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Gold standard case presentation
Cigarette smoking is the most important risk factor for development of COPD. The causal relationship of smoking and COPD is fully established. Studies have established “dose-response relationship” for smoking and lung function but considerable variability is present among individuals.
In early stages of COPD, physical examination may be normal. Patients having more severe disease may have a prolonged expiratory phase. Signs of hyperinflation such as barrel shaped chest, increased resonance on percussion may be present. On auscultation, expiratory wheezing, decreased breath sounds, crackles at the base of lungs may be present. Chest x-ray is not required for making a diagnosis of COPD. It is typically performed to look for complication such as pneumonia, pneumothorax, and heart failure during acute exacerbations. Increased hyperlucency, flat diaphragm and long narrow cardiac shadow is visible on postero-anterior view of chest x-ray.
The major components of in-hospital management of exacerbations of COPD include reversing airflow limitation with inhaled short-acting bronchodilators and systemic glucocorticoids, treating infection, ensuring adequate oxygenation. Respiratory status, heart rate and rhythm, and fluid status should be monitored regularly. Arterial blood gas measurement should be performed to check for respiratory acidosis, confirm the oxygen saturation, and to monitor hypercapnia.
Supplemental oxygen therapy is of critical importance in management of acute condition. The target of oxygen therapy should be pulse oxygen saturation (SpO2) of 88 to 92 percent or arterial oxygen tension (PaO2) of approximately 60 to 70 mmHg.
Inhaled short-acting beta adrenergic agonists (e.g., salbutamol (aka albuterol) and levalbuterol) are the mainstay of therapy for an exacerbation of COPD. Onset of action is rapid and effectively produces bronchodilation. Beta adrenergic agonists may be combined with a short acting anticholinergic agent like ipratropium.
Systemic glucocorticoids are added to the bronchodilator therapies to improve symptoms and lung function, and decrease the length of hospital stay. Oral administration of glucocorticoids appears equally efficacious to intravenous glucocorticoids for treating most exacerbations of COPD. Intravenous glucocorticoids should be considered for patients with a severe exacerbation, who respond poorly to oral glucocorticoids, who are unable to take orally or who may have impaired absorption of oral medication.
There is good clinical evidence to suggest use of glucocorticoids in patients of COPD both in setting of acute exacerbation and stable COPD. Both systemic and inhaled glucocorticoids are widely prescribed for patients with chronic obstructive pulmonary disease (COPD).
Systemic (oral or intravenous) glucocorticoids improve symptoms, hasten recovery, reduced treatment failure and increased the rate of improvement in lung function. Hospitalized patients with COPD exacerbation also benefit from systemic glucocorticoid therapy. The benefits of glucocorticoids appear to be greatest in the first 72 hours after administration. Oral therapy appears to be equally effective if patients are able to take orally. Intravenous glucocorticoids should be considered in cases of failure to respond with oral regimen, very severe, exacerbation or in patient having poor oral absorption.
The mainstays of drug therapy of stable symptomatic COPD are inhaled bronchodilators (beta agonists and anticholinergics) with or without inhaled glucocorticoids depending upon the severity, risk of exacerbations, and response to therapy.
Inhaled glucocorticoids are part of the stepwise approach to management of stable COPD, which is intended to control symptoms, decrease exacerbations, and improve patient function and quality of life. Inhaled corticosteroids are not recommended as monotherapy for stable COPD patients because inhaled bronchodilators have greater benefits with fewer adverse effects.
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Question 1 of 11
1. Question1 point(s)
What level of deoxygenated blood is required for cyanosis to occur?CorrectIncorrect
Question 2 of 11
2. Question1 point(s)
What is the clinical definition of Chronic Bronchitis?CorrectIncorrect
Question 3 of 11
3. Question1 point(s)
What is the definition of a bullus?CorrectIncorrect
Question 4 of 11
4. Question1 point(s)
When does alpha 1 antitrypsin tend to manifest? More than one answer may be correct.CorrectIncorrect
Question 5 of 11
5. Question1 point(s)
What is the definition of COPD?CorrectIncorrect
Question 6 of 11
6. Question1 point(s)
Which of the following 12-lead electrocardiogram changes would be consistent with a diagnosis of COPD?CorrectIncorrect
Question 7 of 11
7. Question1 point(s)
Do macrolide and fluoroquinolone doses need to be increased or decreased with concomitant use of beta2 agonists and anti-muscarinic agents?CorrectIncorrect
Question 8 of 11
8. Question1 point(s)
Which one of the following vaccinations should all patients with COPD be recommended to have unless there is a contraindication?CorrectIncorrect
Question 9 of 11
9. Question1 point(s)
What are the indications for long term oxygen therapy in COPD? There maybe more than one right answer.CorrectIncorrect
Question 10 of 11
10. Question1 point(s)
In the assessment for long term oxygen therapy, how should you assess a patient’s potential need?CorrectIncorrect
Question 11 of 11
11. Question1 point(s)
What is the best marker in the assessment of severity in COPD?CorrectIncorrect