Continuing Medical Education examination
Obesity and asthma: Possible mechanisms Instructions for category 1 Continuing Medical Education credit The American Academy of Allergy, Asthma & Immunology is accredited as a provider of Continuing Medical Education (CME) by the Accreditation Council for Continuing Medical Education. Test ID no.: mai00150 Contact hours: 1.0 Expiration date: April 30, 2010 Category 1 credit can be earned by reading the text material and taking this CME examination online. For complete instructions, visit the Journal’s Web site at www.jacionline.org.
The Editors thank the Kaiser Permanente-Los Angeles Medical Center Allergy/Immunology training program for developing this CME examination. The individuals who contributed to its preparation were Amber Burnette, MD, Patricia Gomez-Dinger, DO, Michael Kaplan, MD, and Caroline Spagnola, MD.
Learning objectives: ‘‘Obesity and asthma: Possible mechanisms’’ 1. To understand that mechanical factors in obesity can increase the risk for asthma. 2. To identify the most important adipokines and their effects on airway hyperresponsiveness, airway inflammation, and cytokine production in the lung. 3. To understand the proposed mechanisms by which comorbidities of obesity contribute to the asthmatic phenotype.
CME items Question 1. Which of the following asthma outcome(s) is/are improved by either surgical or diet-induced weight loss? A. prevalence B. severity C. hospitalizations D. (all of the above) Question 2. Which of the following mechanical factors resulting from obesity does not contribute to the development of airway narrowing and airway hyperresponsiveness (AHR)? A. reduced functional residual capacity B. low tidal volume C. small airway closure in the supine position D. reduced forced vital capacity Question 3. Which of the following mechanical factors causes airway smooth muscle shortening and airway narrowing? A. low tidal volume resulting in actin-myosin crossbridge attachment B. low tidal volume causing increased actin-myosin crossbridge detachment C. higher PAO2 contributing to systemic inflammation of obesity D. low tidal volume causing hypoventilation and hypercapnea, resulting in increased smooth muscle contractility
Question 4. Which of the following cytokines has not been associated with obesity-related inflammatory conditions, such as type 2 diabetes, atherosclerosis, and asthma? A. TNF-b B. vascular endothelial growth factor C. IL-6 D. eotaxin Question 5. The M2 phenotype expressed by adipose tissue macrophages in lean mice decreases local adipose tissue inflammation by — A. increasing IL-10 and IL-6 expression and diminishing production of TNF-a and IL-1RA. B. increasing IL-10 and IL-1RA expression and diminishing expression of IL-6 and TNF-a. C. increasing TNF-a and IL-6 expression and diminishing production of IL-10 and IL-1RA. D. increasing TNF-a and IL-1RA expression and diminishing production of IL-10 and IL-6. Question 6. Increasing blood leptin levels during allergen challenge of sensitized mice causes which of the following responses? A. It increases lymphocyte influx into perivascular lung tissue. B. It increases eosinophil influx into perivascular lung tissue. C. It augments allergen-induced AHR. D. It increases TH2 cytokine expression by CD41 T cells in the lung parenchyma. J ALLERGY CLIN IMMUNOL
J ALLERGY CLIN IMMUNOL VOLUME 121, NUMBER 5
Question 7. Increasing serum adiponectin levels by 50% during allergen challenge of sensitized mice causes which of the following effects? A. It increases allergen-induced AHR, airway inflammatory cell chemotaxis, and TH2 cytokine expression in lung tissue. B. It increases allergen-induced AHR and TH2 cytokine expression in lung tissue but decreases airway inflammatory cell chemotaxis. C. It increases allergen-induced AHR but decreases TH2 cytokine expression in lung tissue and airway inflammatory cell chemotaxis. D. It decreases allergen-induced AHR, airway inflammatory cell chemotaxis, and TH2 cytokine expression in lung tissue. Question 8. Which of the following is the correct activity for adiponectin receptor adipo R2? A. It binds high-molecular-weight (HMW) adiponectin and augments the effects of acute ozone exposure on pulmonary inflammation. B. It binds trimeric adiponectin and activates hepatic adenosine monophosphate kinase, thus inhibiting liver gluconeogenesis. C. It binds HMW adiponectin and has anti-inflammatory effects that include suppressing synthesis of TNF-a and monocyte chemotactic protein-1. D. It binds HMW adiponectin and suppresses antioxidant genes, thus promoting an inflammatory response.
Question 9. All of the following statements regarding dyslipidemia and allergic asthma are true except: A. Feeding a cholesterol-supplemented diet to allergensensitized mice led to decreased lung levels of IL-5, eosinophils, and lymphocytes. B. The presence of free fatty acids leads to increased synthesis of proinflammatory cytokines and chemokines by CD11c1 macrophages in obese mice. C. TH2 cytokines upregulate the expression of AP2 (fatty acid binding protein) in airway epithelium of obese mice. D. Hypercholesterolemia may be a risk factor for asthma in children and adolescents independent of their body mass index. Question 10. Which of the following statements regarding asthma and the comorbidities of obesity is correct? A. The increased risk of asthma in the obese is directly related to gastroesophageal reflux and sleep-disordered breathing. B. Treatment of the obese asthmatic with continuous positive airway pressure improves quality of life by increasing the patient’s functional residual capacity while the patient is supine. C. Peribronchial edema and increased endothelin levels are associated with gastroesophageal reflux. D. In mice, hyperglycemia directly contributed to increased airway hyperresponsiveness and thus correlated with the obese pulmonary phenotype.