Respiratory Flashcards
What is the definition and epidemiology of ARDS?
ARDS is a syndrome of acute and persistent lung inflammation with increased vascular permeability (non-cardiogenic pulmonary oedema). It is characterised by:
• Acute onset
• Bilateral infiltrates consistent with pulmonary oedema
• Hypoxaemia
• No clinic evidence of increased left atrial pressure
Annual UK incidence is 1 in 6000 (not uncommon).
What is the aetiology of ARDS?
ARDS is the severe end of ‘Acute Lung Injury’. It is caused by severe insult to the lungs and other organs, which causes the release of inflammatory mediators. This causes increased vascular permeability, pulmonary oedema, impaired gas exchange, and decreased lung compliance.
Common causes include: • Sepsis • Aspiration • Pneumonia • Pancreatitis • Trauma/burns • Transfusion, transplantation, and drug overdose.
What are the clinical features of ARDS?
Patients present with risk factors (severe injury to lungs), and rapid deterioration of lung function. Dyspnoea, respiratory distress, cough.
Examination
On examination of patient, notice cyanosis, tachypnoea, tachycardia, widespread inspiratory crepitations. Hypoxia unresponsive to oxygen treatment.
How is ARDS investigated?
CXR: Bilateral alveolar and interstitial shadowing.
Bloods:
• FBC, U&E, LFTs
• ESR/CRP
• ABG shows low oxygen partial pressure.
• Blood culture to detect underlying infection
• Plasma BNP (low) may distinguish ARDS from heart failure.
Urine and sputum culture to detect underlying infection.
Echocardiography: severe aortic or mitral dysfunction or decreased left ventricular ejection fraction favours haemodynamic oedema over pulmonary oedema.
Pulmonary artery catheterisation can be used to determine whether pulmonary oedema is cardiogenic if diagnosis is still in doubt after measuring BNP levels and carrying out an echocardiography.
Bronchoscopy can be used to exclude differentials.
What is the definition and epidemiology of Aspergillus Lung Disease?
Definition: Lung disease associated with Aspergillus fungal infection. It is fairly uncommon and tends to affect the elderly and immunosuppressed.
What are the different types of Aspergillus Lung Disease?
Inhalation of the ubiquitous Aspergillus spores can produce three different clinical features:
- Aspergilloma - Growth of A. fumigatus mycetoma ball in pre-existing lung cavity (post-TB, infarct or abscess).
- Allergic bronchopulmonary aspergillosis affects patients with asthma, cystic fibrosis and sinusitis. Aspergillus colonisation of the airway leads to immune response causing.
- Invasive aspergillosis - invasion of Aspergillus into lung tissue and fungal dissemination. Secondary to immunosuppression (e.g. neutropenia, steroids, AIDS).
What are the clinical features of Aspergillus Lung Disease?
Aspergilloma
Asymptomatic, haemoptysis, which may be massive. A large aspergilloma may cause tracheal deviation.
Allergic Bronchopulmonary Aspergillosis
Patients usually present as difficult to control asthma, recurrent episodes of pneumonia with wheeze, cough, fever and malaise. On examination there is dullness on affected lung, decreased breath sounds, and wheeze.
Invasive Aspergillosis
Presents as dyspnoea with rapid deterioration. Looks like sepsis.
How can Aspergillus Lung Disease be investigated
Aspergilloma
CXR shows a round opacity, with a crescent of air around it. A CT or MRI can be used if still unclear.
Sputum Culture may be negative if there is no communication between the cavity and bronchial tree.
ABPA
As it is caused by an immune reaction to Aspergillus, an immediate skin test reactivity to Aspergillus antigens.
Bloods will show eosinophilia, and increased IgE and IgG. Also specific antibodies to A. fumigatus.
CT and CXR are used as imaging modalities.
Invasive Aspergillosis
Detection of Aspergillus in cultures or by histologic examination. Usually prompted by risk factors and clinical signs.
What is the definition and epidemiology of Asthma?
Asthma is a chronic inflammatory airway disease characterised by reversible airway obstruction, airway hyper-responsiveness and bronchial inflammation. Note that asthma is a chronic condition, but is a disease that can be exacerbated upon exposure to triggers. Asthma is very common, affecting 10% of adults, and 5% of children. Acute asthma is an important emergency, as it still causes 1000-2000 deaths in the UK annually.
