History and exam
Your Organizational Guidance
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Astma bij volwassenen: diagnose en monitoring in de eerste lijnPublished by: Werkgroep Ontwikkeling Richtlijnen Eerste Lijn (Worel)Last published: 2020Asthme chez l’adulte : diagnostic et surveillance en soins de santé primairesPublished by: Groupe de Travail Développement de recommmandations de première ligneLast published: 2020Key diagnostic factors
common
recent upper respiratory tract infection
With a recent sinusitis or common cold, symptoms are typically exacerbated.
dyspnea
Precipitated by allergen exposure, exposure to cold air, tobacco smoke, or particulates; worse with emotions such as laughing hard.
May wake the patient from sleep.
cough
Precipitated by allergen exposure, exposure to cold air, tobacco smoke, or particulates; worse with emotions such as laughing hard.
May wake the patient from sleep.
expiratory wheezes
Precipitated by allergen exposure, exposure to cold air, tobacco smoke, or particulates; worse with emotions such as laughing hard.
Polyphonic, high-pitched expiratory wheezes are typical of asthma.
Auscultation sounds: Polyphonic wheeze
Auscultation sounds: Expiratory wheeze
nasal polyposis
Appear as single or multiple polyps in the nasal cavity.
Risk factors
strong
family history
A parental history of asthma is a major risk factor for early development of asthma.[1]
Multiple genes are implicated that predispose people to hyper-responsiveness to environmental etiologic triggers.
allergens/irritants
Common allergens include cats, dogs, cockroaches, dust mites, fungal spores, environmental tobacco smoke, fumes from chemicals (e.g., bleach), and pollen from trees, weeds, and grass.[30]
Other indoor air pollutants linked to increased asthma symptoms and exacerbations include those from wood burning, natural gas, cooking, and evaporative volatile organic compounds.[20][21][22]
Workers commonly affected by occupational allergens include bakers, farmers, carpenters, and people involved in manufacturing plastics, foams, and glues. See Occupational asthma.
atopic disease history
History of eczema, atopic dermatitis, and allergic rhinitis is strongly associated.[16] The progression from eczema/atopic dermatitis to allergic rhinitis to subsequent asthma has been termed the "allergic or atopic march."[31] Association is possibly due to genetic variants in shared susceptibility genes.[16][31]
cigarette smoking
vaping
Vaping (electronic nicotine delivery system or e-cigarette use) has been associated with higher rates of asthma and asthma exacerbations (including reports of status asthmaticus).[19][33][34] It is thought to exert its effects by increasing the risk of obstructive lung function impairment.[17][18][19]
respiratory viral infection early in life
nasal polyposis
The prevalence of chronic rhinosinusitis with nasal polyps is higher in patients with asthma compared with the general population, and is associated with greater disease severity.[36][37] The two conditions share pathophysiologic processes including airway remodeling and eosinophilia.[37] Chronic rhinosinusitis with nasal polyps is more commonly associated with adult early- or late-onset versus childhood asthma.[36]
low socioeconomic status
Socioeconomically disadvantaged groups are more likely to live in areas with the poorest air quality and worst housing conditions, while being exposed to more psychosocial stress and having poorer diets.[24] These factors increase the risk of asthma, poor asthma control, and acute exacerbations. Socioeconomic status (e.g., education and income) can also affect access to healthcare. Communities of color (e.g., Black and Hispanic people) are disproportionately affected by lower socioeconomic status in the US.[24]
weak
obesity
High body mass index increases the likelihood of developing asthma, while significant weight loss can improve asthma control.[38][39] One study found that adults with a history of, or current asthma were significantly less likely to be physically active than those without asthma.[40][41] Obesity is also a major risk factor for the development of chronic obstructive pulmonary disease in asthmatic patients.[42]
Postulated mechanisms include reduced lung and tidal volume (promoting airway narrowing), low-grade systemic inflammation, effect of comorbidities, or a common etiology.[43][44] Growing evidence suggests a specific, female-predominant phenotype of asthma in people with obesity, whereby patients are less responsive to typical asthma medications and generally have a poorer prognosis.[38][39][45]
gastroesophageal reflux
Prevalent in patients with poorly controlled asthma.[46] The link between gastroesophageal reflux disease (GERD) and the development of asthma remains unclear, but could be related to chronic irritation and inflammation of the airways following exposure to gastric contents.[47][48] A Cochrane review found that treatment for GERD moderately improved lung function and use of rescue medication in patients with moderate-to-severe asthma and comorbid GERD; however, the effect of GERD treatment on exacerbations and hospital utilization is uncertain.[49]
obstructive sleep apnea
The prevalence of obstructive sleep apnea (OSA) in patients with asthma is approximately two to three times higher than in the general population.[50] Both conditions share risk factors including obesity, rhinitis, and gastroesophageal reflux disease.[48][50] Patients with asthma should be screened for symptoms suggestive of OSA and, if positive, referred for sleep testing to confirm the diagnosis.[51]
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