First Aid, Chapter 7 Hypersensitivity Disorders, COPD Flashcards Preview

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Flashcards in First Aid, Chapter 7 Hypersensitivity Disorders, COPD Deck (15)
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1
Q

What is the definition of COPD?

A

Progressive airflow limitation characterized by FEV1/FVC

2
Q

What are the GOLD criteria for COPD?

A

GOLD 1:

FEV1 ≥ 80% predicted = Mild GOLD 2: 50% to

3
Q

In severe COPD, what is respiratory mortality related to?

A

In severe COPD, an inverse relationship between body mass and respiratory mortality has been described.

4
Q

In COPD, what cells cause airway inflammation and how? What do they release? How does tobacco play a role?

A

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).

5
Q

In COPD, what cells in the sputum are markers of viral and bacterial exacerbations?

A

Sputum eosinophils are a marker of viral exacerbation, whereas sputum neutrophils are seen in both bacterial and viral exacerbations.

6
Q

What airways does chronic bronchitis involve? What are the symptoms?

A

Chronic bronchitis involves inflammation of small- and medium-sized airways, with symptoms of dyspnea, chronic cough, and sputum production.

7
Q

What tissue does emphysema involve? What are signs and symptoms? What are teh two types?

A

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
8
Q

What is the loss of function in smokers vs. non-smokers in COPD?

A

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).

9
Q

What stage of COPD is hyperinflation seen in?

A

Moderate to severe.

10
Q

What causes the reduced diffusion capacity for carbon monoxide along with hypoxemia in COPD?

A

Destruction of the alveolar-capillary interface (particularly with emphysema) and alveolar hypoventilation

11
Q

What are the major differences seen in treatment of COPD vs. Asthma?

A

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.
12
Q

Why is COPD less responsive to inhaled corticosteroids than asthma?

A
  • 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.
13
Q

How does smoking cessation help in COPD?

A

Smoking cessation is critical and returns rate of loss of lung function almost to normal.

14
Q

What is the only treatment that prolongs life in COPD?

A

Supplemental oxygen decreases mortality.

15
Q

What are COPD adjuvant treatments? What treatment preserves lung function in adjunct to ICS?

A

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.

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