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

Contrast aspergilloma and invasive aspergillosis.

Aspergilloma: a fungal ball colonising a pre-existing cavity (e.g. old TB), causing haemoptysis; CXR shows a rounded opacity with an air crescent (Monod sign); treat with surgery/embolisation if bleeding. Invasive aspergillosis: tissue-invasive infection in the immunocompromised/neutropenic, with the CT 'halo sign'; treat with voriconazole, high mortality.

What is the typical presentation and treatment of Pneumocystis jirovecii pneumonia (PCP)?

Occurs in the immunocompromised (HIV with $CD4 < 200$ cells/$\mu$L). Features: dry cough, progressive exertional dyspnoea, desaturation on exertion, often a relatively clear CXR or bilateral perihilar infiltrates, raised LDH. Treatment: high-dose co-trimoxazole; add corticosteroids if $PaO_{2} < 9.3$ kPa (hypoxia).

What are the characteristic clinical, HRCT and histological features of idiopathic pulmonary fibrosis (IPF)?

Clinical: progressive exertional dyspnoea, dry cough, bibasal fine 'velcro' inspiratory crackles, finger clubbing, age $> 60$. HRCT/histology: usual interstitial pneumonia (UIP) pattern — subpleural, basal predominant reticulation, honeycombing and traction bronchiectasis with minimal ground glass. Spirometry shows a restrictive pattern with reduced TLCO.

Which antifibrotic drugs slow disease progression in IPF and how?

Pirfenidone (an antifibrotic/anti-inflammatory agent) and nintedanib (an intracellular tyrosine kinase inhibitor). Both slow the rate of decline in $FVC$. Corticosteroids/immunosuppression are NOT beneficial in IPF (unlike in other interstitial lung diseases) and the triple therapy of prednisolone/azathioprine/NAC increased mortality.

What restrictive lung function pattern is seen in interstitial lung disease, including the $FEV_{1}/FVC$ ratio and gas transfer?

A restrictive pattern: reduced $FEV_{1}$ and $FVC$ with a preserved or increased $\frac{FEV_{1}}{FVC} \geq 0.7$ (often $> 0.8$), reduced total lung capacity, and a reduced transfer factor ($TLCO$/$DLCO$) reflecting impaired alveolar gas exchange.

What are the typical features of sarcoidosis and the radiographic (Scadding) staging?

A multisystem non-caseating granulomatous disease, often young adults with bilateral hilar lymphadenopathy, erythema nodosum, raised ACE and hypercalcaemia. Scadding stages: 0 normal; I bilateral hilar lymphadenopathy (BHL); II BHL + pulmonary infiltrates; III infiltrates without BHL; IV pulmonary fibrosis.

What is Lofgren syndrome and what is its prognosis?

An acute presentation of sarcoidosis comprising the triad of bilateral hilar lymphadenopathy, erythema nodosum and arthralgia/arthritis, often with fever. It carries an excellent prognosis with spontaneous resolution in the majority and usually requires only symptomatic treatment (NSAIDs).

Contrast acute and chronic hypersensitivity pneumonitis (extrinsic allergic alveolitis) including zonal predominance.

A type III/IV hypersensitivity to inhaled organic antigens (e.g. bird fancier's, farmer's lung). Acute: flu-like illness with cough/dyspnoea 4–8 h post-exposure, resolving on removal. Chronic: progressive fibrosis. Characteristically upper/mid-zone predominant (contrasting with IPF's lower-zone). Management: antigen avoidance and corticosteroids.

Which connective tissue diseases are associated with interstitial lung disease, and which ILD pattern predominates?

Rheumatoid arthritis, systemic sclerosis, polymyositis/dermatomyositis (anti-Jo-1/antisynthetase), Sjogren's and SLE. The commonest pattern is non-specific interstitial pneumonia (NSIP, ground glass, more steroid-responsive), except RA which often causes UIP. Systemic sclerosis ILD may be treated with mycophenolate or cyclophosphamide.

State Light's criteria for distinguishing an exudative from a transudative pleural effusion.

An effusion is exudative if ANY one is met: pleural/serum protein ratio $> 0.5$; pleural/serum LDH ratio $> 0.6$; pleural LDH $> \frac{2}{3}$ of the upper limit of normal serum LDH. If none are met, it is a transudate.

Give common causes of transudative versus exudative pleural effusions.

