IM28.1-26 | Obstructive Airway Diseases — Practice Quiz

Correct. The GOLD (Global Initiative for Chronic Obstructive Lung Disease) diagnostic criterion for COPD is a post-bronchodilator FEV1/FVC ratio below 0.70 (the fixed ratio). This confirms persistent, largely irreversible airflow limitation. The absolute FEV1 then grades severity: GOLD 1 (FEV1 ≥80% predicted), GOLD 2 (50–79%), GOLD 3 (30–49%), GOLD 4 (<30%).

COPD diagnosis by GOLD criteria requires a post-bronchodilator FEV1/FVC < 0.70. Absolute FEV1 alone, FVC, smoking history, or percentage predicted values are not the diagnostic criterion — the ratio is. In this patient FEV1/FVC = 1.8/3.2 = 0.56, confirming fixed airflow obstruction.

Correct. GINA defines significant bronchodilator reversibility as FEV1 increasing by ≥12% AND ≥200 mL from baseline after a short-acting beta2-agonist. This patient shows a 380 mL (18%) increase — both criteria met. This pattern of variable, reversible airflow limitation is a hallmark of asthma. Unlike COPD, airflow limitation in asthma is not fixed; it responds substantially to bronchodilators.

Asthma is characterised by variable, reversible airflow obstruction. GINA's reversibility criterion is FEV1 increase ≥12% AND ≥200 mL after short-acting beta2-agonist. This patient's 380 mL (18%) increase meets both thresholds, confirming reversibility — the key distinction from the fixed obstruction of COPD.

Correct. Respiratory tract infections — viral (most commonly rhinovirus, influenza, parainfluenza) and bacterial (Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis) — account for approximately 70-80% of COPD exacerbations. Air pollution is the second most common environmental trigger. Features of infection (purulent sputum, fever, recent URTI) are hallmarks of infective exacerbations as in this case.

Respiratory tract infections (viral and bacterial) are by far the most common triggers for acute COPD exacerbations, accounting for ~70-80% of cases. Air pollution, non-compliance, and cardiac events (PE, LVF) are important secondary causes but far less frequent than infection. Purulent sputum and fever in this case point strongly to an infective trigger.

Correct. Acute severe asthma management (GINA/BTS) requires simultaneous: (1) controlled supplemental oxygen to target SpO2 94-98%; (2) repeated/continuous nebulised SABA (salbutamol); (3) nebulised ipratropium (added in acute severe/life-threatening asthma for additional bronchodilation); (4) systemic corticosteroids (IV hydrocortisone 100 mg 6-hourly or oral prednisolone 40-50 mg) — steroids should NOT be deferred. IV magnesium sulfate is added if no improvement after 1 hour.

Acute severe asthma requires immediate combination therapy: controlled oxygen (SpO2 target 94-98%), nebulised salbutamol + ipratropium, AND systemic corticosteroids (not deferred). High-flow uncontrolled oxygen is not appropriate — target SpO2 94-98%, not 100%. Steroids are started from the outset, not waited on.

Correct. GOLD 2023 recommends long-acting bronchodilators (LABA and/or LAMA) as the cornerstone of stable COPD maintenance therapy. With FEV1 55% predicted (GOLD 2) and significant symptoms plus 2 exacerbations, this patient is GOLD Group E and should receive LABA+LAMA combination. ICS is added (as triple therapy ICS/LABA/LAMA) if eosinophil count ≥300 cells/microL or continued exacerbations on LABA+LAMA. Unlike asthma, ICS is NOT first-line alone in COPD. Systemic steroids are not used long-term (side effects). Theophylline is a third-line add-on.

GOLD guidelines recommend long-acting bronchodilators (LABA and/or LAMA) as the foundation of stable COPD treatment. ICS is not first-line in COPD — it is added only in selected patients with high eosinophils or persistent exacerbations despite LABA+LAMA. Systemic steroids are not for stable disease management.

