Respiratory Flashcards
Define chronic obstructive pulmonary disease
Non-reversible long-term deterioration in air flow through the lungs caused by damage to lung tissue (almost always due to smoking).
2 main types:
* Chronic bronchitis: clinical diagnosis. Daily productive cough for 3+ months, in at least 2 consecutive years. Hypertrophy and hyperplasia of mucous glands, chronic inflammation cells infiltrate bronchi > hypersecretion, ciliary dysfunction, luminal narrowing.
* Emphysema: pathological diagnosis. Permanent enlargement and destruction of airspaces distal to the terminal bronchiole. Destruction of elastin layer causes trapped air distal to blockage (large air sacs = bullae). Centriacinar emphysema = respiratory bronchioles only, smokers. Panacinar emphysema = A1AT deficiency.
Describe the epidemiology for COPD
40-60 years, smokers, males, miners/coal workers
Describe the aetiology for COPD
Smoking, pollution, genetics (A1AT)
Describe the risk factors for COPD
Smoking, increasing age, second-hand smoke exposure, occupational exposure (mining, dust, cotton, wool), pollution (heating fuel, outdoor pollutants), genetics (alpha-1-antitrypsin deficiency)
Describe the pathophysiology for COPD
Obstructed airflow through airways > difficulty ventilating the lungs > shortness of breath and prone to infection. Unlike asthma, not reversible with a bronchodilator.
Patients may experience exacerbations; if due to infections they are called infective exacerbations (H. influenza, S. pneumonia.)
What are the key presentations for COPD
Long-term smoker, shortness of breath, cough, sputum, wheeze, recurrent respiratory infections.
Barrel chest/hyperinflation, hyper-resonance on percussion, distant breath sounds on auscultation.
Describe the clinical manifestations for COPD
Signs: Chronic bronchitis: ‘blue bloaters’, chronic productive cough, purulent sputum, dyspnoea, cyanosis, peripheral oedema, haemoptysis, obesity
Emphysema: ‘pink puffers’, dyspnoea/tachypnoea, minimal cough, pink skin, pursed lip-breathing, accessory muscle breathing, cachexia (body/muscle wasting), hyperinflation (barrel chest), weight loss
What is the gold standard investigation for COPD
Clinical presentation + spirometry (FEV1/FVC <0.7 = obstruction. Bronchodilator irreversible = COPD. Bronchodilator reversible = asthma)
Describe the first line investigations for COPD
Spirometry (FEV1/FVC < 0.7 = shows obstruction. Overall lung capacity is better than their ability to forcefully expire air quickly).
DLCO (diffusion capacity of CO across lung. COPD = low). Pulse oximetry (low O2)
Chest x-ray (hyperinflation, exclude lung cancer/other pathology)
ABG (type 2 respiratory failure – raised pCO2, low pO2).
FBC (chronic hypoxia > polycythaemia). BMI (weight loss - lung cancer). ECG. Serum alpha-1-antitrypsin levels. Sputum culture.
Other: Grades: MRC dyspnoea scale
Grade 1: breathless on strenuous exercise
Grade 2: breathless walking up a hill
Grade 3: breathless that slows on the flat
Grade 4: stop to catch breath after 100m walking on flat
Grade 5: unable to leave house due to breathlessness
What are the differential diagnosis for COPD
Asthma, bronchiectasis, fibrosis, congestive heart failure, lung cancer
Describe the management for COPD
General: stop smoking!! Pneumococcal vaccine, annual flu vaccine
1st line – SABA short acting beta agonist (e.g., salbutamol or terbutaline) OR SAMA short acting muscarinic antagonist (e.g., ipratropium bromide)
2nd line – if no asthmatic/steroid response: LABA long-acting beta agonist (salmeterol), LAMA long-acting muscarinic antagonist (tiotropium). If asthmatic/steroid response: LABA long-acting beta agonist (salmeterol), ICS inhaled corticosteroids (budesonide)
3rd line – LTOT long term oxygen therapy
Describe the complications for COPD
Infective exacerbations: acute worsening of symptoms – SOB, cough, wheeze, sputum. Triggered by infection (H. influenza, S. pneumonia). ABG – raised CO2 > acidosis. Type 2 respiratory failure (raised pCO2, low pO2).
Treatment: steroids (hydrocortisone/prednisolone) + nebulised bronchodilators (salbutamol/ipratropium bromide) + antibiotics (amoxicillin).
Other complications: cor pulmonale, recurrent pneumonia, depression
Define asthma
Chronic, inflammatory condition causing episodes of reversible airway obstruction, airway hyperresponsiveness and inflamed bronchioles, due to bronchoconstriction and excessive secretion production.
Describe the aetiology for asthma
Hypersensitivity of the airways, triggered by: cold air, exercise, cigarette smoke, air pollution, allergens (pollen, cats, dogs, mould), time of day (early morning, night)
Describe the risk factors for asthma
Allergens, atopy, smoking, previous respiratory tract infection, hygienic hypothesis: Growing up in very hygienic environment
Describe the pathophysiology for asthma
Overexpressed TH2 cells in airways exposed to trigger > TH2 cytokine release, IgE production, eosinophil recruitment > IgE mast cell degranulation releasing histamines, leukotrienes, tryptase. Eosinophilia: release of toxic protein > bronchial constriction, mucus hypersecretion
Define Atopic triad and Samter’s triad
Atopic triad: atopic rhinitis, eczema, asthma. Samter’s triad: asthma, aspirin allergy, nasal polyps.
What are the key presentations of asthma
Episodes of wheeze (widespread, polyphonic – multiple musical notes starting and ending at same time), breathlessness, chest tightness and dry cough.
Atopy (family/personal history of eczema/asthma/hayfever).
Diurnal variability (typically worse at night).
What is the gold standard investigation for asthma
Spirometry with reversibility testing. Obstructive pattern: FEV1 <80% of predicted normal, FEV1/FVC ratio <0.7. Bronchodilator reversible (>12% FEV1 improved).
Describe the first line investigations for asthma
FeNO (fractional exhaled nitric oxide - raised), spirometry (obstruction FEV1:FVC <0.7), peak flow measurement, chest x-ray (normal/hyperinflated), FBC (raised eosinophils or neutrophils)
What are the differential diagnosis for asthma
Cystic fibrosis, COPD, bronchiectasis, alpha-1-antitrypsin deficiency
Describe the management for asthma
Management 1st line – SABA short acting beta 2 adrenergic receptor agonists (salbutamol) – bronchodilation
2 – add ICS inhaled corticosteroids (budesonide) – reduce inflammation and reactivity of airways
3 – add LRTA leukotriene receptor antagonist (montelukast) – block leukotriene effects (inflammation, bronchoconstriction, mucus secretion)
4 – add LABA long-acting beta agonist (salmeterol)
5 – increase ICS dose
For exacerbations OSHITME: oxygen, SABA salbutamol, Hydrocortisone (ICS), Ipratropium bromide, Theophylline, MgSO4, escalate (ventilation – BiPAP bilevel positive airway pressure)
Describe the complications for asthma
Exacerbation, airway remodelling, oral candidiasis/dysphonia (voice disorders) from inhaled steroids
Define tuberculosis
Infectious granulomatous caseating disease caused by mycobacterium tuberculosis bacteria
Describe the epidemiology for tuberculosis
Majority of cases in Africa and South Asia, cause of death for most people with HIV
Describe the aetiology for tuberculosis
Mycobacterium tuberculosis complex (TB causing): M. tuberculosis, M. africanum, M. microtis, M. bovis
Describe the risk factors for tuberculosis
Living/travel to TB area, immunocompromised (e.g. HIV), homeless/crowded housing, IVDU, smoking, alcohol, increasing age
Describe the pathophysiology for tuberculosis
Aerobic, non-motile, non-sporing slightly curved bacilli with a thick waxy mycolic acid capsule. Acid-fast bacilli – stains red/pink with Ziehl Neelsen stain. Slow growing. Resistant to phagolysosomal killing and able to remain dormant by granuloma formation.
