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Stack #183272
| Question | Answer |
|---|---|
| beable to recognize the inhaled glucoorticosteroids used in COPD. We only use the med to high dose | beclomethasone, budesonide, flunisolide, fluticasone, mometasone, triamcinolone, ciclesonide |
| what are the most common side effects seen with ICS | dry cough raspy vocie, bruising, skin thinning |
| what extra side effects do you see with systemic corticorids | osteoporosis, diabeties, glucoma and cateracts |
| which two ICS are 2nd generations that claim fewer side effects but not proven | fluticasone and mometasone |
| a medium dose of mometasone would be dosed how often | qd but for a higher dose use bid |
| what is the new drug that claims less systemic side effects by being metobolized in the lung | ciclesonide |
| at what stage do you recommend a glucocorticosteroids in COPD | at stage 3 you should add |
| the two glucocorticosteroids that are not used often because of increased frequency | beclomethasone and triamcinolone |
| if you need to give glucocorticosteroids by nebulizers what drug do you give | budesonide Pulmicort respules. only approved for children but could consider in adults with increased doses |
| what is the new black box warnings on spiriva (titropium)and also with ipratopium bromide | increased cardiovascular death and MI. SO YOU WOULD NOT WANT TO USE IN PATIENTS WITH PREVIOUS HISTORY OF MI HINT HINT |
| what is the onse of action for titropium and when do you expect to see max effect | 30 min onset with max effect seen in one week. only dosed once a day because DOA is 24 hours |
| the black box warning with long acting beta 2 agonist and their effects seen in COPD patients | this warning is not really seen with COPD patients like it is seen with asthma patients |
| what is the difference with salmeterol and formoterol | the onset with fomoterol is 5-10 minutes which is the same as seen with albuterol. |
| what are the nebulizer formulas seen with COPD | albuterol and levalbuterol, arformoterol (LABA) and duoneb (como of ipratropium and albuterol combined) |
| what symptoms need to be present to recommend an antibiotic | increased sputum producting and purulence together would be enough or increased dyspnea and sputum purulence. You don't need to give antibiotic with only dyspnea and production. |
| if you want to increase mucociliary clearance what class of drugs should be recommended | B agonists |
| what is the goal of oxygen therapy | to get oxygen saturation >90% |
| what are the monitoring parameters of oxygen therapy | monitor arterial blood gas for hypercapnia and should be considered for patients with acute respiratory failure |
| what vaccines should be give to COPD patients | flu for all patients and pneumonia for >65 and recommend in all other ages |
| what part of smoking is the cause of Cyp 1a2 interactions | hydrocarbons in cigeretts. it is not the nicotine that is why nicotine patch is still ok with theophylline |
| what are the main two side effects seen with theophylline and toxic concentrations | arrhythmias and seizures/ should only give teh sustained release formular in COPD if ever give (rarely precribed since the merge of LABA) |
| what drugs are inducers of CYP 1A2? what does it mean to be an inducers | inducers increase the metabolism and therfor the clearance. these drugs are hydrocarbons, hypethyroidiam, phenytoin, phenobarbital, rifampin, and carbmazepine |
| what drugs are inhibitors of CYP 1A2? what does it mean to be and inhibitor | they will block the metabolism of other drugs by causing down regulation of CYP enzyme. This will increase levels of theophylline. these drugs included cimetidine, macrolides, and fluoroquinolones antibiotics. clarithromycin, cipro |
| what is the starting dose of theophylline and what class of drug is this | it is a methylxanthine and should be started with 200mg bid and titrated upward to a target trough of 8-15 mcg/ml. tradionally the therapeutic range was 10 to 20. once stable and nothing changes monitor doses once to twice yearly |
| what is the most common side effect of long acting anticholinergic | dry mouth is biggest complaint |
| which short acting bronchodilators beta 2 agonist has a longer onset of action | levalbuterol. this is xopenex and is without the S racemate in the mixture. proposed to be less side effects but so for not proven |
| the three short acting slective b2 agonist are | albuterol, levalbuterol, and pirbuterol |
| what are the four long acting bronchodilators | tiotropium, salmeterol, formoterol, and arformoterol |
| what do bronchodilators do for patients | they reduce the tone of airway smooth muscle by relaxation thus minimizing airflow limitation increasing the exercise capacity, decreasing air trapping and relieve symptoms such as SOB. |
| what can't bronchodilators do for patients | they are not associated with significant improvements in pulmonary function measurements such as FEV1 |
| when patient has intermittent symptoms they are considered mild class one and should be on what pharmacological treatment | short acting bronchodilators, rarely see doctor at this point |
| when symptoms become more persistent what pharmacological treatment should be used | add regualr treatment for long acting bronchodilators and rehibilitation therapy |
| when a patients FEV1 gets bellow 50 they are considered to be in class three severe and should be on | inhaled glucocorticosteroids |
| how is the diagnosis of COPD made | using spirometry. and ratio less than 70% indicates airway obstruction. an improvement in FEV1 of less than 12% following inhalation of rapid acting bronchodilator is considered to be evident of irreversible airflow obstruction |
| what inflammatory cells predominate in COPD and which in asthma | neutrophil COPD and eosinophils and mast cells in asthmas. ICS work better on eosinopils and mast cells which is why they work better for asthma |
| which three pathogens are seen most frequently with COPD | S. pneumoniaeH. influenzaeM. catarrhalis |
| Chronic bronchitis is defined as | obstruction in small airways-chronic productive cough |
| Emphysema | change in pulmonary structure |
Created by:
lainylaina