Respiratory : Airways Disease

• Asthma: Asthma: What It Is | Diagnosing Asthma | Treating Asthma: AIR and MART | Asthma Review and Risk | Severe Asthma and Biologics | Occupational Asthma | Asthma in Special Situations | Asthma Mimics
• COPD: COPD: What It Is | Diagnosing and Assessing COPD | Treating Stable COPD | Oxygen and Home NIV | Advanced COPD | Alpha-1 Antitrypsin Deficiency
• Suppurative lung disease: Bronchiectasis | Cystic Fibrosis | Primary Ciliary Dyskinesia | Allergic Bronchopulmonary Aspergillosis
• Revision: Drug Reference Table | Spot the Diagnosis | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🌬️ Airways disease is the commonest group of lung conditions - asthma affects over 5 million people in the UK and COPD over 1 million. Both narrow the airways, but they behave differently: asthma is variable and inflammatory, while COPD is fixed and progressive. This chapter also covers bronchiectasis and cystic fibrosis, where damaged airways fill with infected mucus.
Your four questions for every patient: Is the obstruction variable (asthma) or fixed (COPD)? Is there type 2 (eosinophilic) inflammation? Is the inhaler technique and adherence right? Are smoking, triggers and infections being tackled?

Asthma: What It Is

Mechanism: Chronic inflammation of the airways makes them hyper-responsive. Triggers cause:

• Smooth muscle contraction (bronchospasm).
• Swelling of the airway wall.
• Mucus production.

The narrowing is variable and at least partly reversible. Most asthma is "type 2" (eosinophilic, allergic) - driven by IL-4, IL-5 and IL-13 - which responds well to steroids.

Risk factors:

• Atopy - eczema, hay fever, food allergy.
• Family history.
• Early viral infections.
• Smoking (including passive) and air pollution.
• Obesity.
• Occupational exposures.

Triggers:

• Viral infections.
• Allergens - house dust mite, pollen, pets, moulds.
• Exercise; cold air.
• Smoke; pollution.
• Drugs - beta-blockers (including eye drops), NSAIDs and aspirin in some people.
• Stress; hormones (premenstrual).

Clinical pattern:

• Wheeze, breathlessness, chest tightness, cough.
• Variable over time, often worse at night and early morning.
• Triggered by the factors above.
• Between attacks, the examination may be normal.

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Diagnosing Asthma

Asthma is over-diagnosed and under-diagnosed, so the BTS/NICE/SIGN guideline (2024) requires an objective test as well as a typical history.

Adults - test in this order:

• 1. Blood eosinophils or FeNO: A raised eosinophil count (above the lab reference range) or FeNO of 50 ppb or more confirms asthma when the history is typical.
• 2. Spirometry with bronchodilator reversibility: An FEV1 rise of 12% or more and 200 mL or more (or 10% or more of predicted) confirms asthma.
• 3. Peak flow variability (if spirometry is delayed or unavailable): Twice-daily readings for 2 weeks; variability of 20% or more confirms asthma.
• 4. Bronchial challenge test (specialist): Hyperresponsiveness confirms asthma. A normal test suggests another diagnosis.

Points to remember:

• Test before starting inhaled steroids if possible - they reduce FeNO, eosinophils and variability.
• If the patient is very unwell, treat first and test later.
• Normal spirometry between attacks does not exclude asthma.
• Record the evidence for the diagnosis in the notes.

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Treating Asthma: AIR and MART

The big change (BTS/NICE/SIGN 2024): People aged 12 and over should not use a salbutamol (SABA) inhaler alone. Relying on SABA without inhaled steroid is linked to severe attacks and asthma deaths. Treatment is now built around a combined inhaled steroid plus formoterol inhaler (e.g. budesonide/formoterol). Formoterol works within minutes, so the same inhaler can be both the reliever and the preventer.

Adult pathway:

• Step 1 - Newly diagnosed: AIR (anti-inflammatory reliever). A low-dose ICS/formoterol inhaler used as needed for symptoms.
• Step 2 - Not controlled, or very symptomatic or recent severe attack at diagnosis: low-dose MART (maintenance and reliever therapy). The same ICS/formoterol inhaler is taken regularly (e.g. 1 puff twice daily) and as needed.
• Step 3 - Moderate-dose MART (e.g. 2 puffs twice daily plus as needed).
• Step 4 - Still not controlled on moderate-dose MART despite good adherence and technique:
  • Check FeNO and blood eosinophils.
  • If either is raised, refer to a specialist (possible severe asthma).
  • If neither is raised, try adding a leukotriene receptor antagonist (montelukast) or a LAMA for 8–12 weeks, then refer if still uncontrolled.
• Step down to the lowest effective treatment once well controlled for at least 3 months.

