W14 COPD And Smoking Cessation Flashcards
COPD learning objectives
● For treatment of COPD, list the
major classes of drugs, examples of
drugs within those classes, and their
common adverse effects.
● Based on GOLD guidelines,
recommend medication therapy for a
COPD patient on initial diagnosis, as
well as for treatment escalation.
● Be familiar with the different types
of inhalers and their advantages and
disadvantages.
● Recommend pharmacologic agents to
facilitate smoking cessation based on
patient-specific factors.
COPD symptoms and diagnosis
—dyspnea that is persistent and/or progressing
—chronic cough +/- wheezing
—chronic sputum production
—recurrent lower respiratory tract infections
—risk factors, incl family history
—spirometry :
FEV1«FVC
post- bronchodilator
FEV1/FVC<0.7 indicates irreversible airflow limitation, more likely COPD than asthma
COPD
Goals of treatment
Preventative measures
ANS: PNS vs SNS : how do you achieve bronchodilation?
⭐️
symptom reduction
● relieve symptoms
● improve exercise tolerance
● improve health status
risk reduction
● prevent disease progression
● prevent/treat exacerbations
● reduce mortality
No medication has conclusively shown to slow lung function decline or prolong survival in COPD.
Preventative measures
these should be addressed and optimized at every follow-up visit
—⭐️smoking cessation and avoidance of environmental exacerbants
—⭐️vaccination: influenza, pneumonia, pertussis, COVID-19
—physical activity (incl cardiovascular health)
—pulmonary rehab if group B-D
⭐️this is especially important in COPD, since no medication has conclusively shown to slow lung function decline or prolong survival in COPD
Autonomic Nervous System
—parasympathetic (ACh, cholinergic) → bronchoconstriction
—sympathetic (NE, a,ß receptors) → bronchodilation
⭐️thus, to achieve bronchodilation:⭐️
● enhance the sympathetic system (β2-agonist), and/or
● block the parasympathetic system (anticholinergic, aka
antimuscarinic)
How do you achieve bronchodilation?
What is bronchodilation?
to achieve bronchodilation (↓bronchial tone):
● enhance the sympathetic system (β2- agonist),
and/or
● block the parasympathetic system (anticholinergic, aka antimuscarinic)
What should you be cautious about with BB and COPD patients?
Which are non-selective
Which are non-selective + alpha blocker ?
caution giving beta-blockers to patients w/ asthma, COPD,
etc. particularly agents that are not β1-selective and can cause β2 blockade (propranolol, carvedilol, labetalol)
β1,β2 non-selective: O → Z
—ex: propranolol, timolol:
—avoid in bronchospastic disease non-selective β-blockade
Non-selective BB AND ɑ1 blockade
—carvedilol, labetalol
ɑ1 blockade adds vasodilation
-olol = no ɑ activity
-ilol or -alol = ɑ activity
c
short-acting β2-selective agonists (SABA)
Which 2 agents?
⭐️albuterol (VentolinTM, ProventilTM)
● rescue inhaler of choice for most patients!
Anyone with COPD should have this (or other
SABA or SAMA) and ideally carry it with them
at all times.
● adverse effects/limitations
○ cardiovascular: tachycardia
○ neurologic: headache, jittery
● caution/avoid if patient has
○ uncontrolled HTN / CVD
levalbuterol (Xopenex)
● pure (R)-isomer of albuterol which is responsible for the bronchodilation effect
● theoretically more efficacy and less tachycardia, but $$ and benefits over albuterol are not well proven
terbutaline
—oral or injectable agent, rarely used chronically, utility in acute exacerbations in addition to albuterol
long-acting β2-selective agonists (LABA)
● ⭐️ formoterol
● ⭐️ salmeterol
● ⭐️ vilanterol
● arformoterol
● olodaterol
generally considered equivalent/interchangeable often coformulated with an inhaled corticosteroid (ICS) or long-acting muscarinic antagonist (LAMA)
adverse effects / limitations
—fewer than albuterolcompared to LAMAs
—lesser efficacy in reducing exacerbations and hospitalizations
⭐️only for chronic control - never use for rescue!
short-acting muscarinic antagonists (SAMA)
(see notebook)
⭐️ipratropium (AtroventTM)
adverse effects
● dry mouth
● nausea
● metallic taste
muscarinic receptors exist throughout the rest of the body!caution/avoid if patient has
● narrow-angle glaucoma
● urinary obstruction, including BPH
compared to SABAs
● similar efficacy and characteristics; ipratropium
technically takes longer to work (15-20min, vs
5min for albuterol)
● often combined (albuterol-ipratropium inhaler or
neb), especially for COPD
● in general, short-acting bronchodilators (SABA and
SAMA) do not reduce frequency or severity of COPD
exacerbations the way long-acting bronchodilators
do
don’t get it mixed up w/ tiotropium (a LAMA)!
