Respiratory
Asthma
Reversible airway obstruction — bronchoconstriction, inflammation, and remodeling
Asthma is a chronic inflammatory airway disease characterized by reversible bronchoconstriction, mucosal edema, mucus plugging, and over years, structural remodeling. Triggers include allergens, viral infections, exercise, cold air, and aspirin. The pathology involves Th2-driven eosinophilic inflammation in most patients, producing IL-4, IL-5, and IL-13 that recruit eosinophils, drive IgE class switching, and increase mucus production. Diagnosis rests on episodic symptoms plus reversible airflow obstruction (FEV1 improvement ≥12% after bronchodilator). Treatment is staged, with inhaled corticosteroids as the cornerstone and biologics now reserved for severe phenotypes.
- Global prevalence~262 million people
- Reversibility criterionFEV1 increase ≥ 12% post-bronchodilator
- First-line controllerInhaled corticosteroid + LABA (combination)
- Rescue therapyShort-acting beta-2 agonist (albuterol)
- Severe asthma biologicsOmalizumab, mepolizumab, dupilumab
- Status asthmaticus mortality1-3% in hospitalized cases
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Why asthma matters
- Primary care. Asthma affects ~7% of adults and is one of the most common chronic conditions managed in general practice.
- Pediatrics. Childhood asthma drives school absence, ER visits, and hospitalizations; early ICS shapes long-term lung function.
- Emergency medicine. Acute severe asthma can deteriorate within hours; rapid bronchodilator-steroid pathways save lives.
- Anesthesia. Poorly controlled asthma raises perioperative bronchospasm risk; preoperative optimization reduces complications.
- Public health. Air pollution, tobacco smoke, and occupational exposures all worsen incidence and severity.
- Pharmacology. Asthma drugs span the full spectrum — small molecules, inhaled steroids, biologics, and now oral inhibitors of TSLP signaling.
- Sports medicine. Exercise-induced bronchoconstriction is common in elite endurance athletes and amenable to specific management.
Common misconceptions
- "Albuterol alone is enough." SABA-only treatment increases mortality; ICS is required for any persistent asthma.
- "Asthma is purely allergic." Non-allergic, neutrophilic, and obesity-related phenotypes exist and respond differently to therapy.
- "Steroid inhalers stunt children's growth permanently." Modest height effects of ~1 cm have been documented but do not progress with continued use.
- "Wheezing means asthma." Cardiac asthma, vocal cord dysfunction, and foreign bodies all wheeze; misdiagnosis is common.
- "Status asthmaticus needs immediate intubation." Intubation is high-risk in asthma; aggressive medical therapy first, intubation only when truly necessary.
- "Asthma is outgrown." Many adults experience recurrence after apparent remission; airway hyperresponsiveness often persists.
Frequently asked questions
What's the underlying biology?
Most asthma is type 2 inflammation. Allergen exposure activates dendritic cells that prime Th2 cells, which release IL-4, IL-5, and IL-13. IL-4 drives B cells to make IgE; IL-5 expands and activates eosinophils; IL-13 promotes mucus hypersecretion and smooth muscle hyperreactivity. Mast cells degranulate on IgE cross-linking, releasing histamine, leukotrienes, and prostaglandin D2 that constrict airways within minutes. Repeated cycles drive subepithelial fibrosis and smooth muscle hypertrophy — airway remodeling.
How is asthma diagnosed?
Clinical pattern of episodic wheeze, cough, chest tightness, and dyspnea — often nocturnal or exercise-induced. Spirometry shows obstruction (FEV1/FVC reduced) that reverses substantially with bronchodilator. If baseline spirometry is normal, methacholine challenge or peak flow variability over time can document hyperresponsiveness. Fractional exhaled nitric oxide (FeNO) above 25-50 ppb suggests eosinophilic inflammation. Allergen-specific IgE and blood eosinophil count help phenotype severe disease.
How is acute asthma treated?
Repeated inhaled short-acting beta-2 agonists (albuterol via spacer or nebulizer), ipratropium for moderate-severe attacks, and systemic corticosteroids within the first hour. Magnesium sulfate IV is added for severe attacks not responding. Oxygen titrated to SpO₂ 93-95%. Failure to respond, rising pCO₂, or exhaustion mandate intensive care and consideration of intubation — though ventilating an asthmatic is dangerous because of breath-stacking and high airway pressures.
What about chronic management?
GINA stepwise approach. Step 1-2: low-dose ICS as needed or daily, increasingly with formoterol (a fast-onset LABA) as combined controller and reliever. Step 3-4: medium-dose ICS-LABA, with tiotropium or LTRA add-on. Step 5: high-dose ICS-LABA, biologics (omalizumab for allergic, mepolizumab/benralizumab for eosinophilic, dupilumab for type 2 high), oral steroids as last resort. SABA-only treatment is no longer recommended at any step.
What are the biologics?
Omalizumab is anti-IgE for severe allergic asthma. Mepolizumab and reslizumab target IL-5; benralizumab targets the IL-5 receptor and depletes eosinophils. Dupilumab blocks IL-4Rα, inhibiting both IL-4 and IL-13 signaling. Tezepelumab targets TSLP, an upstream alarmin, and works across phenotypes including non-eosinophilic. These agents reduce exacerbations 50-70% in selected patients but cost tens of thousands per year, requiring biomarker-based selection.
Why do attacks kill?
Death from asthma is from progressive ventilation-perfusion mismatch leading to hypoxemia, then hypercapnia and respiratory acidosis from fatigue. A "silent chest" — no wheeze because air movement is too low — is ominous. Patients can deteriorate rapidly; near-fatal attacks share risk factors of prior intubation, frequent ED visits, oral steroid dependence, poor adherence, and psychosocial stress. Most asthma deaths are preventable with appropriate controller therapy.
Is exercise asthma the same?
Exercise-induced bronchoconstriction is a manifestation of airway hyperresponsiveness rather than a separate disease. Cooling and drying of the airway during high-minute-ventilation exercise triggers mast cell degranulation and bronchoconstriction 5-10 minutes after exertion. Pre-exercise SABA prevents most cases; daily ICS reduces underlying responsiveness. In athletes, leukotriene receptor antagonists are useful and not banned by WADA.