Correct. AAT deficiency follows autosomal codominant inheritance — both alleles are expressed and contribute to the AAT level. The alleles are designated by the Pi (protease inhibitor) system: PiMM is normal; PiZZ homozygotes have AAT levels ~15% of normal and the highest risk of emphysema and liver disease; PiMZ heterozygotes have intermediate levels (~60%) with mild-moderate increased risk. Cigarette smoking dramatically accelerates emphysema in PiZZ individuals by increasing neutrophil elastase load. Emphysema in a young non-smoker should always prompt AAT testing.

AAT deficiency is autosomal codominant — both alleles contribute to AAT serum level. PiZZ homozygotes (AAT ~15% of normal) have the highest risk of early emphysema, even without smoking. Young non-smokers with emphysema should be tested for AAT deficiency (serum AAT + Pi typing).

Correct. The 5As of smoking cessation counselling: Ask (screen every patient for tobacco use), Advise (provide a brief, clear, personalised recommendation to quit), Assess (assess readiness and motivation to change), Assist (provide quitting methods: NRT, varenicline, bupropion, behavioural support), Arrange (arrange follow-up and referral). The 'Advise' step is specifically the non-judgmental, direct clinical recommendation.

In the 5As framework: Ask = screen for use; Advise = give a clear, personalised recommendation to stop; Assess = gauge readiness; Assist = offer NRT/pharmacotherapy/counselling; Arrange = schedule follow-up. Advise is the step where the clinician directly tells the patient to stop, with a personalised reason.

Correct. PEFR zones (% of personal best): Green = ≥80% (good control, continue usual treatment); Yellow = 50-80% (caution zone — increase SABA, may need systemic steroids, seek medical review); Red = <50% (danger zone — immediate medical attention, emergency bronchodilators, likely systemic steroids, consider hospitalisation). 290/480 = 60.4% — this is in the Yellow zone. Action: use reliever inhaler, re-check PEFR, contact physician for guidance on stepping up treatment.

PEFR zones: Green ≥80%; Yellow 50-80%; Red <50% of personal best. 290/480 = 60% — Yellow zone. Yellow means caution: the patient should increase reliever use and seek medical review for possible treatment step-up. Red (<50%) requires emergency treatment.

Correct. LTOT criteria (GOLD/BTS): indicated when resting PaO2 ≤7.3 kPa (55 mmHg) on air, or ≤8 kPa (60 mmHg) with cor pulmonale/polycythaemia/nocturnal desaturation. This patient (PaO2 7.0 kPa, SpO2 88%) meets criteria. LTOT must be prescribed for ≥15 hours/day (including sleep) at a flow rate to achieve PaO2 ≥8 kPa (SpO2 ≥90%). The flow rate is titrated carefully (usually 1-2 L/min) to avoid suppressing hypoxic drive in CO2-retaining patients. High-flow uncontrolled oxygen is dangerous — target SpO2 88-92% in COPD with hypercapnia during acute illness.

LTOT is prescribed when resting PaO2 ≤7.3 kPa (≤55 mmHg). The prescription: ≥15 hours/day at the lowest flow rate that achieves PaO2 ≥8 kPa (SpO2 ≥90%). This is titrated supplemental oxygen — not high-flow, and not PRN. In this CO2-retaining patient, high-flow oxygen can suppress hypoxic drive and worsen hypercapnia.

Correct. Sensitiser-induced occupational asthma involves two phases: (1) sensitisation — on initial exposure, the immune system develops specific IgE (or T-cell) responses to the occupational antigen (e.g., isocyanates, flour, latex, wood dust, laboratory animals); (2) disease expression — on subsequent exposures, even at low concentrations, re-exposure triggers an immediate and/or late-phase allergic airway response. The characteristic feature is a latency period (months to years) before symptoms appear. Irritant-induced asthma (RADS) occurs acutely from a single high-level toxic exposure without a sensitisation phase.

Sensitiser-induced occupational asthma requires a latency period (the sensitisation phase) before symptoms appear. Unlike irritant-induced (RADS), it involves immune sensitisation (usually IgE-mediated) to a specific occupational antigen. Subsequent low-level exposures then trigger allergic airway inflammation. The work-related pattern with improvement on holidays is the clinical hallmark.