Obstructive Lung Disease Flashcards
Type of airflow in small airways
laminar
Why is flow turbulent in large airways and laminar in small airways
- high flow rate in large airways causes turbulent flow, and low flow rate in small airways allow for laminar flow
Large airway disease process
- greater changes in pressure are required to change airflow
- insensitive to most changes in diameter or pressure
- clinically significant changes in airflow require very large changes in driving pressure or airway diameter
Large airway diseases
- obstructive apnea
- aspiration of foreign body
- airway tumors
Small airway disease process
- changes in flow are linearly related to changes in pressure but exponentially related to changes in airway radius
- small changes in diameter produce substantial changes in flow
Small airway diseases
- asthma
- COPD
Differences in total cross sectional area b/w large and small airways
- cross sectional area increases exponentially from large to small airways
- therefore there is a lot less resistance in the smaller airways
Significance of larder cross sectional area of small airways
- young adults who smoke have substantial airway inflammation but have few, if any, symptoms of COPD until the disease has progressed for decades
Dynamic changes in airway diameter during respiratory cycle
- expansion during inhalation
- compression during exhalation
Significance of airway expansion during inhalation and compression during exhalation
- will hear wheezes during exhalation before you will during inhalation
How loss of elastic tissue in COPD effects airflow resistance
- emphysema patient airways will collapse during exhalation, b/c damage to walls have made them weak
Clinical relevance of wheezing during different points of respiratory cycle
- progression of disease follow wheezing
- wheezing during end of exhalation is early disease followed by wheezing throughout exhalation and finally with late disease patient will have wheezing during inhalation
Spirometry parameters and values
- FVC: volume exhaled during very forceful and prolonged exhalation
- FEV1: volume exhaled in the first second-normal is 80%
- FEV1/FVC: percentage of vital capacity exhaled in 1 second-normal is 80%, obstructive diseases
Flow-volume loop: explain steady exhalation slope
- steady flow out of lung b/c you can’t use expiratory muscles past a certain point or they will collapse airways
Flow-volume loop: obstructive disease
- airways collapse easier so the exhalation slope will be steeper and won’t reach as high
Large airway obstruction: location
- oropharynx, trachea, main bronchi
Large airway obstruction diseases
- tumors of trachea
- benign fibrous structures and scarring
- functional disorder: sleep apnea
- aspiration of foreign bodies
Clinical features of large airway obstruction
- dyspnea: not changed by medical management (ineffective steroids)
- stridor: MONOphonic wheeze
- KEY feature includes presence during inhalation only or both inhalation and exhalation; not altered or improved with coughing**
Asthma statistics
- 1/12 people have asthma (2009), increased from 1/14 (2001)
- 1 in 2 people with asthma have at least one attack every year
- $56 billion medical costs, about $3,300 per person
- 3,404 deaths in 2010
- slightly more prevalent in women for all ages
Asthma pathophysiology
- airway epithelial damage
- maintenance of inflammatory cell & cytokine environment in airways including lymphocytes, eosinophils, neutrophils, plasma/mast cells
- airway remodeling
Airway remodeling in asthma
- increased thickness of basement membranes
- increased mass of airway smooth muscle
- goblet cell metaplasia with mucus hypersecretion
- increased airway angiogenesis and lymphangiogenesis
How is asthma different from COPD
asthma is predominantly an AIRWAY disease and does not lead to lung parenchyma disease
Cell most commonly associated with asthma
- Type-2 helper cell cytokine mediated eosinophilic airway inflammation
Phenotypes of asthma
- early onset allergic disease w/ TH2 response
- TH2 response but not allergic syndrome
- exercise induced
- obesity related
- neutrophil dominated
Clinical syndrome of asthma
- chronic disease involving inflammation of pulmonary airways
- hyperresponsiveness resulting in lower respiratory obstruction
- REVERSIBLE
Development of asthma
- chronic airflow results from airway remodeling
- acute hyperresponsiveness: bronchoconstriction, airway edema, mucus plug formation
- symptoms
Symptoms of asthma
- coughing, particularly at night
- wheezing
- chest tightness
- dyspnea w/ exertion and shortness of breath at rest
Physical exam in asthma patients
- wheezing
- prolonged exhalation
- hyperresonance to percussion
- diminished air entry breath sounds
- accessory muscle use
Asthma staging
- normal,mild intermittent, mild persistent: FEV1>80%
- moderate persistent: FEV1 60-80%
- severe persistent: FEV1
Cornerstone of asthma treatment
- control of underlying inflammation for ALL patients with persistent symptoms
Controller treatment of asthma
- corticosteroids: inhaled and oral-mometasone, beclomethasone, fluticasone, prednisone
- LABA: 12-24 hr response for smooth muscle relaxation-inhaled salmeterol, formoterol
- leukotriene inhibitors
Rescue/Reliever treatment of asthma
- B-2 agonists: albuterol-primary rescue medication
- OVERUSE a marker and risk factor for increased mortality
Type of airflow in large airways
turbulent
Step therapy in asthma
- mild intermittent
- mild persistent
- moderate persistent
- severe persistent
Step therapy mild intermittent
- symptoms 80%
- medication: no daily control, as needed albuterol
Step therapy mild persistent asthma
- symptoms 2/month
- FEV1>80% predicted
- medications: low dose steroids, long active bronchodilator, leukotriene inhibitor
Step therapy moderate persistent asthma
- symptoms daily
- exacerbations >2/week
- affects activity, sleep
- night time symptoms >1/week
- FEV1 60-80%
- medications: high or moderate dose inhaled corticosteroids, long acting bronchodilator, leukotriene inhibitors
Step therapy sever persistent asthma
- symptoms: continuous
- frequent exacerbations and night time symptoms
- limits activity and work
- FEV1
COPD disease type
- airflow obstruction
- NOT reversible
COPD pathophysiology
- damage (usually due to smoking)
- inflammation
- abnormal response to inhaled toxins
- inflammatory and structural changes persist even after smoking cessation
COPD pathogenesis
- response to toxin
- lung inflammation: oxidative stress, impaired repair, tissue destruction, protease/antiprotease balance
Airflow limitation components
- irreversible component: fibrosis and narrowing of airways
- dynamic component: loss of elastic recoil due to tissue destruction
- reversible component: acute inflammation, mucus plugging and smooth muscle contraction
Causes of COPD
- TOBACCO SMOKING: 85-90% of COPD due to primarily cigarette smoking
Clinical features of COPD
- dyspnea
- age of onset 40-60
- cough, wheezing, chronic sputum production
- recurrent respiratory infections
COPD diagnosis
- dyspnea: progressive and persistent
- chronic cough or sputum production
- history of exposure to cigarettes or other causes
- SPIROMETRY is required to make diagnosis
COPD classification
- Mild: FEV1>80%
- Moderate: FEV1 50-80%
- Severe: FEV1 30-50%
- Very Severe: FEV1
COPD treatment
- substantial overlap w/ asthma
- pharmacologic therapy has NOT been shown to improve mortality
- anticholinergic treatment more prominent with COPD than asthma (inhaled ipratropium bromide, tiotropium)
- leukotriene inhibitors less frequently used
