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Lecture 5
hypersensitivity and introduction to immunopharmacology
| Question | Answer |
|---|---|
| Innate | directly activated by pathogens; defends multicellular organisms against infection |
| adaptive | pathogens and innate IS activated |
| Innate IS | first line of defense against invading pathogens --> quick response |
| Innate IS | exists prior to infection, not enhanced by repeated infection, generally not antigen-specific --> no memory, responds to pathogen in same way |
| Innate IS | consists of the following components: mechanical (skin/epidermis, mucus), biochemical (antimicrobial peptides, proteins, complement, enzymes, interferons, acidic pH, free radicals), cellular (neutrophils, monocytes, macrophages, nk cells) |
| Adaptive IR | lymphocytes carry out both classes of responses |
| Adaptive IR | antibody-mediated (humoral immunity) = B cells secrete antibodies (Ig) that neutralize the virus |
| Adaptive IR | cell-mediated = T cells kill the virus-infected cells |
| Adaptive IS | activated from innate response when innate processes not sufficiently coping with infection; leads to: production of antibodies -- effectors of humoral immunity; activation of T lymphocytes --effectors of cell-mediated immunity |
| Adaptive IS | may involve antigen-presenting cells (APCs), including dendritic cells (CDs), macrophages, and B lymphocytes |
| hypersensitivity | inappropriate immune responses can lead to extensive tissue damage |
| Autoimmunity | reactivity against self antigens |
| Immunodeficiency | failure of immune system to protect the body adequately from infection due to absence or insufficiency of some component process or substance |
| Antigen | a toxin or other foreign substance which induces an immune response in the body, especially the production of antibodies |
| Antibodies | compounds of protein and sugars circulating in blood stream created by the immune system to fight germs and foreign substances |
| Hypersensitivity classifications and types: antibody-mediated | type I= reaction mediated by IgE antibodies; Type II=cytotoxic reaction mediated by IgG or IgM; Type III=reaction mediated by immune complexes |
| Hypersensitivity classifications and types: cell-mediated | type IV=delayed reaction mediated by cellular response |
| Type I Hypersensitivity: happens ___, sometimes within _____. reaction mediated by ___antibodies; re-exposure to antigen --> IgE-mediated mast cell and basophil degranulation | quickly, minutes, IgE |
| Type I Hypersensitivity: results in ___, hay fever, urticaria(hives), bronchoconstriction, hypotension, face/lip swelling | anaphylaxis |
| Type I Drug Allergy: allergen crosslinks IgE on mast cell --> triggers ___ and mediator release | degranulation |
| Type I Drug Allergy: common causes of type I reactions | food allergies, animal source, environmental factors, medications |
| Type I Drug Allergy: ____reaction to allergen | systemic (hives, anaphylaxis) |
| Localized Type I Reactions | hay fever, rhinitis, hives, asthma |
| Systemic Type I Reactions | anaphylaxis or anaphylactic shock, severe bronchoconstriction, some arterial beds may contract; if coronary artery contracts --> chest pain, dilation of capillary beds --> hypotension, edema |
| Treatment of Type I Hypersensitivity: epinephrine = first line therapy | increases vasoconstriction and peripheral vascular resistance --> relieves hypotension; decreases airway or mucosal edema --> relaxes bronchiolar smooth muscle --> relieves bronchospasm |
| Treatment of Type I Hypersensitivity: bronchodilators | inhaled or nebulizer beta-agonists (albuterol); treats bronchospasm |
| Treatment of Type I Hypersensitivity: antihistamines | relieves hives, pruritis; adjunctive therapy (not mono therapy); H1 antagonist(Benadryl) or H2 antagonist (Pepcid) |
| Treatment of Type I Hypersensitivity: glucocorticoids | no acute role in treatment of anaphylaxis b/c of delay in onset of action; rationale for use --> decrease biphasic and protracted reactions that may happen in anaphylaxis |
| Treatment of Type I Hypersensitivity: supplemental oxygen, IV fluids, glucagon or vasopressors, ___ | atropine |
| Type II hypersensitivity: also known as ___ | cytotoxic hypersensivity |
| Type II hypersensitivity: antibodies produced by immune response bind to antigens on healthy cells --> cells recognized by ____or ____ --> initiates a ____response --> production of ____against antigen ---> destroys ____cells | macrophages or dendritic cells; B cell; antibodies (IgM/G); host |
| Type II hypersensitivity: antigens may be ____ | extrinsic or intrinsic |
| Type II hypersensitivity: cytotoxic mechanisms=___system. Membrane ___complex (MAC) forms channels that interfere with phospholipid bilayer ---> ____and death. Antibody-dependent cell-mediated _____(ADCC) | complement; attack; cell lysis; cytotoxicity |
| Type II hypersensitivity: ADCC=cells with ___antigen tagged with antibodies (M/G) --> tagged cells recognized by ___cells and macrophages --> death of tagged cells | foreign, natural killer |
| Type II hypersensitivity Reactions | cytotoxic/antibody-mediated, tissue specific. Examples are hemolytic reactions and transfusion reactions |
| Type III Hypersensitivity: ____ complex-mediated reactions. Occurs ____after antigen exposure | immune, 1-3 hours |
| Type III Hypersensitivity: immune complexes deposit on vessel ____--> activate complement and ____--> release of pro inflammatory ____, enzymes, reactive oxygen species --> ____damage | wall, neutrophils, cytokines, tissue |
