Respiratory

A chronic inflammatory airway disease with reversible airflow obstruction and bronchial hyperresponsiveness. It presents with episodic wheeze, cough and breathlessness with diurnal variation (worse at night/early morning) and triggers. NICE/BTS/SIGN 2024 (NG245) made anti-inflammatory reliever (AIR) and MART the backbone — SABA-only treatment is OUT. Recognising and grading an acute attack (especially life-threatening features) is the high-yield emergency skill.

A progressive disease of largely irreversible airflow obstruction, almost always from smoking (consider alpha-1 antitrypsin deficiency in the young/non-smoker). Diagnosis needs post-bronchodilator spirometry showing obstruction (FEV1/FVC <0.7). Management is smoking cessation (the only intervention that alters the course) + inhalers stepped by phenotype, pulmonary rehab, vaccines, and recognising/treating exacerbations and chronic type 2 respiratory failure.

A clinical phenotype with features of both asthma and COPD — persistent airflow obstruction (like COPD) with significant variability/reversibility and eosinophilic/atopic features (like asthma). It typically affects older smokers with an atopic/asthma history and tends to have more frequent exacerbations. The practical point is that the ICS-responsive (eosinophilic) component means inhaled corticosteroids are central, unlike pure COPD.

Permanent, abnormal dilatation of the bronchi resulting from a vicious cycle of infection, inflammation and impaired mucociliary clearance. It presents with a chronic productive cough of large volumes of (often purulent) sputum and recurrent chest infections. HRCT (signet-ring sign, tramlines) is diagnostic. Causes include post-infective, cystic fibrosis, immunodeficiency, ABPA and ciliary dyskinesia; Pseudomonas colonisation is a key issue.

Repetitive collapse of the upper airway during sleep causing apnoeas/hypopnoeas, intermittent hypoxia and fragmented sleep. It presents with snoring, witnessed apnoeas and daytime sleepiness, typically in an overweight, middle-aged man. It is diagnosed by sleep study and treated with weight loss and CPAP. It is important because of road-traffic-accident risk (DVLA), hypertension and cardiovascular consequences.

Infection and consolidation of the lung parenchyma. Community-acquired pneumonia (CAP) is graded by CURB-65 to decide setting and antibiotics; the commonest organism is Streptococcus pneumoniae. Recognise the atypical and aspiration patterns, hospital-acquired pneumonia, and the high-yield organism clues. CXR consolidation confirms it; the severity score drives where and how the patient is treated.

A chest infection without the consolidation of pneumonia. Acute bronchitis is usually a self-limiting viral infection of the large airways (cough ± sputum, often after a coryzal illness) and generally does NOT need antibiotics. The skill is distinguishing it from pneumonia (no focal signs/consolidation) and using antibiotics judiciously (stewardship) — reserving them for higher-risk patients or signs of pneumonia.

Suppurative complications of chest infection. Empyema is pus in the pleural space (a complicated parapneumonic effusion), suspected when a patient with pneumonia has persistent/swinging fever; pleural fluid that is purulent, pH <7.2, low glucose or organism-positive needs a chest DRAIN. Lung abscess is a localised cavity of pus (air-fluid level on imaging) from aspiration, obstruction or necrotising infection, treated with prolonged antibiotics ± drainage.

Infection with Mycobacterium tuberculosis, presenting after weeks-to-months with cough, weight loss, night sweats, fever and haemoptysis. It is high-yield because of the chronic presentation, the apical/cavitating CXR, the importance of risk factors (immigration from high-prevalence areas, HIV, immunosuppression), and the standard RIPE regimen with its specific drug toxicities. Latent TB is treated to prevent reactivation. (Cross-references the Infection content-map domain.)

Accumulation of fluid in the pleural space. The fundamental split is transudate (low protein — heart/liver/renal failure, hypoalbuminaemia) vs exudate (high protein — infection, malignancy, PE, inflammation), separated by Light's criteria. Diagnostic aspiration (with pleural fluid analysis) is the key step; a purulent/low-pH effusion is an empyema needing a drain.

Air in the pleural space causing partial/complete lung collapse. Primary spontaneous (tall thin young smoker, no lung disease), secondary spontaneous (underlying lung disease — COPD/CF), traumatic/iatrogenic, or tension (a one-way valve causing cardiorespiratory collapse). The BTS 2023 pathway is symptom-based (single algorithm), but the one rule that overrides everything: TENSION pneumothorax is a clinical diagnosis treated with IMMEDIATE decompression — never wait for a CXR.

A group of diffuse parenchymal lung diseases causing inflammation and/or fibrosis of the interstitium, with a RESTRICTIVE pattern and reduced gas transfer (DLCO). Idiopathic pulmonary fibrosis (IPF) is the commonest progressive form (basal/peripheral honeycombing, antifibrotics); others are drug-induced, connective-tissue-disease-associated, hypersensitivity pneumonitis, sarcoidosis and pneumoconioses. Progressive exertional breathlessness with fine crackles and clubbing is the picture.

A multisystem granulomatous disease of unknown cause, characterised by non-caseating granulomas, most often affecting the lungs and intrathoracic lymph nodes. It ranges from an acute self-limiting form (Löfgren syndrome — bilateral hilar lymphadenopathy + erythema nodosum + arthralgia, good prognosis) to chronic pulmonary fibrosis and extra-pulmonary disease. Bilateral hilar lymphadenopathy on CXR is the classic finding.

Lung diseases caused by inhaled occupational or environmental agents, where the EXPOSURE HISTORY is the diagnostic key. Asbestos causes pleural plaques, asbestosis (fibrosis) and mesothelioma (+ raises lung-cancer risk, multiplied by smoking). Silicosis and coal-worker's pneumoconiosis are nodular fibroses; hypersensitivity pneumonitis (extrinsic allergic alveolitis) is an immune reaction to organic antigens (e.g. farmer's/bird-fancier's lung). Many are compensable industrial diseases.

A leading cause of cancer death, dominated by smoking. Split into non-small-cell (NSCLC — adenocarcinoma, squamous, large-cell) and small-cell (SCLC — aggressive, often paraneoplastic, usually disseminated at presentation). Presents with cough, haemoptysis, weight loss, breathlessness or an incidental mass; paraneoplastic syndromes and metastatic/local complications are high-yield. Urgent (2-week-wait) referral and CT-guided diagnosis/staging direct treatment.

Failure of the respiratory system to oxygenate and/or clear CO2. Type 1 (hypoxaemic, low PaO2 with normal/low CO2 — V/Q mismatch: pneumonia, PE, oedema, ARDS). Type 2 (hypercapnic, high CO2 — alveolar hypoventilation: COPD, neuromuscular, opioids, chest-wall). ARDS is severe non-cardiogenic pulmonary oedema with refractory hypoxia and bilateral infiltrates. Respiratory arrest is the terminal endpoint (→ cross-ref acute_care).

An autosomal recessive multisystem disease (commonest CFTR mutation ΔF508) in which defective epithelial chloride transport produces thick, viscous secretions affecting the lungs, pancreas, gut and reproductive tract. It is diagnosed in childhood (newborn screening, sweat test) but its burden is increasingly an adult respiratory one — recurrent infections, bronchiectasis and progressive lung disease — with multidisciplinary care and, now, transformative CFTR-modulator therapy. (Paediatric diagnosis/screening detail is on the child_health page.)