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60 Cards in this Set
- Front
- Back
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What are the stages and treatments for COPD?
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Stage 0 (at risk) - STOP SMOKING, influenza, pneumovax vaccine
Stage I (FEV1>80%) - add short acting bronchodilators PRN Stage II (50-80) - add tiotropium DOC, or SABA/LABA. Pulmonary rehab Stage III (30-50) - ICS Stage IV (<30) - oxygen tx, surgery |
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What is the tx for intermittent asthma? Persistent asthma? Pregnancy?
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ALL pts with asthma should have a rescue bronchodilator.
Persistent: Use an ICS, add a LABA if needed, have SABA as rescue inhaler. Acute exacerbation: steroid Pregnancy: ICS (budesonide is good), for SABA use albuterol, for steroid in acute exac use prednisone. |
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What are the long acting bronchodilators for asthma?
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ICS, LABA, mast cells stabilizers, methylxanthines, leukotriene modifiers, and IgG Ab
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What are the inhaled corticosteroids (ICS)?
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Fluticasone > Budesonide > Beclomethasone > Flunisolide > Triamcinolone (potency)
10-20 puffs triamcinolone = 2-3 puffs fluticasone |
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What are the 2 formulations of ICS?
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1) Meter dose inhaler (MDI)
2) Dry powder inhaler (DPI) - less AE |
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What is the MOA of ICS?
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Nonspecific anti-inflammatory effects of mediators (CYTOKINES, eo's, mast cells, etc)
PREVENTS epithelial cell destruction, airway remodeling Reduces airway hyper-responsiveness INCREASES beta receptor responsiveness --> ICS and BA are SYNERGISTIC |
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What are the AE of ICS?
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Dose-dep, less serious toxicity versus systemic steroids:
Decrease growth velocity (same final height) At HIGH dose, decrease bone density at spine/hip, skin bruising/thinning Topical: hoarseness, dysphonia, throat irritation, CANDIDIASIS |
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How can you minimize the AE of ICS?
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Dose at lowest effective dose.
MDI - spacer improves efficacy. Gargle/rinse/spit |
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What is the use of ICS?
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Long term control!! Preferred at ALL stages of PERSISTENT asthma
Used in comb with LABA, reduces inflammation/sx's, brochospasm, morbidity/mortality Reduces need for oral corticosteroids |
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What should you give for post-menopausal women on high doses of ICS?
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Calcium + Vit D bc decreases bone density
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What are the mast cell stabilizers?
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Cromolyn (MDI, DPI) and Nedocromil (MDI only) -- "crom"
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What is the MOA of mast cell stabilizers?
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INHIBIT mast cell DEGRANULATION (histamines, leukotrienes)
Inhibit release of mediators from eo's, epithelial cells Decrease airway hyperresponsiveness |
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What are the AE of mast cell stabilizers?
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Rare and limited to local effects (no systemic)
Coughing in first 2 weeks (SABA can reduce cough), unpleasant taste |
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What is the use of mast cell stabilizers?
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Long term alternative to children with MILD persistent asthma
Use in peds, safe and effective in allergy-based asthma but LOW efficacy Comb with ICS: Nedocromil is added on; also preventative, exercise induced asthma |
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What are the LABAs?
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Long-acting Beta Agonists
Salmeterol, Formoterol |
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How are the combinations of ICS and LABA formulated?
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Dose of LABA stays constant even if ICS dose increases to prevent TACHYPHYLAXIS
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What is the MOA of LABAs?
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Directly STIMULATE beta2 receptors -> bronchial SM relaxation (increase camp, decrease intracellular calcium)
Lipophilic side chain lets drugs stay at receptor longer than other BA ICS and BA are SYNERGISTIC |
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What are the AE of LABA?
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Same as SABA
Cardiac stimulation: tachycardia, QT prolongation Muscle tremor (stim muscle receptors) Nervousness/anxiety Hypokalemia, Hyperglycemia (careful with DIGOXIN and DIABETICS) |
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What is the use of LABA?
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Long-term control! Most effective ADD-ON to ICS in moderate - severe persistent asthma
Onset too slow for quick relief Do NOT exceed recommended dose -> tachyphylaxis Also preventative for exercise induced asthma (take early) |
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What are the methylxanthines?
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Theophylline and Aminophylline (IV, PO)
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What is the MOA of methylxanthines?
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Unknown, BRONCHODILATION
Inhibits phosphodiesterase, relaxes SM Adenosine antagonism in CNS Increase mucociliary clearance and diaphragm contractility Decrease eo's |
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What are the kinetics of methylxanthines?
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Narrow tx index, follows Michaelis-Mentin (nonlinear increases)
Cyt p450 (CYP3A4, CYP1A2), age-dependent: 1-9yo, highest ability to metabolize (<1, elderly no) Inc metab: smoking, charcoal broiled foods, seizure meds, rifampin Deb metab: cirrhosis, CHF, drugs |
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What are the AE of methylxanthines?
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Serum conc > 20mcg/ml: N/V, nervousness, tremors, tachycardia, HA, insomnia
>30: arrhythmias, hypokalemia, hyperglycemia, seizure, hypotension, coma |
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What is the use of methylxanthines?
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Long-term: ADD-on to ICS (laba better)
Use alone in mild persistent (ICS better) Narrow TI, MM kinetics, AE - do NOT increase dose Caffeine, charcoal foods, caffeine affect theophylline, aminophylline |
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What are the leukotriene modifiers?
