COPD Flashcards
What is COPD?
Chronic Obstructive Pulmonary Disease
* Lung condition characterized by chronic pulmonary symptoms (cough, dyspnea,
sputum) and evidence of airflow limitation
* WHO Defenition: Heterogeneous lung condition characterized by chronic
respiratory symptoms (dyspnea, cough, expectoration, exacerbations) due to
abnormalities of the airway (bronchitis, bronchiolitis) and/or alveoli
(emphysema) that cause persistent, often progressive, airflow obstruction”
* COPD patients often report they are “hungry” for air
* Usually progressive and not fully reversible
Prevalence of COPD
Prevalence: Around 6% of US adults
* Prevalence increases with age, and mostly occurs in patients ≥ 40 years old
Mortality of COPD
Mortality: Generally in the top 5 leading
causes of death in the US annually
COPD Clinical Risk Factors:
- Envornmental Exposures (smoking, pullution, etc.)
- Persistent Asthma, airway hyperresponsiveness, allergies, or atopy
*Infections (Childhood pneumonia, Tuberculosis, HIV)
Molecular (genetic) Risk Factors of COPD:
Gene polymorphisms
* Alpha 1-antitrypsin (AAT) deficiency
* Connective tissue disorders
Clinically significant COPD develops in ___% of smokers
15
How Cigarette smoking leads to COPD:
- smoking Interferes with ciliary motility, damages epithelium
- Inhibits alveolar leukocytes from clearing bacteria
- Induces macrophages to release neutrophil chemotactic factors
- Causing tissue destruction
Non-reversible (persistent) airflow limitation
Defined as the reduced ability to
exhale efficiently, with a postbronchodilator FEV1/FVC < 0.7
Non-reversible (persistent) airflow limitation in the airways
: Small airway narrowing or obstruction
- Usually caused by Chronic Bronchitis and/or Chronic Obstructive Asthma
Non-reversible (persistent) airflow limitation in the alveoli
enlargement of the airspaces
accompanied by destruction of the airspace walls
- Usually caused by Emphysema
COPD pathology of the airways
Various factors lead to chronic inflammation, increased numbers of goblet cells, mucus gland hyperplasia, fibrosis, narrowing/reduction in the number of small airways, and airway collapse (more prominent in chronic bronchitis)
COPD pathology of the lung parenchyma
Permanent dilation or destruction of the alveolar ducts, alveolar sacs, and alveoli (more prominent in emphysema)
Emphysema
Defined as specific structural changes associated with COPD
* Permanent enlargement of air spaces
* Destruction of alveolar walls
* Lacks obvious fibrosis
Emphysema: “pink puffer”
- Less surface area for gas exchange
- Collapse of alveoli during
expiration - Body compensates through
hyperventilation
Emphysema classifications
Centriacinar (centrilobular)
● Localized to the proximal respiratory bronchioles
● Focal destruction, predominantly upper lung zones
Panacinar (panlobular)
● Destroys the entire alveolus uniformly
● Predominantly lower half of lungs
Paraseptal (distal)
● Localized around the septae of the pleura, adjacent to foci of fibrosis
● Airflow often preserved but can lead to spontaneous pneumothorax
Emphysema radiologic findings
- Flattening of the diaphragm
- ↑ retrosternal air space (Usually >2.5cm)
- Long, narrow heart shadow
Alpha-1 Antitrypsin
- A protein produced in the liver which
acts in the lungs and liver - Protects the lungs from damage
caused by neutrophil elastase, an
enzyme that disrupts connective tissue
and causes inflammation
Alpha-1 antitrypsin Deficiency (AATD)
- Autosomal co-dominant genetic disease
- Severe disease is rare (<100,000 in the US)
- Present in 2% to 3% of patients with COPD
- Increases risk of developing emphysema
Alpha-1 Antitrypsin Deficiency (AATD) symptoms
- Mild disease may have no symptoms and go undiagnosed
- Shortness of breath, wheezing, chronic
