Obstructive Lung Disease Flashcards Preview

MODHIII - Unit 3 > Obstructive Lung Disease > Flashcards

Flashcards in Obstructive Lung Disease Deck (47)
Loading flashcards...

Type of airflow in small airways



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


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

1. airway epithelial damage
2. maintenance of inflammatory cell & cytokine environment in airways including lymphocytes, eosinophils, neutrophils, plasma/mast cells
3. 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

1. early onset allergic disease w/ TH2 response
2. TH2 response but not allergic syndrome
3. exercise induced
4. obesity related
5. neutrophil dominated


Clinical syndrome of asthma

- chronic disease involving inflammation of pulmonary airways
- hyperresponsiveness resulting in lower respiratory obstruction


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



Step therapy in asthma

1. mild intermittent
2. mild persistent
3. moderate persistent
4. 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