| Type III Hypersensitivity: may be ___induced. Example ____ | drug; vasculitis (inflammation of vessel walls; drug-induced examples=antibiotics and NSAIDs) |
| Type III Hypersensitivity: diseases involved | serum sickness, post streptococcal glomerulonephritis, systemic lupus erythematosus, rheumatoid arthritis |
| Type III Hypersensitivity: serum sickness | immune system reacts to medications containing proteins (immune complexes form between human proteins and nonhuman proteins), occurs 1-2 weeks after exposure, examples of medications=vaccinations, immune modulating agents, antivenom |
| Type IV Hypersensitivity: also known as____ | cell mediated hypersensitivity or delayed type hypersensitivity |
| Type IV Hypersensitivity: ____lymphocyte mediated. CD4/Helper T-cells induce hypersensitivity reactions through cytokine recruitment of ____ | T, inflammatory cells |
| Type IV Hypersensitivity: typically starts ___after exposure and lasts for many days. Due to time it takes to recruit and activate T cells | 2-3 days |
| Type IV Hypersensitivity: Examples | purified protein derivatives (PPD) , medications, poison ivy, contact dermatitis, graft vs. host disease(GVHD) |
| Hypersensitivity Reactions (ACID): Type I = IgE mediated, quick onset after exposure | ALLERGIC, bee stings, latex, certain medications |
| Hypersensitivity Reactions (ACID): Type II = Cytotoxic/antibody mediated, IgG/M | CYTOTOXIC; hemolytic reactions, good pasture's syndrome, hyper acute graft rejection |
| Hypersensitivity Reactions (ACID): Type III = immune complex/IgG/M mediated | IMMUNE COMPLEX DEPOSITION; hypersensitivity pneumonitis, SLE, serum sickness |
| Hypersensitivity Reactions (ACID): Type IV = delayed or cell mediated | DELAYED; chronic graft rejections, PPD test, latex, nickel, poison ivy |
| Immunopharmacology definition | refers to medications that suppress, modulate, or stimulate immune functions |
| Immunosuppressants definition | prevent rejection of organ or tissue grafts; diseases caused by dysregulation of immune response |
| Augmentation of immune response or balance component of immune system | cancer, AIDS, autoimmune/inflammatory disease |
| Mechanisms of Pharmacologic immune suppression 1**: suppression of ____ | gene expression (glucocorticoids) |
| Mechanisms of Pharmacologic immune suppression 2**: attack on clonal expanding ___ | lymphocyte lines (general cytotoxic methods) |
| Mechanisms of Pharmacologic immune suppression 3**: inhibition of ____ | intracellular signals (JAK-STAT, mTOR) |
| Mechanisms of Pharmacologic immune suppression 4**: neutralization/disruption of ____ | cytokine signals |
| Mechanisms of Pharmacologic immune suppression 5**: depletion of ____ | B/T cells (B and T cell targeting mabs) |
| Mechanisms of Pharmacologic immune suppression 6**: inhibition of ___ | APC co-stimulation |
| Mechanisms of Pharmacologic immune suppression 7**: inhibition of lymphocyte/___ | target cell interaction |
| Mechanisms of Pharmacologic immune suppression ***: Generally, need to do a ____to screen for ___before using, avoid ____ | PPD, TB, live vaccines |
| Adverse Effects Common to Most Immune Suppressants: immune suppression risks | malignancy (lymphoma, skin cancer, leukemias); infection (TB, hep), vaccinate prior to initiation, no live vaccines while on biologic DMARD or other immunosuppressant. Baseline monitoring for many of these drugs (TB-PPD), |
| Adverse Effects Common to Most Immune Suppressants: monoclonal antibodies and injectable proteins | injection reaction, allergic reaction, anti-antibodies (recognize other antibodies_ |
| Adverse Effects Common to Most Immune Suppressants: monoclonal antibodies and injectable proteins | worsening heart failure or new onset heart failure |
| Adverse Effects Common to Most Immune Suppressants: monoclonal antibodies and injectable proteins | neurologic reactions: PML, opic neuritis, activation of MS |
| Cytotoxic Medications: with autoimmune diseases and vasculitis, immune system is ___and produces ____at rapid rate | hyperactive, autoantibodies |
| Cytotoxic Medications: cytotoxic medications have greatest effect on ____--> suppress cells involved in hyperactive ____ | rapidly dividing cells, immune response |
| Cytotoxic Medications: immunosuppressive and ___ effects. Examples are | anti-inflammatory, methotrexate and azathioprine |
| Cytotoxic Drug Side Effects: bone marrow suppression | neutropenia, anemia, thrombocytopenia |
| Cytotoxic Drug Side Effects: GI effects | diarrhea, stomatitis |
| Cytotoxic Drug Side Effects: alopecia. Hyperuricemia | when cells die, purines from DNA metabolized to uric acid --> hyperuricemia |
| Cytotoxic Drug Side Effects: tumor lysis syndrome | hyperuricemia, hyperkalemia, hyperphosphatemia, azotemia, hypocalcemia |
| Glucocorticoids: inhibit phospholipidase A2--> blocks release of arachidonic from ____ | membrane phospholipid |
| Glucocorticoids: ____ inflammation and immune response | decrease |
| Glucocorticoids Effects on Inflammation: act on both inflammatory cells and ___to reduce inflammation | structural cells |
| Adverse Effects | Cushing-like syndrome, cataracts, hyperglycemia, topical therapy (skin atrophy, ecchymosis, purple striae) |
| Discontinuation: sudden cessation may lead to serious consequences if ___of HPA axis is present | suppression; acute adrenal insufficiency may be fatal; dose should be tapered |
| Immune suppression takeaway points: benefit = stops ___. Risks: =____ | auto-immune processes. infection (fever), cancer, injection reactions |
Created by:
bluedolphin7
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