People already on SABA plus a separate inhaled steroid: Consider switching to ICS/formoterol AIR or MART at review.

Montelukast: MHRA warning about neuropsychiatric reactions (sleep disturbance, depression, suicidal thoughts) - warn patients and carers.

💡 Clinical Pearl: Before stepping up, check four things: inhaler technique, adherence, triggers (smoking, allergens, occupation) and the diagnosis itself. Most "uncontrolled asthma" is one of these.

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Asthma Review and Risk

Review at least once a year, and after every attack:

• Symptom control: Asthma Control Questionnaire or Asthma Control Test; night waking; reliever use; activity limitation.
• Attacks: Courses of oral steroids, emergency visits, admissions.
• Inhaler technique - watch the patient use it; choose the right device.
• Adherence - check prescription records.
• Triggers and comorbidities: Smoking, rhinitis, reflux, obesity, anxiety, dysfunctional breathing.
• Written personalised asthma action plan - what to do when symptoms worsen.
• Vaccinations: Influenza; COVID-19 (and pneumococcal if eligible).
• Consider the inhaler's environmental impact - dry powder inhalers have a lower carbon footprint than metered-dose inhalers, where suitable.

Warning signs of high risk of a fatal attack (National Review of Asthma Deaths):

• Previous near-fatal attack or ICU admission.
• Hospital admissions or emergency visits in the past year.
• Heavy reliever use - frequent SABA prescriptions.
• Low use of inhaled steroids; poor adherence.
• Psychological or social problems.
• Recent discharge after an attack.

These patients need urgent review and close follow-up.

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Severe Asthma and Biologics

Definition: Asthma that stays uncontrolled despite high-dose treatment with good adherence and technique, after comorbidities and triggers have been addressed. It affects about 5% of people with asthma, but causes a large share of attacks and costs.

Assessment in a specialist severe asthma centre:

• Confirm the diagnosis.
• Check adherence (including FeNO suppression testing).
• Look for comorbidities - rhinosinusitis and nasal polyps, reflux, obesity, inducible laryngeal obstruction, dysfunctional breathing, anxiety.
• Phenotype the asthma: Blood eosinophils, FeNO, IgE, allergen sensitisation.
• Look for ABPA and EGPA.

Biologic treatments (injected monoclonal antibodies; NICE technology appraisals - specialist use):

• Omalizumab (anti-IgE): Severe allergic asthma with raised IgE.
• Mepolizumab, reslizumab (anti-IL-5) and benralizumab (anti-IL-5 receptor): Severe eosinophilic asthma.
• Dupilumab (anti-IL-4 receptor alpha - blocks IL-4 and IL-13): Type 2 asthma with raised eosinophils and FeNO. Also treats nasal polyps and eczema.
• Tezepelumab (anti-TSLP): Acts "upstream" and works in both eosinophilic and non-eosinophilic severe asthma.
• Typical NICE criteria: Frequent attacks needing oral steroids (often 3–4 or more a year), or long-term maintenance oral steroids, with the biomarker thresholds specific to each drug.

Why it matters: Biologics reduce attacks by about half, and allow many patients to stop maintenance oral steroids - which otherwise cause osteoporosis, diabetes, cataracts, weight gain and adrenal suppression.

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Occupational Asthma

• What it is: Asthma caused by something at work. It accounts for about 1 in 6 cases of adult-onset asthma.
• Common causes:
  • Isocyanates (spray painting - the commonest).
  • Flour and grain (bakers).
  • Wood dust.
  • Latex (healthcare).
  • Laboratory animals.
  • Glutaraldehyde, cleaning products.
  • Solder flux (colophony).
  • Hairdressing chemicals (persulfates).
• Clues: Adult-onset asthma, or asthma that worsens, which improves on days off and holidays. Rhinitis often comes first.
• Diagnosis:
  • Serial peak flow at least 4 times a day for 3–4 weeks, at work and away from work.
  • Specific IgE or skin prick tests.
  • Specialist challenge tests.
• Management:
  • Early removal from exposure gives the best chance of recovery.
  • Involve occupational health.
  • The patient may be entitled to Industrial Injuries Disablement Benefit.
  • Work-exacerbated asthma (pre-existing asthma made worse by work) is different - improve control and reduce exposure.