Transudates (protein $< 25$ g/L): heart failure, liver cirrhosis/hypoalbuminaemia, nephrotic syndrome, hypothyroidism, Meigs syndrome. Exudates (protein $> 35$ g/L): pneumonia (parapneumonic), malignancy, TB, pulmonary embolism, pancreatitis, rheumatoid/autoimmune disease, empyema.

What pleural fluid findings indicate an empyema or complicated parapneumonic effusion requiring chest drainage?

Drainage is indicated if the fluid is frankly purulent/turbid, is culture or Gram-stain positive, or has pleural fluid $pH < 7.2$. A low glucose and high LDH also support a complicated effusion. Chest tube drainage plus antibiotics is required; persistent collections may need fibrinolytics or surgery (VATS).

How does primary spontaneous pneumothorax management differ by size and symptoms (BTS approach)?

In a primary pneumothorax: if the patient is asymptomatic and the rim is $< 2$ cm, discharge with review. If $> 2$ cm or breathless, perform aspiration (14–16G); if aspiration fails (still $> 2$ cm/symptomatic), insert a chest drain. The $2$ cm rim is measured at the level of the hilum and approximates a $\sim 50\%$ volume loss.

What is a tension pneumothorax and its immediate management?

A one-way valve allowing air into the pleural space under pressure, causing mediastinal shift, raised JVP, tracheal deviation away from the side, hypotension and cardiac arrest. It is a clinical diagnosis — do NOT wait for a CXR. Immediate treatment: large-bore needle decompression (2nd intercostal space mid-clavicular line, or 4th/5th space anterior axillary), then a chest drain.

Outline the Wells score use and diagnostic pathway for suspected pulmonary embolism.

The two-level Wells score stratifies probability: $\leq 4$ = PE unlikely (do a D-dimer; if negative, exclude); $> 4$ = PE likely (proceed directly to CTPA). If CTPA is delayed, give interim anticoagulation. A positive D-dimer in the 'unlikely' group also warrants CTPA. V/Q scanning is an alternative in renal impairment/contrast allergy/pregnancy.

What ECG and ABG changes may be seen in pulmonary embolism?

ECG: sinus tachycardia (commonest), and the classic but uncommon $S_{1}Q_{3}T_{3}$ pattern (deep S in lead I, Q wave and inverted T in lead III), right bundle branch block, right axis deviation. ABG: type 1 respiratory failure with hypoxaemia and hypocapnia (respiratory alkalosis from hyperventilation), and a raised A–a gradient.

How is a massive (high-risk) PE defined and managed differently from a stable PE?

Massive/high-risk PE causes haemodynamic instability (sustained hypotension, $SBP < 90$ mmHg). It is treated with systemic thrombolysis (e.g. alteplase) unless contraindicated, or embolectomy. Haemodynamically stable PE is treated with anticoagulation alone (a DOAC first-line, or LMWH bridging to warfarin).

What is the diagnostic threshold for obstructive sleep apnoea using the Apnoea-Hypopnoea Index (AHI)?

OSA severity by AHI (events per hour of sleep): mild $5 \leq AHI < 15$; moderate $15 \leq AHI < 30$; severe $AHI \geq 30$. An apnoea is $\geq 90\%$ airflow reduction for $\geq 10$ s; a hypopnoea is a partial reduction with desaturation/arousal. Diagnosis combines AHI with symptoms (e.g. Epworth score).

What is the first-line treatment for moderate-to-severe OSA and its key benefits?

Continuous positive airway pressure (CPAP), which splints the upper airway open during sleep. It improves daytime somnolence, quality of life and blood pressure control, and reduces road-traffic-accident risk. Adjuncts: weight loss, avoiding alcohol/sedatives, and mandibular advancement devices for milder disease.

Define obesity hypoventilation syndrome (Pickwickian syndrome) and its diagnostic criteria.

The triad of obesity ($BMI \geq 30$ kg/m$^{2}$), chronic daytime hypercapnia ($PaCO_{2} > 6$ kPa / $45$ mmHg while awake), and sleep-disordered breathing, in the absence of another cause of hypoventilation. Management: weight loss and non-invasive ventilation (NIV/BiPAP), often with CPAP if coexisting OSA.

Distinguish type 1 from type 2 respiratory failure by arterial blood gas values.

Type 1 (hypoxaemic): $PaO_{2} < 8$ kPa with a normal or low $PaCO_{2}$ — a V/Q mismatch problem (e.g. PE, pneumonia, pulmonary oedema). Type 2 (hypercapnic/ventilatory): $PaO_{2} < 8$ kPa with $PaCO_{2} > 6$ kPa — an alveolar hypoventilation problem (e.g. COPD, neuromuscular weakness, sedation).