What is the aetiology of Asthma?
Aetiology is not completely known, but development of asthma can be attributed to genetic and environmental factors:
• Genetic factors: family history, genes that confer atopy (the tendency to produce abnormally high levels of IgE for an otherwise harmless foreign environmental substance).
• Environmental factors: predominant theory concerning early childhood exposure to allergens (Hygiene hypothesis).
What are the triggers of Asthma?
Triggers for asthma exacerbations include:
• Environmental allergens such as grass pollen, domestic pets, dust mites
• Viral infections from Rhinovirus, Parainfluenza virus and RSV
• Cold air
• Emotions
• Irritants such as perfume or cigarette smoke.
• Drugs, typically NSAIDs, β-adrenoceptor antagonists
• Atmospheric pollution such as sulphur dioxide, ozone and particulates
• Occupational sensitizers.
What are the clinical features of Asthma?
Patients complain of symptoms after exposure to a trigger. Some patients will report all three of the classic symptoms, while some only two:
• Wheezing (high-pitched whistling sound usually during inspiration)
• Coughing (usually worse at night)
• Breathlessness or Dyspnoea
On examination, patient may be tachypnoea, prolonged expiratory phase, polyphonic wheeze and a hyper-inflated chest.
How is a severe and life-threatening asthma attack defined?
A severe attack manifests as: • PEFR (Peak Expiratory Flow Rate) of <50% predicted. • Pulse >110bpm • Respiratory Rate >25/min • Inability to complete sentences
A life-threatening attack manifests as:
• PEFR <33%
• Silent chest, cyanosis, bradycardia, hypotension, confusion and coma
What are the complications of Asthma?
Complications include: growth retardation (in children), chest wall deformity, recurrent infections, pneumothorax, respiratory failure and death.
How is Asthma investigated?
In an acute setting: • Peak flow and pulse oximetry and ABG • CXR to exclude other causes such as pneumonia • FBC, CRP, U&Es • Blood and sputum cultures
In a chronic setting:
• PEFR monitoring and seeing if improvement after administration of β2-agonist
• Spirometry pattern of asthma, that resolves with bronchodilation
Skin prick test may help identify allergens
How is Asthma managed?
ACUTE:
• Resuscitate (ABC),
• Monitor O2 stats, ABG and PEFR.
• Immediately start on nebulised salbutamol and ipratropium if needed.
• IV hydrocortisone, followed by 40mg oral prednisolone.
• IV Magnesium Sulphate, Aminophylline or Salbutamol of not improving
• If PCO2 increasing, get anaesthetic help
CHRONIC ‘stepwise’ therapy:
- For mild intermittent and exercise-induced asthma: Inhaled short-acting β2-agonist as required, such as salbutamol or levosalbutamol.
- For mild persistent: As step 1 + low-dose inhaled steroids such as fluticasone.
- For moderate persistent: As step 2 + long-acting β2-agonist such as salmeterol. If inadequate control with LADA then increase steroid dose.
- For severe persistent: As step 3 + increase steroid dose and add fourth drug such as a leukotriene antagonist or β2-agonist tablet.
- As step 4 + addition regular oral steroids.
What is the prognosis of Asthma?
Many children improve as they get older. Adult-onset tends to be more chronic.
What is the definition and epidemiology of Bronchiectasis?
Bronchiectasis is a lung airway disease characterised by chronic bronchial dilation, impaired mucociliary clearance and frequent bacterial infections. It is not uncommon, affecting 1 in 1000. Most often arises initially in childhood.
What is the aetiology of Bronchiectasis?
Severe inflammation in the lungs causes fibrosis and dilation of the bronchi. This is followed by pooling of mucus, predisposing to further cycles of infection, damage and fibrosis to bronchial walls. Causes include:
• Idiopathic in up to 50% of cases.
• Post-infectious: prior childhood viral respiratory infections (i.e measles, influenza, pertussis), prior infections with mycobacteria or severe pneumonia, exaggerated response to Aspergillus fumigatus.
• Immunodeficiency
• Genetic causes such as cystic fibrosis (often treated separately due to range of additional clinical problems), ciliary dyskinesia.
• Obstruction of bronchi, gastric reflux disease, inflammatory disorders.
What are the clinical features of Bronchiectasis?
