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Respiratory Flashcards

1
Q

What is asthma?

A

Chronic inflammatory condition characterised by exacerbations of bronchoconstriction (reversible airway obstruction).

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2
Q

Is asthma a restrictive or obstructive disease?

A

Obstructive.

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3
Q

What are risk factors for the development of asthma?

A

Family history, history of atopy, exposure to tobacco smoke, exposure to pollutants.

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4
Q

Give examples of asthma triggers.

A

Infection, exercise, animals, cold/damp, dust and strong emotions.

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5
Q

What are the clinical features of asthma?

A

Episodic symptoms of wheeze, dry cough, shortness of breath and chest tightness.

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6
Q

What is heard on auscultation in a person with asthma?

A

Bilateral widespread polyphonic wheeze.

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7
Q

What formal tests can be done in the diagnosis of asthma?

A

Spirometry with reversibility testing.

Fractional exhaled nitric oxide (FeNO).

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8
Q

Spirometry: What is FEV1?

A

Forced expiratory volume 1 is the volume of air exhaled at the end of the first second of forced expiration.

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9
Q

Spirometry: What is FVC?

A

Forced vital capacity is the volume of air exhaled after maximal expiration following full inspiration.

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10
Q

What are the typical results of spirometry in a person with asthma?

A

FEV1 significantly reduced.
FVC normal.
FEV1/FVC < 70%.

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11
Q

What are the results of spirometry in a person with asthma following reversibility testing?

A

FEV1 improvement of ≥ 12%.

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12
Q

Describe how FeNO test is used in the diagnosis of asthma.

A

Nitric oxide is produced by three types of nitric oxide synthases… one of which is inducible and levels tend to rise in inflammatory cells. The level of nitric oxide is measured.

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13
Q

What are the results of the FeNO test in a patient with asthma?

A

Adults ≥ 40 ppb.

Children ≥ 35 ppb.

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14
Q

Outline the six step asthma treatment ladder.

A
  1. SABA (salbutamol).
  2. ICS (beclometasone).
  3. LTRA (montelukast).
  4. LABA (salmeterol).
  5. MART.
  6. Theophylline.
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15
Q

Asthma: How do SABA/salbutamol work?

A

Relax smooth muscles of the airways.

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16
Q

Asthma: What is a potential side effect of SABA?

A

Fine tremor.

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17
Q

When should asthma management progress beyond SABA?

A

Using salbutamol inhaler more than twice per week.

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18
Q

Asthma: What are side effects of ICS (in adults and children)?

A 
Oral candidiasis. 
Stunted growth (children).
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19
Q

What is acute asthma?

A

The rapid worsening of asthma symptoms as a result of a trigger (infection, exercise, cold weather, allergens).

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20
Q

What is the presentation of acute asthma?

A

Breathlessness, wheeze, dry cough and chest tightness.

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21
Q

What is heard on auscultation in acute asthma?

A

Symmetrical expiratory wheeze with reduced air entry throughout.

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22
Q

How is the severity of acute asthma graded?

A

Peak expiratory flow rate (PEFR).

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23
Q

What is the PEFR in moderate acute asthma?

A

50-75% of best/predicted.

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24
Q

What are the characteristics of an episode of severe asthma attack?

A

PEFR 33-50% of best/predicted.
Pulse rate >110.
Respiratory rate >25.
Too breathless to complete sentences.

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25
Q

What are the characteristics of an episode of life-threatening asthma attack?

A 
PEFR < 33% of predicted. 
Oxygen saturations < 92%. 
Silent chest. 
Poor respiratory effort. 
Altered consciousness. 
Cyanosis.
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26
Q

What are the initial findings on ABG in acute asthma?

A

Respiratory alkalosis as tachypnoea leads to a fall in carbon dioxide.

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27
Q

How may ABG results show deterioration in an episode of acute asthma?

A

If pCO2 is normal or there is hypoxia = concerning (patient is tiring).
If there is respiratory acidosis = very concerning.

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28
Q

What is the management of moderate acute asthma?

A 
Give oxygen. 
Nebulised 5mg salbutamol. 
Nebulised ipratropium bromide. 
Steroids (e.g. intravenous hydrocortisone). 
Antibiotics (if infection suspected).
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29
Q

What is the management of severe acute asthma?

A

Moderate management +
Intravenous aminophylline.
Intravenous salbutamol.

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30
Q

What is the management of life-threatening acute asthma?

A

Severe management +
Intravenous magnesium sulphate.
ICU and intubation.

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31
Q

What is chronic obstructive pulmonary disease (COPD)?

A

Progressive obstructive lung disease characterised by long-term breathing problems with poor airflow.

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32
Q

What is the most common cause of COPD?

A

Smoking (typically a 20 pack-year history).

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33
Q

Suggest two causes (other than smoking) of COPD.

A 
Air pollution (wood combustion, cooking fires). 
Alpha-1 antitrypsin deficiency.
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34
Q

Describe the pathophysiology of COPD.

