Chronic obstructive pulmonary disease (COPD): Clinical

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Chronic obstructive pulmonary disease (COPD): Clinical

USMLE® Step 2 questions

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USMLE® Step 2 style questions USMLE

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A 62-year-old woman comes to the physician due to dyspnea and a productive cough for the past several months. Past medical history is significant for hypertension. The patient has a 42-pack-year smoking history. She has tried multiple times to quit smoking by herself, but these attempts have been unsuccessful.Temperature is 37.0°C (98.6°F), pulse is 88/min, respirations are 14/min, blood pressure is 132/84 mm Hg, and oxygen saturation is 95% on room air. Physical examination reveals diffuse bilateral wheezes and rales. Pulmonary function testing (PFT) is performed, and the diagnosis of chronic obstructive pulmonary disease (COPD) is confirmed. Which of the following medications would be most effective in stopping the progression of this patient’s disease?  


Chronic obstructive pulmonary disease, or COPD is characterized by obstruction of airflow due to either inflammation of the airways, or chronic bronchitis, and destruction of the alveolar wall with dilation of the airspaces, or emphysema.

These events are due to inflammation that’s often triggered by inhalation of toxic substances, like tobacco smoke, as well as occupational pollutants like dust and silica.

Most people have elements of both chronic bronchitis and emphysema, so they’re often clumped together under the term COPD.

Alright, now chronic bronchitis is characterized by an inflammatory process that leads to increased mucus production, which obstructs the airways and leads to air trapping behind those mucus plugs.

Chronic bronchitis is clinically defined as having a productive cough for more than 3 months each year for 2 or more consecutive years.

Now, zooming in for a moment, the body maintains a balance between elastases, which destroy elastin in the alveolar wall and respiratory bronchioles, and anti-elastases, which stop elastase from doing just that.

In emphysema an inflammatory response to tobacco smoke tips the balance towards elastases, causing excessive destruction of the alveolar wall.

Without elastin, the elastic recoil that normally maintains the patency of the alveoli and respiratory bronchioles during exhalation is lost, and so these small airways collapse when the person tries to breathe out.

If air can’t get out, it becomes trapped in the alveoli, causing the airspaces to “puff up”.

Also, by destroying the alveolar-pulmonary capillary interface, gas exchange is impaired, resulting in hypoxemia and retention of carbon dioxide or CO2.


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