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Aniasthmatic/Antiinf
Anti-Inflammatory/Antiasthamtic Agents
| Question | Answer |
|---|---|
| What are the causes of lung inflammation? | Diseases Infections Inhalation of toxic substances Trauma |
| What is the immune response? | The bodies natural defense mechanism. |
| What is the function of the immune response? | To neutralize, destroy and eliminate antigens. |
| What are antigens? | Any foreign substance |
| How does humoral immunity work?(circulating immunity) | B-lymphocytes produce antibodies (IgG, IgM,IgA,IgD) |
| How do T-lymphocytes work? | They remove or destroy directly or indirectly. (cell mediated immunity) |
| What does the antibody IgG do? | It is the most common 80% of immunoglobulins in plasma. Protects against childhood diseases |
| What does IgM do? | 10% of immunoglobulins; numbers increase in chronic infections. |
| What does IgE do? | It's involved in hypersensitivity reactions, allergic rhinitis, allergic asthma; bound to mast cells |
| What does IgA do? | Mucous membranes in respiratory tract;Transfer immunity to the child. |
| Describe Mast Cell Chemical Mediator Release. | Mast cells are found throughout the body. Antigens attatch to mast cells Mast cells become sensitized. Await re-exposure. Upon re-exposure antigen-antibody reaction occurs causing rupture of mast cell. Histamine/Chemotactic factors are released. |
| What are the two types of asthma? | Allergic Asthma and non-allergic asthma |
| Describe allergic Asthma. | Most common. Caused by external agents Treated with allergy shots. |
| Describe non-allergic asthma | caused by infection, cold air, exercise, stress. No immune response occurs (mast cells degranulate and burst) |
| How is non-allergic asthma treated? | With prophylactic antiashtmatic agents that prevent mast cells from bursting. |
| Describe the early phase inflammatory response. | Local vasodilation, increased vascular permeability, redness and wheal formation. Immediate response is bronchial contraction, wheezing, cough dyspnea, hypoxemia |
| What almost always reverses the early phase inflammatory response? | Bronchodilators |
| Describe the late phase response. | Slow imflammatory process that develops 6-8 hours later. Can be serious Treatment is aimed at stopping the inflammatory progression before it occurs at this stage |
| What happens during the late phase response? | Hypersecretion of mucus and mucus swelling occurs. Traffic jam of cellular debris piles up |
| What class is geared towards the late phase response? | Corticosteroids. |
| What does the endocrine system do? | Secretes hormones into the blood stream. |
| What does the adrenal medulla secrete? | Norepinephrine Epinephrine |
| What does the adrenal cortex secrete? | steroids |
| What are the two classes of corticosteroids? | Mineralcorticoids Gluccocorticoids |
| What are mineralcorticoids? | Corticosteroids with salt-retaining activity that are important for electrolyte balance and fluid volume |
| What are gluccocorticoids? | affect carbohydrate, protein and fat metabolism. Have anti infmallatory activity and supress immune response. |
| What does the hypothalamic Pituitary Adrenal Axis do? (HPA) | Controls corticosteroid release. Responsible for normal fluctuation in steroid blood levels |
| Describe HPA. | Hypothalamus stimulated. CRF (corticotropin releasing factor) released by anterior pitutiary gland. ACTH (Adrenocorticotropic Hormone released. Causes steroids to be released by adrenal cortex. This is a biofeeback mechanism. |
| Three mechanisms of action of the HPA. | Block or diminish late-phase asthma response. Remove circulatory lymphocytes. Inhibit macrophage and leukocyte processing of antigens. |
| What are three more mechanism of actions of the HPA. | Enhance responsiveness of B2 receptors. Time dependent (cellular biochemical effects are immediate, clinical response takes longer.) |
| What are corticosteroid effects on inflammation? | Block arachidonic acid metabolites (leukotrienes and prostoglandins) Decrease monocytes, eocinophils and basophils. Decrease lymphocytes and macrophages Inhibit late-phase inflammation Increase Beta 2 receptors and responsiveness. |
