Flashcards in Chronic Obstructive Pulmonary Disease Deck (18):
1. Define chronic bronchitis.
chronic bronchitis: hyper secretion of mucus and structural abnormalities in the bronchi accompanied by chronic cough (both chronic simple bronchitis or chronic obstructive bronchitis)
2. Describe the epidemiology and natural history of COPD.
COPD is the 4th leading cause of death and second only to CAD for SS-compensated disability
dominant feature is progressive airflow obstruction, after age 20, FEV declines 20-40mL per year, smoking increases this decline
3. Understand the evidence for cigarette smoking and its contribution to COPD.
smoking can worsen the progression of disease, smoking is recognized as the major cause of COPD and can caused increased mortality in those with COPD
risk of COPD is proportional to the dose and duration of cigarette smoking age and baseline lung function
4. Explain the pathological changes and changes in lung mechanics that result form smoking.
pathologic changes in smoking-related emphysema (centrilobar emphysema)
emphysema represents loss of elastic and/or collagen fiber continuity, major determinants of alveolar shape, and tissue elasticity--- leads to abnormalities in pressure volume relationships including hyperinflation and expiratory airflow limitation
pathologic lesions of the respiratory bronchioles in smokers include: acute and chronic inflammatory cels, infiltrates of airway walls, enlarged smooth muscle elements, fibrosis of airway walls (dysplasia) and metaplasia of lining epithelium
5. Explain how smoking influences protease levels and their role in the development of emphysema.
90% of smokers compared to 10-15% of older nonsmokers show some emphysema at death, there is positive correlation between severity and pack-year exposure
advanced emphysema is found in 0% nonsmokers, 12% 1ppd smokers
6. Appreciate the many factors that influence the development of COPD and specifically understand how alpha-1-antiprotease deficiency contributes to COPD.
heritable deficiency in alpha-1-antiprotease cases severe panlober emphysema, cigarette smoke increase lung protease levels
different individuals present different combinations of innate susceptibility and environmental insult including older age and male gender; alpha-1-antiprotease deficiency, second hand smoke, workplace exposure
7. Analyze clinical, PFT and arterial blood gas information in chronic bronchitis and emphysema.
symptoms: DOE, chronic cough, sputum, wheezing, hemoptysis, orthopena and LEE; barrel chest, hyper resonant percussion, deminished breath sounds, prolonged expiratory phase, rhonchi
8. Compare and contrast PFTs and arterial blood gasses seen in COPD to those in other lung diseases.
invariably low FEV,/FVC and FEV1; normal or increased TLC (over inflation), FRC and RV (gas trapping), reduction in DLCO
blood gases: hypoxemia and hypercapnea may be present
9. Illustrate how to make a diagnosis of chronic bronchitis or emphysema.
10. Understand the mechanisms of airway narrowing in COPD.
loss of elastic recoil- loss of radial traction
lumen occlusion by mucus
airway wall thickening and bronchospasm
11. Explain the changes in lung volumes that occur as COPD progresses.
VC and FVC reduced due to slowing of expiratory airflow and premature airway closure at abnormally high lung volumes resulting in increased residual volume
hyperinflation may be present due to loss of elastic recoil
12. Describe the mechanism of why COPD patients have hypoxemia.
low ventilation-perfusion V/Q relationships, hypoxemia corrects with low amounts of supplemental oxygen
some patients may have matched reduction in ventilation and perfusion
shunt is not, unless there is a complication that leads to alveolar filling
13. Analyze the V/Q relationships seen in COPD.
V/Q mismatch with emphasis on low V/Q, alveolar hyperventilation and low mixed venous O2
14. Describe the pathophysiologic mechanisms that contribute to the development of cor pulmonale and pulmonary hypertension in patients with COPD.
alveolar hypoxia-- pulmonary arteriolar vasoconstriction cause increased pulmonary vascular resistance and right ventricular failure
additionally: destruction of pulmonary capillary bed, polycythemia and elevated blood volume
15. Discuss the principles of management of chronic bronchitis or emphysema.
bronchodilators (anticholinergics, B agonists, theophylline)
tx. of acute exacerbations: corticosteriods, antibiotics, hospitalization and ventilatory assistance
tx. of hypoxemia (if PaO2<55-60)
16. Compare and contrast "pink puffers" and "blue bloaters" in terms of clinical presentation, PFTs and ABGs.
clinical presentation: cyanotic, HTN, overweight, volume overload-edema, associated with sleep disordered breathing v. well perfused, no heart failure, no cyanosis, characteristic pursed-lip breathing
PFT: FEV1 and FVC are much greater in the blue bloater, FEV1/FVC is much more decreased as compared to pink puffer
ABGs: blue bloater pH is low, O2 is very low, hypercapic; pink puffer: sats are somewhat normal at rest, lower PaO2, exercise brings down sats and pH
difference in patient is the responsiveness of respiratory center to derangement in blood gases
1. Define emphysema.
emphysema: destructive process with dissolution of alveolar walls with airspace enlargement and loss of pulmonary capillaries that surround the alveoli; presents with dyspnea and moderate to sever airflow obstruction