COPD Flashcards
What is COPD?
Chronic airflow obstruction due to chronic bronchitis and/or pulmonary edema
NOT ACUTE, doesn’t go away, not completely reversible
Airflow obstruction is FEV1/FVC ratio < 0.70
Also can be viewed as persistent post-bronchodilator FEV1/FVC < 0.70 not due to dz other than COPD)
What is the definition of chronic bronchitis?
Persistent cough & sputum production for at least three months in at least two consecutive years
Leads to airflow obstruction vie intramural & intraluminal pathways
What is the definition of emphysema?
Destructino of acinar walls –> loss of radial traction on airways & increased lung compliance –> hyperinflation, poor lung mechanics
What are the risk factors for COPD?
Cigarette smoke
Occupational dust/chemicals
Environmental tobacco smoke
Air pollution
Genetic variation
Can FEV1 change if you quit smoking? Even if you’re really old?
Yes!
If you quit smoking, FEV 1 improves over the years: improves based on how long ago you quit smoking
What is alpha-1 antitrypsin deficiency?
Autosomal codominant disorder caused by mutation in the SERPINA1 gene
Mutations/deficiencies are correlated with emphysema risk
2% of COPD patients have sever A1A deficiency, esp younger patients with basilar emphysema
Can also cause liver dz
Treatment = IV pooled plasma alpha-1-antitrypsin
What does alpha-1-antitrypsin do?
Inhibits neutrophil elastase; consequence is the break down of alveolar walls
What happens to compliance in emphysema? Result?
Increased compliance
Leads to increased lung volume at lower pressures! Both for residual volume and inspiratory volume
What happens to the alveolar walls in COPD?
Loss of A1A –> loss of alveolar walls –> loose structure of the lung –> change elastic properties of the lung = hyperinflation due to increased compliance
Why does COPD/loss of alveolar walls lead to obstruction of the airway?
You also lose the radial traction that’s normally on your airways pulling it open –> airway collapses down (extraluminal cause of airway obstruction)
What happens to airway during forced expiration in COPD?
Loss of radial traction –> airways start to collapse; leads to something that you have to overcome during forced expiration; can eventually close down all the way
Results in a lower overall pressure in alveoli during forced expiration
“floppy airways” = bronchomalatia
What happens to the flow volume loop during COPD?
Lower flow at a given volume!
What happens to gas exchange in COPD? What’s the mechanism?
Mild hypoxemia (severe is rare)
Due to areas of Low V/Q, Alveolar hypoventilation, but NOT R–>L shunt!
What’s abnormal about ventilation in COPD?
Increased dead space ventilation (emphysemous regions are poorly perfused, increased work of breathing)
Alveolar hypoventilation
What’s the clinical presentation of COPD?
Half are asymptomatic
Half are symptomatic: cough, sputum production, chronic bronchitis, exertional dyspnea, muscular wasting
During an exacerbation: change in sputum, wheezing, increased dyspnea
What findings do you have on the physical exam in COPD?
Early dz=normal
Later dz = barrel chest, bilaterally diminished breath sounds, skeletal muscle atrophy
During exacerbation: wheezing, ronchi, cyanosis
Chx in COPD?
Big dark lungs
Flat diaphragm (seen better in lateral xray)
Also in CT you can see the airspaces
How do you diagnose COPD?
Clinical presentaiton
Airflow obstruction on spirometry that’s not reversible with bronchodilator
Exclude alternative cause
Which test is used to diagnose and to stage COPD?
Spirometry
If FEV1/FVC is < 0.70 = COPD
Then use FEV1 for staging
You can further use ABG to stage: PaO2/PaCO2
Why is staging important?
It determines how you manage COPD: each stage gets all the stages less severe than it
Stage 1: risk factor reduction, vaccination, short-acting inhalde beta 2 agonist
Stage 2: long acting inhaled bronchodilators, pulm rehab
Stage 3: inhaled corticosteroids
Stage 4: long term O2 therapy, surgical therapy
What is Varenicline?
Chantix- smoking cessation drug; partial agonist of alpha4beta2 subumint of nicotinic acetylcholine receptor
Stimulats it (which reduces withdrawal) while blocking nicotine from binding (reduces reward)
33% 6 month quit rate
Take until you’ve quit for 12 weeks and then for 12 weeks after they quit
Poorly tolerated: nausea, HA, insomnia, weird dreams, depression, suicidal thoughts, CV events
What are the 2 main classes of drugs used to treat COPD?
Symptom relief and controllers
Which drug classes are for symptom relief?
Short acting beta2 agonist (SABA)
Short acting anti-cholinergic
They come in a combo formulation
Which drug classes are controllers?
Long acting beta-2 agonist (LABA)
Long acting anti-cholinergic
Glucocorticoid (which can come in a formulation with LABA)
What is the overall effect of these drugs
Better lung function
Reduced exacerbation
Patient feels better
No mortality benefit
What are the side effects of beta-2 agonists?
tremor, tachycarida, hypokalemia, LABA: possibly death
Anti-cholinergics SE:
dry mouth
CV events (maybe)
Glucocorticoids SE?
Oral thrush
Cataracts
Osteoporosis
Pneumonia in COPD patients
What is Roflumilast?
PDE-4 inhibitor: used in patients who can’t tolerate other treatments
SE= diarrhea, weight loss
Decreases airway inflammation/promotes smooth muscle relaxation
Improves FEV1, decreases exacerbation
Which antibiotic is commonly used to treat COPD?
Azithromicin
Decreases exacerbations, improves quality of life
SE= hearing decrements, microbial resistance, CV risk
What are the indications for long-term O2 therapy in COPD?
Chronic hypoxemia: PaO2 <55 mmHg, SpO2<88%
Or PaO2 56-59, SpO2 <89% with one of the following: hematocrit >55%, cor pulmonale, or dependent edema
Improves survival, pulm hemodynamics, exercise capacity
Which 2 surgeries can you do to treat COPD?
(1) LVRS: lung volume reduction surgery
remove about 1/4 of each lung
Works for select patients: upper lobe predominant emphysema, low exercise capacity
Improves exercise capacity, quality of life, survival
(2) Lung transplant (possibly improved survival, improved quality of life, improved exercise capacity)
What does an acute exacerbation of COPD look like?
Increased sputum quantity, thickness, change in color
Often with systemic signs of infection/dyspnea
How do you manage acute exacerbation of COPD?
Short acting beta agonists & anti-cholinergics
O2 therapy (but avoid O2 induced hypercapnia)
Systemic antibiotics/corticosteroids
Noninvasive positive pressure ventilation (for acute alveolar hypoventilation/hypercapnia)
COPD summary of therapies