cough, increased sputum production - Decreased exercise capacity
- Frequent respiratory infections
- Symptoms of chronic hepatitis/cirrhosis (like jaundice)
- Unique features of AATD emphysema are younger onset and basilar-predominant pattern of emphysema
Alpha-1 Antitrypsin Deficiency (AATD) testing
- Testing for AATD should be performed on all adults with persistent
airflow obstruction on spirometry, especially if: - Emphysema in a young individual (eg, age ≤45 years)
- Emphysema in a nonsmoker or minimal smoker
- Emphysema characterized by predominant basilar changes
- History of unexplained chronic liver disease
- Various methods exist, but most common is testing serum AAT
levels and targeted genotyping for the most common variants
Chronic Bronchitis
“Blue bloaters”
* Defined by a chronic bronchial
inflammation, leading to a
productive cough over a defined
period. It can be preceded or
followed by development of
airflow limitation
* Chronic Bronchitis is considered
COPD only when permanent
airflow obstruction occurs
Chronic Bronchitis
- Chronic inflammation of the bronchi and
bronchioles - Results in excessive secretions, and
mucus buildup. - Tissues swell and bronchial tubes may
narrow or close off - Fibrosis of bronchial wall can occur
Histological features of chronic bronchitis
- Lymphocytic infiltration
- Enlargement of mucin secreting glands
- Bronchial epithelium may exhibit squamous dysplasia/metaplasia
The difference between asthma and COPD is:
Most patients with asthma
have reversible airflow
obstruction. If the obstruction
is completely reversible, it is
not considered COPD
COPD Signs and Symptoms
3 cardinal
* Dyspnea
* Chronic cough
* Sputum production
others
* Wheezing
* Chest tightness
Typical Onset/Presentations of COPD:
- Patients with very sedentary lifestyles, but few complaints:
- Patients presenting with dyspnea and chronic cough:
- Patients who present with episodes of increased cough, purulent sputum,
wheezing, fatigue, and dyspnea that occur intermittently, with or without
fever:
Systemic manifestations of COPD
- Obesity
- Depression or anxiety
- Osteoporosis
- Advanced Disease:
- Weight loss
- Anemia
- Pulmonary hypertension
- Cor pulmonale
Limitated expiratory flow + Preserved inspiratory flow =
It takes longer to exhale than it does to inhale
Exam for COPD:
● Limitated expiratory flow + Preserved inspiratory flow
= It takes longer to exhale than it does to inhale
● Hyperinflation of the lungs (eg, increased resonance to percussion)
● Decreased breath sounds, wheezes, crackles at the lung bases
● Distant heart sounds
Exam - End-stage findings of COPD:
● Accessory respiratory muscle use
● Depressed diaphragm with limited movement.
● Positions that relieve dyspnea, like leaning forward and weight supported on the palms or elbows (tripod position)
● Expiration through pursed lips
● Cyanosis
● Elevated jugular venous pressure
● Peripheral edema
Emphysema exam findings:
● Tachypnea
● Hyperresonance with percussion
● Diffusely diminished breath sounds
● Patients are often thin
● Increased anteroposterior diameter
of the chest (“barrel chest”)
Chronic Bronchitis exam findings
- Hypercapnia
- Hypoxemia
- Cyanosis
COPD Lab Testing
- Lab testing is not diagnostic
- Check BNP for heart failure
- Serum chemistries
- Elevated serum bicarbonate may indicate chronic hypercapnia
- Testing for alpha-1 antitrypsin (AAT) deficiency
Exercise Capacity: can help evaluate risk of mortality - Six-minute walking distance, evaluating for desaturation
COPD Imaging
- Imaging is not needed to diagnosis of COPD, but is helpful for other reasons
- Chest X-Ray:
- CT-Scan: More sensitive and specific
COPD pulmonary function testing
SPIROMETRY
* Essential for the diagnostic evaluation of patients with suspected COPD.