TB spreads via respiratory droplets. TB phagocytosed but resists phagolysosomal killing and forms caseating granuloma > T cells recruited and central region of granuloma undergoes caseating necrosis to form Ghon focus in upper lungs > Ghon focus spreads to nearby lymph nodes forming Ghon complex > if TB spreads systemically = miliary TB, if infection in containing within granulomas (dormant, asymptomatic) it is latent TB.
What are the key presentations for tuberculosis
Productive cough (sputum), cough > 3 weeks, haemoptysis, breathlessness, chest pain, lymphadenopathy
Weight loss, low grade fever, anorexia, night sweats, malaise, pyrexia
Describe the clinical manifestations for tuberculosis
Signs of bronchial breathing, dullness on percussion, decreased breathing, fever, crackles.
Extrapulmonary: meningitis, skin changes (erythema nodosum), TB pericarditis symptoms, joint pain (spinal TB – Pott’s disease of spine)
What is the gold standard investigation for tuberculosis
Sputum culture (positive)
Describe the first line investigations for tuberculosis
Chest x-ray (fibronodular opacities on upper lobes), sputum acid-fast bacilli smear 3x (Ziehl Neelsen stains red/pinkusing Lowenstein Jensen culture), biopsy (shows caseating granuloma), sputum culture (positive), FBC (raised WBCs), NAAT (positive for M. tuberculosis)
Diagnosing latent TB: tuberculin skin test ‘Mantoux’ (tuberculin injected in skin and look for induration – thickening/hardening - of 5mm or more), interferon gamma release assay (mixing blood with TB antigens, if a person has already had TB, their WBCs will release interferon gamma)
What are the differential diagnosis for tuberculosis
Covid-19, community acquired pneumonia, lung cancer, sarcoidosis
Describe the management for tuberculosis
Acute TB intensive phase therapy:
* R: rifampicin – 6 months, bactericidal > blocks protein synthesis, SE: red urine, hepatitis
* I: isoniazid – 6 months, bactericidal > blocks cell wall synthesis, SE: neuropathy, hepatitis Give pyridoxine/vit B6 to reduce neuropathy side effects
* P: pyrazinamide – 2 months, bactericidal initially, less effective after, SE: gout, arthralgia, rash, hepatitis
* E: ethambutol – 2 months, bacteriostatic > blocks cell wall synthesis, SE: optic neuritis
Latent TB treatment: isoniazid and rifampicin
All cases must be notified to Public Health England. BCG vaccine available (live attenuated TB)
Describe the complications for tuberculosis
Transmission of TB, ARDS, pneumothorax, emphysema, bronchiectasis
Define pneumonia
Inflammation of the substance of the lungs. It is an acute lower respiratory tract infection. Bacterial infection of the distal airways and alveoli with the formation of an inflammatory exudate.
Community-acquired (pneumonia acquired outside hospital or healthcare facilities),
Hospital-acquired (acute lower respiratory tract infection defined by acquired after at least 48 hours of hospital admission and is not incubating at the time of admission),
Atypical pneumonia (bacterial pneumonia caused by organisms that are not detectable on gram stain and cannot be cultured using standard methods)
Pneumonia in immunocompromised patients (e.g., pneumocystis jirovecii pneumoniae in HIV patients)
Describe the epidemiology for pneumonia
CAP: extremes of ages, Pneumocystis pneumonia is most common in HIV
Describe the aetiology for pneumonia
Bacterial infection:
Community acquired – 1. Streptococcus pneumoniae, 2. Haemophilus influenzae, 3. Mycoplasma pneumoniae.
Hospital acquired – aerobic gram-negative bacilli, e.g., pseudomonas aeruginosa, E. coli, Klebsiella pneumoniae.
Atypical – mycoplasma pneumoniae, Chlamydophila pneumoniae, listeria pneumophila.
Also, viral (influenza, covid-19, CMV) and fungi infection (pneumocystis jirovecii).
Describe the risk factors for pneumonia
Age, smoking, COPD, residence in healthcare setting, poor hygiene, multidrug-resistant bacteria
Describe the pathophysiology for pneumonia
Lower airways should always be sterile in a healthy person.
Invasion and overgrowth of a pathogen in lung parenchyma > overwhelming of host immune defences > production of intra-alveolar exudates and sputum
What are the key presentations for pneumonia
Fever, productive cough (purulent sputum), pleuritic chest pain, dyspnoea, rigors, confusion, haemoptysis, night sweats.
Rusty sputum is characteristic of strep pneumoniae.
Atypical pneumonia: headache, low grade fever, dry cough, malaise
Describe the clinical manifestations for pneumonia
Signs: Increased respiratory rate and heart rate, hypotension.
Dullness to percussion, decreased air entry, bronchial breath sounds (harsh breathing sounds on inspiration and expiration), coarse crackles.
Symptoms: Dyspnoea, tachypnoea, malaise, cough, myalgia, fatigue, headache
What is the gold standard investigation for pneumonia
Chest x-ray shows consolidation: air that fills lung airways is replaced with something else (fluid or solid). Air bronchogram – fluid filled alveoli.
* Pneumonic lesions: multi-lobar – s. pneumonia, s. aureus, legionella.
* Multiple abscesses: s. aureus.
* Upper lobe: Klebsiella but exclude TB first
Describe the first line investigations for pneumonia
FBC (raised WCC), CRP raised, pulse oximetry/ABG (low arterial O2), U&Es (raised urea), blood culture (organism growth), sputum culture and gram stain (growth),
Chest x-ray (consolidation, multi-lobar: s. pneumoniae, s. aureus. Multiple abscesses: s. aureus)
Other: CURB-65 score (to assess severity, 1 point for each):
* Confusion (abbreviated mental test score <8)
* Urea > 7
* Respiratory rate > 30
* BP < 90 systolic AND/OR <60 diastolic
* Age > 65
Score: 0-1 (outpatient treatment), 2 (short-stay inpatient treatment OR hospital-supervised outpatient treatment), 3-5 (manage as high-severity pneumonia)
What are the differential diagnosis for pneumonia
Covid-19, bronchitis, COPD exacerbation, congestive heart failure, tuberculosis
Describe the management for pneumonia
Maintaining O2 saturation between 94-98% (88-92% in COPD patients), analgesia (NSAIDs or paracetamol), IV fluids
CURB-65 guided treatment:
0-1: oral amoxicillin at home
2: consider hospitalising, amoxicillin (IV or oral) + macrolide (clarithromycin, erythromycin)
3+: consider ITU, IV co-amoxiclav + macrolide (clarithromycin + erythromycin)
Atypical pneumonia: 1st line – clarithromycin. Pneumocystis jirovecii pneumonia – co-trimoxazole (trimethoprim/sulfamethoxazole)
Describe the complications for pneumonia
Sepsis, pleural effusion, empysema, lung abscess, ARDS
Describe the prognosis for pneumonia
5-20% mortality
Define cystic fibrosis
Autosomal recessive condition affecting CFTR gene (cystic fibrosis transmembrane conductance regulatory gene on chromosome 7) which codes for chloride channels. Mutation affects mucus glands, resulting in thick mucus plugs.
