9/21- COPD Flashcards
Spectrum of Obstructive Lung Diseases (picture)
What is COPD (definition)
- Onset
Preventable and treatable disorder of the airways characterized by airflow limitation that is not fully reversible
- Onset in midlife
- Airflow limitation usually progressive and associated with abnormal inflammatory response to particles or gases primarily caused by cigarette smoking
Epidemiology of COPD
- Affected
- Diagnosed
- Deaths
- Disability
- 24 million affected in US
- Only 50% diagnosed (12 million)
- Estimated 130,000 deaths, being the #3 COD in the US (2012)
- #2 cause of disability (prob most common by 2020)
Affected populations in COPD
- Age
- Gender
Age: 70% are under 65 yo
- COPD > diabetes and asthma in pts 45-64
Gender: women > men (5x)
- Deaths in women > men as well
What is chronic bronchitis?
A clinical disorder
- Chronic cough on most days for at least 3 mo/year
- At least two consecutive years
- Cough and sputum production not due to any other specific causes
What is emphysema?
A disease in which airspaces distal to the terminal bronchioles are enlarged with destruction of alveolar walls.
(defined in anatomic-pathologic terms)
What are risk factors for COPD?
- Host factors
- Exposures
- Other
Host factors:
- Genetics (not all smokers get COPD)
- Gender
- Airway hyperreactivity
Exposures:
- Smoking
- Environmental pollution
- Perinatal events and childhood infection
- Recurrent infections
- Occupational and environmental exposure (e.g. coal dust, silica)
- Socio-economic status and (poor) diet
Others:
- Preexisting bronchial hyperreactivity (Dutch hypothesis)
What is the relationship between smoking and COPD?
- Smoking is the predominant risk factor for development of COPD (>90% of pts with COPD)
- Dose-response relationship of FEV1 to the intensity of cigarette smoking
What is the most important genetic risk factor for COPD?
- Mechanism (chrom)
- Alleles
- Inheritance
- Normal function
Alpha-1 anti-trypsin deficiency
- Deficiency of the protein from deficiency alleles of the AAT gene on chrom 14
Alleles:
- Normal = M, causes production of normal AAT
- S allele: slightly reduced levels
- Z allele: markedly reduced levels
- Null alleles may rarely be present
Inheritance:
- Autosomal recessive
- 1/3000 inherit, but only minority recognized - Not all pts with PiZZ develop COPD
- AAT def accounts for under 1% of COPD in US
Function:
- AAT-protein has potent protease inhibitor activity; protects normal lung tissue from proteolytic attack during inflammation
- Normal levels are 120-200 mg/dL
When should you screen for AAT deficiency?
- COPD in a never-smoker
- Premature onset of COPD (moderate to severe impairment, by/before age 50)
- A predominance of basilar (lower lobe) emphysema
- Family Hx of AAT def or COPD onset before age 50
- Cirrhosis without apparent risk factors
- Bronchiectasis, esp. w/o risk factors for the disease
What is the pathophysiology of COPD?
- What are the 2 main components of COPD?
- Environment/occupational exposures and childhood respiratory infections (and other risk factors) act on genetic susceptibility
- CD8 lymphocyte and neutrophil activation (MCP-1) and release of proteases
- Protease activation and tissue destruction (protease inhibitors knocked out)
- Airway inflammation and remodeling
Overall result = airflow limitation
2 main components of COPD:
- Airway wall thickening and inflammation (presentation = chronic bronchitis)
- Destruction of lung tissue (presentation = emphysema)
How many COPD patients have never smoked?
~10%
What cell types play a big role in COPD? Asthma?
COPD
- Macrophages
- Neutrophils
- CD8 lymphocytes
(elevated inflammatory mediators: IL-8, TNF-a, LTB-4, oxidants and imbalance in protease/anti-proteases)
Asthma
- CD4 lymphocytes
- Eosinophils
How does cigarette smoking predispose people to COPD?
- Smooth muscle hypertrophy
- Replacement of Clara cells with mucus-secreting cells; less surfactant and more mucus
- Small airway, goblet cell metaplasia
- Neutrophil activation; elastases destroy walls of terminal bronchioles and alveolar ducts
All result in airway narrowing -> dyspnea
What are the structural changes in COPD (histological/micro-anatomical)?
- Goblet cell hyperplasia/metaplasia
- Mucus gland hypertrophy
- Increased smooth muscle mass
- Airway fibrosis
- Alveolar destruction
Mucociliary dysfunction:
- Mucus hypersecretion
- Reduced mucociliary transport
- Mucosal damage
Airflow limitation in COPD is caused by what?
- Loss of alveolar attachments
- Loss of elastic recoil
- Increased smooth muscle contraction
What are the end results of the pathologic changes seen in COPD?
- Airflow obstruction
- Hyperinflation
- Impaired gas exchange
What factor of COPD correlates more directly with patient-reported outcomes?
Hyperinflation (increased airway resistance)
What are the clinical features expected in a COPD patient’s history?
- Smoking history
- Cough with sputum production
- Exertional dyspnea: usually gradual and progressive, constant
- RV failure (cor pulmonale) symptoms like pedal edema
What is expected upon inspection of COPD patient? Palpation? Percussion?
Inspection
- Thin, asthenic (more in emphysema)
- Tachypnea
- Use of accessory muscles
- Tripod position
- Barrel chest
- Cyanosis rare
- Nicotine stained fingernails
- Hoover’s sign-inward movement of rib cage with inspiration
- Elevated JVD (if RHF)
Palpation:
- Barrel chest
Percussion:
- Enlarged lung volumes
What is seen here?
Left: pink puffer
- Muscle wasting
- Use of intercostals/accessory neck muscles
- Pursed lips
Right: blue bloater
- Cyanosis seen in lips
Various patterns of disease seen in COPD?
What do flow volume loops look like in COPD?
- Scooped/spooned expiratory portion (obstructive disease)
- Hyperinflation indicated by increased RV and TLC
- Lower peak and slower flow
What x-ray view is best to diagnose COPD? What will be seen?
Lateral
- Can see air trapping and flattened diaphragm
What is seen here?
Asthma
What is seen here?
Chronic bronchitis
What is seen here?
Emphysema
What are nonpharmacologic approaches to COPD management?
All stages of disease
- Smoking cessation
- Avoidance of indoor and outdoor occupational exposures
Vaccinations
- Influenza
- Pneumococcal – no documented evidence
Optimizing nutrition
Oxygen Pulmonary rehabilitation
Surgical interventions (LVRS, transplantation)
What can cause bronchiectasis?
- Infection-most common
- Virulent bacterial, influenza, Pertussis childhood infection and Tuberculosis
- ABPA
- Slow growing endobronchial tumors, foreign body aspiration, stenosis
- Impaired pulmonary defense: immunoglobulin deficiency, primary ciliary disorder, cystic fibrosis
- Toxic inhalation, yellow-nail syndrome
What is seen here?
Classic for bronchiectasis
- “Signet ring” sign
- Can see thickening of airway wall (not here)
