Membership of the Royal College of Physicians (MRCP UK) Respiratory Medicine Syllabus

Respiratory Medicine syllabus — full chapter and topic list

Expand any chapter to see its topics and sub-topics. This is the whole examinable outline for Respiratory Medicine in Membership of the Royal College of Physicians (MRCP UK), not a summary of it.

1. 1

   Airways Disease

   4 topics

   • Asthma diagnosis and chronic management
     • Stepwise pharmacological therapy
     • Acute severe and life-threatening asthma
   • Chronic obstructive pulmonary disease
     • Inhaled therapy and exacerbation management
     • Long-term oxygen therapy criteria
   • Bronchiectasis and cystic fibrosis
   • Occupational and environmental lung disease
2. 2

   Respiratory Infections

   4 topics

   • Community-acquired pneumonia
     • CURB-65 severity scoring
   • Hospital-acquired and aspiration pneumonia
   • Tuberculosis
     • Latent versus active TB
     • Multidrug-resistant TB management
   • Fungal lung disease and opportunistic infection
3. 3

   Interstitial and Pleural Disease

   5 topics

   • Idiopathic pulmonary fibrosis
     • Antifibrotic therapy
   • Sarcoidosis and hypersensitivity pneumonitis
   • Connective tissue disease-associated lung disease
   • Pleural effusion
     • Light's criteria
   • Pneumothorax management
4. 4

   Pulmonary Vascular and Sleep Disorders

   4 topics

   • Pulmonary embolism
     • Wells score and diagnostic pathways
     • Anticoagulation and thrombolysis
   • Obstructive sleep apnoea and CPAP
   • Obesity hypoventilation and respiratory failure
     • Non-invasive ventilation indications
   • Arterial blood gas interpretation
5. 5

   Thoracic Oncology

   4 topics

   • Lung cancer presentation and staging
     • Non-small cell versus small cell management
   • Mesothelioma and pleural malignancy
   • Solitary pulmonary nodule evaluation
   • Paraneoplastic syndromes in lung cancer

Respiratory Medicine flashcards for Membership of the Royal College of Physicians (MRCP UK)

20 of 51 cards from the Respiratory Medicine deck — real questions with worked answers.

1. What spirometry findings confirm a diagnosis of asthma in an adult, and what bronchodilator reversibility threshold is significant?

   An obstructive pattern with $\frac{FEV_{1}}{FVC} < 0.7$, plus a positive bronchodilator reversibility of an increase in $FEV_{1} \geq 12\%$ AND $\geq 200$ mL after a short-acting bronchodilator. FeNO $\geq 40$ ppb and peak flow variability also support the diagnosis.

2. Outline the current (BTS/SIGN/NICE) stepwise pharmacological management of chronic asthma in adults.

   Step 1: low-dose ICS (or ICS-formoterol as MART). Step 2: add LABA (combined ICS/LABA). Step 3: increase to medium-dose ICS or add LTRA/LAMA. Step 4: high-dose ICS, add LAMA, refer to specialist. Step 5: oral corticosteroids and biologics (e.g. anti-IgE omalizumab, anti-IL5). Use lowest dose maintaining control; MART regimens are increasingly first-line.

3. What are the features of acute severe versus life-threatening asthma?

   Acute severe: PEF $33$–$50\%$ best/predicted, RR $\geq 25$/min, HR $\geq 110$/min, inability to complete sentences. Life-threatening: PEF $< 33\%$, $SpO_{2} < 92\%$, silent chest, cyanosis, poor respiratory effort, bradycardia/arrhythmia/hypotension, exhaustion, confusion, and a normal or raised $PaCO_{2}$ (a normal $CO_{2}$ is a red flag).

4. How is COPD severity graded by airflow obstruction using the GOLD/post-bronchodilator $FEV_{1}$?

   Requires $\frac{FEV_{1}}{FVC} < 0.7$. GOLD 1 (mild): $FEV_{1} \geq 80\%$ predicted; GOLD 2 (moderate): $50$–$79\%$; GOLD 3 (severe): $30$–$49\%$; GOLD 4 (very severe): $< 30\%$ predicted.

5. What are the criteria and survival benefit of long-term oxygen therapy (LTOT) in COPD?

   Offered when $PaO_{2} \leq 7.3$ kPa on air, or $PaO_{2}$ $7.3$–$8.0$ kPa with secondary polycythaemia, peripheral oedema or pulmonary hypertension. Must be used $\geq 15$ hours/day. It improves survival only in chronic hypoxaemia. Do not offer to current smokers (fire risk and reduced benefit).

6. Which interventions improve survival/mortality in COPD?

   Smoking cessation, LTOT in chronically hypoxaemic patients, lung volume reduction surgery in selected patients, and lung transplantation. Most pharmacotherapy (bronchodilators, ICS) improves symptoms and exacerbations but has limited proven mortality benefit; vaccination reduces morbidity.

7. What is the inheritance and underlying genetic defect in cystic fibrosis?

   Autosomal recessive mutation in the CFTR gene on chromosome 7, encoding a cAMP-regulated chloride channel. The commonest mutation is $\Delta F508$ (deletion of phenylalanine at position 508). Defective chloride/water transport produces thick secretions affecting lungs, pancreas, gut and reproductive tract.

