Possible to have both asthma and COPD
1. Describe the pathophysiology, clinical manifestations, and treatment of chronic obstructive pulmonary disease
(COPD) and asthma. Risk factors, interventions
a. COPD
i. Description
1. Preventable and treatable disease
2. 3rd leading cause of death in USA
3. Systemic disease as a result of chronic inflammation
4. Slowly progressive resp disease of airflow obstruction
5. Other associated resp diseases
a. Chronic bronchitis = inflammation and irritation of bronchial tubules
i. Productive cough for 3mo in each of 2 consecutive years
ii. Ciliary function dec narrow and thickening damaged alveoli and
fibrosis resp infections
b. Emphysema = causes SOB
i. Abnormal, permanent enlargement of air spaces + destruction of alveoli
walls hypoxemia
ii. w/o obvious fibrosis
ii. Pathophysiology
1. Airflow limitation is progressive and associated w/abnormal inflammatory response to
noxious particles/gases
a. Happens through:
i. Proximal and peripheral airways
ii. Lung parenchyma
iii. Pulm vasculature
2. Body attempts to repair inflammation
a. Prox airways = inc goblet cells more mucus
b. Peri airways = thickening of wall exudate in airway and airway narrowing
c. Parenchyma = wall destruction dec loss of alveolar attachments
d. Pulm vasculature = thickening, scarring, dec SA hypertrophy of SM (pulm HTN)
iii. Risk factors
1. Age
2. Environment (smoking)
3. 2nd hand smoking
a. Depresses scavenger cells + ciliary cleaning mechanism trapped air distended
alveoli and dec lung capacity
b. Inc goblet cells more mucus infection lung damage
4. Prolonged/intense exposure to dust, chemicals, pollution (indoor and outdoor)
5. Genetic makeup
a. Deficient in Alpha-antitrypsin = enzyme protect lung parenchyma
b. Gene environment interactions (smoking, air pollution, infectious agents, allergies)
iv. Assessment
1. Spirometry = evaluate airflow obstruction
a. Grades 1-4
2. Arterial blood gas measurements
3. Chest X-ray
4. CT
5. Screen for alpha-antitrypsin deficiency
, v. Manifestations
1. Chronic cough
2. Sputum production
3. Dyspnea
4. Weight loss bc dyspnea interferes w/eating
5. Barrel chest (1:1 ratio diameter)
6. Resp insufficiency and infection
7. Musculoskeletal wasting
8. Metabolic syndrome
9. Depression
vi. Treatment
1. Goals
a. Relieve symptoms
b. Slow progression of disease
c. Improve exercise tolerance
d. Prevent/manage complications
e. Improve overall health
2. Lifestyle
a. Quit smoking and 2nd hand smoke, pollution,
3. Medical
a. Bronchodilators
i. Relax SM around airways dilation
ii. Inhalers straight to lungs
iii. Via
1. PMDI, NB, PO pill or liquid, powder, spacers/valved chambers
iv. Short acting
1. PRN for trouble breathing
v. Long
1. Ongoing symptoms
2. Still take if no symptoms
3. Better to improve long term
4. More expensive
b. Corticosteroids
i. Reduce inflammation in lungs
ii. Don’t use alone
iii. If severe COPD use long acting broncho + corticosteroids
iv. PO corticosteroids only used in acute flare-ups/exacerbations; not used
routinely
1. Help get over flare-up
2. Lower relapse and hospitalization chances
c. Methylxanthines
d. Phosphodiesterase 4 inhib (PDE-4)
i. Given if no relief of symptoms from other meds
ii. Lower COPD exacerbation
iii. Inc QOL
4. Vaccinations
a. Antibiotics control bacterial lung infections esp during acute flare-ups
b. Flu and pneumoniae prevent illness and hospitalization
, 5. Oxygen therapy
a. Supplemental oxygen via nasal cannula
b. For severe COPD or less than 55% O2 sat
c. Don’t give too much oxygen retention of CO2
d. Helps
i. Better breathing/sleep and exercise tolerance
ii. Improve physical activity
iii. Lower chance of death from COPD
iv. Inc baseline resting arterial O2 to 60mm and O2 saturation to 90%
6. Pulm rehab
a. Exercise program
b. Disease management training
c. Nutrition
d. Psych counseling
e. Goals:
i. Stay healthy
ii. Carry on w/ADLs
iii. Eat healthy
iv. Sleep well
v. Manage disease
7. Surgery
a. Sever not improved w/med therapy
b. LVR (lung volume reduction)
i. Removal of damaged tissue
ii. Helps breath better, improve QOL
iii. Only a few select people
c. Lung transplant
i. Rejection and infection of lungs possible
d. Bullectomy = removal of bulla
vii. Complications
1. Resp insufficiency and failure
2. Dry mouth, headache, cough, resp arrest
3. Pneumonia
4. Chronic atelectasis (complete/partial collapse of lung/lobe)
5. Pneumothorax = collapsed lung
a. Air leaks into space between lung and chest walls (pleural cavity)
6. Cor pulmonale = alt in structure/function of RV
a. Pulm hypertension common link
viii. Management
1. Stop smoking
2. Reduce risk factors
3. Manage exacerbations
a. Exacerbation = acute change in resp symptoms
i. Can be due to change in meds
b. Roflumilast (daliresp) can reduce risk of exacerbations w/severe COPD
c. Identify cause and admin specific treatment
d. Supplemental oxygen rapid assessment short acting bronchodilator PO/IV
