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177 Cards in this Set
- Front
- Back
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What is COPD?
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progressive disease characterized by airflow limitation that is not fully reversible and is associated with an abnormal inflammatory response of the lungs to noxious particles or gas
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Is mortality from COPD increasing or decreasing?
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increasing, 4th leading cause of death
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What is the primary cause of COPD?
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cigarette smoking
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What other risk factors for COPD?
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genetics, environmental exposures (occupational dusts, chemicals), air pollution
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What is the only management strategy proven to slow progression of COPD?
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smoking cessation
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When is oxygen therapy indicated?
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resting PaO2 (partial pressure alveolar oxygen) less then 55mmHg or a PaO2 less than 60mmHg and evidence of right sided HF, polycythemia, or impaired neurologic function
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What is the mainstay of COPD tx?
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bronchodilators
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What pts need inhaled CS?
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severe COPD and frequent exacerbations
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When is antimicrobial tx used in acute exacerbations of COPD?
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increased dyspnea, increased sputum volume, increased sputum purulence
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Is COPD preventable?
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yes
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Is COPD treatable?
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yes
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What are the most common conditions comprising COPD?
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chronic bronchitis and emphysema
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What is chronic bronchitis associated with?
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chronic or recurrent excessive mucus secretion into the bronchial tree with cough that is present on most days for at least 3 months of the year for at least 2 consecutive years if other causes of chronic cough have been excluded
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How is emphysema defined?
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anatomic pathology: abnormal permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of their walls yet without obvious fibrosis
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What are contributors to chronic airflow in COPD ?
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pathophysiologic features: small airways disease and parenchymal destruction
most COPD pt have features of both |
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What causes small airway disease and parenchymal destruction?
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inflammation
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What is the underlying problem that sustains the inflammatory response?
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persistent exposure to noxious particles or gases
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What is the result of inflammation?
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chronic airflow limitation that characterizes COPD
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How many deaths from COPD each year?
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more than 100,000
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What is the only leading cause of death to increase over the last 30 years?
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COPD, projected to be the 3rd leading cause of death by 2020
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Is mortality rate for COPD higher for males or females?
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males, female death rate has doubled over the last 25 years
number of female deaths higher than males |
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What race has higher mortality from COPD?
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whites
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What is the primary cause of COPD?
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cigarette smoking
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What % of people smoke?
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25%
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What is the 2nd leading cause of disability?
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COPD
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How much more likely are smokers to die from COPD than nonsmokers?
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12-13x
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What are host factors?
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not modifiable but identify pts at high risk of COPD: genetic predisposition (alpha1-antitrypsin), airway hyperresponsiveness, impaired lung growth
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What are environmental exposures?
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modifiable factors (if avoided may reduce risk of disease), particles that are inhaled and result in inflammation and cell injury: tobacco smoke, occupational dusts and chemicals, air pollution
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Does total burden of inhaled particles play a role in development of COPD?
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yes, significant
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How action does cigarette smoke have in causing COPD?
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components of tobacco smoke activate inflammatory cells, which produce and release the inflammatory mediators characteristic of COPD
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How is risk of COPD in pipe and cigar smokers compared to cigarette smokers?
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lower, but higher than nonsmoker
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What parts of smoking are predictive of COPD mortality?
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age of starting, total pack years, and current smoking status
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What % of smokers develop COPD?
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15-20%
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Do all smokers who have equivalent smoking histories develop the same degree of pulmonary impairment?
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no, suggests that other host and environmental factors contribute to the degree of lung dysfunction
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What is the rate of loss of lung function determined primarily by?
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smoking status and history
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Does secondhand or environmental tobacco smoke increase risk of COPD?
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yes, children and spouses of smokers at increased risk
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What jobs increase risk of death from COPD?
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gold and coal mining, glass and ceramic industries with exposure to silica dust, exposure to cotton dust or grain dust, toluene diisocyanate, or asbestos
others: chronic exposure to open cooking or heating fires |
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What pt does air pollution worsen symptoms?
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pt with existing pulmonary dysfunciton
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Do individuals exposed to the same environmental risk factors have the same chance of developing COPD?
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no
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What genetic link to COPD?
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hereditary deficiency of alpha1-antitrypsin (AAT)
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How is AAT-associated emphysema inherited?
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autosomal recessive pattern
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What is consequence of AAT (alpha1-antitrypsin) deficiency?
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protease-antiprotease imbalance
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What % of COPD is from AAT (alpha1-antitrypsin) deficiency?
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less than 1%
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Where is AAT (alpha1-antitrypsin) synthesized?
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hepatocytes
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What is the primary role of AAT (alpha1-antitrypsin)?
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protect cells, especially thos in the lung, from destruction by elastase released by neutrophils
may inhibit 90% elastase |
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When is the protective effect of AAT (alpha1-antitrypsin) significantly diminished?
