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

Correct. GOLD 2023 simplified ABCD to ABE: Group A (low symptoms, low exacerbation risk), Group B (high symptoms, low exacerbation risk), Group E (high exacerbation risk — ≥2 moderate exacerbations or ≥1 hospitalisation in past year). This patient: FEV1 38% (GOLD 3), 3 hospitalisations = Group E (exacerbation-driven). GOLD E initial therapy: LABA + LAMA. If blood eosinophils ≥300 cells/microL, ICS can be added upfront (triple therapy). ICS is not universally contraindicated — it reduces exacerbations in appropriate patients; theophylline is a third-line add-on, not step-up.

GOLD 2023 groups ABE: Group E = ≥2 moderate exacerbations or ≥1 hospitalisation. With 3 hospitalisations and FEV1 38% predicted, this is GOLD E. Recommended treatment is LABA + LAMA; triple therapy (ICS/LABA/LAMA) is preferred when blood eosinophils ≥300 cells/microL. Theophylline is third-line. ICS is not contraindicated in COPD — it is guideline-recommended in selected patients.

Correct. The SMART study and subsequent trials established that LABA monotherapy (without ICS) in asthma significantly increases the risk of serious and fatal asthma exacerbations. The mechanism: LABAs produce bronchodilation and symptom relief, masking underlying eosinophilic airway inflammation (T2 pathway); the patient feels better but airway inflammation continues unchecked, increasing risk of sudden fatal attacks. All asthma guidelines (GINA, NHP) mandate that LABAs in asthma must always be prescribed in fixed-dose combination with ICS — never as sole asthma controller therapy.

LABA monotherapy in asthma is dangerous because it relieves bronchoconstriction without suppressing underlying eosinophilic inflammation, masking worsening disease and increasing fatal asthma risk (SMART trial). GINA guidelines strictly require that any LABA prescribed for asthma must be combined with ICS — this is a non-negotiable safety requirement, not a cost or severity restriction.

Correct. Non-invasive ventilation (NIV — BiPAP) is the treatment of choice for acute hypercapnic respiratory failure (type 2) in COPD when pH 7.25-7.35 (acidaemia) and PaCO2 is elevated, and the patient has not responded adequately to initial medical treatment within 1 hour. pH 7.28 is below the 7.35 threshold, indicating significant respiratory acidosis. NIV reduces mortality, reduces need for intubation, and reduces length of stay compared to medical therapy alone. Increasing FiO2 would worsen hypercapnia. Immediate intubation is indicated if NIV fails or is contraindicated (patient unable to protect airway, severe agitation, haemodynamic instability).

Acute hypercapnic respiratory failure in COPD with pH 7.25-7.35 that does not respond to medical treatment within 1 hour is a clear indication for NIV (BiPAP). pH 7.28 confirms respiratory acidosis. Increasing FiO2 would worsen CO2 retention. Immediate intubation is not the first escalation step — NIV is tried first unless there is a contraindication. Further delay is inappropriate given the acidaemia.

Correct. A near-silent chest in asthma is a life-threatening sign — it indicates such severe bronchoconstriction that air movement is barely sufficient to generate wheeze. This patient has multiple life-threatening features (SpO2 89%, unable to speak, RR 32, PEFR unmeasurable, silent chest). Life-threatening asthma requires: (1) high-flow controlled oxygen (target SpO2 94-98%); (2) continuous nebulised salbutamol; (3) IV magnesium sulfate 1.2-2 g IV over 20 min (bronchosmolytics); (4) IV hydrocortisone. Anaesthetic referral for intubation should be made simultaneously if no rapid response. Absence of wheeze in asthma is a dangerous sign, not reassurance.

A silent chest in severe asthma is ominous — it means airflow is so restricted that there is insufficient velocity to produce wheeze. This is a LIFE-THREATENING feature. Immediate treatment: controlled oxygen, continuous nebulised salbutamol + ipratropium, IV hydrocortisone, IV magnesium sulfate 1.2-2 g over 20 minutes, and prepare for possible intubation. Never interpret a silent chest as improvement.

Correct. In moderate COPD (GOLD 2), patients can maintain near-normal PaCO2 by increasing respiratory rate and effort — compensatory hyperventilation driven by hypoxic and hypercapnic stimuli. CO2 retention (hypercapnia) typically appears in severe to very severe disease (GOLD 3-4, FEV1 < 50%) when the respiratory muscles fatigue and cannot sustain the increased work of breathing, or when respiratory drive becomes impaired. This is the distinction between 'pink puffers' (emphysema-predominant, hyperventilate, maintain PaCO2 at cost of increased work of breathing) and 'blue bloaters' (bronchitis-predominant, tolerate higher PaCO2).

Normal PaCO2 in moderate COPD reflects maintained compensatory hyperventilation — the patient works harder to blow off CO2 and maintains normocapnia. CO2 retention emerges when this compensation fails in severe disease (GOLD 3-4) due to muscle fatigue. Normal PaCO2 does NOT mean obstruction is mild — in this patient FEV1/FVC 0.55 confirms moderate obstruction. It means compensation is still effective.

