First Aid, Chapter 7 Hypersensitivity Disorders, COPD Flashcards
What is the definition of COPD?
Progressive airflow limitation characterized by FEV1/FVC
What are the GOLD criteria for COPD?
GOLD 1:
FEV1 ≥ 80% predicted = Mild GOLD 2: 50% to
In severe COPD, what is respiratory mortality related to?
In severe COPD, an inverse relationship between body mass and respiratory mortality has been described.
In COPD, what cells cause airway inflammation and how? What do they release? How does tobacco play a role?
Neutrophils and macrophages play a major role in COPD. Activated macrophages and neutrophils release matrix-degrading enzymes (including matrix metallo-, serine, and cysteine proteases) that cause the parenchymal lung destruction that underlies emphysema. Nicotine in cigarette smoke may also enhance tissue destruction by inhibiting tissue inhibitors of matrix metalloproteinases (TIMPs).
In COPD, what cells in the sputum are markers of viral and bacterial exacerbations?
Sputum eosinophils are a marker of viral exacerbation, whereas sputum neutrophils are seen in both bacterial and viral exacerbations.
What airways does chronic bronchitis involve? What are the symptoms?
Chronic bronchitis involves inflammation of small- and medium-sized airways, with symptoms of dyspnea, chronic cough, and sputum production.
What tissue does emphysema involve? What are signs and symptoms? What are teh two types?
Emphysema involves destruction of elastic tissue in terminal airspaces, loss of lung elastic recoil, and parenchymal loss. Signs and symptoms include dyspnea and hypoxemia.
- Centrilobular emphysema: Involves upper lobes; associated with cigarette smoke
- Panlobular emphysema: Involves lower lobes; seen with α1-antitrypsin deficiency
What is the loss of function in smokers vs. non-smokers in COPD?
There is an accelerated loss of lung function in smokers with a decline in FEV1 of almost 60 mL/year (compared with a normal loss of 30 mL/year typical of nonsmokers).
What stage of COPD is hyperinflation seen in?
Moderate to severe.
What causes the reduced diffusion capacity for carbon monoxide along with hypoxemia in COPD?
Destruction of the alveolar-capillary interface (particularly with emphysema) and alveolar hypoventilation
What are the major differences seen in treatment of COPD vs. Asthma?
Medications useful for COPD include:
- Short- and long-acting anticholinergics, which improve symptoms and airflow while decreasing hyperinflation in COPD. -Long-acting β agonists, which are used only with inhaled corticosteroids for asthma, can be used as isolated agents for COPD.
- Although inhaled corticosteroids (ICS) are a mainstay of treatment for persistent asthma, ICSs are considered only for moderate-to-severe COPD with symptoms despite bronchodilators.
Why is COPD less responsive to inhaled corticosteroids than asthma?
- Histone acetyltransferase acetylates (unwinds) the DNA-histone complex, leading to the generation of nuclear factor kappa B (NFκB) and activator protein 1 (AP-1), which are proinflammatory transcription factors.
- Histone deacetylases (HDACs) deacetylate (compacts) DNA, which suppresses gene transcription of NFκB and AP-1 (thus less inflammation).
- Corticosteroids increase HDACs in asthma, but not in COPD.
How does smoking cessation help in COPD?
Smoking cessation is critical and returns rate of loss of lung function almost to normal.
What is the only treatment that prolongs life in COPD?
Supplemental oxygen decreases mortality.
What are COPD adjuvant treatments? What treatment preserves lung function in adjunct to ICS?
Pulmonary rehabilitation, lung volume reduction surgery, and/or lung transplant for some patients. Use of anticholinergic therapy as adjunct to ICS has been shown to preserve lung function.