A

Long-term exposure to irritants causes an inflammatory response in the lungs, resulting in a narrowing of the small airways and breakdown of lung tissue. Damage causes obstruction to the flow of air making the lungs more difficult to ventilate.

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35
Q

What are the clinical features of COPD?

A

Dyspnoea, breathlessness, productive cough, wheeze and a history of recurrent respiratory infections.

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36
Q

Describe how breathlessness progresses over the disease-course of COPD.

A

Breathlessness is initially on exertion but later becomes chronic. Everyday activities (getting dressed) become more difficult.

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37
Q

How is a diagnosis of COPD made?

A

Based on clinical presentation + lung function testing (spirometry) which demonstrates a FEV1/FVC ratio of < 0.7

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38
Q

What spirometry results classify COPD into stage 1 (mild)?

A

FEV1/FVC < 0.7

FEV1 > 80% of predicted

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39
Q

What spirometry results classify COPD into stage 2 (moderate)?

A

FEV1/FVC < 0.7

FEV1 50-79% of predicted

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40
Q

What spirometry results classify COPD into stage 3 (severe)?

A

FEV1/FVC < 0.7

FEV1 30-49% of predicted

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41
Q

What spirometry results classify COPD into stage 4 (very severe)?

A

FEV1/FVC < 0.7

FEV1 < 30% of predicted

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42
Q

In COPD what is demonstrated by spirometry following bronchodilator therapy / reversibility testing?

A

Obstructive picture does not show a dramatic response with beta-2 agonists, unlike in asthma.

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43
Q

What is found on chest x-ray in an individual with COPD?

A

Hyperinflation.
Bullae.
Flat hemidiaphragm.

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44
Q

What may FBC reveal in patients with COPD?

A

Polycythaemia (raised Hb).

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45
Q

Why do some patients with COPD have polycythaemia?

A

Increased haemoglobin is a response to chronic hypoxia.

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46
Q

What are the initial steps (lifestyle) in the management of COPD?

A

Encourage immediate smoking cessation, offer nicotine replacement therapy.

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47
Q

What vaccinations should be offered to people with COPD?

A

Annual influenza vaccine.

One-off pneumococcal vaccine.

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48
Q

What is the first-line pharmacological management of COPD?

A 
Salbutamol (SABA). 
Ipratropium bromide (SAMA).
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49
Q

What is the pharmacological management of COPD following SABA and SAMA use?

A

Determine whether patient is steroid-responsive. If not give salmeterol (LABA) + tiotropium (LAMA). If steroid-responsive give salmeterol (LABA) + beclometasone (ICS).

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50
Q

Give examples of additional pharmacological management options in COPD.

A

Oral theophylline.
Oral mucolytic (carbocisteine)
Prophylactic azithromycin.
Long-term oxygen therapy.

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51
Q

What are the most common causes of infective exacerbations of COPD?

A

Haemophilus influenzae.

Streptococcus pneumoniae.

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52
Q

What are the clinical features of exacerbations of COPD?

A

Worsening dyspnoea, cough, wheeze and an increase in sputum production.

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53
Q

How are arterial blood gasses used in the management of exacerbations of COPD?

A

Determine the presence/extent of carbon dioxide retainment, hypoxia and respiratory failure.

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54
Q

COPD: What is indicated by low pH and raised pCO2 on ABG?

A

Respiratory acidosis.

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55
Q

COPD: What is indicated by raised bicarbonate on ABG?

A

Chronic retainment of CO2… kidneys have responded by increasing bicarbonate production to maintain a normal pH.

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56
Q

COPD: What is indicated by low pO2 on ABG?

A

Hypoxia and respiratory failure.

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57
Q

COPD: What is indicated by low pO2 and normal pCO2 on ABG?

A

Type 1 respiratory failure.

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58
Q

COPD: What is indicated by low pO2 and raised pCO2 on ABG?

A

Type 2 respiratory failure.

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59
Q

What are the risks of giving a patient with COPD too much oxygen?

A

Too much oxygen can suppress the patients respiratory drive, slowing their breathing rate and leading to more CO2 retention.

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60
Q

What are the target oxygen saturations for a patient with COPD retaining CO2?

A

88-92%.

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61
Q

What is the pharmacological management of an exacerbation of COPD?

A 
Increase SABA use. 
Consider nebuliser. 
Oral prednisolone. 
Antibiotics. 
Mucolytics (carbocisteine).
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62
Q

What is non-invasive ventilation?

A

An alternative to intubation that involves placing a tight fitting mask on the face to forcefully blow air into the lungs… supporting the lungs in respiratory failure due to obstructive disease.

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63
Q

What are the two types of non-invasive ventilation?

A

BiPAP.

CPAP.

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64
Q

Describe BiPAP.

A

Bilevel positive airway pressure involves a cycle of high and low pressure that corresponds to the patient’s inspiration and expiration.

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65
Q

When is BiPAP used?

A

Type 2 respiratory failure (e.g. in COPD).

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66
Q

What are the criteria for initiation of BiPAP?

