{"title": "Chapter 4: Pulmonary Disorders", "flashcards": [{"q": "Define type 1 and type 2 respiratory failure with blood gas criteria.", "a": "Type 1 (hypoxaemic): PaO₂ <8 kPa, PaCO₂ normal or low. Causes: V/Q mismatch (PE, pneumonia, pulmonary oedema). Type 2 (hypercapnic): PaO₂ <8 kPa AND PaCO₂ >6 kPa. Causes: COPD exacerbation, neuromuscular disease, chest wall deformity, CNS depression."}, {"q": "What is the CURB-65 score for pneumonia severity?", "a": "Confusion (AMTS ≤8), Urea >7 mmol/L, Respiratory rate ≥30/min, Blood pressure <90 systolic or ≤60 diastolic, age ≥65. Score 0–1: low severity (community treatment); 2: consider hospital admission; ≥3: high severity (hospital, consider ITU if ≥4–5)."}, {"q": "Name the GOLD spirometric grading for COPD.", "a": "Post-bronchodilator FEV₁/FVC <0.70 confirms obstruction. GOLD 1 (mild) FEV₁ ≥80%; GOLD 2 (moderate) 50–79%; GOLD 3 (severe) 30–49%; GOLD 4 (very severe) <30% predicted. GOLD ABCD groups also incorporate symptom burden and exacerbation history."}, {"q": "What is the Wells score for pulmonary embolism and which score makes PE likely?", "a": "Variables: clinical signs of DVT (3pts), PE is most likely diagnosis (3), HR >100 (1.5), immobilisation/surgery ≤4 weeks (1.5), prior DVT/PE (1.5), haemoptysis (1), malignancy (1). Score >4 = PE likely; ≤4 = PE unlikely (proceed to D-dimer). D-dimer only useful if score ≤4."}, {"q": "What oxygen target should be used in COPD exacerbation?", "a": "Target SpO₂ 88–92% in patients at risk of hypercapnic respiratory failure. Uncontrolled high-flow oxygen can suppress hypoxic drive and worsen CO₂ retention. Titrate oxygen using nasal cannulae at 1–2 L/min or 24–28% Venturi mask. If pH <7.35 and PaCO₂ >6 kPa despite medical therapy, start NIV."}, {"q": "What are the indications for pleural drainage in pleural effusion?", "a": "Empyema (frank pus); complicated parapneumonic effusion (pH <7.2, glucose <2.2 mmol/L, LDH >1000 IU/L, or positive culture); massive effusion causing haemodynamic or respiratory compromise; malignant effusion for symptom relief. Thoracentesis for diagnostic purposes requires no drainage threshold."}, {"q": "Define status asthmaticus and name three markers of life-threatening severity.", "a": "Status asthmaticus: severe acute asthma unresponsive to initial bronchodilator therapy. Life-threatening markers: SpO₂ <92%, PaO₂ <8 kPa, PaCO₂ normal or raised (exhaustion), peak flow <33% predicted/best, silent chest, cyanosis, bradycardia, dysrhythmia, hypotension, exhaustion, altered consciousness."}, {"q": "What is the treatment for tension pneumothorax?", "a": "Immediate needle decompression — 2nd intercostal space mid-clavicular line (14–16G cannula) or 4th/5th ICS anterior axillary line — without waiting for imaging. Do not delay for CXR if clinical diagnosis is certain. Follow immediately with intercostal chest drain insertion."}, {"q": "Name the HRCT pattern of usual interstitial pneumonia (UIP) in IPF.", "a": "Bilateral, basal, subpleural honeycombing with or without peripheral traction bronchiectasis or bronchiolectasis. Ground-glass opacity is minimal. Upper lobe, diffuse, or peribronchovascular predominance argues against UIP. UIP on HRCT in the right clinical context is sufficient to diagnose IPF without biopsy."}, {"q": "What is the mechanism of action of montelukast in asthma?", "a": "Montelukast is a cysteinyl leukotriene receptor 1 (CysLT1) antagonist. It blocks the bronchoconstrictor, pro-inflammatory, and mucus-secreting effects of leukotrienes (LTC4, LTD4, LTE4) generated via the 5-lipoxygenase pathway. Particularly effective in aspirin-exacerbated respiratory disease and exercise-induced bronchoconstriction."