Respiratory

Question 1

What is the definition and epidemiology of ARDS?

Answer 1

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).

Question 2

What is the aetiology of ARDS?

Answer 2

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.

Question 3

What are the clinical features of ARDS?

Answer 3

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.

Question 4

How is ARDS investigated?

Answer 4

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.

Question 5

What is the definition and epidemiology of Aspergillus Lung Disease?

Answer 5

Definition: Lung disease associated with Aspergillus fungal infection. It is fairly uncommon and tends to affect the elderly and immunosuppressed.

Question 6

What are the different types of Aspergillus Lung Disease?

Answer 6

Inhalation of the ubiquitous Aspergillus spores can produce three different clinical features:

1. Aspergilloma - Growth of A. fumigatus mycetoma ball in pre-existing lung cavity (post-TB, infarct or abscess).
2. Allergic bronchopulmonary aspergillosis affects patients with asthma, cystic fibrosis and sinusitis. Aspergillus colonisation of the airway leads to immune response causing.
3. Invasive aspergillosis - invasion of Aspergillus into lung tissue and fungal dissemination. Secondary to immunosuppression (e.g. neutropenia, steroids, AIDS).

Question 7

What are the clinical features of Aspergillus Lung Disease?

Answer 7

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.

Question 8

How can Aspergillus Lung Disease be investigated

Answer 8

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.

Question 9

What is the definition and epidemiology of Asthma?

Answer 9

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.

Question 10

What is the aetiology of Asthma?

Answer 10

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).

Question 11

What are the triggers of Asthma?

Answer 11

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.

Question 12

What are the clinical features of Asthma?

Answer 12

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.

Question 13

How is a severe and life-threatening asthma attack defined?

Answer 13

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

Question 14

What are the complications of Asthma?

Answer 14

Complications include: growth retardation (in children), chest wall deformity, recurrent infections, pneumothorax, respiratory failure and death.

Question 15

How is Asthma investigated?

Answer 15

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

Question 16

How is Asthma managed?

Answer 16

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:

1. For mild intermittent and exercise-induced asthma: Inhaled short-acting β2-agonist as required, such as salbutamol or levosalbutamol.
2. For mild persistent: As step 1 + low-dose inhaled steroids such as fluticasone.
3. For moderate persistent: As step 2 + long-acting β2-agonist such as salmeterol. If inadequate control with LADA then increase steroid dose.
4. For severe persistent: As step 3 + increase steroid dose and add fourth drug such as a leukotriene antagonist or β2-agonist tablet.
5. As step 4 + addition regular oral steroids.

Question 17

What is the prognosis of Asthma?

Answer 17

Many children improve as they get older. Adult-onset tends to be more chronic.

Question 18

What is the definition and epidemiology of Bronchiectasis?

Answer 18

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.

Question 19

What is the aetiology of Bronchiectasis?

Answer 19

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.

Question 20

What are the clinical features of Bronchiectasis?

Answer 20

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.

Question 21

What are the complications of Bronchiectasis?

Answer 21

Massive haemoptysis, respiratory failure and cor pulmonale.

Question 22

How can Bronchiectasis be investigated?

Answer 22

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.

Question 23

How is Bronchiectasis managed?

Answer 23

The three principles of managing bronchiectasis is as follows:
1. Identify, and when possible, treat the cause.

2. 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.
3. Maintain or improve pulmonary function.
   a. Minimising active chronic infection
   b. Reducing the frequency and severity of exacerbations
   c. Using bronchodilators regularly (beta-agonists).

Question 24

What is the definition and epidemiology of COPD?

Answer 24

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.

Question 25

What is the aetiology of COPD?

Answer 25

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.

Question 26

[What is the pathophysiology of COPD]?

Answer 26

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.

Question 27

What are the symptoms of COPD?

Answer 27

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.

Question 28

What are the examination features of COPD?

Answer 28

* 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).

Question 29

How can COPD be investigated?

Answer 29

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.

Question 30

How is COPD managed?

