2 COPD Flashcards
Highest prevalence of COPD is among…
65-74 year olds
Men and women affected almost equally
Morbidity increases with age and is greater in males
Global Initiative for Chronic Obstructive Lung Disease (GOLD) definition:
Chronic obstructive pulmonary disease is a common, PREVENTABLE and TREATABLE disease that is characterized by 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.
What are the three clinical subtypes of COPD?
Chronic Bronchitis (predominant)
Emphysema (predominant)
Chronic Obstructive Asthma
Patients with Chronic Bronchitis are described as…
“Blue Bloaters” due to CYANOSIS and OVERWEIGHT body habitus
Hypoxemia and respiratory acidosis more common
Cor pulmonale from pulmonary HTN (b/c problems with both getting air in and out)
Patients with Emphysema are described as …
“Pink Puffers” because of pursed-lip breathing, skin color, and thin body habitus
Use a lot of accessory muscles to breath
Chronic bronchitis is defined as a chronic productive cough for ____________ with no other cause.
3 or more months during 2 consecutive years
Leads to structural changes:
• Mucous gland enlargement —> hyper secretion
• Bronchial squamous metastasis
• Loss of ciliary transport
In Chronic Bronchitis, inflammation of bronchial wall and infiltration of sub-mucosal layer is caused by ________
Neutrophils (vs eosinophils in asthma)
Chronic bacterial colonization and airway hyper-reactivity are thought to play an important role
Obstruction in chronic bronchitis is ….
Both inspiratory and expiratory
Hypoxemia and hypercapnia result form impeded ventilation
There is less parenchymal damage than emphysema
Pathologic enlargement of the air spaces distal to the terminal bronchioles due to destruction of the alveolar walls
Emphysema
Destructive process not clearly understood (may be too much elastase or too little antitrypsin activity)
Protease enzyme secreted by neutrophils and macrophages during inflammation
Neutrophil elastase - it destroys bacteria and host tissue (ie - elastin)
An inhibitor of neutrophil elastase
Alpha-1 Antitrypsin
When in deficiency there is breakdown of the lung structure by elastase
Describe what happens to the alveoli in emphysema
Reduced alveolar surface area available for gas exchange
Decreased elastic recoil
Loss of alveolar supporting structure = airway narrowing
Obstruction in emphysema is …
Mostly during exhalation
Not associated with significant hypoxemia until later in disease severity
Destruction of capillary beds in emphysema results in …
Reduced DLCO (diffusing capacity for carbon monoxide)
Chronic inflammation in asthma is primarily mediated by…
Eosinophils
Airway hyper-reactivity —> increased secretions, mucosal edema, constriction of bronchial smooth muscle —> airway obstruction
Is asthma reversible or irreversible?
Reversible!
Most common risk factor for COPD
Cigarette smoking - 80% of COPD patients, most have smoked at least 20 cigarettes a day for 20 or more years
Other risk factors: • Environment/occupation • Second hand smoke exposure • Airway hyper-responsiveness (asthma) • Genetic RF: alpha-1 antitrypsin deficiency (<1% of all cases)
How does cigarette smoking cause COPD?
Stimulates elastase enzymatic activity, causing degenerative changes in elastin and alveolar structures
Causes release of cytotoxic oxygen radicals from WBCs in lung tissue
Amount and duration contribute to disease severity
Examples of environmental exposures that can lead to COPD
Air pollution
Coal miners
Grain handlers
Metal molders
Workers exposed to dust
Cooking with biomass fuels (1/3 of the world)
A hereditary syndrome resulting in the early onset of emphysema (<1% of US cases)
Alpha-1 antitrypsin deficiency
Features of emphysema present at a younger age (≤45)
AAT is a protease inhibitor - inhibits elastase and several other proteolytic enzymes
The process of lung destruction is accelerated in smokers with AAT deficiency
Classic presentation of COPD
Dyspnea, chronic cough, and sputum production
Sx onset in 5th or 6gh decade of life
Most common early symptom is DYSPNEA ON EXERTION
Common comorbidities of COPD
CVD (HTN, CAD, stroke)
DM
Renal insufficiency
Osteoporosis
Psychiatric illness
Cognitive dysfunction
Gross physical exam findings in emphysema
Tripod positioning
Cyanosis
Tobacco staining of fingers (because the idiot is still smoking)
JVD, use of accessory muscles (neck and shoulder)
Pursed lip breathing
Why do patients with emphysema purse their lips?
In COPD, ordinary breathing allows early bronchial collapse on exhalation
Pursed-lip breathing achieves resistance to outflow at the lips, raising intrabronhial pressure, keeping the bronchi open. More air can thus be expelled.
