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12 questions about Asthma and airway function , make them strong
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Here are 12 strong, high-yield questions on asthma and airway function suitable for advanced students, clinicians-in-training, or exam prep. They emphasize pathophysiology, diagnosis, interpretation, and management — many are multi-part or vignette-based to test clinical reasoning.
1. Explain in detail how Type 2 (Th2) airway inflammation causes acute bronchoconstriction and chronic airway narrowing. Include the key cells, cytokines, IgE, mediators, and the link between inflammation and structural airway remodeling.
2. A 28-year-old presents with episodic wheeze and dyspnea. Baseline spirometry: FEV1 65% predicted, FEV1/FVC = 0.68. After 400 µg salbutamol, FEV1 improves to 78% predicted. Interpret these findings with respect to diagnostic criteria for asthma, and discuss alternative diagnoses you would consider if bronchodilator response were absent.
3. Describe the principle of bronchial provocation testing using methacholine (or histamine). State the usual diagnostic threshold(s), how to interpret results, and three clinical or pharmacologic factors that can produce false-positive or false-negative tests.
4. Define airway remodeling in asthma. List at least four structural changes that contribute to fixed airflow limitation, discuss the cellular mechanisms driving each change, and comment on their reversibility with current therapies.
5. Case: A 45-year-old with known asthma arrives in the ED in distress. Exam: accessory muscle use, RR 34, audible wheeze. ABG on room air: pH 7.36, PaCO2 48 mmHg, PaO2 56 mmHg. a) Interpret the ABG. b) Explain the pathophysiologic significance of rising PaCO2 in an acute asthma attack. c) Outline the immediate management priorities and indications for intubation.
6. Compare and contrast eosinophilic (Type 2) asthma and non-eosinophilic/neutrophilic asthma in terms of typical triggers, biomarkers (blood/sputum eosinophils, FeNO), steroid responsiveness, and targeted biologic treatment options.
7. For each of the following medication classes used in asthma — short-acting β2-agonists (SABA), inhaled corticosteroids (ICS), long-acting β2-agonists (LABA), long-acting muscarinic antagonists (LAMA), systemic corticosteroids, leukotriene receptor antagonists (LTRA), and anti-IgE/anti-IL5/anti-IL4R biologics — state the primary mechanism of action, typical onset of effect, main clinical indication, and one important adverse effect or safety concern.
8. Explain how ventilation–perfusion (V/Q) mismatch produces hypoxemia in asthma. Why is hypoxemia often present with low or normal PaCO2 early in an exacerbation, and why does the development of hypercapnia signal impending respiratory failure?
9. Peak expiratory flow (PEF) is used for home monitoring. a) Define clinically significant diurnal variability and the usual thresholds used for diagnosis/monitoring. b) List factors that can make PEF measurements unreliable. c) How would you use PEF trends to adjust treatment?
10. Pediatric focus: Describe key differences in diagnosing and managing asthma in children under 5 years versus school-aged children/adolescents. Include discussion of viral-triggered wheeze phenotypes, limitations of spirometry, and when to trial controller therapy.
11. Occupational asthma: List clinical features and history elements that distinguish occupational asthma from adult-onset non-occupational asthma. Describe the diagnostic approach (including timing of symptoms, workplace exposure assessment, serial peak flow, and specific inhalational challenge) and immediate workplace/medical actions when suspected.
12. A 52-year-old woman with severe, uncontrolled asthma is already on high-dose ICS/LABA and regular tiotropium with persistent symptoms and two hospitalizations in the past year. Construct a stepwise management plan including: assessment for modifiable contributors, adjunct pharmacologic options (with rationale for selecting biologic therapies and criteria for each), nonpharmacologic interventions, and indications for referral for bronchial thermoplasty or specialist airway center.
If you want, I can convert these into multiple-choice items, add model answers with key points, or tailor them to undergraduate, postgraduate, or board-exam difficulty. Which would you prefer?
1. Explain in detail how Type 2 (Th2) airway inflammation causes acute bronchoconstriction and chronic airway narrowing. Include the key cells, cytokines, IgE, mediators, and the link between inflammation and structural airway remodeling.
2. A 28-year-old presents with episodic wheeze and dyspnea. Baseline spirometry: FEV1 65% predicted, FEV1/FVC = 0.68. After 400 µg salbutamol, FEV1 improves to 78% predicted. Interpret these findings with respect to diagnostic criteria for asthma, and discuss alternative diagnoses you would consider if bronchodilator response were absent.
3. Describe the principle of bronchial provocation testing using methacholine (or histamine). State the usual diagnostic threshold(s), how to interpret results, and three clinical or pharmacologic factors that can produce false-positive or false-negative tests.
4. Define airway remodeling in asthma. List at least four structural changes that contribute to fixed airflow limitation, discuss the cellular mechanisms driving each change, and comment on their reversibility with current therapies.
5. Case: A 45-year-old with known asthma arrives in the ED in distress. Exam: accessory muscle use, RR 34, audible wheeze. ABG on room air: pH 7.36, PaCO2 48 mmHg, PaO2 56 mmHg. a) Interpret the ABG. b) Explain the pathophysiologic significance of rising PaCO2 in an acute asthma attack. c) Outline the immediate management priorities and indications for intubation.
6. Compare and contrast eosinophilic (Type 2) asthma and non-eosinophilic/neutrophilic asthma in terms of typical triggers, biomarkers (blood/sputum eosinophils, FeNO), steroid responsiveness, and targeted biologic treatment options.
7. For each of the following medication classes used in asthma — short-acting β2-agonists (SABA), inhaled corticosteroids (ICS), long-acting β2-agonists (LABA), long-acting muscarinic antagonists (LAMA), systemic corticosteroids, leukotriene receptor antagonists (LTRA), and anti-IgE/anti-IL5/anti-IL4R biologics — state the primary mechanism of action, typical onset of effect, main clinical indication, and one important adverse effect or safety concern.
8. Explain how ventilation–perfusion (V/Q) mismatch produces hypoxemia in asthma. Why is hypoxemia often present with low or normal PaCO2 early in an exacerbation, and why does the development of hypercapnia signal impending respiratory failure?
9. Peak expiratory flow (PEF) is used for home monitoring. a) Define clinically significant diurnal variability and the usual thresholds used for diagnosis/monitoring. b) List factors that can make PEF measurements unreliable. c) How would you use PEF trends to adjust treatment?
10. Pediatric focus: Describe key differences in diagnosing and managing asthma in children under 5 years versus school-aged children/adolescents. Include discussion of viral-triggered wheeze phenotypes, limitations of spirometry, and when to trial controller therapy.
11. Occupational asthma: List clinical features and history elements that distinguish occupational asthma from adult-onset non-occupational asthma. Describe the diagnostic approach (including timing of symptoms, workplace exposure assessment, serial peak flow, and specific inhalational challenge) and immediate workplace/medical actions when suspected.
12. A 52-year-old woman with severe, uncontrolled asthma is already on high-dose ICS/LABA and regular tiotropium with persistent symptoms and two hospitalizations in the past year. Construct a stepwise management plan including: assessment for modifiable contributors, adjunct pharmacologic options (with rationale for selecting biologic therapies and criteria for each), nonpharmacologic interventions, and indications for referral for bronchial thermoplasty or specialist airway center.
If you want, I can convert these into multiple-choice items, add model answers with key points, or tailor them to undergraduate, postgraduate, or board-exam difficulty. Which would you prefer?
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