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plasma levels less than 11 micromolars (80mg/dL)
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Which variant of AAT (alpha1-antitrypsin) represents 95% of clinical cases of AAT associated emphysema?
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homozygous Z deficiency (ZZ)
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What level of AAT do S variant have?
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60% of normal
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What level of AAT do homozygous Z variant (ZZ) have?
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10% of normal
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What level of AAT do heterozygous Z variant (SZ) have?
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40% of normal
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Are S variant at increased risk of COPD?
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no
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Do homozygous or heterozygous Z variant have an increased risk of COPD?
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homozygous
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Are pts with null, null phenotype at risk for emphysema?
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yes, produce virtually no AAT
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When do pts with AAT deficiency develop COPD?
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early age (20-50 years)
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How much annual decline in forced expiratory volume in 1 second (FEV1) in healthy nonsmokers?
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25mL/year
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How much decline in FEV1 in pts with homozygous Z deficiency?
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54mL/year for nonsmokers
108mL/year for current smokers |
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How is diagnosis of AAT deficiency made?
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clinical suspicion, diagnostic testing of serum concentrations, genotype confirmation
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Who should be screened for AAT deficiency?
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develop COPD at early age or strong family history of COPD
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When is genotype testing done?
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if AAT concentration is low
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What other host factors can influence risk of COPD?
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airway hyperresponsiveness and lung growth
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What is COPD characterized by?
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chronic inflammatory changes that lead to destructive changes and the development of chronic airflow limitation
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What all does the inflammatory process in COPD involve?
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airways, pulmonary vasculature, and lung parenchyma
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What kind of inflammation is seen in COPD?
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neutrophilic in nature, macrophages and CD8+ lymphocytes also play major roles
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What do inflammatory cells release that plays a major role in COPD?
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TNF-alpha, IL-8, LT B4
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What is the stimulus for activation of inflammatory cells and mediators?
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exposure to noxious particles and gas through inhalation
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What is the most common etiologic factor in COPD?
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tobacco smoke
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What other processes play a major role in the pathogenesis of COPD?
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oxidative stress and an imbalance between aggressive and protective defense systems in the lungs (proteases and antiproteases)
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What is responsible for the increased oxidative stress present in COPD?
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altered interaction between oxidants and antioxidants in the airways
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How does cigarette smoke cause damage?
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oxidants generated by cigarette smoke reacts with and damages various proteins and lipids, leading to cell and tissue damage
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Can oxidants promote inflammation directly?
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yes, and exacerbate the protease-antiprotease imbalance by inhibiting antiprotease activity
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What does AAT inhibit?
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several proteases, including neutrophil elastase
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What action does elastase have?
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attacks elastin, a major component of alveolar walls
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What is present in the inherited form of emphysema?
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an absolute deficiency of AAT
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What causes imbalence seen in cigarette smoking associated emphysema?
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increased protease activity or reduced activity of antiproteases
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Does the response to antiinflammatory therapy differ in inflammation from COPD and asthma?
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yes
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What is the difference in inflammation in COPD and asthma?
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the inflammatory cells that predominate differ: neutrophils play a major role in COPD and eosinophils and mast cells in asthma
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How do mediators of inflammation differ between COPD and asthma?
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COPD: LTB4, IL-8, TNF-alpha
asthma: LTD4, IL-4, IL-5 |
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How does increase in macrophage differ in COPD and asthma?
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COPD: large increase
Asthma: small increase |
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What lymphocytes are increased in COPD and asthma?
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COPD: CD8+ T lymphocytes
Asthma: CD4+ Th2 lymphocytes |
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What consequences of COPD?
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squamous metaplasia of epithelium, parenchymal destruction, mucus metaplasia, glandular enlargement
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What consequences of Asthma?
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fragile epithelium, thickening of basement membrane, mucus metaplasia, glandular enlargement
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What all is affected in COPD?
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large and small airways, lung parenchyma, and pulmonary vasculature
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What is result of inflammatory exudate?
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increase in the number and size of goblet cells and mucus glands
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What happens to mucus secretion in COPD?
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increased
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What happens to ciliary motility in COPD?
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impaired
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What happens to smooth muscle and connective tissue in the airways in COPD?
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thickened
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Is inflammation in central or peripheral airways in COPD?
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both
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What does the chronic inflammation result in?
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repeated injury and repair process that leads to scarring and fibrosis
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What happens to airway in COPD?
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narrowing, more prominent in smaller peripheral airways
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What causes decrease in FEV1 in COPD?
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inflammation in the airways
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What causes blood gas abnormalities in COPD?
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impaired gas transfer due to parenchymal damage
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What does parenchymal change affect?
