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PP Ch 3
Pathophysiology Chapter 3
| Question | Answer |
|---|---|
| Immune system | Specific defense mechanism that responds to foreign substances, cells, toxins or proteins; ID’s & removes foreign material from the body; uses Ags on the surface of cells to determine “self” cells from “non-self” cells. |
| Antigens (Immunogens) | Unique cell surface structure made of ptns, polysacc’s, or glycopns |
| Antigens Found on “self” cells | MHC/HLA proteins label cells of the individual; Immune system ignores “self” cells |
| Found on “non-self” or foreign cells | Immune system recognizes spec non-self Ags as foreign; Devo of spec response to particular Ag (Ab produxn); Memory cells made to respond quickly to Ag in case it reappears in the body |
| 2 Mechanisms of Immune Response | Humoral Immunity & Cell-Mediated Immunity |
| Humoral immunity | Antibodies are produced to protect body |
| Cell-mediated immunity (CMI) | Lymphocytes are programmed to attack non-self cells to protect the body |
| Humoral & CMI Work Together | Antibodies “tag” foreign cells by identifying cells with “non-self” antigens; Immune cells are able to destroy the “tagged” cells |
| Components of the Immune System | Lymphoid Structures, Immune Cells, Tissues (Immune Cell Development) |
| Lymphoid Structures | Lymph nodes, Spleen, Tonsils, Intestinal lymphoid tissue (MALT), Lymphatic circulation |
| Immune Cells | Lymphocytes, Macrophages (Both identify and remove foreign material) |
| Tissues – Immune Cell Development | Bone marrow (Origination of immune cells); Thymus (Maturation of immune cells (T-lymphocytes)) |
| Macrophages | Initiate immune response; Develop from monocytes; Engulf foreign material; Display Ags of foreign material to lymphocytes; Secrete chemicals (monokines & interleukins)- Activates additional lymphocytes and inflammation; Present throughout the body |
| T-lymphocytes | “Cell-mediated” immunity; From BM stem cells; Further differentiation in thymus; Include: Cytotoxic T-killer cells, Helper T cells, Memory T cells |
| B-lymphocytes | “Humoral” immunity; Responsible for Ab production; Mature in BM - Proceed to spleen and lymphoid tissue; Include: Plasma cells; Produce new Abs |
| B-memory cells | Can quickly re-form antibodies in repeated antigen exposure |
| Antibodies (Immunoglobulins) | Proteins produced by Plasma B-lymphocytes; Bind to specific foreign antigens so they can be destroyed |
| Complement system | Group of inactive proteins (C1 to C9) circulating in blood; Becomes activated when antigen-antibody complex binds to C1; Causes phagocytosis of the foreign cell, chemotaxis, and further inflammation |
| Chemical mediators | Involved in inflammation and immune reactions (histamine, interleukins); Causes chemotaxis and inflammation |
| Two Components of the Immune Response | Primary Response & Secondary Response |
| Primary Immune Response | First exposure to antigen; 1 to 2 weeks for antibody titer to reach efficacy |
| Secondary Immune Response | Repeat exposure to the same antigen; More rapid response with efficacy in 1 to 3 days |
| 4 Ways Immunity is Acquired | Active Natural Immunity, Active Artificial Immunity, Passive Natural Immunity, Passive Artificial Immunity |
| Active immunity | requires the person’s own body to develop antibodies or T-cells in response to an antigen in the body |
| Active natural immunity | Natural exposure to antigen (i.e. infection); Development of antibodies |
| Active artificial immunity | Antigen purposefully introduced to body; Stimulation of antibody production; Immunization; booster immunization |
| Passive immunity | occurs when antibodies are transferred from one person to another; gives immediate, short-term protection (no memory) |
| Passive natural immunity | Antibodies (IgG) transferred from mother to fetus (Across placenta, Through breast milk); Protection of infant for the first few months of life or until weaned |
| Passive artificial immunity | Injection of antibodies; Short-term protection |
| Hypersensitivity | an unusual and/or damaging immune response to normally harmless substances; Are distinguished by the mechanism in which they cause tissue injury |
| 4 Types of Hypersensitivity Reactions | Type I: Allergic reactions; Type II: Cytotoxic hypersensitivities; Type III: Immune complex hypersensitivity; Type IV: Cell-mediated or Delayed hypersensitivity |