Describe the epidemiology for cystic fibrosis
Most diagnosed in childhood, 90% before 8 yo
Describe the aetiology for cystic fibrosis
Autosomal recessive mutation in cystic fibrosis transmembrane conductance regulatory (CFTR) gene on chromosome 7 (delta-F508)
Describe the risk factors for cystic fibrosis
Family history, both parent carriers, Caucasians
Describe the pathophysiology for cystic fibrosis
Mutation in CFTR gene leads to a defect in chloride secretion and sodium absorption across airway epithelium. Normal CFTR secretes Cl- and Na+ (+H20) into ductal secretions making them thin and watery. Defect causes thicker secretion due to Cl- and Na+ retention.
Also impaired mucociliary clearance as mucus is thicker > increases stagnation > increases infection risk and difficulty breathing, and increased risk of bronchiectasis.
What are the key presentations for cystic fibrosis
Respiratory: Productive cough and mucus plugs, dyspnoea, recurrent infection (pseudomonas aeruginosa), bronchiectasis, pneumothorax.
Neonates: meconium ileus (bowel obstruction – baby’s first poo is thicker and stickier so causes blockage), failure to thrive.
GIT: thick secretions, exocrine pancreatic insufficiency (malabsorption, steatorrhea), bowel obstruction.
Other: males = atrophy of vas deferens (infertility), very salty sweat.
Describe the clinical manifestations for cystic fibrosis
Low weight and height, nasal polyps, finger clubbing, crackles and wheezes on auscultation, abdominal distention.
What is the gold standard investigation for cystic fibrosis
Sweat test (>60mmol/L Cl-): pilocarpine applied to skin, electrodes send small current causing sweat production, sweat is absorbed and sent to lab for chloride concentration. Diagnostic = over 60mmol/L
Describe the first line investigations for cystic fibrosis
Sweat test (>60mmol/L Cl-)
Chest x-ray (bronchiectasis, hyperinflation)
Faecal elastase decreased (normally elastase produced by pancreas and found in faeces – pancreatic exocrine insufficiency and bowel obstruction decreases it)
Genetic testing (CFTR mutation chromosome 7 – delta-F508) by amniocentesis or chorionic villous sampling
Other: Newborn bloodspot test
What are the differential diagnosis for cystic fibrosis
Primary ciliary dyskinesia, asthma, GORD, coeliac disease
Describe the management for cystic fibrosis
1st line - Respiratory physiotherapy (mobilise mucus from walls – vibrating chest wall devices, positive expiratory pressure devices)
Inhaled mucolytics (dornase alfa), inhaled bronchodilator (salbutamol), empirical antibiotics for infection (tobramycin), anti-inflammatory (azithromycin, ibuprofen), pancreatic enzyme supplementation, CFTR modulator (ivacaftor)
Describe the complications for cystic fibrosis
Infections: s. aureus, h. influenza, p. aeruginosa. Male infertility, chronic respiratory failure, diabetes mellitus, arthritis.
Define bronchiectasis
Chronic inflammation of bronchi/bronchioles resulting in permanent dilation
Describe the aetiology for bronchiectasis
Post-infection (most common): TB, pneumonia, H. influenzae, S. pneumoniae
Other: cystic fibrosis, asthma, HIV, ABPA (allergic bronchopulmonary aspergillosis)
Describe the risk factors for bronchiectasis
Cystic fibrosis, immunosuppressed, previous infections, congenital bronchial airway disorders
Describe the pathophysiology for bronchiectasis
Irreversible dilation and loss of cilia > mucus hypersecretion which increased risk of infection due to decreased muco-ciliary clearance.
Usually affects lower lobes
What are the key presentations for bronchiectasis
Chronic, productive, foul-smelling cough with lots of sputum. Dyspnoea, recurrent respiratory tract infections
Describe the clinical manifestations for bronchiectasis
Signs: Finger clubbing, coarse inspiratory crackles, wheeze, haemoptysis, rhinosinusitis
Symptoms: Fever, fatigue, weight loss
What is the gold standard investigation for bronchiectasis
High resolution chest CT (thickened, dilated bronchi – signet ring sign - and cysts at the end of bronchioles. Big broncho:arterial ratio)
Describe the first line investigations for bronchiectasis
Sputum culture (H. influenzae, S. pneumoniae, P. aeruginosa),
spirometry (obstructive FEV1:FVC <0.7),
chest x-ray (cystic shadows, thickened bronchial walls),
FBC (raised WCC), low serum immunoglobulins
Other: Cystic fibrosis sweat test as bronchiectasis is common in CF, primary ciliary dyskinesia testing
What are the differential diagnosis for bronchiectasis
COPD, asthma, pneumonia
Describe the management for bronchiectasis
Conservative = Respiratory physiotherapy to clear secretions (e.g., postural drainage). Airway pharmacotherapy (mucolytics, inhaled corticosteroids, inhaled bronchodilator)
Antibiotics if infection (H. influenzae and S. pneumoniae = amoxicillin. P. aeruginosa = piperacillin/tazobactam).
Describe the complications for bronchiectasis
Empyema, lung abscess, respiratory failure, cor pulmonale
Define pleural effusion
Fluid collects between visceral and parietal pleural surfaces of the thorax
Describe the aetiology for pleural effusion
Transudate (protein <25g/L) = due to increased hydrostatic pressure or low oncotic pressure. E.g., congestive heart failure, liver cirrhosis, nephrotic syndrome, hypalbuminaemia
Exudate (protein >35g/L) = due to inflammation causing increased vascular permeability. E.g., cancer, TB, pneumonia, rheumatoid arthritis
Describe the risk factors for pleural effusion
Congestive heart failure, pneumonia, malignancy, pulmonary embolism
Describe the pathophysiology for pleural effusion
Rate of fluid formation > rate of fluid removal. Normal pleural space has some fluid for lubrication.
Exudate effusion: alteration of local factors like inflammation leading to capillary leakage of high protein (>35g/L) and LDH fluid into pleural space
Transudate effusion: mediated by systemic factors like elevated portal pressure from cirrhosis, heart failure or hypalbuminaemia, leading to low protein (<25g/L) and LDH fluid in pleural space
What are the key presentations for pleural effusion
Dyspnoea, dullness to percussion (due to increased fluid), cough, quieter breath sounds, pleuritic chest pain
Describe the signs of pleural effusion
Tracheal deviation away from effusion if it is massive
What is the gold standard investigation for pleural effusion
Chest x-ray (decreased costophrenic angles – blunting. Excess fluid appears white. Fluid in lung fissures. Tracheal and mediastinal deviation)
Describe the first line investigations for pleural effusion
Chest x-ray (blunting of costophrenic angle), pleural ultrasound (pleural fluid), thoracocentesis (identifies underlying cause. Sample pleural fluid: protein, LDH, pH, lactate, microscopy, WCC. Transudate – translucent. Exudate - cloudy)
What are the differential diagnosis for pleural effusion
Pneumothorax (hyper-resonant percussion), congestive heart failure, pulmonary embolism
Describe the management for pleural effusion
1st line - Chest drain/pleural aspiration. If recurrent, pleurodesis – surgical fusing of pleural layers to prevent fluid build-up.