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Asthma in Special Situations

• Pregnancy:
  • Asthma may improve, stay the same or worsen.
  • Continue all usual asthma medicines, including inhaled and oral steroids - uncontrolled asthma is far more dangerous to the baby than the drugs.
  • Treat acute attacks as in non-pregnant patients.
  • Use regional rather than general anaesthesia where possible in labour.
• Aspirin-exacerbated respiratory disease (Samter's triad):
  • Asthma, nasal polyps, and reactions to aspirin and NSAIDs.
  • Avoid NSAIDs (paracetamol is usually tolerated).
  • Leukotriene antagonists may help; specialist desensitisation; dupilumab for polyps.
• Exercise-induced symptoms: Usually means poorly controlled asthma - improve maintenance treatment. ICS/formoterol can be taken before exercise.
• Eosinophilic granulomatosis with polyangiitis (EGPA):
  • Late-onset severe asthma with very high eosinophils.
  • Sinusitis.
  • Neuropathy (mononeuritis multiplex).
  • Rash; cardiac and kidney involvement.
  • About 40% are ANCA-positive.
  • Specialist immunosuppression; mepolizumab.
• Older adults: Asthma and COPD often overlap. Check inhaler technique - arthritis and cognitive problems affect device use.

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Asthma Mimics

• Inducible laryngeal obstruction (vocal cord dysfunction):
  • The vocal cords close inappropriately on breathing in, causing sudden throat tightness and noisy breathing.
  • Often in young women and people with anxiety or reflux.
  • Normal oxygen during attacks; poor response to asthma treatment.
  • Diagnosis: Laryngoscopy during symptoms.
  • Treatment: Speech and language therapy.
• Dysfunctional breathing (breathing pattern disorder): Sighing, air hunger, tingling, chest tightness, often with anxiety. Physiotherapy breathing retraining.
• COPD - smokers, fixed obstruction.
• Heart failure ("cardiac asthma").
• Central airway obstruction - tumour, tracheal stenosis, goitre, foreign body. Monophonic wheeze; abnormal flow–volume loop.
• Bronchiectasis; ABPA; obliterative bronchiolitis.
• Chronic cough from reflux, rhinitis or ACE inhibitors.

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COPD: What It Is

Mechanism: Chronic obstructive pulmonary disease is long-term, largely irreversible airflow obstruction caused by inhaled damage - mainly smoking. Two processes combine:

• Chronic bronchitis and small airways disease: Inflamed, narrowed small airways and excess mucus.
• Emphysema: Destruction of the alveolar walls, so the lungs lose their elastic recoil and air is trapped (hyperinflation). Gas exchange surface is lost.

Causes:

• Tobacco smoking - about 90% in the UK.
• Occupational dusts and fumes (coal, silica, cadmium).
• Biomass fuel smoke (worldwide).
• Alpha-1 antitrypsin deficiency.
• Poor lung growth in childhood (prematurity, early infections).
• Cannabis smoking.

Clinical pattern:

• Over 35, a smoker or ex-smoker.
• Exertional breathlessness; chronic cough; regular sputum.
• Frequent winter "bronchitis"; wheeze.
• Signs in advanced disease:
  • Hyperinflated chest, pursed-lip breathing.
  • Reduced breath sounds.
  • Cor pulmonale (raised JVP, ankle oedema).
  • Weight loss and muscle wasting.
• Clubbing is not a feature of COPD - look for cancer or bronchiectasis.

Comorbidities: Cardiovascular disease, lung cancer, osteoporosis, depression and anxiety, diabetes and frailty are all common and affect survival.

