Obstructive Lung Disease Flashcards
What does IL-4 do?
directs B lymphocytes to synthesize IgE
What does IL-5 do?
regulates eosinophil production and maturation
What does IL-13 do?
leads to airway eosinophilia, mucous gland hyperplasia, airway fibrosis and remodeling
What are the primary T lymphocytes involved in the pathogenesis of asthma?
Th2 CD4+ T lymphocytes
A 22-year-old male is seen for evaluation of his asthma. He was born at a gestational age of 42 weeks by planned cesarean section to a 19- year-old mother. During pregnancy his mother took herbal pills containing vitamin K. Which of these perinatal factors is associated with the development of childhood asthma?
Delivery by cesarean section. Prematurity (birth between 23-27 weeks gestational age), neonatal jaundice, and prenatal exposure to maternal smoking are other risk factors. Maternal age and vitamin K use have not been shown to be risk factors.
There is no gold standard for the diagnosis of asthma. It is a clinical diagnosis based on history, patient characteristics, physical findings, and the results of other evaluations.
New-onset asthma, although possible, is rare in older adults. The majority of cases are diagnosed in childhood, with most of the remaining cases diagnosed in their teens and twenties.
Baseline spirometry should be obtained in all patients with a suspected diagnosis of asthma.
Spirometry can be normal in a patient with asthma.
Absolute contraindications to bronchoprovocation testing?
SMUK:
Severe airflow limitation (FEV1 < 50% predicted or < 1 L)
Myocardial infarction or stroke in last 3 months
Uncontrolled hypertension (systolic blood pressure > 200 mm Hg or diastolic blood pressure > 100 mm Hg)
Known aortic aneurysm
A false positive bronchoprovacation test can occur in patients with?
ABCs
Allergic rhinitis Bronchitis
Congestive heart failure, COPD
cystic fibrosis
Total serum IgE levels should be measured in patients with moderate-to- severe persistent asthma who are being considered for omalizumab therapy or in patients suspected of having ABPA.
A 55-year-old patient with asthma had three episodes of fever with worsening dyspnea as well as sputum production with brownish mucus plugs in the last 2 months. Chest radiographs show fleeting infiltrates and an HRCT shows central bronchiectasis. Serum IgE levels are elevated (1200 ng/mL) with peripheral blood eosinophilia (700/mL).
What is the most likely diagnosis? Which test should be done next?
Allergic bronchopulmonary aspergillosis.
A skin-prick test checking reactivity to Aspergillus fumigatus should be performed.
Medications associated with EGPA:
COIL
Cocaine
Omalizumab
Inhaled glucocorticoids Leukotriene-modifying
agents
The most direct way to establish the diagnosis of exercise-induced asthma is via exercise challenge testing.
In patients with poorly controlled asthma who experience frequent episodes of exercise- induced bronchoconstriction, the most important strategy is to improve overall asthma control.
In the development of Occupational asthma (OA), the most important factor is the intensity of exposure.
In a symptomatic patient with ongoing exposure, normal spirometry, and a negative nonspecific bronchoprovocation test excludes the possibility of Occupational asthma.
The cornerstone of therapy for OA is to avoid further exposure to the sensitizing agent.
After complete avoidance of exposure, OA improves gradually then plateaus after about 2 years.
Reactive airways dysfunction syndrome (RADS) and Irritant Induced Asthma (IrIA) symptoms are not reproduced by inhalation challenge with low levels of offending workplace agents, while symptoms of immunologic OA are reproduced in those conditions.
After complete cessation of exposure, RADS and IrIA usually improve with time, but some patients continue to have symptoms for at least 1 year and residual physiologic abnormalities like bronchial hyperreactivity can last for several years.
What are symptoms that typically begin within 30 minutes to 3 hours following NSAID use:
ABCDEF
Asthma-like symptoms (acute asthma exacerbation)
Bronchospasm and laryngospasm (might be severe enough to require intubation)
Congestion and conjunctival redness
Diffuse abdominal cramps (less common)
Epigastric pain (less common) and edema (usually periorbital)
Facial flushing
The only way to definitively diagnose NSAID sensitivity is via aspirin challenge testing. However, it is rarely used clinically for establishing the diagnosis of AERD. It is mostly performed as a part of a protocol when aspirin desensitization is indicated.
Although other COX-1– inhibiting NSAIDs can be used safely in AERD patients who have been successfully desensitized with aspirin, only subsequent aspirin therapy has been shown to slow the regrowth of nasal polyps and improve asthma symptoms.
Successfully desensitized patients should continue taking 325 mg of aspirin or equivalent dose of another COX-1–inhibiting NSAID daily to maintain their desensitized state.
It is important for patients to understand that medication use is required to control airway inflammation, even in the absence of symptoms.
Never use inhaled long- acting bronchodilators alone in the treatment of asthma. Studies suggest they may increase risk of asthma-related death when not combined with an inhaled corticosteroid.
Anti-IgE therapy is not a first-line therapy for the majority of asthma patients, but it can be considered in patients with atopic asthma refractory to standard therapy.
A history of severe and/or frequent exacerbations puts patients at increased risk for experiencing a fatal exacerbation.
Epithelial cells –> TGFβ –> small airway fibrosis
Macrophages–> LTB4 and IL-8 –> neutrophil and T-cell chemoattractant –> increase d inflammation
What are the primary lymphocytes involved in pathogenesis of COPD?
A: CD8+ cytotoxic T cells