Congestive heart failure – loop diuretics (furosemide, bumetanide), infection – empirical antibiotics (co-amoxiclav, metronidazole), malignant – therapeutic thoracocentesis
Describe the complications for pleural effusion
Empyema, pleural fibrosis, lobar collapse, pneumothorax following thoracocentesis
Define pneumothorax
Air in pleural space, causing ipsilateral collapse.
Classification: Spontaneous (without trauma or precipitating event),
Traumatic (penetrating or blunt injury to chest),
Iatrogenic (accidental consequence of medical interventions, e.g., central line, mechanical ventilation),
Lung pathology,
Tension pneumothorax (emergency, one way valve – air enters pleural space but cannot exit)
Describe the epidemiology for pneumothorax
Tall thin males, connective tissue disorder, smokers, trauma
Describe the aetiology for pneumothorax
Spontaneous or secondary to trauma, iatrogenic, lung pathology
Describe the risk factors for pneumothorax
Smoking, family history, male, tall and slender build, young age, presence of underlying lung disease
Describe the pathophysiology of pneumothorax
Normally intrapleural pressure is negative. Pleural space is a vacuum (no air). Breach in pleura causes abnormal connection between pleural space and airways.
Tension PTX – air enters pleural space but cannot exit. Increased positive pressure in chest. Collapse of ipsilateral lung and compression of contralateral lung, trachea, heart and other structures.
What are the key presentations for pneumothorax
Stable patient. Sudden onset one-sided pleuritic chest pain, dyspnoea, or cough. Hyper-resonant percussion. Decreased ipsilateral breathing sounds.
Tension PTX: cardiopulmonary deterioration – hypotension (imminent cardiac arrest), respiratory distress, low sats, tachycardia, shock. Severe chest pain. Increasing intrapleural pressure, worse with every breath
Describe the signs of pneumothorax
Evidence of trauma or tension pneumothorax on examination (tracheal deviation to contralateral side, ipsilateral reduced breath sounds, reduced air entry on ipsilateral side hyperresonance on percussion, hypoxia)
What is the gold standard investigation for pneumothorax
Chest x-ray (excess air appears black. Tracheal deviation to contralateral side. Reduced/absent lung markings between lung margin and chest wall. Visible rim between lung margin and chest wall)
Describe the first line investigations for pneumothorax
Erect chest x-ray (reduced/absent lung markings between lung margin and chest wall. Visible rim between lung margin and chest wall)
Bloods – clotting abnormalities. Chest USS. CT chest. ABG is stats <92% on room air.
What are the differential diagnosis for pneumothorax
Pulmonary embolism, myocardial infarction, asthma/COPD exacerbation
Describe the management for pneumothorax
Small primary spontaneous pneumothorax (visible rim <2cm) and not SOB: self-healing, consider discharge and follow-up chest x-ray.
Large primary spontaneous pneumothorax (visible rim >2cm) and/or SOB: needle aspiration and remove air with syringe, if not <2cm on repeat chest x-ray insert chest drain and supplemental O2 if needed. Chest drain triangle of safety: 5th intercostal space, midaxillary line, anterior axillary line.
If recurrent, pleurodesis (surgical fusion of pleura to stop pleural space filling)
Tension PTX: cardiac arrest call, high flow O2, immediate decompression. Unless due to trauma: insert large bore cannula into pleural space through 2nd intercostal space at midclavicular line. Hiss sound confirms diagnosis.
Describe the complications for pneumothorax
Effusion, haemorrhage, empyema, respiratory failure, cardiac arrest
Describe the prognosis for pneumothorax
Tension pneumothorax fatal if treatment delayed
Define tension pneumothorax
Caused by trauma to the chest wall that creates a one-way valve that lets air in but not out. Can lead to tracheal deviation away from side of the pneumothorax .
Describe the management of tension pneumothorax
Insert a large bore cannula into the second intercostal space in the midclavicular line
Define empyema
Presence of pus in pleural space
Describe the aetiology for empyema
Bacterial pneumonia
Describe the risk factors for empyema
Pneumonia, iatrogenic intervention in pleural space, alcohol, diabetes mellitus
Describe the pathophysiology for empyema
End-stage process of pleural inflammation. Pleural fluid accumulation > bacterial invasion > formation of pus
What are the key presentations for empyema
Infection and significant pleura effusion, recent pneumonia, pyrexia and rigors. Productive cough, pleuritic chest pain, dyspnoea.
What is the gold standard investigation for empyema
CT chest
Describe the first line investigations for empyema
Blood cultures, WBC and CRP raised, chest x-ray (blunting of costophrenic angle, effusion on affected side), thoracocentesis (pleural fluid sample: protein, LDH, pH, glucose, WCC, culture)
What are the differential diagnosis for empyema
Pleural effusion, pneumothorax, pneumonia
Describe the management for empyema
1st line – urgent chest drain.
Prolonged course of antibiotics (cefuroxime/ceftriaxone, metronidazole, co-amoxiclav)
Describe the complications for empyema
Sepsis, respiratory failure
Describe the prognosis for empyema
15-20% mortality
Define interstitial lung disease and idiopathic pulmonary disease
Interstitial lung disease: conditions that affect lung parenchyma causing inflammation and fibrosis. Idiopathic pulmonary fibrosis: Formation of scar tissue in lungs with no known cause.
Describe the epidemiology for idiopathic pulmonary fibrosis
Most common interstitial lung disease. 2/3 are over 60, more common in males
Describe the aetiology for idiopathic pulmonary fibrosis
Idiopathic
Describe the risk factors for idiopathic pulmonary fibrosis
Smoking, occupational (e.g., dust), drugs (amiodarone, methotrexate, cyclophosphamide, nitrofurantoin), viruses (CMV, EBV), autoimmune conditions (SLE, rheumatoid arthritis)
Describe the pathophysiology for idiopathic pulmonary fibrosis
Progressive scarring can lead to type 1 respiratory failure (low pO2, normal/low pCO2)
What are the key presentations for idiopathic pulmonary fibrosis
Dyspnoea, dry unproductive cough, bibasal inspiratory crackles, finger clubbing
Describe the symptoms for idiopathic pulmonary fibrosis
Weight loss, fatigue, malaise
What is the gold standard investigation for pulmonary fibrosis
High resolution chest CT: ground glass appearance of lungs and traction bronchiectasis (dilation of bronchioles)
Describe the first line investigations for pulmonary fibrosis
Spirometry = restriction (FEV1:FVC >0.7) but FVC is decreased <0.8.
Chest x-ray (abnormal opacities). Serology: antinuclear antibodies, rheumatoid factor, anti-cyclic citrullinated peptide (normal or slightly raised)
Other: lung biopsy and histology
What are the differential diagnosis for pulmonary fibrosis
Asbestosis, sarcoidosis, hypersensitivity pneumonitis, non-specific interstitial pneumonia
Describe the management for pulmonary fibrosis
Pharmacological: pirfenidone (pyridine – anti fibrotic and inflammatory), nintedanib (kinase inhibitor – antifibrotic properties)
Non-pharmacological: smoking cessation, physiotherapy, vaccines up to date
Surgery: lung transplant last resort. Consider proton pump inhibitor
Describe the complications for pulmonary fibrosis
GORD, pulmonary hypertension, pulmonary infection, lung cancer
Describe the prognosis for pulmonary fibrosis
2-5 years from diagnosis
Define sarcoidosis
Interstitial lung disease: conditions that affect lung parenchyma causing inflammation and fibrosis.