}], "quiz": [{"q": "Which organism most commonly causes hospital-acquired pneumonia (HAP) in ventilated patients?", "opts": ["Streptococcus pneumoniae", "Gram-negative enteric bacilli (Pseudomonas, Klebsiella, E. coli) and Staphylococcus aureus", "Mycoplasma pneumoniae", "Legionella pneumophila"], "ans": 1, "exp": "VAP and HAP are predominantly caused by Gram-negative bacilli (Pseudomonas aeruginosa, Klebsiella pneumoniae, Enterobacter, E. coli) and Staphylococcus aureus (including MRSA). Antibiotic choice must reflect local resistance patterns and be de-escalated after 48–72 hours based on culture results."}, {"q": "What is the mechanism of oxygen toxicity in patients with COPD given uncontrolled high-flow oxygen?", "opts": ["Pulmonary vasoconstriction", "CO₂ retention from suppression of hypoxic ventilatory drive and reversal of hypoxic pulmonary vasoconstriction (Haldane effect)", "Pulmonary oedema", "Oxygen free radical damage to airways"], "ans": 1, "exp": "In COPD, high-flow O₂ suppresses hypoxic drive, reverses hypoxic pulmonary vasoconstriction (increasing V/Q mismatch via Haldane effect), and can cause CO₂ retention leading to respiratory acidosis. Careful titrated oxygen to SpO₂ 88–92% prevents worsening hypercapnia."}, {"q": "A patient with known IPF is admitted with acute dyspnoea and new bilateral ground-glass opacities without infection. What is the most likely diagnosis?", "opts": ["Community-acquired pneumonia", "Acute exacerbation of IPF (AE-IPF)", "Pulmonary embolism", "Acute pulmonary oedema"], "ans": 1, "exp": "AE-IPF is defined as acute (within 30 days), unexplained respiratory deterioration with new bilateral ground-glass opacities or consolidation superimposed on an IPF background pattern, without an identifiable cause. Mortality exceeds 50%. High-dose corticosteroids are used despite limited evidence."}, {"q": "Which inhaled therapy combination is recommended first-line for GOLD group E COPD (high symptoms, ≥2 exacerbations)?", "opts": ["LABA alone", "LAMA/LABA combination, with ICS added if blood eosinophils ≥300 cells/µL", "ICS alone", "SABA alone"], "ans": 1, "exp": "GOLD 2024 recommends LAMA/LABA for group E COPD with frequent exacerbations. ICS is added (triple therapy: LAMA/LABA/ICS) when blood eosinophils ≥300 cells/µL. ICS without LABAs are not recommended as monotherapy. Roflumilast and azithromycin are add-on options for persistent exacerbations."}, {"q": "What is the significance of a pleural fluid pH <7.2?", "opts": ["Indicates viral pleuritis", "Indicates exudate requiring drainage (complicated parapneumonic or empyema)", "Confirms malignant effusion", "Is a normal finding in transudates"], "ans": 1, "exp": "Pleural fluid pH <7.2 in a parapneumonic effusion indicates a complicated effusion requiring intercostal chest drain insertion. Below this threshold, spontaneous resolution with antibiotics alone is unlikely. pH <7.0 strongly suggests empyema. Always send pleural fluid for glucose, LDH, pH, Gram stain, culture, and cytology."}, {"q": "What is the pathophysiology of cor pulmonale?", "opts": ["Left ventricular failure causing pulmonary hypertension", "Right ventricular dysfunction secondary to pulmonary hypertension from chronic lung disease", "Cardiomyopathy from oxygen toxicity", "Arrhythmia from hypoxaemia"], "ans": 1, "exp": "Cor pulmonale is right heart failure secondary to chronic pulmonary hypertension from lung disease (most commonly COPD, IPF, or OSA). Chronic hypoxic pulmonary vasoconstriction → pulmonary hypertension → right ventricular hypertrophy and eventual dilatation and failure. Signs: raised JVP, peripheral oedema, loud P2, right parasternal heave."}, {"q": "Which drug is used for pulmonary arterial hypertension (PAH) in patients with connective tissue disease?", "opts": ["Beta-blockers", "Endothelin receptor antagonists (macitentan, ambrisentan) ± PDE-5 inhibitors", "ACE inhibitors", "Furosemide alone"], "ans": 1, "exp": "Combination therapy with endothelin receptor antagonists (ERAs) and PDE-5 inhibitors (sildenafil, tadalafil) is first-line for PAH. The AMBITION trial demonstrated superiority of upfront ambrisentan + tadalafil combination over monotherapy. Prostacyclin analogues are added in refractory cases."