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22 Cards in this Set
- Front
- Back
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Bronchioles contain smooth muscle that respond to _____ |
inputs from ANS |
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Sympathetic input stimulates Parasympathetic input |
beta2 adrenergic receptors - to relax bronchiole SM and increase SM - bronchodilation Induces bronchoconstriction |
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Major features of asthma |
Airway obstruction Airway inflammation Airway irritability - hyper-responsiveness |
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Causes of asthma |
Air pollutants allergens chemicals in food drugs including NSAIDS, ASA and Beta blockers Respiratory infections Stress |
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Goals of therapy |
reduce intensity and frequency of asthma symptoms (cough, chest tightness, wheezing and SOB) - decrease night time waking, increase lung function, decrease need for beta agonists (less than 2 days per week) Reduce adverse effects associated with asthma - recurrent exacerbations and need for ER or hospital, prevent reduced lung growth in children and loss of function in adults |
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Aerosols |
Topical administration - small particles of liquid or fine solid particles - limit systemic side effects -Nebulizers - emergency -Dry powder inhalers -Metered dose inhalers - puffers - use a propellant to deliver the medication into the lungs |
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Relievers vs. controllers |
Relievers: beta-adrenergic agonists - short acting (SABA) and muscarinic antagonists Controllers: Glucocorticoids (inhaled and oral), long acting beta-adrenergic agonists (LABA), leukotriene antagonists and lipaxygenase inhibitors, methylxanthines and IgE antibodies (omalizumab) and mast cell stabilizers |
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How does an allergen cause histamine release ane leukotriene formation |
Allergen binds to IgE receptors on the mast cells which activate Gq proteins which cleave PIP into IP3 and DAG and increase Ca2+ release from the endoplasmic reticulum and cause histamine release Ca2+ also activating phospholipase A2 which facilitates the formation on AA which can be converted to prostaglandin via COX1 and 2 as well as Leukotrienes via lipoxygenase |
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How do Leukotrienes and Histamine cause airway SM constriction |
They bind to Gq protein receptors on SM cell and cause increased Ca2+ release and contraction of the muscle |
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Beta 2 adrenergic agonists function by |
Binding to B2 receptors on airway smooth muscle and activating Gs proteins which convert adenylate cyclase into cAMP - which inhibits Ca2+ release and promotes relaxation They also open potassium channels so more can leave the cell (making it less reactive) |
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Beta 2 adrenergic agonists as treatment Routes of administration Side effects |
1st line! they are the most effective and rapid acting bronchodilator -short and rapid acting (salbutamol) - reliever -Long and slow acting (salmeterol) - controller Nebulizer - severe Inhaler - short acting Oral - long acting, pediatric night time control - increased AE AE: Tremor, tachy (increased sympathetic drive) |
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Anticholinergics (Muscarinic antagonists) - Ipratropium function as treatment/when is it used Side effects |
Block muscarinic receptors in the smooth muscle of the bronchi 2nd line therapy - only affective in2/3 of clients with asthma, slower acting than Short acting beta agonist (SABA) - may be combined with these (Combivent) Most commonly used in COPD and bronchitis Fewer adverse effects are associated with inhaled route of administration (dry mouth and sedation) |
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How does asthma lead to long term damage |
Allergen induces transcription factors that indcuce DNA transcription and synthesis of proteins that form inflammatory cytokines in the mast cell and T-Lymphocytes. These cytokines cause increased immune cell recruitment which produce cytotoxic compounds that generate airway remodelling, inflammatory effects and also cause bronchoconstriction |
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Glucocorticoid drugs when do you take them and how? what do they do? |
-Daily administration Severe: prednisone - IV or oral Moderate: beclomethasone - inhaled (spacer device for children) Suppress airway inflammation reduce airway hyper-responsiveness and airway obstruction, preventing asthma attacks! |
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Two methods of glucocorticoid action |
1) They directly inhibit the transcription factor for DNA that would normally lead to the formation of inflammatory cytokines 2) It binds to receptors to form a complex that gets taken through the cell membrane and binds to response elements that act directly on DNA and cause down regulation of the genes responsible for the formation of these inflammatory cytokines They also increase the production of proteins that inhibit phospholipase A2 - shutting down the AA cascade (stoping the formation of leukotrienes) and they inhibit COX2 |
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Adverse effects of glucocorticoid therapy |
Low dose - throat irritation, oral candidiasis High dose - adrenal insufficiency, osteoporosis |
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Leukotriene receptor antagonists function by when are they used route side effects |
bind to leukotriene receptors in bronchiolar SM inducing bronchodilatory and immunomodulatory effects (Controller) -2nd line compared to glucocorticoid - can be used in combination -Weaker effects compared to beta adrenergic agonists at bronchodilation Oral - montelukast (singulair) - take once per day -Available in chewable tablet to take at night SE: nausea and headache (mild) |
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Mast cell stabilizer (e.g. Cromolyn - Intal) - when is it used how does it work |
Used when client has asthma that is related to a specific trigger that is predictable - eg. cat dander - take it in advance so you don't have an attack -Less effective compared to glucocorticoids at improving airway obstruction, hyper-responsiveness and inflammation -No bronchodilatory effect - prevent constriction in response to antigen -Aerosol -Prevents allergen induced increase in Ca2+ - decreasing inflammatory response, bronchoconstriction and histamine release |
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Lipoxygenase inhibitors (e. Zileutron) function used for adverse effects and contraindications |
oral inhibits the formation of all leukotrienes Used for the prevention of asthma attacks, minimal adverse effects contraindicated in clients with liver disease |
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Methylxanthines (eg. Theophylline) route? functions by used for side effects |
oral admin Inhibits phosphodiesterase (PDE) which degrades cAMP -increased Ca2+ sequestering - induces bronchodilation -control nocturnal asthma - slow release -GI distress, irritability, insomnia, headache, nausea and vomiting (not everyone experiences these) |
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IgE antibodies (eg. Omalizumab) |
-SC injection -Only used for allergic forms of asthma (with a heavy immune component) -Reduces the production of IgE -Downregulates IgE receptors -Significant mast cell stabilizing effects expensive - reserved for moderate-severe asthma that does not respond to glucocorticoids SE: joint pain (arms,legs and ears), dizziness, fatigue, skin rash, anaphylaxis (1-2/1000 users) |
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Important considerations for pharmacological management |
SABA always a part of therapy to stop an attack if it occurs - as severity increases we use multiple drugs -glucocorticoids are the best controllers |
