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93 Cards in this Set
- Front
- Back
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carries unoxygenated blood
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pulm artery
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typically normal in COPD pts
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increase in C02
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where does the decrease in gas exchange occur with COPD
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alveolar level
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airflow limitation that is not reversible
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COPD
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what happens with the airflow limitation in copd
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progressive and associated with an abnormal inflammatory response of the lung to noxiois particles or gases
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types of copd (2)
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-emphysema
- chronic bronchitis |
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what causes airflow limitation in copd
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inflammatory response throughout proximal and peripheral airways, parenchyma, pulm vasculature
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what can chronic inflammation and bodys response lead to with copd
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changes and narrowing in the airways
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peripheral airway inflammation causes what (4)
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- thickening of airway wall
- peribronchial fibrosis -exudate in airway -narrowing of airway lumen |
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S&S of copd (5)
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- pulm vasculature w/thickening of lining
-hypertrophy of smooth muscle - inflam and structural changes in parenchyma - proximal airway increased # goblet cells -enlarged submucosal glands |
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why does hypersecretion occur with COPD
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helps to clear airway but too much can eventually obstruct airway
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hypertrophy of smooth muscle can lead to what
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pulm HTN
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causes a decrease in airway passage
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thickening and stiffining of wall
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cough and sputum production at least 3 mths in 2 consecutive years
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chronic bronchitis
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what does irritation from chronic bronchitis cause
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- mucus secreting glands and goblets to increase in # and increase mucus production
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too much mucus (plug) results in what
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decreased ciliary function
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in chronic bronchitis, if the alveoli become damaged and fibrosed, what happens
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alters the alveolar macrophage function (increases susceptibility to resp infections)
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impaired gas exchange from destruction of walls of overdistended alveoli
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emphysema
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what happens if alveoli become overdistended
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they lose elasticity
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in empyshema, what does the destruction of walls cause
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-decrease in alveolar suface area in contact with cap bed (dead space and impaired gas exchange)
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S&S of emphysema with progression (3)
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- decreased C02 elimination
- hypercapnia - resp acidosis |
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in emphysema, as pulmonary cap bed decreases in size what happens (3)
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- PVR increases
- then requires increased R vent pressure - leading to R sided heart failure |
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risk factors for COPD (5)
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- cigarette smoking
- pipe,cigar smoking - second hand smoke -prolonged/intense exposure to dust and chemicals - indoor/outdoor air pollution |
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host factors for COPD (3)
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- 1 in 6 never smoked
- gene-environment interaction - alpha1-antitypsin deficiency |
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what does the alpha1-antitypsin do
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protects parenchyma
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manisfestations of COPD (7)
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- chronic porgressive disease
- chronic cough, sputum produc - dyspnea on exertion - cough and sputum may precede air flow limitation by years - wt loss - resp insuff/infections - r/f acute and chronic resp failure |
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mild-mild airflow limitation
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stage 1
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moderate- worsening airflow limitation. stage typically seek medical help
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stage II
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severe, further airflow limitation. almost always impacts quality of life
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stage III
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very severe, quality of life appreciably impaired, exacerbations may be life threatening
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stage IV
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Assessment and Dx for COPD (5)
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- Hx&Px
- pulm function studies - ABG for baseling 02 and gas exchange - CXY to r/o other dx - if <45- alpha1-antitypsin deficiency screening |
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changes mainly in center of secondary lobule, preserving peripheral portions of acinus
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centrilobular (centroacinar)
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S&S of centrilobular emphysema (7)
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- vent-perfusion disproportion
- resulting in chronic hypoxemia - hypercapnia - polycythemia - episodes of R sided heart failure - central cyanosis - resp failure |
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destruction of bronchiole, alveolar duct, and alvolvus
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panlobular (panacinar) all branches of alveoli
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S&S of panlobular (5)
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- all airspaces in lobule enlarged
- little inflammation - hyperinflated chest (barrel) - marked dyspnea on exertion - wt loss |
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why does expiration with panlobular require active effort
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to create and sustain enough + pressure to move air out
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causes barrel chest
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hyperinflation
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causes wt loss
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WOB burning up calories
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can cause clogging at microvascular level
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polycythemia
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may not occur for several years with COPD
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sputum production and dyspnea
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maximum volume of air can be exhaled during forced maneuver
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forced vital capacity (FVC)
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volume expired in 1 second of maximal expiration after maximal inspiration (how wuickly lungs can be emptied)
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forced expiratory volume in 1 second (FEV1)
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what can influence FEV1 (4)
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- age
-sex -height - ethnicity |
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expressed as % of the FVC1, gives a clincally useful index of airflow limitation
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FEV1/FVC ratio
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normal FEV1/FVC ratio in adults
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70-80%
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<70 FEV1/FVC ratio