More specific physical exam findings in Emphysema
Lungs:
Barrel chest (increased AP diameter)
Prolonged expiration
Increased resonance on percussion (b/c of air trapping)
Decreased breath sounds (distant), wheezing, and crackles at base
Heart: S3 gallop (if cor pulmonale), RV lift
ABD:
Hepatomegaly, pulm HTN if cor pulmonale
Ext:
Muscle wasting, peripheral edema
Altered structure (hypertrophy or dilation) and/or impaired function of the RIGHT ventricle that results from pulmonary HTN associated with diseases of the lung, vasculature, upper airway, or chest wall
Cor Pulmonale
Most common cause of cor pulmonale
COPD
Diagnostic study required for the diagnosis of COPD
Spirometry
Will also do a CBC, BNP, cardiac enzymes, metabolic panel, AAT but spirometry is diagnostic
Other tests: Pulse ox, ABG, EKG, sputum exam, CXR/HRCT
The amount of air forcefully exhaled during maximal forced expiration
Forced Vital Capacity (FVC)
Normal is 80-120%
Compared to Forced Expiratory Volume in 1 second (FEV1)
What is the FEV1/FVC ratio?
% of FVC expired in 1 sec
Normal is 70-80%
How does spirometry diagnosis of COPD work?
First perform a pre and post-bronchodilator spirometry test
(FEV1/FVC <0.7 is consistent with an obstructive pattern)
Next review post-bronchodilator FEV1% predicted to determine GOLD grade I-IV
In addition to FEV1/FVC < 0.7 and a decreased FEV1, COPD patients will have:
Increased Total Lung Capacity (TLC) due to air trapping
If severe emphysema, will also have decreased Diffusing Capacity of Carbon Monoxide (DLCO) because there’s not good air exchange occurring in capillary beds
What will you see on CBC in COPD patients?
Usually normal but useful to rule out anemia as cause of dyspnea
Chronic bronchitis pt may have polycythemia secondary to chronic hypoxia
Leukocytosis may be present during acute exacerbations of COPD
How to use Pulse Oximetry in COPD patients
If <92%, assess further with arterial blood gas
Arterial Blood Gas really only done inpatient
• Usually mild to moderate hypoxemia without hypercapnia (CO2 retention)
• As disease progresses hypoxemia worsens and CO2 increases (respiratory acidosis)
When should you do a sputum culture on COPD patients?
When in-patient and unresponsive to initial abx treatment
Possible EKG findings in COPD
Tachycardia
R atrial enlargement
R axis deviation and/or RVH
Pathognomonic CXR findings for emphysema
Blebs (focal areas of blackness) or Bullae (larger blebs)
Why do we do a CXR in COPD?
Obtain to exclude other diagnoses and assess for comorbities
See signs of air trapping - increased AP diameter, hyperinflation, hyperlucency, flat diaphragms
Blebs or bullae
Perivascular or peribronchial markings may be present in chronic bronchitis
CXR findings more suggestive of emphysema
Hyperinflation (possibly with bullae)
Flattening of diaphragms
Enlargement of retrosternal air space
CXR findings more suggestive of chronic bronchitis
Cardiac enlargement
Pulmonary congestion
Increased lung markings
Do we need to do a chest CT on COPD patients?
Helpful but not needed for routine Dx
Obtain if SSx suggest a complication of COPD (PNA, pneumothorax, large bullae), alternate Dx (PE), or if considering lung volume reduction surgery (HRCT)
GOLD strategy for staging
Step 1 - Determine if obstructive pattern (FEV1/FVC ratio < 0.7)
Step 2 - Determine severity (GOLD Grade 1-4, based on percent FEV1)
Step 3 - Assess symptoms (use patient rating scale)
Step 4 - Determine exacerbation risk (use frequency of exacerbations in past year)
What are the four GOLD grades?
GOLD 1 = Mild (FEV1 ≥ 80% predicted)
GOLD 2 = Moderate (50% ≤FEV1, <80% predicted)
GOLD 3 = Severe (30% ≤FEV1, <50% predicted)
GOLD 4 = Very Severe (FEV1 <30% predicted)
How to use number of exacerbations to determine further risk of exacerbation
0-1 exacerbations in the past 12 months = Low risk
2 or more exacerbations OR 1 hospitalization for COPD = High risk
How do you prevent progression in COPD?
Stop smoking, you idiot!
How do you relieve symptoms in COPD?
