Asthma

01What asthma is

Three ideas sit at the heart of that definition. First, variable airflow limitation — obstruction that changes hour to hour and day to day, rather than the fixed obstruction of COPD. Second, reversibility: bronchoconstriction that relaxes with a bronchodilator or with time, which is what lets an asthmatic run a race and recover. Third, chronic airway inflammation — most often driven by an allergic, type-2 immune response, which is why corticosteroids, not just bronchodilators, are the disease-modifying treatment.

Asthma is also heterogeneous. Two patients with identical symptoms can have opposite underlying biology: one driven by house-dust-mite IgE and blood eosinophils, another (often older, obese women) with little allergy and normal eosinophils. Recognising this split — endotype, not just appearance — is now the key to choosing therapy, especially biologics.

02Etiology & risk factors

Asthma arises from an interaction between a genetic predisposition and environmental exposures. The single strongest risk factor is atopy — the inherited tendency to make IgE against common environmental proteins. Atopy breeds eczema, allergic rhinitis ("hay fever") and asthma together, often within the same family.

03Phenotypes & endotypes

"Asthma" is not one disease. The modern vocabulary separates phenotype (how it looks clinically) from endotype (the dominant biological pathway). This matters because therapy is increasingly matched to endotype.

04Pathogenesis

The allergic cascade has two phases. In the sensitisation phase, inhaled allergen is presented by dendritic cells to naïve T-cells, which differentiate into Th2 cells producing IL-4, IL-5 and IL-13. IL-4 drives B-cells to switch to IgE; IL-5 recruits and activates eosinophils; IL-13 drives mucus and remodelling. IgE coats mast cells in the airway wall.

On re-exposure, allergen cross-links surface IgE, and mast cells degranulate within minutes — releasing histamine, leukotrienes and prostaglandins. This is the early asthmatic response: smooth muscle contracts, vessels leak, mucus glands fire. A second wave — the late asthmatic response 4–12 hours later — is driven by recruited eosinophils and sustained inflammation, and is the reason symptoms can rebound after an apparent early recovery.

05Airway remodelling

Repeated inflammation does not leave the airway unscathed. Airway remodelling is the structural change that accrues over years: sub-basement-membrane thickening (from deposited reticular collagen), smooth-muscle hypertrophy, goblet-cell hyperplasia, angiogenesis and epithelial shedding.

Remodelling is the bridge between "reversible" and "fixed". It explains why longstanding, poorly-controlled asthma develops a component of irreversible obstruction — and why early, anti-inflammatory control (inhaled steroids) is protective, whereas relying on reliever bronchodilators alone is not. It is also the shared ground with COPD in asthma–COPD overlap.

06Clinical features

The cardinal symptoms are wheeze, breathlessness, chest tightness and cough that are variable — worse at night or in the early morning, with exercise, cold air, allergens or viral infections, and that improve spontaneously or with treatment. A pattern is more important than any single symptom: the patient who is fine at rest but cannot keep up on the stairs, or who coughs only at 3 a.m., is classic.

07Diagnosis & investigations

Asthma is a clinical diagnosis supported by objective tests. There is no single gold-standard test; diagnosis rests on demonstrating variable airflow limitation.

Spirometry

Baseline spirometry in asthma may be normal — the key is reversibility: a significant improvement in FEV₁ after an inhaled bronchodilator (classically ≥12% and ≥200 mL) supports asthma. In children or when baseline is normal, a bronchoprovocation test (methacholine or mannitol) demonstrating bronchial hyper-responsiveness is the next step.

Peak expiratory flow (PEF)

Home peak-flow monitoring captures variability that a single clinic visit misses: a >20% diurnal variation (morning-low, evening-high) over two weeks is diagnostic. It is cheap, portable and still clinically useful.

FeNO

Fractional exhaled nitric oxide is a non-invasive marker of eosinophilic airway inflammation. A high FeNO (>50 ppb in adults) supports a type-2, steroid-responsive phenotype; a low FeNO makes non-adherence or a non-eosinophilic process more likely.

Supporting tests

08Severity & control

GINA (Global Initiative for Asthma) deliberately separates control (current symptom burden) from risk (future exacerbation likelihood) — the two are not the same. A patient can be symptom-free on high-dose therapy yet remain high-risk because of prior intensive care admission or frequent exacerbations. Both dimensions guide stepping.

Asthma is further graded by the step of therapy required to achieve control (GINA steps 1–5). Unlike COPD's severity grades (which are physiological), these steps are treatment tiers — a crucial conceptual difference when comparing the two diseases.

09Management

Modern asthma management rests on four pillars: (1) confirm and monitor the diagnosis and control; (2) avoid triggers and manage comorbidities (rhinitis, reflux, smoking cessation); (3) pharmacological control with the right inhaled regimen; and (4) patient education and a written action plan.

The reliever revolution: anti-inflammatory reliever (AIR)

From 2019, GINA moved away from symptom-driven SABA alone — overuse of short-acting β₂-agonists is itself associated with worse outcomes and death. The preferred approach at every step is an anti-inflammatory reliever: either low-dose ICS–formoterol used both as reliever and maintenance, or (step 1) as-needed ICS–formoterol. This means formoterol — a fast-acting LABA safe enough to use for relief — is combined with an inhaled steroid so every reliever puff also treats inflammation.

Trigger management & non-pharmacological care

10Pharmacology

Asthma drugs split into relievers (rapid bronchodilators) and controllers (anti-inflammatory, disease-modifying). Understanding the receptor biology explains both efficacy and side-effects.

Relievers

Controllers (anti-inflammatory)

Oral corticosteroids

Systemic prednisolone is reserved for exacerbations and refractory disease because of cumulative toxicity (diabetes, osteoporosis, adrenal suppression, cataracts). A short course (e.g. 40 mg for 5 days) is standard for an acute attack; long-term oral steroids are a mark of severe, uncontrolled disease.

Biologics (severe asthma)

For severe eosinophilic or allergic asthma on maximal inhaled therapy, monoclonal antibodies target specific type-2 mediators. Selection is driven by phenotype:

11Acute severe asthma

An asthma attack is an acute, life-threatening worsening of bronchoconstriction, mucus plugging and hypoxaemia. Recognition and aggressive early treatment save lives; the danger is a tiring patient whose CO₂ normalises as they stop generating enough ventilation.

Immediate management

12Special situations

13Prognosis

Many children outgrow their asthma (symptom remission by adulthood), though airway hyper-responsiveness may persist. Adult-onset disease is less likely to remit. Most patients with good adherence and correct technique achieve full, normal lives. The drivers of poor prognosis are uncontrolled eosinophilic disease, frequent exacerbations, smoking, fixed airflow limitation and reliance on SABA alone.