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Diagnosing and Assessing COPD

• Diagnosis (NICE NG115):
  • Symptoms plus risk factors.
  • Post-bronchodilator spirometry with an FEV1/FVC ratio below 0.7 (or below the lower limit of normal).
  • COPD is not diagnosed without spirometry.
• Severity of airflow obstruction (FEV1 % predicted): Mild 80% or more; moderate 50–79%; severe 30–49%; very severe below 30%.
• Initial tests:
  • Chest X-ray (exclude other causes, look for cancer).
  • FBC (anaemia, polycythaemia, eosinophils).
  • BMI.
  • Alpha-1 antitrypsin level if early onset (under 45), minimal smoking or family history.
  • Oxygen saturation (assess for long-term oxygen if 92% or less).
  • ECG and echo if heart disease or cor pulmonale is suspected.
  • CT if symptoms don't fit, or for surgical and valve assessment.
• Assess the impact: MRC dyspnoea scale, the COPD Assessment Test (CAT), exacerbation frequency, and comorbidities.
• Asthmatic or steroid-responsive features (NICE) - these change treatment:
  • Previous diagnosis of asthma or atopy.
  • Raised blood eosinophils.
  • Substantial variation in FEV1 over time (400 mL or more).
  • Substantial diurnal variation in peak flow (20% or more).

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Treating Stable COPD

Foundations - these do the most good:

• Stop smoking - the only measure (with oxygen in selected people) proven to slow decline and improve survival. Offer behavioural support plus drugs (NRT, varenicline where available, bupropion). E-cigarettes are a less harmful alternative to smoking.
• Vaccinations: Annual influenza, pneumococcal, COVID-19 and RSV (for eligible older adults).
• Pulmonary rehabilitation - for MRC grade 3 or more, and after an admission. A 6–8 week exercise and education programme that improves breathlessness, exercise capacity and quality of life, and reduces readmissions.
• Self-management plan and a "rescue pack" (prednisolone and antibiotics) for those who can use it safely.
• Treat comorbidities; nutrition; inhaler technique at every review.

Inhaled treatment (NICE NG115):

• Step 1: A short-acting bronchodilator (SABA or SAMA) as needed.
• Step 2 - still breathless or having exacerbations:
  • No asthmatic features: LABA plus LAMA (combination inhaler).
  • Asthmatic or steroid-responsive features: LABA plus ICS.
• Step 3 - triple therapy (LABA plus LAMA plus ICS):
  • For people still having exacerbations (or severe symptoms) on dual therapy - especially with blood eosinophils of 300 cells/µL or more.
  • ICS increases pneumonia risk. Review the benefit, particularly with low eosinophils.

Further options for frequent exacerbations (specialist):

• Azithromycin long-term prophylaxis:
  • For non-smokers with frequent exacerbations despite optimal treatment.
  • Check ECG (QT), LFTs and sputum for non-tuberculous mycobacteria first.
  • Warn about hearing loss.
• Roflumilast (PDE4 inhibitor): Severe COPD with chronic bronchitis and frequent exacerbations despite triple therapy (NICE TA461).
• Mucolytics (carbocisteine) for chronic productive cough.
• Dupilumab (biologic): NICE (TA1142) recommends it as an add-on for uncontrolled COPD with raised blood eosinophils despite triple therapy (or dual therapy if ICS is unsuitable). Uncontrolled means 1 or more severe, or 2 or more moderate, exacerbations in the past year.
• Oral theophylline: Rarely used - narrow therapeutic range, many interactions.

💡 Clinical Pearl: In COPD, the treatments that make the biggest difference are not inhalers: stopping smoking, pulmonary rehabilitation, vaccination, and oxygen for the right patients.

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Oxygen and Home NIV

Long-term oxygen therapy (LTOT) improves survival when used for at least 15 hours a day in chronic hypoxaemia.

• Assess when stable (at least 8 weeks after an exacerbation), with two arterial or capillary gases at least 3 weeks apart.
• Offer LTOT if:
  • PaO2 below 7.3 kPa, or
  • PaO2 7.3–8.0 kPa plus polycythaemia, peripheral oedema or pulmonary hypertension.
• Do not offer LTOT to people who smoke (or live with smokers) - there is a serious fire and burns risk. Assess home safety.
• Ambulatory oxygen: For people already on LTOT who are mobile. It is not routinely offered for exertional breathlessness alone.
• Palliative oxygen: Not for breathlessness without hypoxaemia - a hand-held fan and other measures work as well.

Home non-invasive ventilation:

• Consider for people with persistent hypercapnia (PaCO2 above about 7 kPa) 2–4 weeks after an admission with acute hypercapnic respiratory failure.
• It reduces readmission and death (HOT-HMV trial).
• Specialist home ventilation service.