Symptoms usually begin after an acute respiratory illness. The cardinal symptom of bronchiectasis is cough with chronic sputum (often daily) production. Sputum is mucoid or purulent, haemoptysis is also common.
Other symptoms include breathlessness, chest pain, malaise, fever, and weight loss.
On Examination
Patient may have clubbing, coarse crepitations (usually at the bases) which shift with coughing. Also notice a wheeze.
What are the complications of Bronchiectasis?
Massive haemoptysis, respiratory failure and cor pulmonale.
How can Bronchiectasis be investigated?
Bronchiectasis is an anatomical diagnosis made when radiological evidence of dilated bronchi are found.
CXR may be normal, or show bronchial wall thickening, ring shaddows and tramlines. Because of the limitations of CXR, diagnosis is based on CT findings.
A HRCT shows thickened or dilated airways. It is the best diagnostic method.
Sputum cultures can reveal the organism causing infection or exacerbation.
FBC can show eosinophilia for bronchopulmonary aspergillosis, or neutrophilia for bacterial infections.
How is Bronchiectasis managed?
The three principles of managing bronchiectasis is as follows:
1. Identify, and when possible, treat the cause.
- Improve quality of life by minimising daily sputum production and reducing frequency of exacerbations.
a. Regular use of self-administered lung clearance techniques - require respiratory physiotherapy.
b. Effective treatment of exacerbations with prolonged courses of appropriate antibiotics.
c. Severe disease may require oral or nebulised prophylactic antibiotic therapy.
d. Long term azithromycin therapy has anti-inflammatory effects that are very effective at reducing daily sputum production. - Maintain or improve pulmonary function.
a. Minimising active chronic infection
b. Reducing the frequency and severity of exacerbations
c. Using bronchodilators regularly (beta-agonists).
What is the definition and epidemiology of COPD?
COPD is a chronic, progressive lung disorder characterised with airflow obstruction with the following:
• Chronic bronchitis - inflammation of the bronchial tubes, leading to a chronic productive cough (that is present for at least 3 months /year for the last 2 years).
• Emphysema - abnormal, permanent enlargement of air spaces distal to the terminal bronchioles (alveoli).
COPD is very common, affecting 8% of the population.
What is the aetiology of COPD?
In developed countries, cigarette smoking accounts for over 90% of cases. However, only 10-20% of heavy cigarette smokers develop COPD, indicating individual susceptibility. Exposure to smoke from solid fuel used for cooking is a major cause of COPD in low- and middle-income countries.
[What is the pathophysiology of COPD]?
Exposure to noxious particles such as oxidants in tobacco smoke, causes excessive inflammatory response in the airways driven mainly by macrophages, CD8 (T-killer) lymphocytes and neutrophils.
This inflammation causes scarring and thickening to the reparatory epithelium that narrows the airways, and increases the number of mucous-secreting cells.
Noxious particles also increase the number of proteinases in the lungs. These are normally neutralised by antiproteinases, but this increase upsets the balance, allowing the proteinases to digest lung tissue.
These processes result in the three main features of COPD:
• Hypersecretion of mucus
• Small airway obstruction
• Alveolar destruction (emphysema)
COPD usually progresses slowly, but its severity increases if the patient has frequent exacerbations and comorbidities.
What are the symptoms of COPD?
Patients will usually present with a productive cough (see definition) that starts out in the morning. As the disease progresses, the cough becomes constant. Patients also present with shortness of breath when exercising, but this progresses to dyspnoea at rest as the disease progresses.
Exacerbations cause increased breathlessness, wheeze, cough and the production of sputum (which may be purulent). These symptoms may be preceded by coryzal symptoms (runny nose and sneezing) suggesting a viral upper respiratory tract infection.
What are the examination features of COPD?
- Inspection: May have respiratory distress (laboured breathing), use of accessory muscles, barrel-shaped overinflated chest, decreased cricosternal distance and may also show cyanosis.
- Percussion: hyper-resonant chest, loss of liver and cardiac dullness.
- Auscultation: Quiet breath sounds, prolonged expiration, wheeze, ronchi (coarse rattling respiratory sound) and crepitations sometimes present.
- Signs of CO2 retention: bounding pulse, warm peripheries, asterixis.
- In late stages, signs of right heart failure (e.g right ventricular heave, raised JVP, ankle oedema).
How can COPD be investigated?