Pharmacotherapy/pulm rehab/Oxygen
Improve exercise tolerance
Manage/prevent exacerbations
Reduce mortality
3 min counseling for smoking cessation can increase quit rate by…
5-10%
Management of COPD for Group A patients (Gold 1-2, 0-1 exacerbations, mMRC 0-1)
Short-acting bronchodilator OR
SABA + SAMA combo used PRN
Management of COPD for Group B patients (Gold 1-2, 0-1 exacerbations, mMRC 2+)
Long-acting bronchodilator (LAMA or LABA)
Management of COPD for Group C patients (Gold 3-4, 2+ exacerbations or hospitalization, mMRC 0-1)
LAMA
Management of COPD for Group D patients (Gold 3-4, 2+ exacerbations or hospitalization, mMRC 2+)
LABA + LAMA, consider ICS + LABA
Mainstay of treatment for COPD
Inhaled ß2-agonists and anticholinergics (short and long acting)
Besides bronchodilation, may provide other effects such as ability to improve mucociliary clearance, diaphragmatic action, and cardiac contractility
Examples of short acting ß2 agonists (SABAs)
Albuterol (Ventolin, ProAir, Proventil)
Usual dose = 2 puffs q4-6 hours (also available in neb form)
Examples of Long-acting ß2-agonists (LABA)
Salmeterol (Serevent)
Formoterol (Foradil)
q12h dosing - every day, not for rescues
Side effects of ß2 agonists
Palpitations
Tachycardia
Insomnia
Tremors
Examples of anticholinergic bronchodilators
Short-acting:
• Ipratropium bromide (Atrovent) - most common
• Ipratropium plus albuterol (Combvent)
• 2 puffs BID-QID, also in neb form
Long-acting:
• Tiotropium bromide (Spiriva) - once daily
• Umeclidinium (Incruse Elliot’s) - once daily
Good bronchodilation, reduces air trapping in lungs, less cardiac stimulation
Side effects of anticholinergics
Dry mouth
Metallic taste
HA
Cough
Examples of LAMA+LABA combo meds
Used in category C/D disease
Bevespi Aerosphere - BID
Utibron Neohaler - BID
Stiolto Respiratory - QD
Anoro Ellipta - QD
Drug that was the standard bronchodilator for many years, but tendency now to avoid use except in refractory cases
Theophylline - a methylxanthine
No long used commonly b/c lots of SE and drug interactions
Debate over benefits:
• Theophylline toxicity common problem
• Can cause tachycardia, arrhythmias, seizures, HA, nausea
• Potential for drug-drug interactions
Examples of corticosteroids
Advair, Dulera, Symbicort, Breo Ellipta
(Inhaled form is available alone or in combo with LABA)
Reduces mucosal edema/inflammation by inhibiting prostaglandins —> decreased secretions
Increases responsiveness to beta-adrenergics
Side effects of corticosteroid use
Oral candidiasis (pt ed=rinse mouth after use)
Bruising
Increased risk of URI
Kind of out of favor now b/c not as effective
Treatment for alpha1 antitrypsin deficiency
Antiprotease replacement therapy in the form of weekly or monthly injections
Used in patients with serum alpha-1 antitrypsin levels <11uM)
Treatment is costly and controversial
Examples of adjunct therapy for COPD patients
Pulmonary rehab (if GOLD stage B-D) - patient ed, exercise training, nutritional counseling and psychosocial support
Oxygen - increases survival (but only if used ≥ 12 hours per day)
• Goal: O2 saturation > 90% during rest, sleep, and exertion
Lung volume reduction surgery —> improved lung recoil
Why do we use supplemental O2 in COPD patients?
Long-term continuous oxygen therapy prolongs survival (min 12 hours/day)
Indicated if chronic dyspnea at rest PaO2 ≤ 55 mmHg or SaO2 ≤ 88%
Caution - high flow O2 may reduce drive to breath and cause resp acidosis (maintain O2 sat 90-92%)
What do we do to minimize complications/exacerbations in COPD patients?
Educate ALL COPD patients about avoidance of risk factors
Influenza vaccination
Pneumococcal vaccination (PPV13 and PCV23)
Regular exercise
Early recognition of pulmonary infection (increased sputum production, fever, worsening dyspnea, fatigue, chest pain, hemoptysis)
How do we define an acute exacerbation of COPD?
Acute change in patient’s baseline dyspnea, cough, or sputum that is beyond normal variability, and sufficient to warrant a change in therapy
Increased dyspnea
Increase in cough frequency/severity
Sputum increases or becomes purulent
Why do we care about acute exacerbations of COPD
Because they contribute to high mortality
70% of acute exacerbations are caused by…
Respiratory illnesses
Pollution also common
Viral infections that most commonly lead to COPD exacerbations
Rhinovirus and influenza
Viral most common, but may lead to secondary bacterial pneumonia
Most common bacterial pathogens causing pneumonia secondary to viral infections
H flu, Strep pneumo, Moraxella catarrhalis, Mycoplasma pneumo, and Pseudomonas (if hospitalized recently or recent abx use)
Outpatient management of an acute exacerbation includes…
Increased dose of short-acting bronchodilators (B2 agonist, add Ipratropium if not already taking)
Oral steroids - 40 mg/day x 5 days (reduces recovery time and hospital time)
Abx (for mod-severe exacerbations)
Consider hospitalization if severe
Meds used in uncomplicated COPD exacerbation with no risk factors (Age <65, FEV1 > 50, <3 exacerbations/year, No cardiac disease)
Advanced macrolide (azithromycin, clarithromycin) OR
Cephalosporins OR
Doxy OR
Bactrim
Meds used in complicated COPD exacerbations with 1 or more risk factors (age >65, FEV1<50, ≥3 exacerbations/year, cardiac disease)
Fluoroquinolone (levofloxacin) OR
Augmentin
If at risk for pseudomonas, use cipro and get sputum culture
Indications for hospitalization in COPD exacerbations
Severe SSx
Severe underlying COPD (FEV1<50%)
Onset of new physical signs (cyanosis, edema, new arrhythmia)
Failure to respond to initial med mgmt
Older age
Insufficient home support
