COPD Flashcards
Define COPD
a respiratory disorder largely caused by smoking, and is characterized by progressive, partially reversible airway obstruction and lung hyperinflation, systemic manifestations, and increasing frequency and severity of exacerbations.”
Main differnce between asthma and COPD
Asthma is rversible, COPD is progressive
Define emphysema
abnormal enlargement of the airspace distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis
Define chronic bronchitis:
Chronic cough for at least 3 months x 2 consecutive years
COPD Epidemiology is primarily…. It results in how many % of deaths?
Cigarette smoking: principal underlying cause of COPD and responsible for about 80% of deaths
What is unique about COPD’s prevelance?
3rd leading cause of death worldwide; only chronic illness with increasing mortality
Risk Factors of COPD
Exposure to Particles
Infections
Socio-economic status
What is the most significant risk factor of COPD?
- SMOKING/EXPOSURE TO 2ND HAND SMOKE
What are some host factors of COPD?
1) Hereditary
1-antitrypsin deficiency predisposes susceptible people to emphysema
1-antitrypsin is a serum protein produced by the liver & normally found in the lungs.
It prevents neutrophil elastase from destroying lung tissue
Accounts for <5% of cases
2) AGE
3) Lung Growth and Development
4) Airway Hyperresposiveness (Hard to seperate and define cause and effect with asthma)
Pathophysiology of COPD Simple
Stimulus (e.g smoking) –> Inflammatory process –> narrowing of perfipheral pathways –> Decreased FEV1
What is noted in COPD patients in regards to pathopjhysiologuy?
A Protease-Antiprotease Imbalance is noted in the lungs of COPD patients. (Protease Mediated destruction of elastin is an important feature of emphysema)
In COPD, what may amplify the inflammatory response?
Oxidative stress may play an important role in amplifying the inflammatory process.
COPD has a specific pattern of what?
Specific pattern of inflammation: CD8+ (cytotoxic) lymphocytes and other Inflammatory cells & mediators induce structural changes in the lung parenchyma & Pulmonary vasculature
COPD –> Increase in residual volume –> GAS TRAPPING
In regards to COPD pathophysiology, these things occur:
Expiratory Flow Limiytation
Lung Hyperinflation
Gas Exchange Abnormality
Mucous Hypersecretionm
What is a hallmark of COPD? Why does it occur?
Expiratory Flow Limitation
Hallmark of COPD
Due to increased resistance from mucosal inflammation, airway remodelling, fibrosis & secretions
In COPD, the lungs will ______upon inhalation. Why does it occur? What is the result?
Lung hyperinflation
Obstruction of the small airways results in air-trapping which causes lung hyperinflation
Develops early in disease and causes exertional dypsnea
In regards to gas exchange, in COPD there is ______ Result?
Gas exchange abnormalities
Result in hypoxemia & hypercapnia
Gas transfer for O2 & CO2 worsens as disease progresses
In regards to mucouis, in COPD there is ______. This results in a _____
Mucous hypersecretion
Results in a chronic productive cough
Not necessarily associated with airflow limitation
What triggers an exacerbation? What occurs during a COPD exacerbation?
Triggered by infection, environmental pollutants or unknown
During exacerbations there is increased hyperinflation and gas trapping, with decreased expiratory flow
With COPD, what other conditions may one have as a result later in life?
Significant Comorbid Illness
Pulmonary hypertension may develop late in course of COPD due to hypoxic vasoconstriction of small pulmonary arteries eventually leading to structural changes
Muscle wasting and cachexia, skeletal muscle dysfunction
Osteoporosis, depression and anemia, metabolic sydrome, cardiovascular, lung cancer
What are some comorbities associated with COPD?
Ischemic heart disease
Congestive heart failure
Arrhythmias
Pulmonary hypertension
Lung cancer
Osteoporosis and Fractures
Skeletal muscle dysfunction
Cachexia and Malnutrition
Glaucoma and Cataracts
Depression
Anxiety and Panic disorders
Metabolic disorders
Three cardinal sx of COPD?
Shortness of breath
Chronic cough
Phlegm
What other sx may be present?
Frequent lung infections
Reduced ability to go about daily activities
Barrel-shaped chest
Fatigue
Unexplained weight loss
End-stage COPD Sx?
Adopt positions that relieve dyspnea relax diaphragm
Use of accessory respiratory muscles
Expiration through pursed lips
Cyanosis
Enlarged liver from right heart failure
How do patients with COPD initially present?
1) Extremely sedentary lifestyle and presents with general fatigue
—> Typically have avoided exertional dyspnea
—> Shifted expectations and limited their activity
2) Patient has complaints of dyspnea and chronic cough
–> Initially noted on exertion only
–> Progressively triggered by less exertion or at rest
–> Morning sputum production
3) Patient who presents with episodes of cough, sputum, wheezing, fatigue and dyspnea
–> May be initially diagnosed as asthma
–> Interval between episodes shortens
Asthma vs COPD: age of onset
Asthma - <40
COPD: <40
Asthma vs COPD: smoking History
Asthma: Not causal, but worsen control
COPD: Usually >10 pack years
Asthma vs COPD: Sputum Production
Asthma: Infrequent
COPD: Often
Asthma vs COPD: Allergies
Asthma: Often
COPD: Infrequent
Asthma vs COPD: Clinical Sx Length/ How long do the sx last?
