Chronic Obstructive Pulmonary Disease

Question 1

1. Define chronic bronchitis.

Answer 1

chronic bronchitis: hyper secretion of mucus and structural abnormalities in the bronchi accompanied by chronic cough (both chronic simple bronchitis or chronic obstructive bronchitis)

Question 2

2. Describe the epidemiology and natural history of COPD.

Answer 2

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

Question 3

3. Understand the evidence for cigarette smoking and its contribution to COPD.

Answer 3

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

Question 4

4. Explain the pathological changes and changes in lung mechanics that result form smoking.

Answer 4

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

Question 5

5. Explain how smoking influences protease levels and their role in the development of emphysema.

Answer 5

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

Question 6

6. Appreciate the many factors that influence the development of COPD and specifically understand how alpha-1-antiprotease deficiency contributes to COPD.

Answer 6

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

Question 7

7. Analyze clinical, PFT and arterial blood gas information in chronic bronchitis and emphysema.

Answer 7

symptoms: DOE, chronic cough, sputum, wheezing, hemoptysis, orthopena and LEE; barrel chest, hyper resonant percussion, deminished breath sounds, prolonged expiratory phase, rhonchi

Question 8

8. Compare and contrast PFTs and arterial blood gasses seen in COPD to those in other lung diseases.

Answer 8

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

Question 9

9. Illustrate how to make a diagnosis of chronic bronchitis or emphysema.

Answer 9

.

Question 10

10. Understand the mechanisms of airway narrowing in COPD.

Answer 10

loss of elastic recoil- loss of radial traction

lumen occlusion by mucus
airway wall thickening and bronchospasm

Question 11

11. Explain the changes in lung volumes that occur as COPD progresses.

Answer 11

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

Question 12

12. Describe the mechanism of why COPD patients have hypoxemia.

Answer 12

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

Question 13

13. Analyze the V/Q relationships seen in COPD.

Answer 13

V/Q mismatch with emphasis on low V/Q, alveolar hyperventilation and low mixed venous O2

Question 14

14. Describe the pathophysiologic mechanisms that contribute to the development of cor pulmonale and pulmonary hypertension in patients with COPD.

Answer 14

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

Question 15

15. Discuss the principles of management of chronic bronchitis or emphysema.

Answer 15

smoking cessation
bronchodilators (anticholinergics, B agonists, theophylline)
tx. of acute exacerbations: corticosteriods, antibiotics, hospitalization and ventilatory assistance
tx. of hypoxemia (if PaO2<55-60)
immunization

Question 16

16. Compare and contrast “pink puffers” and “blue bloaters” in terms of clinical presentation, PFTs and ABGs.

Answer 16

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

Question 17

1. Define emphysema.

Answer 17

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

Question 18

1. Define cor pulmonale.

Answer 18

right ventricular hypertrophy or failure resulting from disease of the lungs