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gas exchanging units of the lungs (alveoli and pulmonary capillaries)
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What kind of emphysema does smoking resul in most commonly?
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centrilobular emphysema, primarily affects respiratory bronchioles
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What kind of emphysema is seen in AAT deficiency?
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panlobular emphysema, extends to the alveolar ducts and sacs
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What vascular changes in COPD?
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thickening of pulmonary vessels, often present early in disease
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What are increased pulmonary pressures early in the disease caused by?
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hypoxic vasoconstriction of pulmonary arteries
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What can persistant chronic inflammation lead to?
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endothelial dysfunction of pulmonary arteries
later, structural changes lead to an increase in pulmonary pressures, especially during exercise |
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What can develop from secondary pulmonary HTN in severe COPD?
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right sided heart failure
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When does mucus hypersecretion start in COPD?
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early in the course of the disease
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What is mucus hypersecretion associated with?
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increased number and size of mucus producing cells
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What are reversible airflow obstruction in COPD?
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mucus and inflammatory cells and mediators in bronchial secretions, bronchial smooth muscle contraction in peripheral and central airways, dynamic hyperinflation during exercise
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What are irreversible airflow obstruction in COPD?
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fibrosis and narrowing of airways, reduced elastic recoil with loss of alveolar surface area, destruction of alveolar support with reduced patency of small airways
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What causes thoracic hyperinflation in COPD?
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chronic airflow obstruction leads to air trapping which results in thoracic hyperinlation
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How is thoracic hyperinflation detected?
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chest radiograph
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What is result of thoracic hyperinflation?
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diaphragm is less efficient muscle of ventilation, predisposes pt to muscle fatigue, especially during exacerbations
other consequence: change in lung volumes, increase in functional residual capacity (amount of air left in lung after exhalation at rest) which limits the inspiratory reserve capacity (amount pt can inhale), increase in dyspnea |
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How is thoracid hyperinflation reduced?
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bronchodilators
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What is the gold standard for diagnosing and monitoring COPD?
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spirometry
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What is the hallmark sign of COPD in spirometry?
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reduction in ratio of FEV1 to forced vital capacity (FVC) to less than 70%
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What syptoms as COPD progresses?
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hypoxemia and/or hypercapnea
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Is there a strong relationship between pulmonary function and arterial blood gas results?
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no
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What FEV1 is significant changes in arterial blood gases usually present?
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less than 1L
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When does hypoxemia and hypercapnia become a chronic problem?
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FEV1 less than 1L
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What is hypoxemia initially associated with?
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exercise
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What is hypoxemia attributed to in COPD?
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hypoventilation of lung tissue relative to perfusion of the area
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What causes the decreased ventilatory drive seen in some COPD pts?
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abnormal peripheral or central respiratory receptors responses
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What is pH in COPD?
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usually normal, kidneys compensate by retaining bicarb
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How does pt present if acute respiratory distress develops?
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PaCO2 rise sharply, pt presents with uncompensated respiratory acidosis
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What consequences of long standing COPD and chronic hypoxemia?
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development of secondary pulmonary HTN
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What is the most common CV complication of COPD?
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pulmonary HTN, can result in cor pulmonale or right sided HF
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What are elevated pulmonary artery pressures attributed to?
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vasoconstriction, vascular remodeling, loss of pulmonary capillary beds
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What can result if elevated pulmonary pressures are sustained?
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cor pulmonale: hypertrophy of the right ventricle in response to increases in pulmonary vascular resistance
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What risks from cor pulmonale?
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venous stasis, thrombosis, PE
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What is result to skeletal muscle mass and overall health in pts with COPD?
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loss of skeletal muscle mass and general decline in overall health status
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Is there systemic inflammation in COPD?
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yes, lead to CV events associated with ischemia, cachexia, and muscle wasting
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What is a COPD exacerbation defined as?
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change in pts baseline symptoms (dyspnea, cough, sputum production) beyond day-to-day variability sufficient to warrant a change in management
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How is diagnosis of COPD exacerbation made?
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subjective measures and clinical judgement
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How do inflammatory mediators change during exacerbation?
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increased: neutrophils and eosinophils increased in sputum
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What symptom may not change during exacerbation?
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chronic airflow limitation
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How does lung hyperinflation change in exacerbation?
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worsened, contributes to worsening dyspnea and poor gas exchange
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What is the primary physiologic change seen in exacerbation?
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worsening of arterial blood gas results
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How is diagnosis of COPD made?
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symptoms: cough, sputum production, dyspnea
history of exposure to risk factors: tobacco smoke and occupational exposures |
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What confirms airflow limitation?
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spirometry
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What is the hallmark finding in spirometry in COPD?
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FEV1:FVC ratio less than 70%
indicates airway obstruction |
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What does a postbronchodilator FEV1 of less than 80% of predicted confirm?