“i” for immediate (short-acting)?
long-acting muscarinic antagonists (LAMA)
compared to ipratropium, more selective for muscarinic receptors and dissociate slower
adverse effects/limitations and precautions - similar to ipratropium
● ⭐️tiotropium
● aclidinium
● umeclidinium
● glycopyrrolate / glycopyrronium
● revefenacin
—generally considered equivalent/interchangeable
—often coformulated with a LABA
⭐️only for chronic control - never use for rescue!
—⭐️ compared to LABAs, greater efficacy in reducing exacerbations and hospitalizations — it is the sole agent in group C ⭐️
Summary of inhaled bronchodilators
⭐️ know them well
B2 agonists
SABA
LABA
Muscarinic antagonists, anti-cholinergics
SAMA
LAMA
Characteristics and usage
Recognise B2 agonists first
Ipratropium = think “immediate”
inhaled corticosteroids (ICS)
Place in therapy
Used in combo with?
Initial therapy criteria
Step up therapy criteria
ADRs
When should it not be used
What are the 4 meds?
Place in therapy
● ⭐️do not use as monotherapy
COPD isn’t as steroid-responsive as asthma, so only use when benefits > risk
○ must combine w/ LABA, or LABA+LAMA
○ no evidence for just ICS+LAMA
● for initial therapy, only for Group D (sickest, most symptomatic) patients if
○ h/o asthma, or
○ ⭐️blood eosinophils ≥300 cells/µL
● for step-up therapy, use if
○ blood eosinophils ≥300 cells/µL, or
○ blood eosinophils ≥100 cells/µL AND ≥2 exacerbations or ≥1 requiring hospitalization
● as with LABAs and LAMAs, ❌ should NOT be used for
rescue during acute exacerbation
adverse effects / monitoring
❌ avoid if patient has recurrent pneumonia or h/o mycobacterial lung disease
● candida/thrush (oral, if used improperly)
● osteoporosis (orthopedic, w/ long-term use)
● cataracts (ophthalmic, w/ long-term use)
memorization tip: -son or -sone = corticosteroid
💊 budesonide
💊 fluticasone
💊 mometasone
💊 beclomethasone
Know the combination inhalers for COPD
—SABA + SAMA
—LAMA + LABA
—ICS + LABA
—ICS + LAMA + LABA
Inhaler terminology
FYI
And technique
MMRC and CAT
MMRC is a dyspnea scale
CAT is a bit more comprehensive, includes coughing, mucous, fatigue etc
The refined ABCD assessment tool
What are the steps?
What are the grades GOLD 1-4
This is for initiating treatment
What is the initial treatment approach for A, B, C D?
Bronchodilator first SABA/SAMA
Then LAMA is a mainstay of therapy
LAMA/LABA is also appropriate, especially if D
Make it a triple therapy with ICS if really sick
Follow up
notes on the f/u pathway
● ABCD only applies to initial tx
● remember to always assess compliance and technique
● COPD meds are usually fixed dosing (dose isn’t titrated like w/ asthma) general step-up/escalation approach:
● + LAMA or LABA if not already taking
● + ICS only if patient qualifies (and 🔺stop ICS if patient has pneumonia or doesn’t respond)
● if maximized on inhaled therapy, considering roflumilast or azithromycin
COPD
Agents for special case scenarios
**methylxanthines (ie, oral theophylline)*(
● slight bronchodilatory effect (inhibits PDE, thus don’t mix w/ roflumilast), reduces airway responsiveness to histamine, adenosine, and allergens
● old-school med; typically reserved for patients unable to optimize inhaler therapy, rarely initiated nowadays
● disadvantages: very narrow therapeutic index, interpatient variability, drug interactions, requires level monitoring
● s/sxs of toxicity: dyspepsia, N/V/D, headache, dizziness, tachycardia, arrhythmias, seizures
mucolytics (ie, N-acetylcysteine)
● may be considered if not on ICS, esp w/ chronic bronchitis
● if nebulized, administer after bronchodilator
● smells like rotten eggs :(
alpha-1 antitrypsin augmentation therapy
● inhibition of alpha-1 proteinases
● may slow progression of emphysema if due to AAT deficiency
❌what’s NOT recommended in the guidelines ❌:
—oral bronchodilators (inhaled prefered)
—oral long-term corticosteroids
—statins
—antitussives (cough suppressants)
—vasodilators
COPD
managing exacerbations
4 steps
1️⃣ SABAs +/- SAMAs
—(ie, albuterol +/- ipratropium) every 4-6 hours until resolution
—definitely use in combination for severe exacerbations
—switch to long-acting bronchodilators once stable (or continue home dose)
2️⃣ Oral or IV corticosteroids (ie, prednisone)
—typically for 5-7 days
3️⃣ Antibiotics?
only if increased sputum purulence, in addition to increased dyspnea and/or sputum volume
—procalcitonin could come into play here, if it’s low, probably not a bacterial infection
—similar organisms and treatments as CAP - azithromycin or clarithromycin, doxycycline, 2nd or 3rd-gen cephalosporins, amox-clav, respiratory fluoroquinolones
—treat for no more than 5-7 days
4️⃣ Oxygen and ventilatory support
COPD, bronchodilator treatment
Escalating therapy
*need to check answers with Dr. Chu