Answer 30

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: 1. Short-acting bronchodilators such as salbutamol or ipratropium to be taken when required. 2. 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 3. All of the above, plus inhaled corticosteroid such as beclomethasone / fluticasone. Add theophylline or phosphodiesterase-4 inhibitor. 4. All of the above, plus supplemental oxygen if PaO2 is  ≤7.3 kPa. Consider lung volume reduction surgery (LVRS). Also get palliative care involved.

Question 31

What is the definition and epidemiology of Idiopathic Pulmonary Fibrosis?

Answer 31

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.

Question 32

What is the aetiology [and pathophysiology] of Pulmonary Fibrosis?

Answer 32

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.

Question 33

What are the clinical features of Pulmonary Fibrosis?

Answer 33

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).

Question 34

How can Pulmonary Fibrosis be investigated?

Answer 34

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.

Question 35

What is the definition and epidemiology of Lung Cancer?

Answer 35

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.

Question 36

What is the aetiology of Lung Cancer?

Answer 36

Cigarette smoking causes 9 out of 10 cases of lung cancer, including passive smoking. Other risk factors include occupational exposure and atmospheric pollution.

Question 37

Describe the different types of Lung Cancer

Answer 37

There are four different histological types: • Adenocarcinomas (40%) - found in peripheral lung, associated with slower growth, but metastases are common at presentation. • Squamous cell carcinomas (30%) - found in central airways, with slower growth and later metastases. • Small-cell carcinoma (20%) - found in central airways, associated with rapid growth and early metastases. • Large-cell carcinoma (10%) found in peripheral lung, associated with slower growth and later metastases.

Question 38

What are the clinical features of Lung Cancer?

Answer 38

The common clinical signs of the primary tumour include: • Cough • Haemoptysis • Systemic symptoms such as tiredness, weight loss and anorexia. Patients can also present with symptoms and signs associated with metastases, often without respiratory symptoms. The following symptoms are less common: • Shortness of breath, commonly caused by lobular collapse secondary to bronchial obstruction, pleural effusions, lymphangitis carcinomatosis or extensive intrapulmonary metastases. • Wheeze caused by bronchial obstruction. • Progressive localised pain, resulting from chest wall or mediastinal invasion.

Question 39

What are the extra clinical features of Non Small-Cell Cancer?

Answer 39

As well as symptoms from primary tumour, symptoms can also be produced due to local invasion: • SVC compression - facial congestion, distention of the neck veins, upper limb oedema. • Brachial plexus - wasting of the small muscles of the hand • Sympathetic chain - Horner's syndrome. Due to metastatic or paraneoplastic syndrome: • Weight loss, fatigue, fits, bone pain or fractures, neuromyopathies. • Clubbing, painful swollen wrists/ankles (hypertrophic osteoarthropathy). • Dermatological signs such as acanthosis nigricans, herpes zoster, dermatomyositis.

Question 40

What are the extra clinical features of Small-Cell Cancer?

Answer 40

Usually metastasised by the time of presentation, producing symptoms of weight loss, fatigue and bone pain. Common signs include supraclavicular lymphadenopathy or hepatomegaly. May also have signs of paraneoplastic syndrome, or symptoms including weakness, lethargy, seizures and muscle fatigability.

Question 41

What are the investigations of Lung Cancer?

Answer 41

The general diagnostic approach in a patient with suspected lung cancer is as follows: 1. CXR to look for a cancer. Tumours often cause a shadow. Enlarged lymph nodes indicate the presence of a tumour even if a shadow is not visible. Other associated signs such as a collapsed lung, pleural effusion or pleural thickening may also be identified. Old CXRs are useful for comparison to assess if a shadow is new or has changed. 2. Further imaging to stage the extent of local disease and detect metastases. A CT scan of the lungs, liver and adrenal glands are essential in all patients with suspected lung cancer. If neurological signs are present, CT/MRI of the brain is necessary to detect cerebral metastases. 3. Biopsy of suspected tumour to confirm diagnosis and for histopathology. This can be through a bronchoscopy, percutaneous needle biopsy, thoracocentesis (needle aspiration) or surgical biopsy. 4. Blood tests to help identify metastases and paraneoplastic syndromes, as well as to assess the patient's background health before treatment. 5. Pulmonary function tests to assess lung reserve if curative therapy is potentially possible.