Give the systematic steps for interpreting an arterial blood gas to classify an acid-base disorder.

1. Assess oxygenation ($PaO_{2}$/$FiO_{2}$). 2. Look at pH: acidaemia $< 7.35$, alkalaemia $> 7.45$. 3. Identify the primary driver via $PaCO_{2}$ (respiratory) and $HCO_{3}^{-}$/base excess (metabolic). 4. Decide whether it is respiratory or metabolic. 5. Assess compensation. 6. For a metabolic acidosis, calculate the anion gap.

How is the anion gap calculated and what are the causes of a raised anion gap metabolic acidosis?

$\text{Anion gap} = [Na^{+}] - ([Cl^{-}] + [HCO_{3}^{-}])$, normal $\approx 8$–$16$ mmol/L. Raised anion gap causes (MUDPILES): Methanol, Uraemia, DKA/diabetic ketoacidosis, Paraldehyde/Propylene glycol, Iron/Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates.

How do you assess respiratory compensation for a metabolic acidosis using Winter's formula?

$$PaCO_{2}\,(\text{mmHg}) = 1.5 \times [HCO_{3}^{-}] + 8 \pm 2$$ The expected $PaCO_{2}$ predicts appropriate respiratory compensation. A measured $PaCO_{2}$ higher than predicted indicates a coexisting respiratory acidosis; lower than predicted indicates a coexisting respiratory alkalosis.

What are the two main histological types of lung cancer and their key clinical/biological distinctions?

Small cell lung cancer (SCLC, $\sim 15\%$): central, strongly smoking-related, neuroendocrine, rapidly metastasising, often with paraneoplastic syndromes; usually treated with chemotherapy not surgery. Non-small cell lung cancer (NSCLC, $\sim 85\%$: adenocarcinoma, squamous, large cell): more amenable to surgical resection if localised, and targeted/immunotherapy options.

Summarise the TNM-based staging concept for lung cancer that determines resectability.

Tumour (T): size and local invasion. Node (N): $N0$ none, $N1$ ipsilateral hilar, $N2$ ipsilateral mediastinal/subcarinal, $N3$ contralateral mediastinal/hilar or supraclavicular. Metastasis (M): $M0$/$M1$. NSCLC is generally resectable up to stage IIIA; $N3$ disease or distant metastases ($M1$) are non-resectable. PET-CT and mediastinal staging (EBUS) guide this.

What is a Pancoast tumour and its characteristic clinical features?

An apical (superior sulcus) lung tumour invading local structures. It causes: Horner syndrome (ptosis, miosis, anhidrosis from sympathetic chain involvement), shoulder/arm pain and wasting in a $C8$–$T1$ distribution (lower brachial plexus), and may cause SVC obstruction. Often squamous cell carcinoma.

What are the features of mesothelioma and its key prognostic and exposure associations?

A malignancy of the pleura strongly linked to asbestos exposure (latency often $> 30$–$40$ years), more with crocidolite/blue asbestos. Features: chest pain, breathlessness, a unilateral pleural effusion, and pleural thickening/nodularity on imaging. Diagnosis needs pleural biopsy. Prognosis is poor (median survival $\sim 8$–$14$ months); it is an industrial/compensatable disease.

How is a solitary pulmonary nodule evaluated and which features suggest malignancy?

Compare with old imaging (stability $> 2$ years suggests benign). Malignant features: size $> 8$ mm, spiculated/irregular margins, upper lobe, age $> 60$, smoking history, growth. Benign features: small, smooth, and certain calcification patterns (central, popcorn, laminated). Assess with volumetry/CT surveillance, PET-CT for indeterminate nodules, and biopsy/resection if suspicious (Brock/Herder risk models).

Which paraneoplastic syndromes are associated with small cell lung cancer?

SCLC (neuroendocrine origin) causes: SIADH (hyponatraemia from ectopic ADH), ectopic ACTH (Cushing's syndrome with hypokalaemic alkalosis), and Lambert-Eaton myasthenic syndrome (antibodies to voltage-gated calcium channels, proximal weakness that improves with repeated effort, autonomic features).

Which paraneoplastic syndromes are characteristically associated with squamous cell lung carcinoma?

Squamous cell carcinoma classically causes hypercalcaemia via secretion of parathyroid-hormone-related peptide (PTHrP), and is also associated with hypertrophic pulmonary osteoarthropathy (clubbing with periostitis and painful wrists/ankles). It is the type most associated with cavitation on imaging.