corticosteroids antibitoics
1. Describe the pathophysiology, clinical manifestations, and treatment of chronic obstructive pulmonary disease
(COPD) and asthma. Risk factors, interventions
a. COPD
i. Description
1. Preventable and treatable disease
2. 3rd leading cause of death in USA
3. Systemic disease as a result of chronic inflammation
4. Slowly progressive resp disease of airflow obstruction
5. Other associated resp diseases
a. Chronic bronchitis = inflammation and irritation of bronchial tubules
i. Productive cough for 3mo in each of 2 consecutive years
ii. Ciliary function dec narrow and thickening damaged alveoli and
fibrosis resp infections
b. Emphysema = causes SOB
i. Abnormal, permanent enlargement of air spaces + destruction of alveoli
walls hypoxemia
ii. w/o obvious fibrosis
ii. Pathophysiology
1. Airflow limitation is progressive and associated w/abnormal inflammatory response to
noxious particles/gases
a. Happens through:
i. Proximal and peripheral airways
ii. Lung parenchyma
iii. Pulm vasculature
2. Body attempts to repair inflammation
a. Prox airways = inc goblet cells more mucus
b. Peri airways = thickening of wall exudate in airway and airway narrowing
c. Parenchyma = wall destruction dec loss of alveolar attachments
d. Pulm vasculature = thickening, scarring, dec SA hypertrophy of SM (pulm HTN)
iii. Risk factors
1. Age
2. Environment (smoking)
3. 2nd hand smoking
a. Depresses scavenger cells + ciliary cleaning mechanism trapped air distended
alveoli and dec lung capacity
b. Inc goblet cells more mucus infection lung damage
4. Prolonged/intense exposure to dust, chemicals, pollution (indoor and outdoor)
5. Genetic makeup
a. Deficient in Alpha-antitrypsin = enzyme protect lung parenchyma
b. Gene environment interactions (smoking, air pollution, infectious agents, allergies)
iv. Assessment
1. Spirometry = evaluate airflow obstruction
a. Grades 1-4
2. Arterial blood gas measurements
3. Chest X-ray
4. CT
5. Screen for alpha-antitrypsin deficiency
, v. Manifestations
1. Chronic cough
2. Sputum production
3. Dyspnea
4. Weight loss bc dyspnea interferes w/eating
5. Barrel chest (1:1 ratio diameter)
6. Resp insufficiency and infection
7. Musculoskeletal wasting
8. Metabolic syndrome
9. Depression
vi. Treatment
1. Goals
a. Relieve symptoms
b. Slow progression of disease
c. Improve exercise tolerance
d. Prevent/manage complications
e. Improve overall health
2. Lifestyle
a. Quit smoking and 2nd hand smoke, pollution,
3. Medical
a. Bronchodilators
i. Relax SM around airways dilation
ii. Inhalers straight to lungs
iii. Via
1. PMDI, NB, PO pill or liquid, powder, spacers/valved chambers
iv. Short acting
1. PRN for trouble breathing
v. Long
1. Ongoing symptoms
2. Still take if no symptoms
3. Better to improve long term
4. More expensive
b. Corticosteroids
i. Reduce inflammation in lungs
ii. Don’t use alone
iii. If severe COPD use long acting broncho + corticosteroids
iv. PO corticosteroids only used in acute flare-ups/exacerbations; not used
routinely
1. Help get over flare-up
2. Lower relapse and hospitalization chances
c. Methylxanthines
d. Phosphodiesterase 4 inhib (PDE-4)
i. Given if no relief of symptoms from other meds
ii. Lower COPD exacerbation
iii. Inc QOL
4. Vaccinations
a. Antibiotics control bacterial lung infections esp during acute flare-ups
b. Flu and pneumoniae prevent illness and hospitalization
, 5. Oxygen therapy
a. Supplemental oxygen via nasal cannula
b. For severe COPD or less than 55% O2 sat
c. Don’t give too much oxygen retention of CO2
d. Helps
i. Better breathing/sleep and exercise tolerance
ii. Improve physical activity
iii. Lower chance of death from COPD
iv. Inc baseline resting arterial O2 to 60mm and O2 saturation to 90%
6. Pulm rehab
a. Exercise program
b. Disease management training
c. Nutrition
d. Psych counseling
e. Goals:
i. Stay healthy
ii. Carry on w/ADLs
iii. Eat healthy
iv. Sleep well
v. Manage disease
7. Surgery
a. Sever not improved w/med therapy
b. LVR (lung volume reduction)
i. Removal of damaged tissue
ii. Helps breath better, improve QOL
iii. Only a few select people
c. Lung transplant
i. Rejection and infection of lungs possible
d. Bullectomy = removal of bulla
vii. Complications
1. Resp insufficiency and failure
2. Dry mouth, headache, cough, resp arrest
3. Pneumonia
4. Chronic atelectasis (complete/partial collapse of lung/lobe)
5. Pneumothorax = collapsed lung
a. Air leaks into space between lung and chest walls (pleural cavity)
6. Cor pulmonale = alt in structure/function of RV
a. Pulm hypertension common link
viii. Management
1. Stop smoking
2. Reduce risk factors
3. Manage exacerbations
a. Exacerbation = acute change in resp symptoms
i. Can be due to change in meds
b. Roflumilast (daliresp) can reduce risk of exacerbations w/severe COPD
c. Identify cause and admin specific treatment
d. Supplemental oxygen rapid assessment short acting bronchodilator PO/IV
corticosteroids antibitoics