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presence of airflow limitation that is not fully reversible
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What is an improvement in FEV1 of less than 12% following inhalation of a rapid acting bronchodilator evidence of?
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irreversible airflow obstruction
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How is reversibility of airflow limitation measured?
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bronchodilator challenge
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Is peak expiratory flow adequate for diagnosis of COPD?
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no, low specificity and high degree of effort dependence
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What preparation for reversibility testing?
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pt should be stable with no respiratory infection
no short acting bronchodilators within 6hrs, LABA within 12hrs, or SR theophylline within 24hrs |
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How is spirometry done in reversibility testing?
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FEV1 before bronchodilator
MDI or nebulizer: 400mcg B agonist, up to 160mcg anticholinergic, or combo FEV1 10-15 minutes after B agonist or 30-45 minutes after combo |
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What is considered reversible in reversibility testing?
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increase in FEV1 greater than 200mL and 12% above prebronchodilator FEV1
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What is stage I: mild COPD?
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FEV1/FVC less than 70%
FEV1 80% or more with or without symptoms |
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What is stage II: moderate COPD?
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FEV1/FVC less than 70%
FEV1 greater than 50% but less than 80% with or without symptoms |
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What is stage III: severe COPD?
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FEV1/FVC less than 70%
FEV1 greater than 30% but less than 50% with or without symptoms |
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What is stage IV: very severe COPD?
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FEV1/FVC less than 70%
FEV1 less than 30% or FEV1 less than 50% with chronic respiratory failure or right heart failure |
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What is the primary tool in classifying COPD according to severity?
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spirometry
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What BMI is associated with increased mortality in COPD?
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less than 21kg/m2
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What is the most troublesome complaint for pt with COPD?
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dyspnea
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What physical findings in later stages of COPD?
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cyanosis of mucosal membranes, "barrel chest" from hyperinflation of lungs, increased respiratory rate and shallow breathing, changes in breathing mechanics
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What is grade 0 dyspnea?
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no dyspnea
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What is grade 1 dyspnea?
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slight dyspnea: SOB when hurrying on level surface or walking up hill
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What is grade 2 dyspnea?
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moderate dyspnea: walk slower than normal due to breathlessness, stop for breath when walking on level surface at own pace
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What is grade 3 dyspnea?
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severe dyspnea: stops for breath after walking 100 yards or after a few minutes on level surface
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What is grade 4 dyspnea?
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very severe dyspnea: too breathless to leave the house or breathless while dressing or undressing
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What is seen of physical exam in COPD exacerbation?
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fever, wheezing, decreased breath sounds
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What does COPD lead to?
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disease progression, poor QOL, possible disability, premature mortality
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Is COPD fatal?
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yes
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What is the most important prognostic indicator in COPD?
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FEV1, avg rate of decline is the most useful measurement to assess the course of COPD
normal: 25-30mL/year much more for smoker |
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Does the number of years smoking affect decline in pulmonary function?
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yes, steeper decline
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Are the rate of decline of blood gases useful to assess progression of disease?
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no
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How often should COPD pt have spirometry?
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annually, to assess disease progression
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What is the survival rate of pts with COPD highly correlated with?
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impairment in FEV1 and age
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What is median survival if FEV1 is 1.4L?
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10 years
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What is median survival if FEV1 is 1L?
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4 years
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What is median survival if FEV1 is 0.5L?
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2 years
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When are arterial blood gases recommended?
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all pts with FEV1 less than 40% of predicted or signs of respiratory failure or right sided heart failure
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What are the leading causes of death from COPD?
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CV complications and lung cancer
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What is an exacerbation?
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change in one or more of the following: worsening dyspnea, increase in sputum volume, increase in sputum purulence
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What is a mild exacerbation?
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one cardinal symptoms plust one of the following: URTI within 5 days, fever without explanation, increased wheezing, increased cough, increased in respiratory or HR more than 20% above baseline
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What is moderate (type 2) exacerbation?
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2 cardinal symptoms
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What is severe (type 3) exacerbation?
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3 cardinal symptoms
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What is an important complication of severe exacerbation?
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acute respiratory failure
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What is obtained to assess the severity of an exacerbation?
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arterial blood gas
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How is diagnosis of acute respiratory failure in COPD made?
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acute change in arterial blood gas
acute drop in PaO2 of 10-15mmHg or acute increase in PaCO2 that decreases pH to 7.3 or less |
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What manifestations of respiratory failure?
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restlessness, confusion, tachycardia, diaphoresis, cyanosis, hypotension, irregular breathing, miosis, and unconsciousness
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How long for return to baseline after exacerbation?
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several weeks
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How many pts are readmitted for another exacerbation within 6 months?
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half
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What are COPD exacerbations associated with?
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significant morbidity and mortality
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