A: Intermittent and variable
C: Persistet and progressive
Asthma vs COPD: Disease Course
A: Stable (withe xacerbations)
C: Progressive (with exacerbations)
Asthma vs COPD: Comorbid Illness
Important for both
Asthma vs COPD: Spirometry
A: often normalizes
C: May improve but never normalizes
Asthma vs COPD: Cause of Airway Inflammation
A: Eiosinophilic
C: Neutrophilic
Asthma vs COPD: ICS response
A: Essential
C: Helpful in pt’s with moderate and frequent AECOPD
Asthma vs COPD: Bronchodilators
A: PRN only
B: Regular tx
Asthma vs COPD: Exercise training
A: Rarely used
C: Essential
Asthma vs COPD: End of life discussions
A: Rare
C: Often essential
A clinical diagnosis of COPD should be considered in any pt who has:
Dyspnea
Chronic Cough
Sputum Production
History of exposure to risk
What is used to diagnose COPD? What is used to stage it?
Spirometry post-bronchodilator FEV1/FVC ratio <0.7 confirms diagnosis
FEV1 is used to stage
Who should be screened for COPD?
Evidence does not currently support population screening with spirometry
-Screen patients who have risk factors:
Smokers/ex-smokers ≥40 who have:
- persistent cough or sputum production
- frequent respiratory tract infections
- progressive activity-related SOB
- evening wheeze
–> if yes –> Spirometry
MRC Scale
STUDY CHART
What is the CAT Test?
Validated, short (8-item) and simple patient completed questionnaire
Reliable measure of the impact of COPD on a patient’s health status
Suspect COPD in people who are:
Age > 40 years
Smokers or ex-smokers – quantify tobacco consumption
Progressive dyspnea, worse with exercise
Spirometry is necessary for COPD ________. Values:
FEV1 / FVC < 70% after bronchodilator
Staging of COPD CTS
STUDY CHART
GOALS of TX COPD
Prevent disease progression
Prevent and treat exacerbations
Alleviate breathlessness and other respiratory symptoms
Improve exercise tolerance and daily activity
Prevent and treat complications of the disease
Improve health status
Reduce mortality
What is the most effective intervention to reduce risk of COPD? Does it stop progression? What should one ask?
Smoking Cessation –> Just slows down the rate of progression (lung function will continue decreasoing if have COPD)
One should: The 5 A’s: Ask, Advise, Assess, Assist, Arrange
In pt education, what should be taught?
Expectations of therapy must be discussed(cannot cure, but improve QOL – progressive life long tx – most likely will add on rather than take away)
Self management plans
prescriptions for oral steroids and antibiotics to fill when needed
advanced care directives
Inhaler technique – select best device for each individual patient
What should be avoided in COPD? Why?
Sedatives/Narcotics: increased sensitivity to respiratory depression especially when sleeping
All COPD pt’s should be encouraged to:
maintain an active lifestyle
What vaccines should people with COPD get?
Annual Influenza vaccine
decreases serious illness / death by 50%
Pneumococcal vaccine
Recommended for all patients with COPD
Covid-19 Vacinne
Who should get long-term oxygen tx? What is the goal?
SEVERE HYPOXEMIA
Does not change pulmonary function
Cornerstone of therapy
improves quality/ duration of life in select patients
Assess patient when stable
goal PaO2 > 60 mmHg
Pharmacological tx is ________. The main stay of tx is…..
Empiric – individuals differ in response to treatment and side effects (start with something and go from there)
Bronchodilators are the mainstay in treatment and are prescribed regularly in COPD; larger doses may be used compared to treatment of asthma.
Pharmacotx difference from asthma:
Compared to asthma:
Muscarinic antagonists have larger role
ICS have less of a role
If bronchodilator fails, confirm compliance and acceptable inhaler technique.
SABA of Choice: Dose:
Slabutamol
Terbutaline
BOTH QID PRN
SAMA of Choice Dose
Ipratropium QID PRN
Can a combo be used? If so, what and dose? WHy?
Salbutamol + ipratropium –> QID PRN
Synergistic –> Better than used alone
What is recommended in all stages of COPD?
PRN use of short acting bronchodilators is recommended in all stages of disease
Higher doses = more bronchodilation
May increase beyond recommended dose in severe disease
SAMA LAMA MOA
Airway muscle tone is partially controlled by cholinergic innervation.
Inhaled anticholinergics competitively inhibit cholinergic receptors in bronchial smooth muscle. This block acetylcholine which reduces cGMP.
Acetylcholine leads to bronchoconstriction.