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Zafirlukast (<7yo, hepatotoxicity), Montelukast (DOC, less AE, given to >1yo)
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What is the MOA of leukotriene modifiers?
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BLOCK leukotriene receptor sites (LTD4, LTE4)
LT: chemotaxis (eo's), bronchoconstriction, mucus production |
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What are the kinetics of the leukotriene modifiers?
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Zafirlukast: p450 inhibitor (inc warfarin, aspirin inc's it, erythromycin dec's it)
Montelukast: phenobarbital decreases it |
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What are the AE's of leukotriene modifiers?
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Zafirlukast: hepatotoxicity (abd pain, nausea, fatigue, lethargy, jaundice, dark urine)
Montelukast: HA |
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What is the use of leukotriene modifiers?
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Long-term add on
Long term in mild persistent asthma, alternative Useful with comorbid allergic rhinitis Useful with aspirin/NSAID induced asthma Exercise induced bronchospasm |
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What is the IgG mAb = anti-IgE Ab?
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Omalizumab
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What is the MOA of omalizumab?
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mAb that BINDS free IgE, blocking attachment to mast cells and basophils, no response to allergens
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How is the anti-IgE ab administered?
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Omalizumab is administered SubQ, dose/freq is determined by baseline IgE and weight
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What are the AE of omalizumab?
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Injection site rxns: bruising, redness, etc
Urticaria Anaphylactic rxns: rare but serious Susceptible to viral and URI, sinusitis, pharyngitis |
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What is the use of Omalizumab?
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Long term - add-on with moderate - severe asthma, in IgE asthma
Must have positive skin test to allergen |
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What are the short-acting asthma drugs?
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SABA, anticholinergics, systemic corticosteroids
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What are the SABAs?
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Albuterol, Pirbuterol, Terbutaline, Levoalbulterol
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What is the MOA of SABAs?
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Directly STIMULATES beta2 receptors -> bronchial SM relaxation (inc camp, dec intracellular calcium)
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What are the AE of SABA?
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Injectable > Oral > Inhaled, thus IV only for emergencies!
Cardiac: tachycardia, prolonged QT Muscle tremor Nervousness/anxiety Hypokalemia, Hyperglycemia (digoxin and diabetics) |
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What is the use of SABAs?
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Short term, DOC! Use PRN in asthma
Prophylaxis, DOC: for exercise induced bronchospasm Monitor frequency of use, associated with inc mortality, drug tolerance |
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What is CI with SABAs?
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BB! avoid, including topical BB.
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What are the anticholinergics?
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Atropine - limited use due to systemic AE, Ipratropium - used, not systemic, (Tiatropium)
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What is the MOA of anticholinergics?
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Compete with ACh at muscarinic receptor, dec cGMP and parasympathetic tone, BRONCHODILATES
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What is the use of anticholinergics?
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Short term relief, limited. NOT used for exercise induced asthma.
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What are the systemic corticosteroids?
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Prednisone - oral, quicker onset, Hydrocortisone, Methylprednisolone (active metabolite of prednisone)
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What are the AE's of systemic corticosteroids?
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(assoc with long-term use)
Glucose intolerance- diabetics! CUSHINGS: moon facies, buffalo hump Growth retardation Osteoporosis, HTN, cataracts, skin thinning, myopathy, impaired wound healing, CNS (mania and depression) Short burst does NOT have severe efects |
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What is the use of systemic corticosteroids?
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Gain RAPID control when initiating long term tx (3-10 days short term), taper
Long term for severe persistent Short bursts can speed recovery, prevent recurrence Short term relief, add on to SABA |
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What are the medications for COPD?
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Anticholinergics, Beta-Agonists, Methylxanthines, and Corticosteroids
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What are the anticholinergics for COPD?
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Atropine - tertiary, causes systemic AE, Ipratropium/Tiotropium - not systemic
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What are the AE of Atropine? Ipratropium/Tiotropium?
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Blurred vision, urinary retention, tachycardia - atropine
Dry mouth worse with tiotropium |
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What is the MOA of the anticholinergics?
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Compete with ACh at muscarinic receptors, dec cGMP and parasymp vagal tone
Cholinergic tone is only REV component of COPD, vagal tone inc airway resistance |
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earthquake (starts with s)
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el sismo
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What are the Beta-Agonists for COPD?
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SABA: Albuterol
LABA: Formoterol, Salmeterol |
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What is MOA of Beta-Agonists in COPD?
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Stimulate Beta-receptors, promote SM relaxation -> increases FEV1
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What is the use of albuterol in COPD?
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DOC for acute exacerbation
Add-on to Ipratropium |
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What is the use of Salmeterol in COPD?
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Same efficacy as Ipratropium, but anticholinergic is still first line
Stage II-IV COPD |
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What is the methylxanthine for COPD?
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Theophylline
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What are the kinetics of theophylline in COPD?
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Michaelis-Menten, dose/response curve flattens at serum conc > 12, aim for 8-15 mcg/ml
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What is the use of theophylline in COPD?
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Toxicity! (neuro, cardio)
Add-on if anticholinergic and BA aren't working |
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What is the use of ICS in COPD?
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NOT fist line, no consistent effects
Add-on in severe COPD (III-IV) with repeated exacerbations, trial 6 weeks - 3 months (pneumonia!) |
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What is the use of Oral CS in COPD?
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NOT first line, no consistent effects
Burst may manage acute SEVERE COPD exacerbation, long term use NOT recommended due to AEs |
