COPD Flashcards
COPD
-Presence of airflow obstruction due to chronic bronchitis or emphysema
Obstruction is generally progressive
-+/- airway hyper-reactivity
-+/- PARTIALLY reversible
-Most patients with COPD have features of both emphysema and chronic bronchitis
key points
-common, preventable and treatable disease
-persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases
-MC respiratory symptoms include dyspnea, cough and/or sputum production -> may be under-reported by pts
-main risk factor is tobacco smoking but other environmental exposures such as biomass fuel exposure and air pollution may contribute
epidemiology of COPD
-14 million Americans diagnosed with COPD
-Equal number thought to be afflicted but remain undiagnosed.
-Fourth leading cause of death in US
-Over 120,000 deaths reported annually
chronic bronchitis
-Clinical diagnosis*
-Excessive secretion of bronchial mucous
-Daily* productive cough for 3 months or more for at least 2 consecutive years*
emphysema
-Pathologic diagnosis*
-Abnormal permanent enlargement of air spaces distal to the terminal bronchiole, with destruction of their walls and without obvious fibrosis
overlap
-emphysema
-COPD
-asthma
-all overlap
risk factors
-CIGARETTE SMOKING
-Occupational dusts and chemicals
-Air pollution
-Airway infection
-Familial factors
-Hereditary factors (deficiency of α1-antiprotease)
emphysema
-excessive lysis of elastin and other structural proteins in lung matrix by elastase and other proteases derived from lung neutrophils, macrophages, and mononuclear cells
-Permanent enlargement of alveolar sacs
-Destruction of tissue and pulmonary capillaries
-Airways floppy (increased compliance)- Destraction of connective tissue
-Air flow obstruction
-V/Q Mismatch
-Cor pulmonale
air trapping in COPD
-loss of alveolar attachments
-thickened (inflammated airway)
-loss of elasticity
-airway collapses on expiration
-a lot of air trapping- trouble breathing out
chronic bronchitis
-Increase in mucous production:
-Hypertrophy bronchial mucous glands (plugging)
-Goblet cells increase in number
-Damaged cilia
-Bronchial mucosa inflammation
-Bronchial smooth muscle hyper-reactivity -> Bronchospasm
-Air flow obstruction
-V/Q mismatch
-Cor Pulmonale
presentation/symptoms of COPD
-3 typical ways in which pts with COPD present:
-Few complaints, but extremely sedentary lifestyle
-Chronic respiratory symptoms (eg, dyspnea on exertion, cough)
-An acute exacerbation (eg, wheezing, purulent cough, dyspnea, +/- fever)
physical exam
-Early in disease:
-normal or prolonged expiration
-Wheezes
-As severity of airway obstruction increases:
-Hyperinflation, decreased breath sounds, wheezes, rhonchi, crackles, distant heart sounds
-Diaphragm may be depressed
-Increased ap diameter
end stage COPD
-Positions that relieve dyspnea
-Accessory muscles
-Expiration through pursed lips
-Paradoxical retraction of the lower interspaces during inspiration (Hoover’s sign)
-Cyanosis
-Asterixis
-Pneumonia
-Pulmonary HTN, cor pulmonale- Enlarged, tender liver, +/-neck vein distention
-Chronic respiratory failure
2 symptom patterns
-with COPD progression 2 symptom patterns tend to emerge:
-pink puffer- emphysema
-blue bloaters- chronic bronchitis
-simplification of anatomy and pathophysiology
-most COPD pts have pathologic evidence of both disorders
type A pink puffer
-DYSPNEA often severe
-Often presenting after age 50
-Cough rare, with scant clear, mucoid sputum
-Thin, wt loss
-Accessory muscles
-Chest is quiet without adventitious sounds
-No peripheral edema
lab, imaging, PFT for pink puffer
-Labs for pink puffer:
-Hemoglobin usually normal (12–15 g/dL)
-PaO2 normal to slightly reduced (65–75 mm Hg) but SaO2 normal at rest
-PaCO2 normal to slightly reduced (35–40 mm Hg)
-Chest radiograph:
-Hyperinflation, flattened diaphragms
-Vascular markings diminished
-Parenchymal bullae
-Pulmonary function tests:
-Airflow obstruction
-Total lung capacity increased
-DLCO reduced
-Static lung compliance increased
type B: blue bloater
-bronchitis predominant
-Mucopurulent chronic cough with frequent exacerbations due to infections
-Often presents in late 30s and 40s
-Dyspnea usually mild
-Frequently overweight and cyanotic but seem comfortable at rest
-Peripheral edema common
-Chest is noisy with rhonchi, wheezes
labs, imaging, PFTs: blue bloater
-Labs:
-Hemoglobin usually elevated (15–18 g/dL)