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Advanced COPD

• Lung volume reduction (for severe emphysema with hyperinflation, after rehabilitation, in non-smokers):
  • Endobronchial valves - one-way valves that collapse a damaged lobe (needs no collateral ventilation between lobes).
  • Lung volume reduction surgery - for upper-lobe-predominant emphysema.
  • Both improve breathlessness, exercise capacity and, in selected patients, survival.
• Lung transplantation: For selected younger patients with very severe disease and no major comorbidity.
• Palliative and supportive care:
  • Breathlessness management - a hand-held fan, breathing techniques, pacing, treating anxiety.
  • Low-dose oral morphine for refractory breathlessness (specialist guidance).
  • Advance care planning, including a treatment escalation plan (NIV, intubation, CPR decisions) before the next crisis.
  • Carer support.
• Signs of poor prognosis:
  • Frequent admissions.
  • Hypercapnia; LTOT.
  • Low BMI and muscle loss.
  • MRC grade 5.
  • Cor pulmonale.
  • Needing NIV.

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Alpha-1 Antitrypsin Deficiency

• Mechanism: Alpha-1 antitrypsin is made in the liver and protects the lungs from neutrophil elastase. In deficiency (inherited - autosomal codominant, PiZZ genotype is the severe form), elastase destroys alveolar walls.
  • The abnormal protein also builds up in the liver and damages it.
• Clinical pattern:
  • Early-onset emphysema (30s–40s), especially in smokers.
  • Basal, panlobular emphysema (usual smoking emphysema is upper lobe).
  • Bronchiectasis.
  • Liver disease - neonatal jaundice, cirrhosis, hepatocellular carcinoma.
  • Rarely, panniculitis or ANCA vasculitis.
• Tests: Serum alpha-1 antitrypsin level, then phenotype or genotype.
• Management:
  • Never smoke.
  • Standard COPD care.
  • Liver monitoring.
  • Family screening.
  • Augmentation therapy (IV alpha-1 antitrypsin) slows emphysema progression, but is not routinely funded on the NHS.
  • Transplant (lung or liver) in severe cases.

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Bronchiectasis

Mechanism: Permanent widening and damage of the bronchi. Damaged airways cannot clear mucus, so bacteria grow, causing inflammation and further damage - a "vicious cycle" of infection, inflammation and airway destruction.

Causes (find one in about half):

• After infection - severe pneumonia, whooping cough, measles, TB.
• Immune deficiency - antibody deficiency (CVID), HIV.
• ABPA (central bronchiectasis in asthma).
• Cystic fibrosis and primary ciliary dyskinesia.
• Connective tissue disease - rheumatoid arthritis.
• Inflammatory bowel disease.
• Aspiration and reflux.
• Non-tuberculous mycobacteria.
• Airway obstruction (tumour, foreign body).
• Alpha-1 antitrypsin deficiency.
• Yellow nail syndrome.

Clinical pattern:

• Daily productive cough with large volumes of sputum.
• Recurrent chest infections; haemoptysis; breathlessness; fatigue.
• Signs: Coarse crackles, wheeze, sometimes clubbing.

Diagnosis: HRCT - dilated airways (bronchus wider than its artery: "signet ring"), no normal tapering, thickened walls.

Investigations for the cause (BTS 2019):

• FBC.
• Immunoglobulins (IgG, IgA, IgM).
• Total IgE and aspergillus-specific IgE and IgG (ABPA).
• Sputum culture - including mycobacteria.
• Spirometry.
• Further tests if indicated: rheumatoid factor and anti-CCP, CF testing (younger patients, upper lobe disease, infertility, malabsorption), PCD testing (lifelong symptoms, sinus and ear disease), alpha-1 antitrypsin, HIV.

Management:

• Airway clearance - daily physiotherapy techniques (active cycle of breathing, oscillating devices); exercise; pulmonary rehabilitation.
• Treat the cause - immunoglobulin replacement, ABPA treatment, reflux.
• Exacerbations:
  • Send sputum first.
  • Antibiotics for 14 days, guided by previous cultures.
• New Pseudomonas aeruginosa: Eradication treatment (e.g. oral ciprofloxacin, sometimes with nebulised colistin).
• Three or more exacerbations a year: Consider long-term macrolide (azithromycin, after excluding NTM and checking QT) or nebulised antibiotics (colistin, gentamicin) if Pseudomonas is present.
• Mucoactive treatment: Nebulised hypertonic saline or carbocisteine for thick sputum.
• Vaccinations.
• Surgery for localised disease or severe haemoptysis (bronchial artery embolisation).