Question 42

What is the definition and epidemiology of Obstructive Sleep Apnoea?

Answer 42

Obstructive Sleep Apnoea is characterised by the recurrent collapse of the pharyngeal airway and apnoea (defined as cessation of airflow for >10s) during sleep, followed by arousal from sleep. Also known as Pickwickian syndrome. Very common affecting 5-20% of men, 2-5% of women >35 years. Prevalence increases with age.

Question 43

What is the aetiology of Obstructive Sleep Apnoea?

Answer 43

Obstructive apnoeas occur when the upper airway narrows because of collapse of the soft tissues of the pharynx when tone in phalangeal dilators decreases during sleep. Associated with: • Excessive weight gain, smoking, alcohol and sedative use • Enlarged tonsils or adenoids in children • Macroglossia, Marfan's syndrome, craniofacial abnormalities.

Question 44

What are the clinical features of Obstructive Sleep Apnoea?

Answer 44

Patients present with excessive daytime sleepiness (at work, driving), unrefreshing/restless sleep. Morning headaches or dry mouth, difficulty concentrating, irritability or mood changes. Partners may report snoring, nocturnal apnoeic episodes or nocturnal chocking. On Examination Patient may have a enlarged tongue, tonsils, long or thick uvula. Larger neck circumference is strongly associated with disease. Obesity and hypertension is common.

Question 45

How can Obstructive Sleep Apnoea be investigated?

Answer 45

Diagnosed with sleep study either by a sleep study centre or portable tests?

Question 46

What is the definition and epidemiology of Pneumoconiosis?

Answer 46

Pneumoconiosis is a fibrosing interstitial lung disease (like idiopathic pulmonary fibrosis), caused by chronic inhalation of mineral dusts. Incidence is increasing in developing countries.

Question 47

What are the types of Pneumoconiosis?

Answer 47

There are many types, common ones include: • Simple: (Coalworker's pneumoconiosis or silicosis) - tends to be asymptomatic • Complicated: Pneumoconiosis results in a loss of lung function (due to progressive massive fibrosis) • Asbestosis: A pneumoconiosis in which diffuse lung fibrosis occurs as a result of prolonged exposure to asbestos.

Question 48

What is the aetiology pf Pneumoconiosis?

Answer 48

It is caused by inhalation of particles of coal dust, silica or asbestos. Therefore risk factors are mainly occupational exposure to any of those dusts.

Question 49

What are the clinical features of Pneumoconiosis?

Answer 49

Occupational history is important, as there may be a long latency between dust exposure and disease process. Simple coal or silica pneumoconiosis tends to be asymptomatic and is only picked up on incidental CXR. If symptomatic, there is usually insidious onset of dyspnoea, and a dry cough. Occasionally black sputum is produced in coalworker's pneumoconiosis. Asbestosis also presents with pleuritic chest pain many years after first exposure. On Examination Examination may be normal in simple pneumoconiosis. There is usually decreased breath sounds in coalworker's pneumoconiosis or silicosis. Asbestosis produces end-inspiratory crepitations and clubbing.

Question 50

How can Pneumoconiosis be investigated?

Answer 50

A CXR (PA and lateral) shows nodular opacities in the upper lobes (as opposed to basilar in idiopathic pulmonary fibrosis). 'Egg-shell calcification' of the hilar lymph nodes are classical in silicosis. A HRCT can also be used. Lung function tests show non-specific signs or are normal. Are used to determine severity and pharmacological treatment.

Question 51

What is the definition and epidemiology of Pneumothorax?

Answer 51

Pneumothorax is air in the pleural space (the potential space between visceral and parietal pleura). Other variants depend on the substance in the pleural space (e.g. blood = haemothorax, lymph = chylothorax). Annual incidence of spontaneous pneumothorax is 9 in 100,000. Mainly affecting 20-40 year olds. Four times more common in males.

Question 52

What is the aetiology of Pneumothorax?