* Performed pre and post bronchodilator administration (like albuterol) to
determine if airflow limitation is reversible.
* Irreversible airflow limitation is a defining physiologic feature of COPD.
* FEV1/FVC is the ratio of forced expiratory volume in 1 second over forced
vital capacity. Less than 70% of predicted defines COPD
Additional Pulmonary Function Testing in COPD:
Lung Volume testing -
* Done using body plethysmography.
* Used to determine whether the reducted FVC is due to air trapping,
hyperinflation, or some other restrictive condition.
Diffusing capacity for carbon monoxide (DLCO):
* Helps clarify the degree of emphysema in smokers with airflow limitation
What will an ABG show in mild to moderate COPD?
mild to moderate hypoxemia without hypercapnia
What will an ABG show in severe COPD?
hypoxemia worsens and hypercapnia may develop
Management goal in COPD
*The goal of COPD management
*Prevent the recurrence of exacerbations
A comprehensive disease management strategy for COPD is associated with _____
a lower hospitalization rate and fewer ER visits
A comprehensive disease management strategy for COPD includes the following:
- Patient education session
- Self-treatment plan for exacerbations
- Monthly follow-up call from a case manager
COPD management program (4 components)
*Assess and monitor disease
*Reduce risk factors
*Manage stable COPD
*Manage exacerbations
Reduce risk factors of COPD
*Vaccines
*Smoking cessation
Pharmacologic treatment for COPD
*Bronchodilators - Central to symptom management
*Inhaled glucocorticosteroids (ICS)
*If used, an ICS should be combined with a long-acting beta 2-agonist
* Oral glucocorticosteroids
Long-term treatment not recommended
Beneficial during exacerbations
* Phosphodiesterase-4 inhibitors (roflumilast)
* AAT augmentation therapy
* Antibiotics: Generally, long-term treatment not recommended in stable COPD.
* Mucoactive agents (N-acetylcysteine)
* Antitussives (benzonatate)
* Regular use contraindicated in stable COPD, no conclusive evidence of benefit
Long-term administration of
oxygen for > ___ hours per day
increases survival
15
Beneficial impact of oxygen therapy in COPD
- Pulmonary hemodynamics
- Hematologic characteristics
- Exercise capacity
- Lung mechanics
- Mental state
Exercise training for COPD
- Patients of all stages benefit from exercise
training programs
*Improves dyspnea and fatigue - Minimum length of an effective program is 6 weeks
- Benefits wane after program ends
COPD patients are the largest single category of ____
lung transplant patients
Pulmonary rehabilitation
- Decreases airflow limitation
- Prevents secondary complications
- Alleviates respiratory symptoms
- Reduces hospitalization in patients with recent exacerbations
- Reduces anxiety/depression and improves exercise tolerance
- Team approach
- Emphasizes the following
COPD Exacerbations
*Exacerbations are characterized by a change in the patient’s
baseline dyspnea, cough, and/or sputum that is beyond normal
day-to-day variations
*Most common causes
*Infection
*Air pollution
* 30% unidentified
T/F COPD Exacerbations often occur in clusters
T - Increased risk of another attack in the 8 weeks following the initial
episode
BODE: What is it?
- Body mass index, airflow Obstruction, Dyspnea and Exercise capacity
- BODE index may be a better predictor of the number and severity of
exacerbations in COPD than FEV1
COPD Exacerbations treatment
- Oxygen therapy
- Inhaled bronchodilators
- Corticosteroids
- Hospitalization
- Initiate LABA before discharge
*Antibiotics if bacterial infection is suspected
Long-term monitoring of COPD
*Patients with severe or unstable disease should be seen
monthly
*When their condition is stable, patients may be seen biannually
*Check theophylline level with each dose adjustment, when
interacting medications are added, and routinely every 6-12
months