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Cystic Fibrosis

Mechanism: An autosomal recessive disease caused by mutations in the CFTR gene (the commonest is F508del). CFTR is a chloride channel. When it fails, secretions in the lungs, pancreas, gut, liver and reproductive tract become thick and sticky. About 1 in 25 white Europeans carries a mutation.

Clinical pattern:

• Lungs:
  • Chronic infection - Staphylococcus aureus, H. influenzae, then Pseudomonas aeruginosa; also Burkholderia cepacia complex, NTM and aspergillus.
  • Bronchiectasis, haemoptysis, pneumothorax.
  • ABPA.
  • Respiratory failure - the main cause of death.
• Upper airways: Nasal polyps, sinusitis.
• Pancreas:
  • Pancreatic insufficiency - fatty stools, poor growth, fat-soluble vitamin deficiency.
  • CF-related diabetes - increasingly common with age.
• Gut: Meconium ileus at birth; distal intestinal obstruction syndrome in adults.
• Liver: CF-related liver disease; gallstones.
• Reproductive: Almost all men are infertile (congenital absence of the vas deferens); women have reduced fertility.
• Other: Osteoporosis; salt loss in heat.

Diagnosis:

• Newborn screening (heel-prick immunoreactive trypsinogen), then a sweat test - chloride of 60 mmol/L or more is diagnostic.
• CFTR genetic testing.
• Milder forms may present in adults with bronchiectasis, pancreatitis or male infertility.

Management (specialist CF centre):

• CFTR modulators - drugs that fix the faulty protein:
  • Elexacaftor/tezacaftor/ivacaftor (Kaftrio) for people with at least one F508del mutation (most patients; NICE TA988).
  • Large improvements in lung function, weight and exacerbations, transforming survival.
  • Monitor LFTs; many interactions (CYP3A).
• Airway clearance physiotherapy; exercise.
• Mucolytics - dornase alfa, hypertonic saline.
• Antibiotics: Eradicate early Pseudomonas; inhaled antibiotics for chronic infection; IV courses for exacerbations.
• Infection control - people with CF must not mix with each other (cross-infection with Burkholderia and Pseudomonas).
• Nutrition: High-calorie diet, pancreatic enzyme replacement with meals, vitamins A, D, E and K.
• Diabetes, bone and liver care.
• Lung transplantation for end-stage disease.

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Primary Ciliary Dyskinesia

• Mechanism: An inherited (usually autosomal recessive) defect in the structure or function of cilia - the tiny hairs that sweep mucus out of the airways.
• Clinical pattern:
  • Lifelong wet cough from birth (neonatal breathing problems).
  • Chronic rhinosinusitis and otitis media (glue ear, hearing loss).
  • Bronchiectasis (often middle and lower lobes).
  • Subfertility - immotile sperm; ectopic pregnancy in women.
• Kartagener syndrome: PCD with situs inversus (organs on the opposite side - dextrocardia) in about half of cases.
• Diagnosis (specialist centres):
  • Low nasal nitric oxide.
  • High-speed video analysis of cilia beating.
  • Electron microscopy; genetic testing.
• Management: Airway clearance, treatment of infections, ENT care - similar to bronchiectasis.

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Allergic Bronchopulmonary Aspergillosis

• Mechanism: An allergic reaction to the fungus Aspergillus fumigatus growing in the airways of people with asthma or cystic fibrosis. It is not an invasive infection. The reaction causes mucus plugging and damages the central airways.
• Clinical pattern:
  • Worsening, hard-to-control asthma.
  • Cough with brown mucus plugs.
  • Fleeting chest X-ray shadows.
  • Fever, malaise.
• Diagnosis:
  • Very high total IgE (often above 1,000 IU/mL).
  • Raised aspergillus-specific IgE (or a positive skin prick test).
  • Aspergillus-specific IgG (precipitins).
  • Blood eosinophilia.
  • CT: central (proximal) bronchiectasis, mucus plugging, "finger-in-glove" shadows.
• Management:
  • Oral prednisolone (tapering course).
  • Itraconazole (antifungal) to reduce the fungal load and steroid needs - check levels and watch for interactions (including steroid interactions causing Cushing's).
  • Biologics (omalizumab, anti-IL-5) in difficult cases.
  • Monitor with IgE levels.