Answer 52

* Spontaneous: Occurs in individuals with previously normal lungs, typically tall thin males. Probably caused by rupture of subpleural bleb. * Secondary: In pre-existing lung disease (COPD, asthma, TB, pneumonia, carcinoma, cystic fibrosis, diffuse lung disease). * Traumatic: Penetrating injury to the chest, often iatrogenic causes (e.g. during subclavian or jugular venous cannulation, thoracentesis, pleural or lung biopsy, or positive pressure assisted ventilation).

Question 53

What are the risk factors for Pneumothorax?

Answer 53

Risk factors include collagen disorders such as Marfan's disease and Ehlers-Danlos syndrome.

Question 54

What are the clinical features of Pneumothorax?

Answer 54

Patient may be asymptomatic if pneumothorax is small. On the other hand, they may present with sudden onset chest pain, dyspnoea, or both. On examination, patients are breathless with reduced expansion. On percussion, affected lung will be hyper-resonant. On auscultation, there will be absent breath sounds on ipsilateral lung as well as reduced or absent vocal resonance. A tension pneumothorax presents with severe respiratory distress, tachycardia, hypotension, cyanosis, distended neck veins and tracheal deviation away from side of pneumothorax.

Question 55

How can Pneumothorax be investigated?

Answer 55

The main differential for sudden onset breathlessness with chest pain is a pulmonary embolism. A chest X-ray readily confirms a pneumothorax. Seen as a dark area of the film where lung markings do not extent to. Fluid level may be seen if there is blood present. In small pneumothoraces, expiratory films may make it more prominent. An ABG may be necessary to determine if there is any hypoxaemia, particularly in secondary disease.

Question 56

How is Pneumothorax managed?

Answer 56

Small (<2cm) primary pneumothoraces resolve spontaneously and are simply monitored. Patients who are symptomatic, or who have a moderate-large (>2cm) pneumothoraces require, or with ANY sized secondary pneumothoraces are treated: 1. Aspiration using a large-bore cannula or catheter with three-way tap: Inserted into the second intercostal space in the midclavicular line. Up to 2.5L of air can be aspirated. Advise to stop diving. Follow up CXR after 2h and 2weeks. 2. If aspiration fails, perform a chest drain with water seal. Advise patients to avoid air travel until follow-up CXR shows resolution. Ensure to give them regular analgesia before you leave the patient.

Question 57

What is the prognosis of Pneumothorax?

Answer 57

After one spontaneous pneumothorax, at least 20% will have another, with the frequency increasing with repeated pneumothoraces.

Question 58

Define pneumonia

Answer 58

Pneumonia refers to an infection of the distal lung parenchyma (alveoli and interstitium).

Question 59

What are the organisms that cause typical and atypical pneumonia?

Answer 59

Typical • Streptococcus Pneumoniae (gram+) • Haemophilus Influenzae (gram-) Atypical • Chlamydia pneumonia and psittaci - contact with birds/parrots (gram-) • Mycoplasma pneumoniae - periodic epidemics (no cell-wall) • Legionella - anywhere with air conditioning (gram-) • Staphylococcus Aureus - anywhere with air conditioning (gram-) [Hospital Acquired] • Pseudomonas Aeruginosa (gram+) [Hospital Acquired] • Anaerobes - aspiration pneumonia

Question 60

What are the clinical features of a typical pneumonia?

Answer 60

Chest symptoms with fever should make you consider pneumonia. Patient may also have rigors, malaise and anorexia. Elderly patients also present with confusion. Chest symptoms include dyspnoea, productive cough (yellow, green or rusty sputum in S. pneumoniae), and pleuritic chest pain. On Examination Signs include pyrexia, respiratory distress, tachypnoea, tachycardia, hypotension and cyanosis. A respiratory examination may show reduced chest expansion, dullness on percussion, increased vocal resonance, bronchial breathing and coarse crepitations on affected side.

Question 61

What can be some clinical features of atypical pneumonia?

Answer 61

Patients may present with a longer period of malaise, complain of headaches, myalgia and diarrhoea/vomiting as well as abdominal pain. They may have no signs of on chest examination.

Question 62

What are the complications of pneumonia?