Sarcoidosis: inflammatory granulomatous disease. Granulomas are nodules of inflammation full of macrophages
Describe the epidemiology for sarcoidosis
Women, 20-40 years, Afro-Caribbean
Describe the aetiology for sarcoidosis
Unknown
Describe the risk factors for sarcoidosis
20-40 years, family history, Scandinavian origin, Afro-Caribbean
Describe the pathophysiology sarcoidosis
Sarcoidosis can affect almost every organ in the body, mostly the lungs (90%+ cases)
Lungs (mediastinal lymphadenopathy, pulmonary fibrosis and nodules), liver (cirrhosis, cholestasis, nodules), eyes (uveitis, conjunctivitis, optic neuritis), skin (erythema nodosum, lupus pernio, granulomas), heart (bundle branch block, heart block, myocardium involvement), kidneys (kidney stones, nephrocalcinosis, interstitial nephritis).
Sarcoidosis is a chronic granulomatous disorder. Granulomas are inflammatory nodules full of macrophages. The cause of these granulomas is unknown.
What are the key presentations for sarcoidosis
Fever, fatigue, dry cough, dyspnoea, extra-pulmonary manifestations (erythema nodosum, lymphadenopathy)
Describe the signs for sarcoidosis
Eye lesions (uveitis), lupus pernio (blue-red nodules on nose, cheeks, and ears)
Lofgren syndrome (specific acute Px of systemic sarcoidosis): triad of erythema nodosum, bilateral hilar adenopathy (lymph nodes of pulmonary hila), polyarthritis (esp. ankles)
What is the gold standard investigation for sarcoidosis
Biopsy and histology (non-caseating granulomas with epithelioid cells)
Describe the first line investigations for sarcoidosis
Raised serum calcium, raised serum ACE (granulomas), raised CRP, raised serum soluble interleukin-2 receptor, raised immunoglobulins, raised urea and creatinine.
Chest x-ray (bilateral hilar adenopathy), high resolution CT chest (bilateral hilar adenopathy and pulmonary infiltrates), MRI (CNS involvement)
Other: Other organ involvement: U&Es, urinalysis, albumin:creatinine ratio, LFTs, ophthalmology, ECG, echocardiogram, USS abdomen/liver/kidney
What are the differential diagnosis for sarcoidosis
Tuberculosis, lymphoma, HIV, hypersensitivity pneumonitis, toxoplasmosis
Describe the management for sarcoidosis
Early stages – self-resolving
Symptomatic – 1st line oral corticosteroids. Bisphosphonates to protect from osteoporosis due to long term steroids. 2nd line methotrexate or azathioprine.
Describe the complications for sarcoidosis
Pulmonary fibrosis, pulmonary hypertension, arrythmias, CNS involvement
Define pulmonary hypertension
Resting mean pulmonary arterial pressure (mPAP) >25mmHg. Increased resistance and pressure of blood in pulmonary arteries, causing strain on the right side of the heart and back pressure of blood into systemic venous system.
Describe the epidemiology for pulmonary hypertension
Women, 20-50 years
Describe the aetiology for pulmonary hypertension
Pre-capillary: pulmonary emboli, left-to-right shunts, primary pulmonary hypertension
Capillary: COPD, emphysema
Post-capillary: backlog of blood, left ventricle failure
Chronic hypoxaemia: living at high altitude, COPD
Describe the pathophysiology of pulmonary hypertension
Reactive pulmonary vasoconstriction when hypoxia (all causes result in hypoxaemia due to reduced perfusion to tissues) > increased pulmonary vascular resistance and pressure, leading to endothelial damage > RVH and failure.
What are the key presentations for pulmonary hypertension
Exertional dyspnoea, lethargy, fatigue, syncope, tachycardia, signs of RHF
Describe the signs for pulmonary hypertension
Right heart failure signs: Accentuated pulmonic component to the 2nd heart sound, tricuspid regurgitation murmur, peripheral oedema, ankle swelling, raised JVP, cyanosis
What is the gold standard investigation for pulmonary hypertension
Right heart catheterisation (>25mmHg)
Describe the first line investigations for pulmonary hypertension
Chest x-ray (enlarged pulmonary arteries, enlarged hilar vessels, right ventricular hypertrophy, pruning),
ECG (RVH, right atrial enlargement – peaked P waves, right axis deviation),
Trans-thoracic echocardiogram (right ventricular systolic pressure >35mmHg, right ventricular hypertrophy)
Describe the management for pulmonary hypertension
Phosphodiesterase-5 inhibitor (sildenafil – Viagra), CCB (amlodipine), endothelin-1-antagonists (ambrisentan, macitentan), prostaglandin analogues (epoprostenol).
Supportive therapy: oral anticoagulants, diuretics for fluid retention, supplemental oxygen, digoxin.
In treatment-resistant patients: balloon atrial septostomy (produces right-to-left shunt that decompressed right atrium and ventricle), lung transplantation
Describe the complications for pulmonary hypertension
Cor pulmonale, right sided heart failure
Describe the prognosis for pulmonary hypertension
30-40% 5-year survival
Define small cell lung cancer
Lung cancer arising from cells lining the lower respiratory tract. The tumour cells are small and densely packed, with scant cytoplasm, finely granular nuclear chromatin, and absence of nucleoli.
Describe the epidemiology for small cell lung cancer
Exclusively cigarette smokers, 15% of bronchial carcinomas
Describe the aetiology for small cell lung cancer
Cigarette smoking
Describe the risk factors for small cell lung cancer
Cigarette smoking, asbestos exposure, environmental tobacco exposure, radon gas exposure
Describe the pathophysiology for small cell lung cancer
SCLC cells contain neurosecretory granules that can release neuroendocrine hormones. This makes SCLC responsible for multiple paraneoplastic effects.
Secondary lung tumours are more common because all blood passes through the lungs so there is a higher risk of metastases
What are the key presentations for small cell lung cancer
Persistent cough, shortness of breath, haemoptysis, chest pain, wheeze, recurrent infections
Describe the clinical manifestations for small cell lung cancer
Signs: Signs of metastases (most commonly liver, bone, adrenal glands, brain): bone pain, headache, seizures, neurological deficit, abdominal pain, Pemberton sign (bilateral arm elevation causes facial plethora – shows SVC obstruction), Horner syndrome (Pancoast tumour – tumour in lung apex metastasises to neck sympathetic plexus causing Horner syndrome – miosis, ptosis and anhidrosis), recurrent laryngeal nerve palsy.
raised ADH > SIADH,
raised ACTH > Cushing’s disease,
Lambert Eaton syndrome.
