Podcast
Questions and Answers
Which drug is a PDE4 inhibitor?
Which drug is a PDE4 inhibitor?
- Roflumilast (correct)
- Caffeine
- Theophylline
- Aminophylline
What is the predominant PDE isoform in inflammatory cells?
What is the predominant PDE isoform in inflammatory cells?
- PDE5
- PDE2
- PDE4 (correct)
- PDE3
Which methylxanthine drug is rarely used now?
Which methylxanthine drug is rarely used now?
- Roflumilast
- Caffeine
- Theophylline (correct)
- Aminophylline
What observation led to the discovery of the effects of methylxanthines on asthma?
What observation led to the discovery of the effects of methylxanthines on asthma?
What is the duration of action of slow-release preparations of theophylline?
What is the duration of action of slow-release preparations of theophylline?
What is the most common adverse effect of theophylline at therapeutic plasma concentration?
What is the most common adverse effect of theophylline at therapeutic plasma concentration?
Which drug is an A1-adenosine receptor blocker?
Which drug is an A1-adenosine receptor blocker?
What is the FDA-approved use of roflumilast?
What is the FDA-approved use of roflumilast?
What is the cost range of roflumilast per month?
What is the cost range of roflumilast per month?
Which enzyme inducer reduces the plasma concentration of xanthines?
Which enzyme inducer reduces the plasma concentration of xanthines?
Which drugs are used primarily to cure acute asthma attacks?
Which drugs are used primarily to cure acute asthma attacks?
What is the main purpose of Alpha1-antitrypsin Deficiency Augmentation Therapy?
What is the main purpose of Alpha1-antitrypsin Deficiency Augmentation Therapy?
What can an imbalance between neutrophil elastase and the elastase inhibitor AAT lead to in patients with AAT deficiency?
What can an imbalance between neutrophil elastase and the elastase inhibitor AAT lead to in patients with AAT deficiency?
What is the treatment strategy to avoid bronchoconstriction in asthma?
What is the treatment strategy to avoid bronchoconstriction in asthma?
In patients with COPD, what leads to alveolar wall destruction and emphysema?
In patients with COPD, what leads to alveolar wall destruction and emphysema?
What is the primary goal of drugs acting on the bronchi as bronchodilators?
What is the primary goal of drugs acting on the bronchi as bronchodilators?
What is the endogenous protease inhibitor involved in AAT deficiency?
What is the endogenous protease inhibitor involved in AAT deficiency?
What is the mechanism of action of bronchodilators in the treatment of asthma?
What is the mechanism of action of bronchodilators in the treatment of asthma?
What is the primary purpose of drugs used in the treatment of asthma and COPD?
What is the primary purpose of drugs used in the treatment of asthma and COPD?
What is the main effect of an imbalance between neutrophil elastase and the elastase inhibitor AAT in patients with AAT deficiency?
What is the main effect of an imbalance between neutrophil elastase and the elastase inhibitor AAT in patients with AAT deficiency?
Which of the following drugs is indicated for COPD but not for asthma?
Which of the following drugs is indicated for COPD but not for asthma?
What is the first-line treatment for inducing persistent chronic bronchodilation in COPD?
What is the first-line treatment for inducing persistent chronic bronchodilation in COPD?
Which class of drugs is much less effective in COPD due to corticosteroid resistance and the nature of inflammation?
Which class of drugs is much less effective in COPD due to corticosteroid resistance and the nature of inflammation?
Which drug can result in downregulation of β2 receptors with chronic treatment?
Which drug can result in downregulation of β2 receptors with chronic treatment?
Which drug class is particularly effective in COPD due to the problem of small airways?
Which drug class is particularly effective in COPD due to the problem of small airways?
Which combination is a fixed LABA/LAMA combination indicated for COPD, not for asthma?
Which combination is a fixed LABA/LAMA combination indicated for COPD, not for asthma?
Which drug decreases the concentration of lymphocytes, monocytes, eosinophils, and basophils, while increasing the concentration of neutrophils, erythrocytes, and platelets?
Which drug decreases the concentration of lymphocytes, monocytes, eosinophils, and basophils, while increasing the concentration of neutrophils, erythrocytes, and platelets?
Which drug class can sensitize the bronchial smooth muscle for β2 agonists by upregulating β2 adrenergic receptor density?
Which drug class can sensitize the bronchial smooth muscle for β2 agonists by upregulating β2 adrenergic receptor density?
Which drug class can significantly improve lung function, dyspnea, symptoms, and health status, and reduce exacerbations in COPD?
Which drug class can significantly improve lung function, dyspnea, symptoms, and health status, and reduce exacerbations in COPD?
Which combination is usually preferred for improving lung function and reducing exacerbations in COPD, but not in asthma?
Which combination is usually preferred for improving lung function and reducing exacerbations in COPD, but not in asthma?
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Study Notes
Treatment Strategies for COPD and Asthma
- In COPD, inflammation is largely corticosteroid-resistant, and there are currently no effective anti-inflammatory treatments.
- The most important therapeutic strategy in COPD is to induce persistent chronic bronchodilation, with LAMA or LABA being the first-line treatment.
- Classes of drugs for asthma and COPD include controllers (anti-inflammatory/immune modulators) such as corticosteroids, leukotriene pathway inhibitors, mast cell degranulation blockers, anti-IgE antibodies, IL-5, and PDE-4 inhibitors, as well as rescue agents (bronchodilators) like β2-adrenergic agonists, muscarinic antagonists, methylxanthines, and PDE-4 inhibitor (roflumilast).
- Inhaled corticosteroids (ICSs) are first-line therapy for chronic asthma but are much less effective in COPD due to corticosteroid resistance and the nature of inflammation.
- Glucocorticoids in asthma have various anti-inflammatory actions, including modulation of immune cell function, reduction in cytokine production, and inhibition of lysosomal enzymes and activity.
- Glucocorticoids decrease the concentration of lymphocytes, monocytes, eosinophils, and basophils, while increasing the concentration of neutrophils, erythrocytes, and platelets.
- Inhaled glucocorticoids like fluticasone, flunisolide, beclomethasone, and budesonide can be used as monotherapy in COPD but are usually combined with LABAs in asthma.
- Chronic treatment with long-acting β2 agonists can result in downregulation of β2 receptors, but corticosteroids sensitize the bronchial smooth muscle for β2 agonists by upregulating β2 adrenergic receptor density.
- Anticholinergics, particularly M3 muscarinic receptor antagonists, are particularly effective in COPD due to the problem of small airways, and have indications for COPD and asthma.
- LAMA, such as tiotropium, aclidinium, umeclidinium, and glycopyrrolate, and LABA/LAMA combinations can significantly improve lung function, dyspnea, symptoms, and health status, and reduce exacerbations in COPD.
- Indacaterol and glycopyrrolate combination (Utibron Neohaler) is a fixed LABA/LAMA combination indicated for COPD, not for asthma, and is effective in improving lung function and reducing exacerbations.
- LABAs are usually combined with ICS in asthma, whereas in COPD, LABA/LAMA combinations are preferred for improving lung function and reducing exacerbations.
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