Answer 62

Lungs: type 1 respiratory failure, pleural effusion, empyema, lung abscess Heart: atrial fibrillation, pericarditis, myocarditis Other: septicaemia, hypotension, cholestatic jaundice, brain abscess, renal failure.

Question 63

How can pneumonia be investigated?

Answer 63

The approach is to establish a diagnosis of pneumonia, followed by identifying the pathogen and finally assessing the severity. Bloods: • FBC (WCC raised), • U&Es (↓Na+ especially in Legionella) • LFTs (legionella can cause LFT derangement). • Blood cultures • ABG (to assess pulmonary function) • Blood film (M. pneumoniae can cause haemolytic anaemia, showing as cold agglutinins) CXR shows lobar or patchy shadowing - kinda 'fluffy' instead of well-demarcated. Sputum MC&S (microscopy, culture and sensitivity) and pleural aspirate. A urine antigen test can detect streptococcus pneumoniae or legionella.

Question 64

How is pneumonia managed?

Answer 64

CURB65 Score: If the patient scores 2 or more they should be admitted into hospital for treatment. A score of 3 or more is severe and consider ITU. ABC resuscitation: • If hypoxic, administer oxygen to maintain PaO2 > 8 and SaO2 > 94%. • If dehydrated or hypotensive, administer fluids. • Treat pain with analgesia such as paracetamol. Antibiotics (for Gram+) • If mild - give oral Amoxicillin • If moderate - give oral or I.V Amoxicillin and Clarithromycin • If severe - give I.V Co-Amoxiclav and Clarithromycin and seek urgent help. Request follow up at 6 weeks.

Question 65

What are the unique features of Streptococcus Pneumoniae?

Answer 65

* Gram + diplococcus. * Alpha haemolytic * Catalase negative * Oxidase negative. Lives in the throats of most people. Most common cause of Community Acquired Pneumonia. Causes a rusty coloured sputum. Causes a lobar pneumonia.

Question 66

What are the unique features of Haemophilus Influenzae?

Answer 66

• Gram - bacilli Common cause of pneumonia in COPD patients. Causes yellow/green sputum.

Question 67

What are the unique features of Mycoplasma pneumoniae?

Answer 67

* Lacks a complete cell wall lol * Most common 'atypical' pneumonia - occurs in epidemics * Associated with AIHA (cold aglutinins). * Transverse myelitis is a complication. * Treated with macrolides such as erythromycin. * Young people who live together common affected.

Question 68

What are the unique features of Chlamydia psittaci and pneumoniae?

Answer 68

They are gram - Psittaci is associated with birds. Pneumoniae is associated with a mild pneumonia in young people, causing small segmental infiltrates.

Question 69

What are the unique features of Legionella?

Answer 69

* Gram - rod * Associated with air conditioning, plumbers, hot tubs * Also associated with smokers. * Causes hypernatraemia, deranged LFTs and altered consciousness * Can be detected by urine antigen detection

Question 70

What are the unique features of Pseudomonas aeroginosa?

Answer 70

* Gram - bacilli * Affects Cystic Fibrosis, bronchiectasis patients, neurtopaenic states e.g. post chemotherapy. * Produces green pigment in culture (pyoverdin) * Causes hospital acquired infections and UTIs. * Not sensitive to many antibiotics originally used for gram negatives.

Question 71

What are the unique features of Staphylococcus aureus?

Answer 71

* Gram + round shaped that is coagulase positive. * Affects elderly and post-influenza * Affects IV Drug Users (in association with staphylococcal endocarditis of tricuspid valve) * Bilateral cavitating bronchopneumonia (not lobar). * Can arise from osteomyelitis.

Question 72

What are the unique features of Pneumocystis jirovecii?

Answer 72

Causes PCP pneumonia in immunocompromised. It is a yeast-like fungus. • Non-productive cough • Marked dyspnoea (out of proportions with CXR). • Boat-shaped organisms on Bronchio-alveolar Lavage • Also causes eosinophilia.

Question 73

What is the definition and epidemiology of PE?