8. What is the diagnostic test and threshold for cystic fibrosis using the sweat test?

   The pilocarpine iontophoresis sweat test: a sweat chloride concentration $> 60$ mmol/L is diagnostic; $30$–$59$ mmol/L is intermediate/borderline; $< 30$ mmol/L makes CF unlikely. Confirmed alongside genetic testing and clinical/newborn screening (raised immunoreactive trypsinogen).

9. What are the commonest organisms colonising the airways in bronchiectasis/cystic fibrosis, and how do they evolve over a CF patient's life?

   Common: Haemophilus influenzae and Pseudomonas aeruginosa. In CF, early colonisation is often Staphylococcus aureus and H. influenzae, progressing in adulthood to Pseudomonas aeruginosa (and Burkholderia cepacia complex, which carries a poor prognosis). Aspergillus and non-tuberculous mycobacteria also occur.

10. What is the imaging modality of choice and a hallmark sign for bronchiectasis?

    High-resolution CT (HRCT) is the gold standard. The hallmark is bronchial dilatation where the internal airway diameter exceeds the accompanying pulmonary artery, giving the 'signet ring sign', plus lack of airway tapering and visibility of bronchi in the peripheral lung.

11. Name the classic occupational lung diseases and their characteristic exposures and zonal distributions.

    Silicosis (silica/mining/quarrying; upper zone, eggshell hilar calcification); Coal worker's pneumoconiosis (coal dust; upper zone); Asbestosis (asbestos; lower zone fibrosis + pleural plaques); Berylliosis (beryllium; granulomatous, sarcoid-like). Silicosis and asbestos increase lung cancer/TB risk.

12. What is Caplan syndrome?

    The combination of rheumatoid arthritis with pneumoconiosis (e.g. coal worker's or silicosis), producing multiple well-defined peripheral pulmonary nodules ($0.5$–$5$ cm) on a background of dust exposure. It represents a hyperimmune response to inhaled dust in seropositive RA patients.

13. How does the CURB-65 score stratify community-acquired pneumonia and guide management?

    One point each for: Confusion (AMTS $\leq 8$), Urea $> 7$ mmol/L, Respiratory rate $\geq 30$/min, Blood pressure ($SBP < 90$ or $DBP \leq 60$ mmHg), Age $\geq 65$. Score $0$–$1$: low risk, consider home; $2$: consider hospital/short stay; $\geq 3$: high risk/severe, consider ICU assessment.

14. Match these CAP clinical clues to the likely organism: rust-coloured sputum; recent influenza; deranged LFTs/hyponatraemia/air-con; dry cough in young adult with cold agglutinins.

    Rust-coloured sputum: Streptococcus pneumoniae. Post-influenza cavitating pneumonia: Staphylococcus aureus. Hyponatraemia/deranged LFTs/air-conditioning: Legionella pneumophila. Young adult, dry cough, erythema multiforme, cold agglutinin haemolysis: Mycoplasma pneumoniae.

15. What organisms cause aspiration pneumonia and which lung regions are typically affected?

    Often polymicrobial, including anaerobes (e.g. Bacteroides, Fusobacterium, Prevotella) and oral streptococci. Affected regions depend on posture: supine aspiration favours posterior segments of upper lobes and superior segments of lower lobes; upright aspiration favours the basal segments of the lower lobes, especially the right (more vertical bronchus).

16. How is hospital-acquired pneumonia (HAP) defined and what organisms predominate?

    Pneumonia developing $\geq 48$ hours after hospital admission, not incubating at admission. Common organisms: Gram-negative bacilli (Pseudomonas aeruginosa, Klebsiella, E. coli, Enterobacter), Staphylococcus aureus including MRSA. Empirical therapy must cover these resistant organisms, unlike CAP.

17. What is the standard first-line drug regimen and duration for fully sensitive pulmonary tuberculosis?

    RIPE: Rifampicin, Isoniazid, Pyrazinamide and Ethambutol for the first 2 months (intensive phase), then Rifampicin and Isoniazid for a further 4 months (continuation phase) — total 6 months. CNS/meningeal TB is treated for 12 months.

18. List the key adverse effects of the four first-line anti-tuberculous drugs.

    Rifampicin: orange secretions, hepatotoxicity, potent enzyme inducer (reduces OCP efficacy). Isoniazid: peripheral neuropathy (give pyridoxine/B6), hepatotoxicity. Pyrazinamide: hepatotoxicity, hyperuricaemia/gout. Ethambutol: dose-dependent optic neuritis (check visual acuity/colour vision).

19. How is latent TB infection detected and managed?

    Detected by tuberculin skin test (Mantoux) or interferon-gamma release assay (IGRA) with a normal CXR and no active disease. Treatment options: isoniazid (+ pyridoxine) for 6 months, or rifampicin plus isoniazid for 3 months. The aim is to prevent reactivation, especially before immunosuppression/biologics.

20. What are the features and treatment of allergic bronchopulmonary aspergillosis (ABPA)?

    A hypersensitivity reaction to Aspergillus fumigatus, often in asthmatics/CF. Features: wheeze, recurrent eosinophilia, fleeting pulmonary infiltrates, central bronchiectasis, raised total IgE and Aspergillus-specific IgE/IgG, positive skin prick. Treatment: oral corticosteroids; itraconazole as a steroid-sparing antifungal.

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