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Drug Reference Table

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Spot the Diagnosis

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Exam-style Scenarios

1. A 28-year-old woman has 3 months of night cough and wheeze. She uses salbutamol most days. FeNO is 58 ppb.
Answer: Asthma confirmed (FeNO 50 ppb or more with a typical history).

• Stop SABA-only treatment.
• Start ICS/formoterol - as low-dose MART, given the daily symptoms (or AIR if symptoms were mild).
• Check technique; give a written action plan; review in 4–8 weeks.

2. A man with asthma on moderate-dose MART still has 4 attacks a year needing prednisolone. Adherence and technique are good. Eosinophils are 0.6 × 10⁹/L.
Answer: Uncontrolled asthma with raised eosinophils.

• Refer to a severe asthma service.
• He may be eligible for an anti-IL-5 biologic, after the diagnosis is confirmed and comorbidities and ABPA excluded.

3. A 67-year-old ex-smoker with COPD (FEV1 45%) is breathless despite LABA/LAMA and has had 2 exacerbations this year. Eosinophils are 0.35 × 10⁹/L.
Answer: Escalate to triple therapy (add ICS) - eosinophils of 300 cells/µL or more predict benefit.

• Check technique.
• Pulmonary rehabilitation; vaccinations; rescue pack.
• Consider dupilumab if exacerbations continue on triple therapy.

4. A woman with COPD who still smokes 10 a day has PaO2 6.9 kPa when stable.
Answer: She meets the oxygen criterion, but LTOT should not be offered while she smokes (fire risk).

• Intensive smoking cessation support.
• Reassess for LTOT once she has stopped.

5. A 45-year-old has chronic daily sputum and recurrent infections. HRCT shows bronchiectasis. Sputum grows Pseudomonas aeruginosa for the first time.
Answer: Bronchiectasis with new Pseudomonas.

• Eradication treatment (e.g. ciprofloxacin ± nebulised colistin).
• Airway clearance physiotherapy.
• Investigate the cause - immunoglobulins, ABPA screen and others.

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Key Points

• Asthma: variable, steroid-responsive airway inflammation. Confirm with FeNO or eosinophils, spirometry with reversibility, peak flow variability or challenge.
• Do not treat asthma with SABA alone (aged 12 and over). Use ICS/formoterol - AIR, then MART.
• Check technique, adherence, triggers and the diagnosis before stepping up.
• Severe asthma with raised eosinophils or FeNO: refer for biologics.
• Occupational asthma: improves away from work - serial peak flows; remove from exposure early.
• COPD: smoking-related, fixed obstruction (post-bronchodilator ratio below 0.7).
• COPD treatment: stop smoking, vaccination, pulmonary rehabilitation; then LABA/LAMA (or LABA/ICS if asthmatic features); triple if exacerbations persist.
• LTOT for at least 15 hours a day if PaO2 is below 7.3 kPa when stable - not for smokers.
• Home NIV for persistent hypercapnia after an acute hypercapnic admission.
• Bronchiectasis: airway clearance, 14-day antibiotics for exacerbations, eradicate new Pseudomonas, find the cause.
• CF: CFTR modulators (Kaftrio) have transformed outcomes.
• ABPA: asthma or CF with very high IgE, aspergillus sensitisation and central bronchiectasis - steroids plus itraconazole.

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Guidelines and Further Reading

• BTS/NICE/SIGN NG245: Asthma - diagnosis, monitoring and chronic asthma management (2024)
• National Review of Asthma Deaths (RCP, 2014)
• NICE NG115: COPD in over 16s - diagnosis and management
• NICE TA1142: Dupilumab for uncontrolled COPD with raised blood eosinophils
• GOLD: Global Strategy for the Diagnosis, Management and Prevention of COPD
• BTS Guideline for bronchiectasis in adults (2019)
• NICE NG78: Cystic fibrosis - diagnosis and management; NICE TA988: CFTR modulators
• BTS Guideline for home oxygen use in adults
• BNF - for current doses