Answer 73

A pulmonary embolism is the occlusion of pulmonary vessels, most commonly by a thrombus that has travelled to the vascular system from another site. PE's are relatively common, especially in hospitalised patients. They occur in 10-20% of those with a confirmed proximal DVT.

Question 74

How can a PE be classified?

Answer 74

Acute pulmonary emboli cause symptoms and signs in a few hours or days. When associated with cardiac arrest or shock, is called a massive pulmonary embolism. A chronic pulmonary embolism is caused by multiple small pulmonary emboli. This causes dyspnoea and pulmonary hypertension that progresses slowly over weeks or months.

Question 75

What is the aetiology of PE?

Answer 75

95% are caused by a thrombus originating from DVT of the lower limbs, or rarely from right atrium in patients with AF. Other agents that can emboli's include amniotic fluid embolus, fat emboli, tumour emboli etc.

Question 76

What is the CURB65 Score?

Answer 76

In deciding where a pneumonia patient should be managed, use the CURB65 tool to assess severity: C = confusion <8 AMT U = urea >7 mmol/L R = respiratory rate ≥30/min B = blood pressure <90 systolic or <60 diastolic Age = ≥65 years If the patient scores 2 or more they should be admitted into hospital for treatment. A score of 3 or more is severe and consider ITU.

Question 77

What are the risk factors for PE?

Answer 77

``` Strong Risk Factors • Increasing age • Diagnosis of a DVT • Surgery within the last 2 months • Bed rest for >5 days or paralysis • Previous thromboembolic event • Family history • Active malignancy • Pregnancy/postprandial period ```

Question 78

What are the clinical features of PE?

Answer 78

Symptoms depend on the size and site of the pulmonary embolus: Small pulmonary embolus may be asymptomatic. There are often no clinical signs. Earliest sign is tachycardia or tachypnoea. A moderate PE causes sudden onset dyspnoea, cough, haemoptysis, and pleuritic chest pain. A large or proximal PE will also cause shock, collapse and acute heart failure or sudden death. Chronic PE patients present with signs of pulmonary hypertension. And have signs of right heart failure. On examination Patient will be tachypnoeic, tachycardic and have low O2 saturation. You may be able to hear a pleural rub. A massive PE can cause shock, cyanosis and signs of right heart strain (↑JVP, left parasternal heave and accentuated S2 heart sound).

Question 79

Describe the Simplified Well's score

Answer 79

1 point for each: - Clinical sign of DVT - Alternative diagnosis less likely than PE - Previous PE or DVT - Heart rate >100bmp - Surgery or immobilisation within 4 weeks - Haemoptysis - Active cancer A PE is deemed likely if the score is 2 or more.

Question 80

How is PE investigated?

Answer 80

A Well's score or Geneva score should be used to assess the likelyhood of PE. If PE is unlikely, perform a D-dimer blood test (high sensitivity but poor specificity) to rule out PE. If D-dimer is positive, or PE probability is likely from score, then use a CTPA (CT Pulmonary Angiogram) to confirm diagnosis of a clot in one or more pulmonary arteries. A ventilation-perfusion scan can also indicate a PE. A normal VQ scan virtually excludes PE. However, the results are often ideterminate, meaning the diagnosis cannot be confirmed or excluded. Furthermore, the scan is difficult to interpret in patients with chronic lung disease. Bloods: • ABG may show hypoxia and hypercapnia. • Consider thrombophilia screen. An ECG may be normal, or more commonly show tachycardia, right axis deviation or RBBB (right heart strain). You may rarely see the classical SI, QIII, TIII pattern. A CXR may be normal and is used to exclude other diseases as cannot show the emboli. However, the lung damage caused but the PE can be visible as areas of atelectasis and wedge-shaped peripheral consolidation. A pulmonary angiography is the gold standard test for PE. However, the procedure is rarely used as it Is invasive.

Question 81

How is a Pulmonary Embolism managed?

Answer 81

Patients with acute PE receive supportive oxygen therapy, analgesics for chest pain and fluids for hypotension. Patients with massive PE require urgent stabilisation in intensive care and are considered for thrombolysis with tPA. Haemodynamically stable patients are anticoagulated to speed clot resolution and prevent further emboli. Patients are first treated for 5-7 days with subcutaneous injections of LMWH. Long-term oral anticoagulation with warfarin starts at the same time, and continued for three months. This is to achieve a therapeutic INR of 2-4. An embolectomy is considered for massive pulmonary emboli, with the patient being at high risk of bleeding. Inferior Vena Cava filters may be inserted for recurrent PE.

Question 82

What is the prognosis of a PE?

Answer 82

For untreated PE, mortality is as high as 30%, but down to 8% with treatment. Patients have an increased risk of thromboembolic events in the future.

Question 83

Define tuberculosis

Answer 83

Tuberculosis is an infectious disease caused by Mycobacterium tuberculosis.

Question 84

What is the epidemiology of PE?

Answer 84

Tuberculosis is the most common fatal bacterial infection worldwide. The incidence of tuberculosis is highest in sub-Saharan Africa and Asia. In Europe and North America, most cases of TB are in immigrants born in high-incidence countries.

Question 85

What are the different types of tuberculosis that affect lungs?

Answer 85

* Primary infection: the initial pulmonary infection with M. tuberculosis. Tends to be asymptomatic, but can cause a progressive and fatal infection. * Latent tuberculosis: dormant M. tuberculosis infection that can reactivate decades after initial infection. * Post-primary/reactivation tuberculosis: progression of latent tuberculosis to active disease. * Pulmonary tuberculosis: active tuberculosis affecting lungs * Extrapulmonary tuberculosis: active tuberculosis affecting other organs. * Miliary tuberculosis: active tuberculosis disseminated by the blood throughout the body. * Bovine tuberculosis: tuberculosis caused by M. bovis and acquired from ingesting infected cows' milk. * Multi-drug-resistant tuberculosis: M. tuberculosis resistant to rifampicin and isoniazid.

Question 86

What are the risk factors for tuberculosis?

Answer 86