Finger clubbing, lymphadenopathy
Symptoms: Cancer symptoms: weight loss, fever, night sweats, pain
What is the gold standard investigation for small cell lung cancer
Bronchoscopy and biopsy (endobronchial lesions, malignant cells, high nuclear to cytoplasm ratio)
Describe the first line investigations for small cell lung cancer
Chest x-ray (central mass, hilar lymphadenopathy, pleural effusion)
CT chest, abdomen, pelvis (lymphadenopathy, mediastinal invasion, staging)
Sputum culture (malignant cells in sputum)
Other: MRI, PET scan, bone scan for metastases
What are the differential diagnosis for small cell lung cancer
Non-small cell lung cancer, pneumonia, secondary lung cancer, carcinoid tumour
Describe the management for small cell lung cancer
1st line – if early = chemotherapy and radiotherapy. Often metastasised at presentation so may response to chemo but will relapse = palliative (radiotherapy, SVC stent, tracheal stent, pain relief)
Describe the complications for small cell lung cancer
SVC compression, tracheal compression, recurrent laryngeal nerve palsy, Horner syndrome (miosis, ptosis, anhidrosis), SIADH, Cushing’s
Describe the prognosis for small cell lung cancer
7% 5-year survival
Define non-small cell lung cancer
Any type of epithelial lung cancer other than small cell lung cancer. Most common types: adenocarcinoma (40%), squamous cell carcinoma (20%), large cell carcinoma (10%), carcinoid tumour.
Describe the epidemiology of non-small cell lung cancer
85% of lung cancers, SCC = smokers, AC = non-smokers
What are the risk factors for non-small cell lung cancer
Cigarette smoking, asbestos, coal, radon exposure, pulmonary fibrosis, COPD, genetics
Describe the pathophysiology for non-small cell lung cancer
Squamous cell carcinoma: most strongly associated with cigarette smokers. Arises from epithelial cells typically in central bronchus. Associated with production of keratin. May secrete PTHrP > hypercalcaemia.
Adenocarcinoma: most common cell type in non-smokers commonly asbestos. Originates from mucus-secreting glandular cells. Metastasises to pleura, lymph nodes, brain, bone, adrenals.
Carcinoid tumour: associated with genetics – MEN-1 mutation and neurofibromatosis. Neuroendocrine secretes serotonin, arises in GI tract, lung symptoms only present with liver mets.
Secondary lung tumours are more common because all blood passes through the lungs so there is a higher risk of metastases
What are the key presentations for non-small cell lung cancer
Persistent cough, shortness of breath, haemoptysis, weight loss, chest pain, wheeze, recurrent infections
Describe the clinical manifestations for non-small cell lung cancer
Signs: Signs of metastases (most commonly liver, bone, adrenal glands, brain): bone pain, headache, seizures, neurological deficit, abdominal pain, Pemberton sign (bilateral arm elevation causes facial plethora – shows SVC obstruction), Horner syndrome (Pancoast tumour – tumour in lung apex metastasises to neck sympathetic plexus causing Horner syndrome – miosis, ptosis and anhidrosis), recurrent laryngeal nerve palsy.
Paraneoplastic effects: raised PTH > hyperparathyroidism/hypercalcaemia,
Hypertrophic pulmonary osteoarthropathy (clubbing, arthritis, periostitis – SCC)
Finger clubbing, lymphadenopathy
Symptoms: Cancer symptoms: weight loss, night sweats, fever, pain
What are the gold standard investigations for non-small cell cancer
Bronchoscopy and biopsy (endobronchial lesions, histological diagnosis)
Describe the first line investigations for non-small cell cancer
Chest x-ray (pulmonary nodules, mass, pleural effusion, lung collapse)
CT chest, abdomen, pelvis (lymphadenopathy, mediastinal invasion, staging)
Sputum culture (malignant cells in sputum)
Other: MRI, PET scan, bone scan for metastases
What are the differential diagnosis for non-small cell cancer
Small cell lung cancer, metastatic cancer, pneumonia, non-Hodgkin’s lymphoma (BALT lymphoma)
Describe the management for non-small cell cancer
Less aggressive than SCLC.
1st line - surgical excision (e.g., lobectomy, segmentectomy/wedge resection, pneumonectomy.) Metastasised = chemotherapy and radiotherapy.
Palliative (radiotherapy, SVC stent, tracheal stent, pain relief)
Describe the complications for non-small cell cancer
SVC compression, tracheal compression, recurrent laryngeal nerve palsy, Horner syndrome (miosis, ptosis, anhidrosis), SIADH, Cushing’s
Describe the prognosis for non-small cell cancer
26% 5-year survival
Define mesothelioma
Lung cancer affecting mesothelial cells of the pleura
Describe the epidemiology for mesothelioma
Males, 40-70 years
Describe the aetiology for mesothelioma
Asbestos exposure (large latent period - typically doesn’t present until decades after exposure)
Describe the risk factors for mesothelioma
Asbestos exposure
What are the key presentations for mesothelioma
Shortness of breath, persistent cough, pleuritic chest pain, recurrent pleural effusions, diminished breath sounds, dullness to percussion
Describe the clinical manifestations for mesothelioma
Signs: Tumour may press on nearby structures, e.g., hoarse voice – recurrent laryngeal nerve palsy
Signs of metastases, e.g., bone pain
Symptoms: Cancer symptoms: weight loss, fever, night sweats, tired all the time, pain
What is the gold standard investigation for mesothelioma
Pleural biopsy (histological diagnosis)
Describe the first line investigations for mesothelioma
Chest x-ray (pleural thickening, pleural effusion, reduced lung volumes).
Chest CT (pleural thickening, pleural effusions, enlarged hilar/mediastinal lymph nodes)
CA-125 (cancer antigen 125) raised – non-selectively raised in many tumours.
What are the differential diagnosis for mesothelioma
Small cell lung cancer, non-small cell lung cancer
Describe the management for mesothelioma
Very aggressive tumour, usually palliative chemotherapy and surgery.
Describe the prognosis for mesothelioma
8 months – 2 years after diagnosis
Define hypersensitivity pneumonitis
Interstitial lung disease: conditions that affect lung parenchyma causing inflammation and fibrosis.
Hypersensitivity pneumonitis: non IgE mediated inflammation of alveoli and distal bronchioles caused by an immune response to inhaled allergens.
Describe the epidemiology for hypersensitivity pneumonitis
Bird fancier’s lung most common
Describe the aetiology for hypersensitivity pneumonitis
Bacteria e.g., thermophilic actinomycetes. Animal proteins e.g., avian proteins in pigeon breeder’s lungs, bird fancier’s lung, farmer’s lung, mushroom farmer’s lung
Describe the risk factors for hypersensitivity pneumonitis
Occupation (e.g., farming, bird-keeping)
Describe the pathophysiology for hypersensitivity pneumonitis
Involves both cellular immunity and deposition of immune complex (type 3 hypersensitivity). Mechanisms attract alveolar and interstitial macrophages leading to progressive development of pulmonary fibrosis
What are the key presentations for hypersensitivity pneumonitis
Acute (hrs after exposure): fever, tachypnoea, dyspnoea, rigors
Sub-acute (weeks-months after): malaise, dyspnoea, dry cough
Chronic (months-years after): little inflammation, fibrosis results in dyspnoea, weight loss, malaise
Describe the symptoms for hypersensitivity pneumonitis
History: exposure to avian proteins/meats/mould/chemicals
What is the gold standard investigation for hypersensitivity pneumonitis
Exposure to allergen + high resolution chest CT: ground glass shadowing
Describe the first line investigations for hypersensitivity pneumonitis
Serum IgG positive. Bronchoalveolar lavage: raised lymphocytes, mast cells.