}, {"q": "What is Cheyne-Stokes respiration?", "opts": ["Rapid deep breathing from metabolic acidosis", "Cyclic alternating crescendo-decrescendo breathing with central apnoeas", "Paradoxical breathing from diaphragmatic paralysis", "Fixed shallow breathing from opioids"], "ans": 1, "exp": "Cheyne-Stokes respiration is characterised by regular cycles of hyperpnoea (crescendo then decrescendo tidal volumes) followed by central apnoeas. It results from delayed chemoreceptor feedback in conditions of prolonged circulation time (HFrEF, post-stroke). It is a marker of poor prognosis in heart failure."}, {"q": "What is the 'step-down' principle in asthma management?", "opts": ["Immediately stopping all medications", "Reducing therapy after ≥3 months of sustained symptom control to the minimum effective dose", "Switching to a different ICS device", "Stopping LABA before ICS"], "ans": 1, "exp": "BTS/SIGN guidelines recommend stepping down asthma therapy after ≥3 months of good control at the current step. Reductions should be gradual (e.g. 25–50% ICS dose reduction) with patient education to recognise deterioration. The goal is achieving control with minimum medication burden and side effects."}, {"q": "What is the diagnostic criterion for obstructive sleep apnoea (OSA)?", "opts": ["Snoring >5 nights/week", "Apnoea-Hypopnoea Index (AHI) ≥5 events/hour with symptoms, or AHI ≥15 regardless", "SpO₂ <90% for >1% of total sleep time", "ESS score >10"], "ans": 1, "exp": "OSA is diagnosed by polysomnography or home sleep testing: AHI ≥5/hr with symptoms (sleepiness, witnessed apnoeas, nocturia) = mild; AHI 15–29/hr = moderate; AHI ≥30/hr = severe. CPAP is first-line treatment for moderate-severe OSA. Continuous positive airway pressure eliminates obstructive events."}, {"q": "Which condition causes bilateral hilar lymphadenopathy on CXR in a young asymptomatic patient?", "opts": ["Tuberculosis", "Sarcoidosis (stage I–II)", "Lymphoma", "Metastatic malignancy"], "ans": 1, "exp": "Bilateral symmetrical hilar lymphadenopathy in a young, often Afro-Caribbean or Scandinavian patient is the classic presentation of stage I–II pulmonary sarcoidosis. Stage I = BHL alone; Stage II = BHL + pulmonary infiltrates; Stage III = infiltrates without BHL. Serum ACE and calcium are elevated in ~50%."}, {"q": "What is the primary mechanism of COPD-related airflow obstruction?", "opts": ["Bronchial smooth muscle hypertrophy", "Chronic inflammation causing small airways fibrosis and remodelling + emphysematous destruction of alveolar walls reducing lung elastic recoil", "Excess mucus production only", "Pulmonary vascular disease"], "ans": 1, "exp": "COPD has two main structural contributors to irreversible airflow limitation: (1) small airways disease — chronic inflammation causing fibrosis, remodelling, and mucus plugging; (2) emphysema — alveolar destruction reducing elastic recoil that normally holds airways open during expiration. Both are smoking-related and permanent."}, {"q": "What percentage of primary spontaneous pneumothorax patients will have a recurrence within 5 years?", "opts": ["5%", "25–50%", "75%", "<5%"], "ans": 1, "exp": "Recurrence rate for primary spontaneous pneumothorax is approximately 25–50% within 2–5 years, with the highest risk in the first year after the initial episode. Chemical pleurodesis or surgical pleurectomy via VATS is recommended after a second ipsilateral episode or first contralateral episode."}, {"q": "What is the key difference between CPAP and BiPAP in non-invasive ventilation?", "opts": ["CPAP delivers higher pressures", "BiPAP provides separate inspiratory (IPAP) and expiratory (EPAP) pressures, supporting ventilation; CPAP delivers a single continuous pressure maintaining airway patency", "BiPAP is only used for OSA", "CPAP generates a backup respiratory rate"], "ans": 1, "exp": "CPAP delivers a single fixed positive pressure throughout the respiratory cycle — splinting the upper airway open and recruiting alveoli. BiPAP (bilevel PAP) provides higher inspiratory pressure (IPAP) to support tidal volume and lower expiratory pressure (EPAP), thereby assisting ventilation and reducing work of breathing. BiPAP is used for type 2 respiratory failure (COPD exacerbation)."