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COPD & alpha-1 antitrypsin flashcards

25 high-yield MRCP Part 1 cards from the Intellect Medicos Respiratory Medicine course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.

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  1. What spirometry finding confirms COPD?

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    Post-bronchodilator FEV1/FVC < 0.7.

    Why? Persistent (not fully reversible) airflow obstruction after a bronchodilator is the defining feature of COPD.

  2. In stable COPD WITHOUT asthmatic features, what inhaler is added if the patient is still limited despite a short-acting bronchodilator (NICE NG115)?

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    A LAMA + LABA combination.

    Why? Dual long-acting bronchodilation improves symptoms and exacerbations. If there ARE asthmatic/steroid-responsive features, LABA + ICS is used instead.

  3. What is the mechanism of action of tiotropium?

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    Long-acting muscarinic (M3) receptor antagonist (LAMA).

    Why? Blocking acetylcholine at airway M3 receptors relaxes bronchial smooth muscle.

  4. Which infection risk is increased by inhaled corticosteroids in COPD?

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    Pneumonia.

    Why? ICS should be used when there are asthmatic features or frequent exacerbations, and patients should be warned about pneumonia risk.

  5. Which two tests should be done before starting long-term azithromycin prophylaxis in COPD (course notes)?

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    An ECG (to exclude QT prolongation) and liver function tests.

    Why? Macrolides prolong the QT interval and can be hepatotoxic.

  6. What is the mechanism of action of roflumilast?

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    Phosphodiesterase-4 (PDE-4) inhibitor.

    Why? It raises cAMP in inflammatory cells, reducing airway inflammation and exacerbations.

  7. When is roflumilast used in COPD (course notes / NICE)?

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    Severe COPD with chronic bronchitis (post-bronchodilator FEV1 < 50% predicted) AND 2 or more exacerbations in the last 12 months despite triple inhaled therapy; started by a specialist.

    Why? It is an oral add-on for severe COPD with frequent exacerbations.

  8. What oral steroid regimen is used for an acute exacerbation of COPD?

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    Prednisolone 30 mg once daily for 5 days.

    Why? A short course speeds recovery and reduces treatment failure. Use IV hydrocortisone if the patient cannot take oral medicine.

  9. In an acute COPD exacerbation, what oxygen target is used BEFORE the ABG is available?

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    SpO2 88–92% (e.g. 28% Venturi mask at 4 L/min).

    Why? Many COPD patients retain CO2, and high-flow oxygen can worsen hypercapnia and acidosis.

  10. What is the most common bacterial cause of an infective COPD exacerbation?

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    Haemophilus influenzae.

    Why? Other common organisms are Streptococcus pneumoniae and Moraxella catarrhalis.

  11. What are the first-choice oral antibiotics for an infective exacerbation of COPD (NICE NG114)?

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    Amoxicillin, doxycycline or clarithromycin.

    Why? Antibiotics are given when sputum is purulent or there are signs of pneumonia; choice depends on allergy and previous cultures.

  12. Why does co-prescribing clarithromycin or ciprofloxacin with theophylline need caution?

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    They inhibit the hepatic cytochrome P450 metabolism of theophylline, raising levels and the risk of toxicity.

    Why? Theophylline has a narrow therapeutic index; levels should be monitored and the dose adjusted.

  13. Name three features of theophylline toxicity.

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    Any three of: nausea and vomiting, tachyarrhythmias, seizures, hypokalaemia, agitation.

    Why? Theophylline is a phosphodiesterase inhibitor and adenosine antagonist with a narrow therapeutic index.

  14. What ABG criteria indicate NIV in an acute exacerbation of COPD (BTS)?

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    Respiratory acidosis (pH < 7.35 with PaCO2 > 6.5 kPa) persisting despite optimal medical therapy.

    Why? NIV (bilevel) supports ventilation and clears CO2; BTS quality standards aim to start it within 60 minutes of the blood gas that prompted the decision.

  15. What PaO2 criteria make a COPD patient eligible for long-term oxygen therapy (LTOT)?

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    PaO2 < 7.3 kPa when stable, or 7.3–8 kPa with secondary polycythaemia, peripheral oedema or pulmonary hypertension.

    Why? LTOT for at least 15 hours a day improves survival in chronic hypoxaemia.

  16. Which COPD patients should NOT be offered LTOT?

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    Those who continue to smoke.

    Why? Smoking near oxygen is a serious fire and burns risk.

  17. LTOT in COPD should be used for at least ______ hours a day.

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    15

    Why? Survival benefit in the trials was seen only with prolonged daily use.

  18. Which pattern of emphysema favours lung volume reduction surgery?

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    Upper-lobe predominant emphysema.

    Why? Removing the worst, hyperinflated upper lobes lets the healthier lung expand. NICE refers for lung volume reduction assessment if FEV1 < 50%, non-smoker, 6-minute walk ≥ 140 m, with hyperinflation and emphysema on CT.

  19. Alpha-1 antitrypsin deficiency is caused by mutations in the ______ gene on chromosome 14.

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    SERPINA1

    Why? A1AT is a serine protease inhibitor made by the liver that protects the alveoli from neutrophil elastase.

  20. Alpha-1 antitrypsin deficiency is caused by mutations in the SERPINA1 gene on chromosome ______.

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    14

    Why? A1AT is a serine protease inhibitor made by the liver that protects the alveoli from neutrophil elastase.

  21. What is the inheritance pattern of alpha-1 antitrypsin deficiency?

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    Autosomal co-dominant.

    Why? Both alleles are expressed, so heterozygotes (e.g. PiMZ) have intermediate levels.

  22. Which A1AT genotype is usually responsible for clinical disease?

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    PiZZ (about 10–15% of normal A1AT levels).

    Why? PiMM is normal; PiMZ and PiSS give about 60%, PiSZ about 40%.

  23. What type of emphysema does alpha-1 antitrypsin deficiency cause?

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    Early-onset panacinar emphysema, mainly in the lower lobes.

    Why? Smoking-related emphysema is typically centriacinar and upper-lobe predominant.

  24. Does NICE recommend IV alpha-1 antitrypsin replacement therapy for A1AT deficiency?

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    No — NICE advises not to offer A1AT replacement therapy.

    Why? Management is smoking cessation, standard COPD treatment, vaccination, screening relatives and, for end-stage disease, transplantation.

  25. Which biologic did NICE recommend in 2026 as an add-on for uncontrolled COPD with a blood eosinophil count of at least 0.3 × 10⁹/L, and what is its target?

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    Dupilumab: a monoclonal antibody against the IL-4 receptor alpha subunit (blocks IL-4 and IL-13 signalling).

    Why? NICE TA1142 (March 2026): add-on to triple therapy (or LAMA + LABA if ICS unsuitable) when there has been ≥ 1 severe or ≥ 2 moderate exacerbations in 12 months. Response is reviewed at 12 months.

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