Correct. A spacer (valved holding chamber) with pMDI: (1) removes the need for precise breath-actuation coordination — the drug aerosol is held in the chamber; (2) slows aerosol velocity, reducing oropharyngeal impaction; (3) increases fine particle fraction delivered to the lungs; (4) significantly reduces oropharyngeal candidiasis and reduces systemic steroid absorption (important for high-dose ICS). DPIs (Turbuhaler, Accuhaler) do NOT use spacers — they require a strong, rapid, deep inhalation; using a spacer with a DPI prevents drug delivery. pMDI drug is actuated on inhalation, not exhalation.

Spacers are used with pMDIs, NOT with DPIs. A spacer improves lung deposition, removes coordination errors, and reduces oropharyngeal candidiasis and systemic steroid absorption with ICS. DPIs (Turbuhaler, Accuhaler) require a fast, deep inspiratory effort without a spacer — the opposite technique from pMDI. pMDI actuation occurs on inhalation.

Correct. GOLD guidelines recommend: (1) annual influenza vaccination for all COPD patients regardless of severity — reduces frequency and severity of COPD exacerbations and associated hospitalisations; (2) pneumococcal vaccination (PCV13 followed by PPSV23) for all patients ≥65 or with significant COPD — reduces incidence of community-acquired pneumonia. The COVID-19 vaccine is now also recommended. Vaccination is a low-cost, high-impact intervention for COPD patients at all severity stages. ICS use does not contraindicate inactivated vaccines.

Influenza vaccination is recommended for ALL patients with COPD at every severity level — it reduces exacerbation frequency and severity. Pneumococcal vaccination is also recommended to prevent pneumococcal pneumonia. These are core GOLD-endorsed preventive interventions. ICS does not contraindicate inactivated vaccines.

Correct. Mepolizumab is a humanised anti-IL-5 monoclonal antibody. IL-5 is the primary cytokine responsible for eosinophil maturation, activation, and survival; blocking IL-5 dramatically reduces peripheral and airway eosinophil counts. It is indicated for severe eosinophilic asthma with blood eosinophils ≥300 cells/microL. Other biologicals: Omalizumab = anti-IgE (for allergic asthma with elevated total IgE); Benralizumab = anti-IL-5 receptor alpha; Dupilumab = anti-IL-4Rα (blocks IL-4 and IL-13, useful in T2-high asthma including eosinophilic and allergic); Tezepelumab = anti-TSLP (broadest T2 coverage).

Mepolizumab targets IL-5 (anti-IL-5), reducing eosinophil production and survival. Omalizumab targets IgE (for allergic high-IgE asthma). Dupilumab blocks the IL-4Rα subunit shared by IL-4 and IL-13 receptors. Tiotropium is a long-acting muscarinic antagonist used for bronchodilation in COPD and add-on in asthma — not a biological.

Correct. Occupational sensitisation to isocyanates (a high-molecular-weight sensitiser) can occur at any point during ongoing exposure — sensitisation is not limited to the first year. The latency period between first exposure and symptom onset is typically 6 months to 4 years but can be longer. Crucially, once sensitised, even very low levels of subsequent exposure trigger airway reactions. The appropriate clinical response is: (1) advise continued exposure without protection is unsafe; (2) recommend respiratory surveillance (serial spirometry + bronchoprovocation where indicated); (3) provide information about personal protective equipment; (4) notify occupational health. Stopping work immediately is not automatically warranted unless symptoms are present.

Five symptom-free years do not protect against future sensitisation to isocyanates. Occupational sensitisation can develop at any point during ongoing exposure, with a latency period of months to years. Surveillance (serial spirometry + symptom monitoring) is required throughout exposure. Once sensitised, the patient must avoid further isocyanate exposure — even minute quantities.

Correct. GINA and major obstetric guidelines consistently advise that ICS should be continued in pregnancy at the minimum effective dose. The key principle: maternal hypoxia from uncontrolled asthma (SpO2 < 95%) poses greater fetal risk (intrauterine growth restriction, premature birth, perinatal mortality) than inhaled corticosteroids at low-moderate doses. Budesonide has the most safety data in pregnancy (FDA Category B). SABAs (salbutamol) are also considered safe for acute relief. Theophylline has a narrow therapeutic index and requires serum monitoring in pregnancy — it is not first-line. LTRAs have limited data; stopping ICS and substituting an LTRA alone would result in undertreatment.

Low-dose ICS should be continued in pregnancy — the risk from uncontrolled asthma (maternal and fetal hypoxia, prematurity) exceeds the risk from inhaled corticosteroids. Budesonide has the best pregnancy safety evidence. Stopping ICS, switching to theophylline (narrow window, monitoring needed), or using LTRA alone would leave the patient undertreated — posing real fetal risk.

Correct. The hierarchy of occupational health controls for preventing occupational lung disease is: (1) Elimination (remove the hazard — not always feasible); (2) Substitution (replace with less hazardous material); (3) Engineering controls (enclosure, local exhaust ventilation, dust suppression at source) — most effective; (4) Administrative controls (work rotation, limiting exposure time); (5) Personal protective equipment (RPE, masks) — last resort as least reliable. Engineering controls targeting the source of dust generation are the most effective primary prevention strategy for byssinosis and occupational OAD. Vaccination and prophylactic bronchodilators do not address the causative exposure.

The hierarchy of occupational control measures prioritises engineering controls (local exhaust ventilation, dust suppression at source) over administrative measures (rotation) and personal protective equipment (which depends on worker compliance). Vaccination and prophylactic inhalers are not primary prevention for occupational exposure. Engineering controls — reducing dust at source — are the most effective and reliable intervention.