-PaO2 reduced (45–60 mm Hg)
-PaCO2 slightly to markedly elevated (50–60 mm Hg)
-Chest radiograph:
-Increased interstitial markings (“dirty lungs”)
-Diaphragms not flattened
-PFTs:
-Airflow obstruction
-Total lung capacity generally normal but may be slightly increased
-DLCO normal
-Static lung compliance normal
classification of severity of COPD
-1- mild COPD- FEV1/FVC < 70%
-FEV1 >= 80% predicted
-2- moderate COPD- FEV1/FVC < 70%
-50% <=FEV1 < 80% predicted
-3- severe COPD- FEV1/FVC < 70%
-30% <= FEV1 <50% predicted
-4- very severe COPD- FEV1/FVC <70%
-FEV1 <30% predicted or FEV1 <50% predicted plus chronic respiratory failure
GOLD ABE assessment tool
-E- any one at risk or who has >= 2 exacerbations OR >= 1 leading to hospitalization
MMRC- modified MRC dyspnea scale
CAT assessment
bronchodilators
-Offer some patients improvement in symptoms, exercise tolerance, and overall health status
-Anticholinergic/Muscarinic antagonists (ipratropium bromide, tiotropium bromide)
-Short acting β2-agonists (eg, albuterol, metaproterenol)
-Long-acting β2-agonists (formoterol, salmeterol)
treatment based on group A, B, E
-group A- CAT<10, mMRC 0-1
-Group B- more symptomatic but still no exacerbations
-Group E- LABA+LAMA (has has exacerbations) -> consider LABA + LAMA + ICS -> prof is hesitant to give steroid ever
steroids (inhaled)
-Improves quality of life
-Decreases severity and # of exacerbations in pts with moderate to severe copd
antibiotics
-Commonly prescribed to outpatients with COPD for the following indications:
-Treat an acute exacerbation/infection
-Not for prophylaxis
-augmenten
-bactrim
-doxy
inhaled medications
-Inhaled Medications are Topical Medications, not Systemic
-They only work if the medication gets to the targeted tissue
-Delivery system/Inhaler Choice and inhaler technique are very important.
-It is very important to demonstrate the inhaler technique and assess patient’s ability to use it properly.
-2020 GOLD Guidelines recommend reassessing inhaler technique and inhaler choice on every visit
pulmonary rehab
-Improve exercise capacity
-Decrease hospitalizations
-Improve Quality of life
-Graded aerobic physical exercise programs (eg, walking 20 minutes three times weekly or bicycling):
-Prevents deterioration of physical condition
-Improves ability to carry out daily activities
-Training of inspiratory muscles
O2 therapy
-Resting hypoxemia (<88%)
-Proved benefits:
-Include longer survival
-Reduced hospitalization needs
-Better quality of life
-Hypoxemic patients who are likely to benefit are:
-Pulmonary hypertension
-Chronic cor pulmonale
-Eythrocytosis
-Impaired cognitive function
-Exercise intolerance
-Nocturnal restlessness
-Morning headache
other treatments
-Human alpha 1 antitrypsin for deficient patients
-Opioids-controversial
-Lung transplantation- Substantial improvements in pulmonary function and exercise performance have been noted after
-Lung volume reduction surgery:
-Bilateral resection of 20–30% of lung volume in selected patients results in modest improvements in pulmonary function, exercise performance, and dyspnea
-Endobronchial Valve placement can achieve the same goal without surgery
-Bullectomy- A single bulla occupies at least 30–50% of the hemithorax
acute exacerbation CXR, spirometry, ABG
-CXR: R/O things that can cause exacerbation -> CHF, pneumonia, pneumothorax
-Spirometry: Not useful in acute setting
-ABG: Useful
acute exacerbation tx?
-Oxygen
-Bronchodilators: beta agonists/anticholinergics or combo
-Oral Steroids:
-40-60 mg Prednisone then taper
-Faster recovery / shorter hospitalizations
-May prolong time to next relapse
-Antibiotics- Approx 50% exacerbations due to infectious etiology
-Non-invasive PPV- decreases need for mechanical vent
prevention
-Largely preventable through elimination of longterm exposure to tobacco smoke.
-Smokers with early evidence of airflow limitation can significantly alter their disease by smoking cessation.
-Slows the decline in FEV1
-Flu and pneumovax
summary
-Obstructive airways disease largely due to smoking
-Not completely reversible like asthma
-Emphysema-Lung destruction and hyperinflation
-Chronic Bronchitis-Airway inflammation and mucous production
-GOLD Guidelines-Degree of obstruction plus exacerbations and symptoms
-Frequently reassess inhaler choice and pt’s ability to properly use the device
-SMOKING CESSATION