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airflow limitation-possibly COPD
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what is recommened for FEV1/FVC ratio <70
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postbronchodilator
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what does FEV1 and FEV1/FVC ratio show in pts with COPD
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decrease in both---generally reflects severity of disease
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mgnt goals for COPD (9)
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- relieve sx
- prevent disease progression - improve exercise tolerance - improve health status - prevent and tx complications - prevent and tx exacerbations - reduce mortality - prevent/minimize SE from Tx |
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what are the 4 components for the mgnt plan of COPD
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- assess and mtr disease
- reduce risk factors - manage stable COPD - manage exacerbations |
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what should be assessed and mtr with the 1st mgnt component (6)
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- med hx
- spirometry - CXR - ABG - alpha-1 antitrypsin def screen - risk factors |
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hwo can risk factors be reduced with COPD (6)
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- smoking cessation
- 5As (ask,advise, assess, assist, arrange) - pharm tx for cessation - smoking prevention - occupational exposures - indoor/outdoor air pollution |
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what are the 5As
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-ask
-advise -assess -assist -arrange |
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what are the pharm tx for smoking cessation (3)
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- nicotine replacement
- bupropion/ nortyptiline -varencicline |
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what do the bronchodilators do (3)
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-alter smooth muscle tone
-reduce airway obstruction -helps sx mgnt |
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used for intermittent relief
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PRN rescue broncho
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what do combo broncs do
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improve efficacy and decrease SE
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what are the beta adrenergic agonists (short) (4)
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- salbutamol (proventil)
- albuterol (ventolin) - fenterol (alupent/isuprel) - terbutaline (brethine) |
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what are the beta adrenergic agonists (long) (2)
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- formoterol (foradil)
- salmeterol (serevent diskus) |
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what are the anticholinergic agents for broncho
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atrovent (ipratropium bromide)
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what are the combo broncs (2)
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- fenoterol/ipratropium (duovent)
- salbutamol/ipratropium (combivent) |
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what are the methyxanthines (2)
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- aminophylline (phyllocontin/truphylline)
- theophylline )theo-dur/slo-bid) |
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reduce the frequency of exacerbations that are stage III or IV w/ repeated exacerbations
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inhaled glucocorticosteriods
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what do glucocorticosteriods increase the likelihood of
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pneumonia
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what are the combine w/long acting beta 2 agonist agents that are more effecitve (3)
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- beclomethasone
- budesonide (pulmicort) - fluticasone propionate (flovent) |
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not recommended for long term tx
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oral glucocorticosteriods
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minimum length of rehab for tx of COPD
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6 wks
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an event characterized by change in baseline dyspnea, cough, and/of sputum beyond normal day to day variations
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exacerbation
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what is the most common cause of infection (2)
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- trachobronchial tree
- air pollution |
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detects electrolyte diturbances, diabetes, and poor nutrition with COPD
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biochemical tests
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identifies polycythemia or bleeding
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CBC
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indicated resp failure
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Pa02 <60 and/or Sa02 <90 w/ or w/o PaC02 >50 when breathin RA
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indication for mech vent
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mod to severe acidosis <7.36, plus hypercapnia
PaC02 45-60 |
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what is long term 02 tx
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>15hrs/day
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when shoudl 02 therapy be initiated (3)
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- Pa02 <55
Sa02 <88 - w or wo hypercapnia |
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what is the goal of 02 therapy
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to increase baseline Pa02 at rest to 60 and Sa02 90%
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removal of affected lobe
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bullectomy
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done if disease is limited to specific area
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lung volume reduction
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when can lung transplantation be considered
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if stage IV pts
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chronic irreversible dilation of brochi and bronchioles
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bronchiectasis
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causes of bronchiectasis (6)
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- airway obstruction
- diffuse airway injury - pulm infections and obstruction of bronchus - genetic disorders (CF) - abnormal host defense - idiopathic causes |
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mgnt for bronchiectasis (2)
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- bronchial drainage
- antimicrobial therapy sometime prophylactic |
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S&S of bronchiectasis (4)
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- chronic cough
-purulent sputum - atelectasis distal to affected area - scarring/fibrosis of lung |
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what happens with bronchiectasis (4)
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-inflammation damages bronchial wall
- thick sputum develops - walls become distended and distorted -usually in lower lobes |
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chronic inflammatory disease that is reacting to a trigger
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asthma
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S&S of asthma (7)
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- hyperresponsiveness
- mucosal edema - mucus production - cough -chest tightness - wheezing - dyspnea |
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what are the most common sx of asthma (3)
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- cough
-dyspnea -wheezing |
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regular use contraindicated with COPD but can use every so often
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antitussives
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may help in pts with viscous sputum but not recommended for routine use
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mucolytic agents
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only to be used to tx infectious exacerbations
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ABX
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reduce serious illness and death in COPD pts by 50%
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influenze vaccine
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used in stage III or IV w/ Hx of exacerbations and chronic bronchitis
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phosphodiesterase 4 inhibitors
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what is a phosphodiesterase 4 inhibitors
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roflumilast
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