Pulmonary function tests: restrictive in acute, mixed in sub-acute or chronic. DLCO reduced.
Chest x-ray: acute/sub-acute: patchy reticulonodular infiltrates. Chronic: fibrosis
Other: Lung biopsy
What are the differential diagnosis for hypersensitivity pneumonitis
Sarcoidosis, pneumoconiosis, viral pneumonia
Describe the management for hypersensitive pneumonitis
Acute: avoidance of allergen, smoking cessation, supplemental oxygen
Sub-acute/chronic: long term low dose corticosteroids (prednisolone)
Describe the complications for hypersensitivity pneumonitis
Lung function deterioration, hypoxaemia, death
Describe the levels of the MRC scale of dyspnoea
0 - No breathlessness except with strenuous exercise
1 - Shortness of breath when hurrying on the level or walking up a slight hill
2 - Walks slower than people of the same age on the level because of breathlessness or has to stop for breath when walking at own pace on the level
3 - Stops for breath after walking about 100 metres or after a few minutes on the level
4 - Too breathless to leave the house or breathless when dressing or undressing
Define type 1 respiratory failure
Inadequate gas exchange leading to hypoxia. PaO2 <8kPa (10.5 – 13.5)
Type 1: hypoxaemia without hypercapnia.
Define type 2 respiratory failure
Inadequate gas exchange leading to hypoxia. PaO2 <8kPa (10.5 – 13.5)
Type 2: hypoxaemia with hypercapnia (PaCO2 < 6kPa. Associated respiratory acidosis)
Describe the aetiology for type 1 resp failure
Type 1: pulmonary embolism, pulmonary oedema, pneumonia, ARDS, pneumothorax, asthma, COPD.
Describe the aetiology for type 2 resp failure
Type 2: motor neuron disease, Guillain-Barre syndrome, COPD, severe asthma, drug toxicity (opioids), stroke, hypothyroidism.
Describe the pathophsyiology for type 1 resp failure
Type 1 is associated with damage to lung tissue which prevents adequate oxygenation of blood however the remaining normal lung is still sufficient to expel carbon dioxide.
Respiratory failure leads to (LAVISH): Low inspired O2, Alveolar hyperventilation, Ventilation/Perfusion mismatch, Impaired diffusion, SHunt (pulmonary AV shunt)
Describe the pathophysiology for type 2 resp failure
Type 2 occurs when alveolar ventilation is insufficient to expel the carbon dioxide being produced. Inadequate ventilation is due to reduced ventilatory effort or inability to overcome increased resistance.
What are the key presentations for hypoxaemia and hypercapnia
Hypoxaemia: dyspnoea, confusion, tachypnoea, tachycardia, cyanosis, arrhythmia
Hypercapnia: headache, change of behaviour, coma, warm extremities
What is the gold standard investigation for resp failure
ABG (type 1: hypoxaemia without hypercapnia. Type 2: hypoxaemia with hypercapnia. pH <7.38)
Describe the first line investigations for resp failure
Pulse oximetry (SpO2 <80%), chest x-ray, blood gas analysis, end-tidal carbon dioxide monitoring (capnometry)
Describe the management for hypoxaemia and hypercapnia
1st line – hypoxaemia: supplemental oxygen (nasal cannula or mask).
If unsuccessful, non-invasive ventilation (non-invasive continuous positive airway pressure CPAP, or bilevel positive airway pressure BiPAP)
Hypercapnia: treat underlying cause
Define occupational lung disease
Interstitial lung disease: conditions that affect lung parenchyma causing inflammation and fibrosis.
Pneumoconioses (occupationally acquired ILD) due to inhalation of mineral dust or metal, e.g., silicon dioxide, asbestos, coal, beryllium
Describe the aetiology of occupational lung disease
Occupational exposure
What are the key presentations for occupational lung disease
Dyspnoea on exertion, dry cough, normal chest examination, crackles on auscultation
Describe the signs for occupational lung disease
Onset > 10 years after initial exposure in asbestosis
Silicosis: eggshell calcification at hilar lymph nodes
What is the gold standard investigation for occupational lung disease
High resolution chest CT (ground glass appearance)
Describe the first line investigations for occupational lung disease
Oxygen saturation reduced. Chest x-ray (silicosis – eggshell calcification), spirometry (restrictive FEV1:FVC >0.7). High resolution chest CT
What are the differential diagnosis for occupational lung disease
Occupational lung diseases: asbestosis, silicosis, coal worker’s lung, berylliosis. Farmer’s lung, bird breeder’s lung, malt worker’s lung
Describe the management for occupational lung disease
Remove exposure, smoking exposure, symptom treatment (oxygen, bronchodilator, corticosteroid)
Describe the complications for occupational lung disease
Asbestosis: mesothelioma, pleural thickening
Pneumonia, bronchitis, COPD
Define Goodpasture’s syndrome
Interstitial lung disease: conditions that affect lung parenchyma causing inflammation and fibrosis.
Goodpasture’s: type 2 hypersensitivity autoimmune anti-glomerular basement disease, where antibodies attack the basement membrane in lungs and kidneys > bleeding from lungs, glomerulonephritis, and kidney failure.
Describe the aetiology for Goodpasture’s syndrome
Autoimmune
What are the key presentations for Goodpasture’s syndrome
Haemoptysis, reduced urine output, oedema, dyspnoea, cough, glomerulonephritis, chest pain, fever, fatigue
What is the gold standard investigation for Goodpasture’s syndrome
Lung and kidney biopsy > IgG deposition, anti-GMB antibodies, crescentic glomerulonephritis
Describe the first line investigations for Goodpasture’s syndrome
Serology = anti-GBM antibodies, abnormal RFTs
What are the differential diagnosis for Goodpasture’s syndrome
SLE, granulomatosis with polyangiitis (Wegener’s), microscopic polyangiitis
Describe the management for Goodpasture’s syndrome
1st line – supportive, corticosteroids (prednisolone), immunosuppressant (cyclophosphamide), plasmapheresis
Describe the complications for Goodpasture’s syndrome
Pulmonary haemorrhage, chronic kidney disease
Define pharyngitis
Upper respiratory tract infection. Acute pharyngitis is characterised by the rapid onset of sore throat and pharyngeal inflammation (with or without exudate)
Describe the epidemiology for pharyngitis
Children
Describe the aetiology for pharyngitis
Viral: EBV, adenoviruses, enterovirus. Bacterial: group A streptococcus (s. pyogenes).
What are the key presentations for pharyngitis
Sore throat, fever, headache, nausea, abdominal pain.
Viral: rhinorrhoea, nasal congestion, cough.
Group A Streptococcus: pharyngeal exudates, cervical adenopathy, fever, absence of cough or rhinorrhoea.
What is the gold standard investigation for pharyngitis
Rapid antigen detection tests for Group A strep, NAAT for GAS. If negative, conventional throat swab culture
Describe the management for pharyngitis
Group A streptococcus = supportive care + antibiotics (phenoxymethylpenicillin, amoxicillin).
Not Group A strep = supportive care (analgesics: paracetamol, ibuprofen, lidocaine).
Describe the complications for pharyngitis
Scarlet fever, rheumatic fever
Define otitis media
Upper respiratory tract infection. Inflammation of the middle ear, associated with effusion and signs of infection.