| What are the immunologic side effects of corticosteroids. | immunosupression, increased susceptibility to infections |
| What are the cardiovascular side effects to corticosteroids? | Edema hypertension |
| What are the CNS side effects to corticosteroids? | Euphoria Insomnia |
| What are dermatologic side effects to corticosteroids? | Thin Skin impaired wound healing bruising altered fat distribution |
| What are endocrinolgic side effects to corticosteroids? | diabetes cushingoid state |
| What are metabolic side effects to corticosteroids? | electrolyte imbalance negative nitrogen imbalance |
| what are musculoskeletal side effects to corticosteroids? | muscle weakness, osteoporosis, growth suspension |
| What are opthalmic side effects to corticosteroids? | glaucoma |
| What is the oral corticosteroid. | prednisone |
| What is the parenteral corticosteroid. | Hydrocortisone (cortef) Methylprednisolone (solumedrol) |
| Cusing syndrome? | Oral-yes Aerosol-No |
| Steroid dependence? | Oral-High risk Aerosol-Low risk |
| Local theraputic effects? | Oral-No Aerosol-yes |
| Risk to growth development in children | oral-yes aerosol-no |
| Ease of use | oral- yes aerosol-no |
| Cost | oral-inexpensive aerosol-expensive |
| local airway reaction | oral-no aerosol-Yes |
| beclamethasone dipropionate | Beclovent Vanceril |
| Budesonide turbuhaler | Pulmicort |
| Ciclesonide HFA | Alvesco |
| Flunisolide | Aerobid |
| Fluticasone | Flovent |
| Triamcinolone acetonide | Azmacort |
| Mometasone furoate | Asmanex |
| Diproprionate HFA | Qvar |
| budesonide, formoterol | Symbicort |
| Advair | low-150 mcg Medium 250 mcg High- 550 mcg |
| Fluticasone (MDI) | low 44 mcg/puff medium 100 mcg/puff high 220 mcg per puff |
| Benefits of daily use. (corticosteroids) | fewer symptoms Fewere severe exacerbations Reduced use of B2 agonist Reduction in airway remodeling. improved lung function. reduced airway inflammation |
| What are the two types of steroid dependency? | psychological desire. physiologic steroid suppression of HPA |
| What are the withdrawal symptoms of steroids | Anorexia Nausea Vomiting Lethargy Headache Hypotension |
| What are antiasthmatics? | Mast cell stabilizers |
| How do antiasthmatics work? | Impair or prevent the inflammatory response from ever beginning. Prevents mast cells from rupturing. |
| What are antiasthmatics used for? | Allergic, nonallergic asthma, allergic rhinitis, and EIB. |
| What is EIB? | Exercise induced bronchospasm |
| What else does antiasthmatics do? | inhibit LAR and prevent BHR |
| What is LAR | Late Asthma reaction |
| What is BHR | bronchohyperresponsiveness |
| Cromolyn Sodium | Intal |
| How does Cromolyn Sodium come? | Solution/DPI |
| Facts about Intal. | Compatible with B2 agonist Prophylactic effect in 4-6 weeks May be an alternate for children with side effects to theophylline |
| Nedocromil Sodium | Tilade |
| How does Tilade come? | MDI |
| Facts about Tilade. | Theraputic effect in 4-6 weeks Side effects (1 in 1000) Non-toxic cough wheeze headache bad taste |
| Prostoglandin facts. | Present in almost all tissues Modulate airway function can alter V/Q classified by chemical structure Very short half life. |
| PgF2 (most common) | bronchoconstriction |
| PgE1, PgE2 | Bronchodilation |
| What are Leukotrine modifiers? | A recent group medication. inhibits leukotriene mediator cascade. |
| What are the two leukotrine modifiers? | Accolate Singulair (maintenance therapy) |
| What agents treat upper airway congestion? | Intranasal Medications, Intranasal corticosteroids, antihistamines,decongestants. |
| Intranasal medications. | Cromolyn (prevents mast cell from degredation). Nasalcrom. |
| Intranasal corticosteroids | Nasocort Nasonex Flonase Rhinocort Beconase |
| Antihistamine | Benadryl Claritin Zyrtec ALlegra |
| Decongestants | Sudafed Afrin (alpha 1 properties) |
Created by:
kparkerlehman
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