``` Risk Factors • Exposure to infection • Birth in an epidemic country • HIV infection • Immunosuppression ```

Question 87

What are the clinical features of tuberculosis?

Answer 87

Tuberculosis presents as a subacute infection with a history of over weeks or months. This includes a history of systemic symptoms such as night sweats, malaise, fevers, anorexia and weight loss. Pulmonary tuberculosis causes a cough and often haemoptysis, which is occasionally severe and life threatening. Dyspnoea is a feature of extensive disease. Examination of the lungs is often normal, but sometimes identify patches of crepitations and bronchial breathing.

Question 88

How can tuberculosis be investigated?

Answer 88

Consider tuberculosis in all patients from a high-incidence country, or high-incidence group who present with focal lung disease or systemic symptoms. A CXR shows fibronodular opacities (cavitations) in upper lobes. The mediastinal nodes are often enlarged. A sputum acid-fast bacilli smear test will be positive for acid-fast bacilli. at least 2 to 3 specimens should be collected minimum 8 hours apart, including an early morning specimen, which is the best to detect M. tuberculosis). Only positive in 50% of patients. A sputum culture is positive in 70-80% of cases, and allows drug sensitivity testing. However, culture takes up to 6 weeks and patients frequently need to be treated before the results are available. If unable to produce sputum culture, a gastric aspirate or bronchoalveolar lavage can be done. Nucleic acid amplification tests are done to confirm that sputum-positive Mycobacteria are M. tuberculosis. Mantoux tests and interferon-y release blood tests identify a cell-mediated immune response to M. tuberculosis. However, mantoux tests are also positive after BCG vaccinations.

Question 89

How is tuberculosis managed?

Answer 89

The standard tuberculosis regimen is: 1. Initial phase (8 weeks) of rifampicin, isoniazid, ethambutol and pyrazinamide. 2. Continuation phase (18 weeks) of rifampicin and isoniazid alone. Multidrug resistant TB is very difficult to treat and requires prolonged treatment with complex and often toxic combinations of anti-mycobacterial agents.

Question 90

What is the prognosis of tuberculosis?

Answer 90

The cure rate for properly treated tuberculosis is 95%. Failure to improve is often due to poor adherence or drug-resistant disease (frequently fatal).