONSE These cells then release chemical mediators such as histamine, serotonin, kinins, SRS-A, and neutrophil factor These chemical substances cause the reactions seen in allergic response

28. IG AND ALLERGIC RESPONSE (CONT.) 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

29. HYPERSENSITIVITIES CONDITIONTYPEWHAT’S HAP’NEN?S/SNRSG ACTIONS TESTSDRUGSVIGILANCE ANAPHYLAXIS I Allergen activates IgE bound to mast cells & release mediators of inflammation SKIN LUNGS GI TRACT HYPOTENSION REMOVE ANTIGEN RAISE HOB 02 MEDS AS ORDERED CBC with emphasis on WBC count and differential Epinephrine Benadryl Intal Careful allergy assessment First dose status protocols MISMATCHED BLOOD II Binding of IgG or IgM antibody to cell-bound antigen activates complement cascade Chills, fever, lower back pain, flushing, ↓ BP, ↑ HR, ↑ RR, vascular collapse Stop blood Maintain IV patency with NS Collect urine Monitor vitals Monitor Urine output Coombs test Urinanalysis Hemo & Hct 2 nurses meticulously check blood before giving Transfuse slowly with frequent VS CHRONIC INFLAMMATION (Lupus) III Formation and deposition of antigen/antibody complexes in tissues that cause damage Vasculitis Arthritis Nephritis Depends on condition e.g. SLE, teach pts. To avoid sun and other stressors CRP ESR ANA WBC w/diff Immuno- Suppressants Steroids Monitor for s/s infection and organ damage CONTACT DERMATITIS IV T-cell and macrophage mediated 24-48 hr post exposure Red, sore,weepy erythematous skin Patch testing Corticosteriods, topical and/or systemic Avoid irritant Burrow’s solution soaks

30. AUTOIMMUNE DISORDERS SLE & AIDS

31. SYSTEMIC LUPUS ERTHEMATOSUS (SLE) Multisystem disease Caused by Type III hypersensitivity Characterized by multitude of antibodies to various organs Associated with presence of antinuclear antibodies (ANA) in blood or tissue which may target DNA or RNA

32. ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) HIV invades cells by attaching to the MHC complex and preferentially infects T cells and related macrophages with the CD4 type of MHC antigen (mainly helper T cells) HIV RNA synthesizes abnormal DNA inside CD4+ cells which merges with normal DNA to become part of a new corrupted T cell DNA Later process is reversed and corrupted DNA produces new HIV RNA New HIV viruses exit the dying cell to infect and kill other CD4+ cells Cycle continues until T cell function is devastated and patient dies from AIDS-related opportunistic infection or malignancy

34. AIDS CONT’D B cell immunity is adversely affected because normal B cell function requires helper T cell support B cells are stimulated by HIV antigens and antigens of the cytomegalovirus (CMV), Epstein-Barr virus, and other infections that occur in AIDS Net effect: both T & B cell function is defective

35. DIAGNOSIS OF HIV & AIDS HIV is the infection, detectable by laboratory tests AIDS is a syndrome, not detected by laboratory data AIDS is a clinical diagnosis proved by the presence of certain AIDS related diseases

36. PROGRESSION OF HIV INFECTION Three phases: 1.Acute Viral Syndrome 2.Chronic infection 3.Progression to clinical AIDS