Describe the aetiology for otitis media
Viral: RSV (respiratory syncytial), rhinovirus, adenovirus, influenza virus
Bacterial: S. pneumoniae, H. influenzae, Moraxella catarrhalis
Describe the risk factors for otitis media
Young age, male, smoking, frequent contact with other children
Describe the pathophysiology for otitis media
Infection of nasal passages, eustachian tube and middle ear causes inflammation and impairs mucociliary action and ventilatory function of eustachian tube. Middle ear effusion develops and grows bacteria.
What are the key presentations for otitis media
Otalgia (ear pain), reduced hearing, preceding URTI symptoms (cough, sore throat), fever, sleep disturbance, irritability in children, coryzal symptoms (rhinorrhoea, nasal congestion)
What is the gold standard investigation for otitis media
Otoscopy (bulging and erythema of tympanic membrane)
Describe the management for otitis media
1st line – analgesia (ibuprofen/paracetamol). If symptoms have not improved after 3 days, Amoxicillin 5–7-day course
Describe the complications for otitis media
Otitis media with effusion, tympanic membrane rupture, mastoiditis
Define sinusitis
Upper respiratory tract infection. Acute sinusitis (aka rhinosinusitis) is inflammation of the mucosal lining of the nasal cavity and paranasal sinuses.
Describe the aetiology for sinusitis
Viral infection. Some cases progress to bacterial sinusitis (S. pneumoniae, H. influenzae, Moraxella catarrhalis)
Describe the pathophysiology for sinusitis
Viral infection > inflammatory response with sinonasal mucosa > oedema and mucus production which blocks ventilation and drainage > decreased mucociliary clearance and stasis of secretions > secondary bacterial infection
What are the key presentations for sinusitis
Viral (peak early and gradually resolve, symptoms <10 days): clear nasal discharge, fever, sore throat.
Bacterial (symptoms >10 days): purulent nasal discharge, nasal congestion, dental/facial pain, headache.
What is the gold standard investigation for sinusitis
Clinical diagnosis (distinguish between viral and bacterial)
Other: Nasal endoscopy, sinus culture
Describe the management for sinusitis
Viral sinusitis = self-limiting disease, treatment is symptomatic (analgesia – paracetamol, ibuprofen. Nasal decongestant spray)
Bacterial sinusitis = symptomatic, antibiotics (amoxicillin)
Define acute epiglottitis
Upper respiratory tract infection. Inflammation of epiglottis, airway emergency especially in children.
Describe the epidemiology for acute epiglottitis
Young children <6 years
Describe the aetiology for acute epiglottitis
Usually H. influenzae, also S. pneumoniae.
Describe the pathophysiology for acute epiglottitis
Infection causes swelling of epiglottis which obstructs the airways.
What are the key presentations for acute epiglottitis
Acute high onset fever (39-40 degrees), toxic appearance (lethargy, poor perfusion, cyanosis, hypo/hyperventilation).
Tripoding breathing (sits leaning forward with arms on knees, tongue out, or stands with arms resting on another surface, e.g., table).
Sore throat, dysphagia, difficulty breathing, decreased oral intake, drooling, stridor.
What is the gold standard investigation for acute epiglottitis
Laryngoscopy during intubation.
Other: Lateral neck radiography if laryngoscopy not possible – thumb print sign (soft tissue sign that looks like thumb pressing into trachea).
Describe the management for acute epiglottitis
1 – secure the airway: direct rigid laryngoscopy and intubation. Mask ventilation follows commonly.
2 – IV antibiotics (cefotaxime, ceftriaxone, clindamycin)
3 – supplemental O2, heliox (lowers gas flow resistance, increases ventilation) and corticosteroids.
Define Croup
Upper respiratory tract infection causing oedema in the larynx. Also called laryngotracheobronchitis.
Describe the epidemiology for croup
Children 6 months - 2 years
Describe the aetiology croup
Parainfluenza virus, influenza, adenovirus, respiratory syncytial virus (RSV)
What are the key presentations for croup
Increased work of breathing, ‘barking’ cough occurring in clusters of coughing episodes, hoarse voice, stridor, low grade fever
What is the gold standard investigation for croup
Clinical diagnosis
Describe the management for croup
1st line – single dose oral dexamethasone. Supportive (fluids, analgesia, nebulised budesonide, nebulised adrenaline).
Describe the complications for croup
Acute respiratory distress syndrome
Define Whooping cough
Upper respiratory tract infection caused by Bordetella pertussis (gram negative bacteria). Coughing fits are so severe that the child is unable to take air between coughs and subsequently makes a loud whooping sound as they forcefully suck in air after the coughing ends.
Describe the epidemiology for whooping cough
Young children < 5 years
Describe the aetiology for whooping cough
Bordetella pertussis
What are the key presentations for whooping cough
Paroxysmal coughing fits. Dyspnoea. Loud inspiratory whoop when coughing ends.
Coryzal symptoms (rhinorrhoea, nasal congestion, sneezing), fever, dry cough.
Describe the key signs for whooping cough
From coughing: syncope, vomiting, pneumothorax, apnoea.
What is the gold standard investigation for whooping cough
Nasopharyngeal swab with PCR testing or bacterial culture.
Other: NAAT nasopharyngeal culture, Anti-pertussis toxin immunoglobulin G
Describe the management for whooping cough
1st line – Macrolides (1 – azithromycin, 2 – clarithromycin/erythromycin). Also co-trimoxazole (trimethoprim/sulfamethoxazole)
Notifiable disease.
Define Wegener’s granulomatosis
Vasculitis is inflammation of blood vessels. Wegener’s granulomatosis affects small blood vessels.
Describe the aetiology for Wegener’s granulomatosis
Autoimmune
Describe the risk factors for Wegener’s granulomatosis
Young adult
Describe the pathophysiology for Wegener’s granulomatosis
Small vessel vasculitis affecting ENT, lungs and kidneys (ELK)
What are the key presentations for Wegener’s granulomatosis
ENT: Saddle shaped nose due to perforated nasal septum, epistaxis, crusty nasal/ear secretions > hearing loss, sinusitis,
Lungs: Cough, wheeze, haemoptysis, dyspnoea
Kidneys: glomerulonephritis > haematuria
Describe the symptoms of Wegener’s granulomatosis
Malaise, fatigue, weight loss, fever, night sweats
What is the gold standard investigation for Wegener’s granulomatosis
cANCA positive + symptoms
Describe the first line investigations for Wegener’s granulomatosis
FBC: raised eosinophils, raised CRP/ESR, tissue biopsy shows granulomas, CT chest shows lung nodules, urinalysis (haematuria), ANCA positive
What are the differential diagnosis for Wegener’s granulomatosis
Small vessel vasculitis: Henoch-Schoenlein purpura (IgA deposits, purpura, joint pain, abdo pain, renal involvement), microscopic polyangiitis (pANCA +ve), eosinophilic granulomatosis with polyangiitis (Churg-Strauss – asthma, pANCA positive, raised eosinophils)
Describe the management for Wegener’s granulomatosis
Corticosteroids (methylprednisolone and prednisolone) and immunosuppressants (rituximab, cyclophosphamide). Plasmapheresis, IV immunoglobulin.
Describe the complications for Wegener’s granulomatosis
Glomerulonephritis, deafness, chronic renal failure
