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Setting: an MBBS final-professional viva. The examiner escalates from definitions to mechanism to management decisions to the corners. Model answers in italics.
[1]Q1 — Definition and the pathognomonic sign (2 min)
Examiner: Define bronchiectasis in one sentence and tell me the single most reliable investigation.
[1]Candidate: Bronchiectasis is the permanent, abnormal dilation of one or more bronchi caused by destruction of the elastic and muscular wall components, sustained by a self-perpetuating cycle of impaired clearance, infection and inflammation. The most reliable investigation is high-resolution CT; the signet-ring sign — a bronchus whose internal diameter exceeds the accompanying pulmonary artery — is the radiological hallmark.[1]
Examiner: Traction bronchiectasis — same disease?
[1]Candidate: No. Traction bronchiectasis is distortion of airways pulled open by peribronchial fibrosis in interstitial lung disease — a completely different mechanism. It is managed by treating the underlying ILD, not with airway clearance antibiotics.[1]
Q2 — Cole's vicious circle and the central mediator (2 min)
Examiner: Walk me through Cole's vicious circle. Name the central mediator and why it matters.
[1]Candidate: The cycle runs in four steps: an initial insult impairs mucociliary clearance; retained secretions become infected; neutrophils release elastase, IL-8, TNF-alpha, MMP-8/9; proteases destroy elastin and muscularis, the wall dilates, and the dilated bronchus clears secretions even more poorly. Neutrophil elastase is the central mediator — it degrades elastin, drives goblet-cell hyperplasia and mucin (MUC5AC) secretion, slows ciliary beat, and inactivates complement and immunoglobulins. Sputum elastase activity tracks exacerbation frequency and FEV1 decline.[6]
Q3 — Microbiology and why Pseudomonas matters (3 min)
Examiner: What is the commonest organism in non-CF bronchiectasis, and which organism changes the prognosis?
[1]Candidate: Haemophilus influenzae is the commonest overall, especially early in the disease. Pseudomonas aeruginosa is the severity organism: it colonises more severe disease, accelerates FEV1 decline, doubles exacerbation frequency, and worsens quality of life and mortality. It forms a biofilm, adopts a mucoid alginate phenotype, and secretes elastases that intensify neutrophil-driven damage. Its presence shifts long-term management toward long-term inhaled antibiotics.[2]
Examiner: You find chronic Pseudomonas with 4 exacerbations a year despite physiotherapy. What do you add?
[1]Candidate: Two things. First, a long-term inhaled antibiotic — nebulised colistimethate or inhaled tobramycin — to suppress bacterial load and reduce exacerbations. Second, a long-term macrolide — azithromycin 250 mg three times weekly — whose benefit is anti-inflammatory and anti-quorum-sensing, not antimicrobial. Before starting I check QTc and LFTs and exclude NTM co-infection, because macrolide monotherapy drives macrolide resistance in NTM.[1]
Q4 — The negative trial and the four pillars (2 min)
Examiner: Name one drug that works in cystic fibrosis but is harmful or useless in non-CF bronchiectasis, and why.
[1]Candidate: Recombinant human DNase (dornase alfa). It degrades extracellular DNA from dead neutrophils, reducing sputum viscosity in CF. In non-CF bronchiectasis the randomised O'Donnell trial showed no clinical benefit and a concerning signal toward increased exacerbations and greater FEV1 decline — it must not be used outside CF.[14]
Examiner: Give me the four pillars of management in one breath.
[1]Candidate: (1) Treat the underlying cause; (2) airway-clearance physiotherapy with mucoactive adjuvants; (3) infection control — acute 14-day antibiotics guided by sputum, long-term macrolide for frequent exacerbators, inhaled antibiotic for chronic Pseudomonas; (4) prevention — vaccination, smoking cessation, pulmonary rehabilitation.[1]
Q5 — Massive haemoptysis (1 min)
Examiner: Your patient coughs 300 mL of bright red blood. Talk me through your first five actions.
[1]Candidate: (1) Protect the airway and the uninvolved lung — place the patient bleeding side down (good lung up); if airway threatened, endobronchial intubation or a dual-lumen tube. (2) High-flow oxygen, large-bore IV access, bloods including group-and-save and coagulation. (3) Resuscitate; correct coagulopathy and any thrombocytopenia. (4) Localise the bleeding — bronchoscopy once stable. (5) Arrange urgent bronchial artery embolisation as first-line definitive therapy; surgical resection is the last resort. I should remember the patient dies of asphyxiation, not exsanguination.[1]
Q6 — ABPA vs NTM (1 min)
Examiner: A 55-year-old woman with asthma has central upper-lobe bronchiectasis, eosinophilia and total IgE 1800 IU/mL. How does her management differ from a 70-year-old thin woman with right middle-lobe and lingula bronchiectasis growing Mycobacterium avium complex?
[1]Candidate: The first is ABPA — asthma, eosinophilia, very high IgE, Aspergillus sensitisation and central/proximal upper-lobe bronchiectasis. Treat with prednisolone 0.5 mg/kg/day tapered, plus itraconazole or voriconazole for steroid-sparing; monitor IgE and eosinophils. The second is the Lady Windermere phenotype of NTM pulmonary disease — elderly, thin, right middle-lobe/lingula disease, minimal cough. NTM requires multidrug therapy guided by species and susceptibility; never give macrolide monotherapy because it drives resistance. Both need airway clearance, but antibiotics differ entirely.[1]
References4ShowHide
- [1]British Thoracic Society Guideline for bronchiectasis in adults. 2019.PMID 30545985
- [2]European Respiratory Society guidelines for the management of adult bronchiectasis. 2017.PMID 28889110
- [6]Inflammation: a two-edged sword — the model of bronchiectasis. 1986.PMID 3533593
- [14]Treatment of idiopathic bronchiectasis with aerosolized recombinant human DNase I. 1998.PMID 9596315