SAMA vs SABA Comparison
Less effective than β2 agonists in asthma
Slower onset of action than SABA
SAMA LAMA A/e
Dry mouth, cough, constipation, urinary retention, headache, metallic taste
Avoid eye contact – can precipitate glaucoma
Rinse mouth after inhalation to decrease dry mouth (less with SAMA)
Cardiovascular (stroke? iffy)
LABA and LAMA Examples. DOSE:
Salmeterol BID
Formeterol BID
Indacterol OD
Oldaterol OD
Vilanterol (Only combo)
Tiotropium OD
Aclindium BID
Glycopyronnium OD
Umeclidium OD
Compare LABA and LAMA
Both improve symptoms
LAMA (tiotropium) may be superior in decreasing exacerbations
LAMAs may be better tolerated (decreased withdrawal in RCTs)
Side effect profiles vary
LAMA: dry mouth, constipation
LABA: headache, dose dependent CV effects (racing heart
ICS COPD
In contrast to asthma, inhaled corticosteroids should not be used as first-line medication.
ICS should not be used as monotherapy
ICS have evidence for reducing exacerbations, but inconsistent evidence for symptom improvement
Patients with a higher eosinophil count may respond better
Consider ICS side effects
Which agent? What should one consider?
evidence, Availability, Onset, Side effects, Guidelines
What LABAS work fast? WHich LAMA?
Formeterol, indacterol, oldaterol LABA
Glycopyrrinium – LAMA
Work within minutes
Prophylatic azithromycin for who?
Recommended in patients who have normal QT interval on electrocardiograms(ECGs), no significant drug interactions with concomitant medications and no evidence of either indolent or active infection with atypical mycobacteria
Reduced exacerbation rates and improved QOL compared to placebo.
Azithromycin group had a higher rate of colonization with macrolide-resistant bacteria, and hearing deficits.
May also see dosed 3 x weekly
on 250mg OD x 1 year
N-acetylcysteine MOA? Dosage form? Dose? USe?
A mucolytic agent with antioxidant properties
Mechanism of action of NAC inCOPDis not clearly understood
Optimal dose of NAC has not been determined
Injectable solution is administered orally
High-dose NAC, 600 mgorally twice daily, may be of benefit in reducing acute exacerbations in those who had 2 or more exacerbations in the previous2-yearperiod
chronic bronchitic phenotype at high risk of exacerbations
Roflimast? MOA? Dose? USe? Spirometry? Rescue?
Phosphodiesterase IV inhibitor
Administered once daily (500 mcg tablet per day)
could be considered for addition to existing triple therapy (LAMA +ICS/LABA) for people withCOPDwho have had at least1 exacerbationin the past year.
Add-on to bronchodilator treatment
chronic bronchitic phenotype at high risk of exacerbations
Improves FEV1, decreases exacerbations
Not be used as a rescue medication
Roflimast S/e?
diarrhea, weight loss, nausea, headache, sleep disturbances
Neuropsych effects – avoid in hx of depression with suicidal ideation
Should theophylline be used in COPD?
NO - No longe rin guidelines
Mild Excaerbation
worsening or new respiratory symptoms without a change in prescribed medications
Moderate Exacerbation
prescribed antibiotic and/or oral corticosteroids
Severe Exacerbation:
requiring a hospital admission or ED visit
Low risk Exacerbation:
if they had 1 or less moderate exacerbation in the last year and did not require an ED visit or hospitalization
High risk exacerbation
if they had at least 2 moderate or 1 severe exacerbation in the last year requiring a hospital admissions/ED visit.
COPD Guidelines
STUDY CHART
In the most severe cases, what is a tx of COPD?
Lung Volume Reduction Surgery
Lung Transplantation –> FEV1 <25% predicted and severe sx
Stepping Up and Down in COPD:
Stepping up:
Usually treatment is progressive and additive
No absolute interval time at which evaluation should be performed after initiating change in therapy
–> consider 6 months after initiating long acting bronchodilator and 12 months after initiating ICS
STEPPING DOWN: QUESTIONABLE
If treatment benefits not realized, or side effects exceed benefits
In patients on ICS at low risk of morbidity and mortality, and exacerbation who have had a long period of stability
Close supervision and monitoring necessary
Taper steroids if considering stopping
Definition of acute exacerbation:
sustained worsening of dyspnea, cough or sputum production leading to an increase in the use of maintenance medications and / or supplementation with additional medications.
Consequences of AECOPD
Reduced health-related QOL
Accelerated decline in Lung function
Increased Mortality
Increased healthr esource ultilzation and costs
Acute Exacerbation TX:
1) Bronchodilators
SAMA and SABA (salbutamol +/-ipratropium) become scheduled
Increase dose and frequency
long-acting inhalers can be continued but should not replace short-acting bronchodilators
2) Steroids (systemic)
Improve spirometry; decrease relapse rate. Restore lung function quicker
Dose:
typically 30-50 mg daily prednisone (or equivalent) x5-14 days
Antibiotics – should be given to:
Patients requiring mechanical ventilation
OR
Patients with at least 2/3 of the cardinal symptoms:
sputum purulence (change in phlegm color to yellow or green)
increased sputum volume
increased dypsnea
ANTIBIOTIC CONSIDERATION:
Study Chart