Spirometry and pulmonary function tests will show an obstructive picture as reflected by ↓PEFR, ↓FEV1:FVC ratio, ↑lung volumes.
CXR may appear normal or show hyperinflation and decreased lung markings, elongated cardiac silhouette.
Bloods: FBC may show secondary polycythaemia.
ABG and pulse oximetry show low oxygen saturation.
ECG and echocardiogram for cor pulmonale - may show right ventricular hypertrophy, arrhythmia and ischaemia.
Sputum and blood cultures in acute exacerbation, to pick antibiotic treatment.
How is COPD managed?
Important to facilitate smoking cessation as soon as possible. Influenza and pneumococcal vaccinations should be offered to all COPD patients.
Inhaled therapies are the mainstay of the pharmacological treatment of COPD. Step-wise therapy:
- Short-acting bronchodilators such as salbutamol or ipratropium to be taken when required.
- Long-acting bronchodilators to be given if (1) is not enough. These include salmeterol / formoterol (beta agonist) or tiotropium (anticholinergic). They can also take short-acting when required. Also start on pulmonary rehabilitation
- All of the above, plus inhaled corticosteroid such as beclomethasone / fluticasone. Add theophylline or phosphodiesterase-4 inhibitor.
- All of the above, plus supplemental oxygen if PaO2 is ≤7.3 kPa. Consider lung volume reduction surgery (LVRS). Also get palliative care involved.
What is the definition and epidemiology of Idiopathic Pulmonary Fibrosis?
Idiopathic pulmonary fibrosis (also called idiopathic fibrosing alveolitis or cryptogenic fibrosing alveolitis) is a progressive lung disease that results in the fibrosis of alveoli (parenchyma) and interstitium (basement membrane and interstitial cells surrounding air spaces).
It is rare (prevalence in UK is around 6 in 100,000), affects men more than women (2:1), and mean age of diagnosis is 67 years.
What is the aetiology [and pathophysiology] of Pulmonary Fibrosis?
The aetiology of pulmonary fibrosis is:
• Largely idiopathic (60% of patients) - there is some link between cigarette smoking, organic or metal dust, GORD, diabetes and infection and idiopathic pulmonary fibrosis.
• Connective tissue diseases such as rheumatoid arthritis and systemic sclerosis can cause interstitial lung disease.
• Certain drugs and chemotherapy can also increases susceptibility.
It is posited that an injury/insult to the lung tissue triggers a pro-inflammatory and pro-fibrotic response. This causes the epithelium (alveolar) to develop mesenchymal properties through the deposition of extracellular matrix proteins, destruction of lung tissue and scarring.
What are the clinical features of Pulmonary Fibrosis?
Pulmonary fibrosis presents with progressive dyspnoea over months and a dry cough. General symptoms like weight loss, fatigue and malaise are common.
On examination
Patient have:
• Reduced chest expansion bilaterally
• Clubbing (15-25%)
• Fine, late inspiratory Velcro crackles that are bilateral and basilar.
• Signs of right heart failure in advanced stages (right ventricular heave, raised JVP and peripheral oedema).
How can Pulmonary Fibrosis be investigated?
A CXR is usually normal on presentation. However, later there is basilar, bilateral and asymmetrical reticular opacities on film.
A HRCT (High Resolution CT) should be ordered for all patients with a suspected diagnosis of IPF. This will show basilar and subpleural predominant areas of increased reticulation, honeycombing and possible traction bronchiectasis.
Pulmonary Function Tests will show restrictive changes (see here): ↓FEV1, ↓FVC, preserved or increased ratio, ↓ lung volumes, ↓ lung compliance and ↓ TLCO.
Blood tests may have normal ABG in early disease. But ↓PCO2 on exercise. One third of patients have rheumatic factor or are ANA positive.
A bronchoalveolar lavage is used to exclude infections and malignancy.
A lung biopsy is the gold standard for diagnosis, but often not appropriate/necessary.
What is the definition and epidemiology of Lung Cancer?
Lung cancers are malignancies arising from the respiratory epithelium. Lung cancer is one of the most common cancers worldwide, accounting for 13% of new cancers. It is also the most common cause of cancer death, with one of the lowest survival rates of any type of cancer.
What is the aetiology of Lung Cancer?
Cigarette smoking causes 9 out of 10 cases of lung cancer, including passive smoking. Other risk factors include occupational exposure and atmospheric pollution.
