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MODHIII - Unit 3 > Obstructive Lung Disease > Flashcards

Obstructive Lung Disease Flashcards

1
Q

Type of airflow in small airways

A

laminar

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2
Q

Why is flow turbulent in large airways and laminar in small airways

A
  • high flow rate in large airways causes turbulent flow, and low flow rate in small airways allow for laminar flow
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3
Q

Large airway disease process

A
  • 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
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4
Q

Large airway diseases

A
  • obstructive apnea
  • aspiration of foreign body
  • airway tumors
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5
Q

Small airway disease process

A
  • 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
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6
Q

Small airway diseases

A
  • asthma

- COPD

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7
Q

Differences in total cross sectional area b/w large and small airways

A
  • cross sectional area increases exponentially from large to small airways
  • therefore there is a lot less resistance in the smaller airways
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8
Q

Significance of larder cross sectional area of small airways

A
  • young adults who smoke have substantial airway inflammation but have few, if any, symptoms of COPD until the disease has progressed for decades
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9
Q

Dynamic changes in airway diameter during respiratory cycle

A
  • expansion during inhalation

- compression during exhalation

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10
Q

Significance of airway expansion during inhalation and compression during exhalation

A
  • will hear wheezes during exhalation before you will during inhalation
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11
Q

How loss of elastic tissue in COPD effects airflow resistance

A
  • emphysema patient airways will collapse during exhalation, b/c damage to walls have made them weak
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12
Q

Clinical relevance of wheezing during different points of respiratory cycle

A
  • 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
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13
Q

Spirometry parameters and values

A
  • 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
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14
Q

Flow-volume loop: explain steady exhalation slope

A
  • steady flow out of lung b/c you can’t use expiratory muscles past a certain point or they will collapse airways
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15
Q

Flow-volume loop: obstructive disease

A
  • airways collapse easier so the exhalation slope will be steeper and won’t reach as high
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16
Q

Large airway obstruction: location

A
  • oropharynx, trachea, main bronchi
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17
Q

Large airway obstruction diseases

A
  • tumors of trachea
  • benign fibrous structures and scarring
  • functional disorder: sleep apnea
  • aspiration of foreign bodies
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18
Q

Clinical features of large airway obstruction

A
  • 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**
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19
Q

Asthma statistics

A
  • 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
20
Q

Asthma pathophysiology

A
  1. airway epithelial damage
  2. maintenance of inflammatory cell & cytokine environment in airways including lymphocytes, eosinophils, neutrophils, plasma/mast cells
  3. airway remodeling
21
Q

Airway remodeling in asthma

A
  • increased thickness of basement membranes
  • increased mass of airway smooth muscle
  • goblet cell metaplasia with mucus hypersecretion
  • increased airway angiogenesis and lymphangiogenesis
22
Q

How is asthma different from COPD

A

asthma is predominantly an AIRWAY disease and does not lead to lung parenchyma disease

23
Q

Cell most commonly associated with asthma

A
  • Type-2 helper cell cytokine mediated eosinophilic airway inflammation
24
Q

Phenotypes of asthma

A
  1. early onset allergic disease w/ TH2 response
  2. TH2 response but not allergic syndrome
  3. exercise induced
  4. obesity related
  5. neutrophil dominated
25
Q

Clinical syndrome of asthma

A
  • chronic disease involving inflammation of pulmonary airways
  • hyperresponsiveness resulting in lower respiratory obstruction
  • REVERSIBLE
26
Q

Development of asthma

A
  • chronic airflow results from airway remodeling
  • acute hyperresponsiveness: bronchoconstriction, airway edema, mucus plug formation
  • symptoms
27
Q

Symptoms of asthma

A
  • coughing, particularly at night
  • wheezing
  • chest tightness
  • dyspnea w/ exertion and shortness of breath at rest
28
Q

Physical exam in asthma patients

A
  • wheezing
  • prolonged exhalation
  • hyperresonance to percussion
  • diminished air entry breath sounds
  • accessory muscle use
29
Q

Asthma staging

A
  • normal,mild intermittent, mild persistent: FEV1>80%
  • moderate persistent: FEV1 60-80%
  • severe persistent: FEV1
30
Q

Cornerstone of asthma treatment

A
  • control of underlying inflammation for ALL patients with persistent symptoms
31
Q

Controller treatment of asthma

A
  • corticosteroids: inhaled and oral-mometasone, beclomethasone, fluticasone, prednisone
  • LABA: 12-24 hr response for smooth muscle relaxation-inhaled salmeterol, formoterol
  • leukotriene inhibitors
32
Q

Rescue/Reliever treatment of asthma

A
  • B-2 agonists: albuterol-primary rescue medication

- OVERUSE a marker and risk factor for increased mortality

33
Q

Type of airflow in large airways

A

turbulent

34
Q

Step therapy in asthma

A
  1. mild intermittent
  2. mild persistent
  3. moderate persistent
  4. severe persistent
35
Q

Step therapy mild intermittent

A
  • symptoms 80%

- medication: no daily control, as needed albuterol

36
Q

Step therapy mild persistent asthma

A
  • symptoms 2/month
  • FEV1>80% predicted
  • medications: low dose steroids, long active bronchodilator, leukotriene inhibitor
37
Q

Step therapy moderate persistent asthma

A
  • 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
38
Q

Step therapy sever persistent asthma

A
  • symptoms: continuous
  • frequent exacerbations and night time symptoms
  • limits activity and work
  • FEV1
39
Q

COPD disease type

A
  • airflow obstruction

- NOT reversible

40
Q

COPD pathophysiology

A
  • damage (usually due to smoking)
  • inflammation
  • abnormal response to inhaled toxins
  • inflammatory and structural changes persist even after smoking cessation
41
Q

COPD pathogenesis

A
  • response to toxin

- lung inflammation: oxidative stress, impaired repair, tissue destruction, protease/antiprotease balance

42
Q

Airflow limitation components

A
  • 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
43
Q

Causes of COPD

A
  • TOBACCO SMOKING: 85-90% of COPD due to primarily cigarette smoking
44
Q

Clinical features of COPD

A
  • dyspnea
  • age of onset 40-60
  • cough, wheezing, chronic sputum production
  • recurrent respiratory infections
45
Q

COPD diagnosis

A
  • dyspnea: progressive and persistent
  • chronic cough or sputum production
  • history of exposure to cigarettes or other causes
  • SPIROMETRY is required to make diagnosis
46
Q

COPD classification

A
  • Mild: FEV1>80%
  • Moderate: FEV1 50-80%
  • Severe: FEV1 30-50%
  • Very Severe: FEV1
47
Q

COPD treatment

A
  • 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

MODHIII - Unit 3 (20 decks)

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