}, {"q": "What is the gold-standard investigation for diagnosing pulmonary embolism?", "opts": ["VQ scan", "CT pulmonary angiography (CTPA)", "D-dimer", "Echocardiography"], "ans": 1, "exp": "CTPA is the gold-standard imaging for PE — fast, widely available, and able to visualise clot to subsegmental level. It also identifies alternative diagnoses (pneumonia, aortic dissection). VQ scan is an alternative when CTPA is contraindicated (renal impairment, contrast allergy, pregnancy preference for lower radiation dose to breast tissue)."}, {"q": "In which clinical context is NIV most strongly contraindicated?", "opts": ["Mild COPD exacerbation with pH 7.38", "Facial trauma or burns preventing mask seal, or inability to protect airway with GCS <8", "Moderate hypercapnia with pH 7.31", "Cardiogenic pulmonary oedema"], "ans": 1, "exp": "NIV requires patient cooperation and an intact airway. Absolute contraindications include: undrained tension pneumothorax, inability to protect the airway (GCS <8, active vomiting, severe agitation), facial trauma/burns preventing mask fit, and haemodynamic instability requiring immediate intubation. These patients need invasive mechanical ventilation."}, {"q": "What is mesothelioma and what is its primary cause?", "opts": ["Primary lung adenocarcinoma", "Malignant tumour of the pleural (or peritoneal) mesothelial cells, caused by asbestos exposure in ≥80% of cases", "Benign pleural fibroma", "Metastatic cancer to the pleura"], "ans": 1, "exp": "Malignant pleural mesothelioma arises from mesothelial cells lining the pleura. It is causally linked to asbestos exposure (latency 20–40 years). It presents with dyspnoea, pleural effusion, and chest wall pain. Median survival is 8–14 months. Management includes cytoreductive surgery (selected), cisplatin-pemetrexed chemotherapy, and immunotherapy (nivolumab + ipilimumab — CheckMate 743 trial)."}, {"q": "Which blood test is most useful in diagnosing allergic bronchopulmonary aspergillosis (ABPA)?", "opts": ["Total IgE and Aspergillus-specific IgE + eosinophil count", "Serum ACE", "ANCA", "Precipitins to Aspergillus"], "ans": 0, "exp": "ABPA diagnostic criteria include: total serum IgE >1000 IU/mL, elevated Aspergillus-specific IgE and IgG, peripheral blood eosinophilia, and central bronchiectasis on CT. It complicates asthma and cystic fibrosis. Treatment is prednisolone ± itraconazole to reduce inflammation and Aspergillus burden."}, {"q": "What is the recommended treatment for Pneumocystis jirovecii pneumonia (PJP) in HIV?", "opts": ["Fluconazole", "High-dose co-trimoxazole (trimethoprim-sulfamethoxazole) for 21 days; adjunctive corticosteroids if PaO₂ <9.3 kPa", "Amphotericin B", "Voriconazole"], "ans": 1, "exp": "High-dose co-trimoxazole (15–20 mg/kg/day trimethoprim component divided TDS-QDS) for 21 days is first-line for PJP. Adjunctive prednisolone is added when PaO₂ <9.3 kPa or A-a gradient ≥35 mmHg to reduce the inflammatory response and improve oxygenation. Second-line: pentamidine or atovaquone."}, {"q": "What lung function pattern is seen in pulmonary fibrosis?", "opts": ["Obstructive (low FEV₁/FVC)", "Restrictive (reduced TLC, FVC, and DLCO with preserved FEV₁/FVC ratio)", "Mixed obstructive and restrictive", "Hyperinflation (increased TLC and RV)"], "ans": 1, "exp": "Pulmonary fibrosis produces a restrictive ventilatory defect: reduced TLC, FVC, and FRC; FEV₁/FVC ratio preserved or elevated (>70%). DLCO is disproportionately reduced (impaired gas transfer). Hyperinflation with increased TLC and RV indicates obstructive disease (emphysema, asthma)."}]}