| Type I hypersensitivity – Allergic reactions | Exposure to allergen – Develop IgE Abs, Mast Cells sensitized on initial exposure to allergen, subsequent exposure causes allergic rxn |
| Common Type I Hypersensitivity reactions | Hay fever/allergic rhinitis: affects nasal mucosa; Food allergies: affects digestive tract mucosa; Atopic dermatitis/eczema: affects skin; Asthma: affects bronchial mucosa; Complications: Anaphylaxis |
| Anaphylaxis/Anaphylactic Shock | Severe, life-threatening; Usually w/in minutes of allergen exposure; C/b mast cells releasing lg amts of chemical mediators (i.e. histamine) into general circulation; Can be caused by: Latex materials, insect stings, nuts or shellfish; various drugs |
| Anaphylaxis/Anaphylactic Shock - Systemic hypersensitivity reaction | Decreased blood pressure due to release of histamine; Bronchoconstriction and edema leading to airway obstruction (Results in severe hypoxia) |
| Anaphylaxis/Anaphylactic Shock - Signs and symptom | Generalized itching or tingling esp. in oral cavity; Coughing; Difficulty breathing; Feeling of weakness; Dizziness or fainting; Sense of fear & panic; Edema around eyes, lips, tongue, hands, feet; Hives (urticaria); Collapse with loss of consciousness |
| Anaphylaxis/Anaphylactic Shock - ED Treatment | Epinephrine: dilates bronchioles; stabilizes blood pressure; Glucocorticoids: decrease immune and inflammatory response; stabilize blood pressure; Antihistamines: decrease inflammatory response; Oxygen; Stabilize BP |
| Type II – Cytotoxic Hypersensitivity | Ag is present on cell membrane - may be normal body component or exogenous; Circulating IgG reacts w/ Ag; Destruction of cell by phagocytosis or cytolytic enzymes (ex. Incomplatible blood transfusion) |
| Type III – Immune Complex Hypersensivity | Ag combines w/ Ab; Forming immune complexes – deposited in tissue; Activation of complement system; Process causes inflammation and tissue destruction; Examples: Glomerulonephritis; Rheumatoid arthritis |
| Type IV – Cell-Mediated or Delayed Hypersensitivity | Delayed response by sensitized T-lymphocytes; Release of lymphokines; Inflammatory response; Destruction of the antigen; Examples: Tuberculin test; Contact dermatitis; Allergic skin rash |
| Autoimmune Disorders | Devo of Abs against own cells/tissues (auto-Abs); Results in loss of self-tolerance; Can affect single organs or tissues or can be generalized; Examples: Hashimoto thyroiditis; SLE; Rheumatic fever; MG; Scleroderma; Pernicious anemia; Graves disease |
| Auto-antibodies | antibodies formed against self-antigens |
| Systemic Lupus Erythematosus (SLE) | Chronic inflamm disease; Affects many organ systems; Lg number circulating auto-Abs against DNA, plts, RBCs, form immune complexes deposited into tissues causes inflammation & necrosis; Vasculitis develops in many organs impairing blood supply to tissues |
| Systemic Lupus Erythematosus (SLE) – Signs & Symptoms | Characteristic facial rash – “butterfly rash”; Affects primarily young women (esp AA, Asians, Hispanics, NAs); S&S vary d/t organ involvement but commonly include: Arthralgia, fatigue, & malaise; CV problems; Polyuria |
| Systemic Lupus Erythematosus (SLE) - Treatment | Usually treated by a rheumatologist; Prednisone (glucocorticoid); Non-steroidal anti-inflammatory drugs |
| Immunodeficiency | Involves partial or total loss of one or more immune system components |
| Primary Immunodeficiencies | Basic developmental failure somewhere in the system (i.e. bone marrow, thymus, etc.) |
| Secondary or Acquired Immunodeficiencies | d/t specific causes; Can occur at any time during the lifespan; C/b Infections, splenectomy, malnutrition, liver disease, immunosupressant drugs, radiation, chemotherapy (cancer) |
| Secondary or Acquired Immunodeficiencies – Complications | Increased risk of infection and cancer; Predisposition to the development of opportunistic infections c/b normal flora - Usually difficult to treat due to immunodeficiency - Prophylactic antimicrobial drugs may be used prior to invasive procedures |
| Secondary or Acquired Immunodeficiencies – Treatment | Use of gamma globulin; bone marrow or thymus transplants |
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