A

Respiratory acidosis (pH < 7.35, pCO2 > 6).

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67
Q

What are the names of the two pressures that compose BiPAP?

A

Inspiratory positive airway pressure (IPAP).

Expiratory positive airway pressure (EPAP).

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68
Q

What is the function of EPAP in BiPAP?

A

Pressure during expiration to prevent airway collapse and allow air to escape the lungs.

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69
Q

Describe CPAP.

A

Continuous positive airway pressure involves continuous flow of air into the lungs to maintain airway expansion so air can travel in and out easier.

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70
Q

When is CPAP used?

A

Obstructive sleep apnoea
Congestive cardiac failure
Acute pulmonary oedema

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71
Q

What is a pulmonary embolism?

A

The result of venous thrombus that passes into the pulmonary circulation and blocks the flow of blood to the lungs.

72
Q

What are risk factors for PE?

A

Malignancy, recent surgery, long haul flights, pregnancy, combined oral contraceptive use, previous thromboembolism and thrombophilia.

73
Q

What VTE prophylaxis can be given to hospital inpatients?

A

Anti-embolic compression stockings.

Low molecular weight heparin (LMWH).

74
Q

What is a contraindication to anti-embolic compression stocking use in VTE prophylaxis?

A

Peripheral arterial disease.

75
Q

What are two contraindications of LMWH use in VTE prophylaxis?

A

Active bleeding.

Existing anticoagulation.

76
Q

What is the clinical presentation of pulmonary embolism?

A

Acute dyspnoea, pleuritic chest pain, haemoptysis, dizziness and syncope. There may also be signs of DVT: unilateral leg swelling and tenderness.

77
Q

What are the clinical signs of pulmonary embolism?

A

Hypoxia, tachycardia, tachypnoea and hypotension.

78
Q

What investigations can be performed in pulmonary embolism?

A

Bloods (FBC, U&E, clotting).
ECG.
D-dimer.
CTPA.

79
Q

What scoring tool can be used to inform the management of pulmonary embolism?

A

Wells score.

80
Q

How does Well’s score inform the management of PE?

A

Low score = low risk = perform a D-dimer.

High score = high risk = perform CTPA.

81
Q

What is D-dimer?

A

A fibrin degradation product (protein fragment in the blood after a clot is degraded by fibrinolysis).

82
Q

Describe the specificity of D-dimer for the investigation of PE?

A

D-dimer has low specificity and can be raised in thrombosis, inflammation, post-op patients, infection and malignancy.

83
Q

What is the treatment of PE?

A

Direct oral anticoagulants (DOACs) such as rivaroxaban.

84
Q

How long should DOACs be continued for following PE?

A

If PE provoked = three months.

If PE unprovoked = six months.

85
Q

How should massive PE with haemodynamic compromise be managed?

A

Thrombolysis (alteplase).

86
Q

What is pulmonary oedema?

A

Liquid accumulation in the tissue and air spaces of the lungs.

87
Q

What causes pulmonary oedema?

A

Left ventricular heart failure (to remove blood aqueately from the pulmonary circulation).
Injury to the tissues or blood vessels of the lungs.

88
Q

What are the findings on chest x-ray in patients with pulmonary oedema?

A 
Alveolar oedema ('bat wings'), Kerley B lines, cardiomegaly, dilated upper lobe vessels and pleural effusion. 
Remember ABCDE.
89
Q

What is the management of pulmonary oedema?

A

Give high flow oxygen and encourage the patient to sit forward.
Give opiates and GTN to encourage vasodilation.
Give furosemide.
Consider CPAP.

90
Q

What is bronchiectasis?

A

Disease of permanent enlargement of the bronchi (airways) secondary to chronic infection or inflammation.

91
Q

Give examples of causes of bronchiectasis?

A

Causes include post-infective (tuberculosis, measles, pertussis, pneumonia), cystic fibrosis, obstruction (malignancy, foreign body) and immune deficiency.

92
Q

What does investigation of bronchiectasis by CT chest reveal?

A

Tram-track appearance.

Signet ring sign.

93
Q

What is the non-pharmacological management of bronchiectasis?

A

Physiotherapy including inspiratory muscle training.

Postural drainage.

94
Q

What is the pharmacological management of bronchiectasis?

A

Antibiotics.
Bronchodilators.
Immunisations.

95
Q

What is pneumonia?

A

An inflammatory condition of lung alveoli that often develops secondary to bacterial infection.

96
Q

Which two pathogens are responsible for most cases of pneumonia?

A 
Streptococcus pneumoniae (50%). 
Haemophilus influenzae (20%).
97
Q

Give examples of three categories of pneumonia?

A

Community acquired pneumonia.
Hospital acquired pneumonia.
Aspiration pneumonia.

98
Q

What is the clinical presentation of pneumonia?

A

Shortness of breath, productive cough (green or brown sputum), fever, haemoptysis, pleuritic chest pain, delirium/acute confusion.

99
Q

What are the signs of pneumonia?

A

Hypoxia, tachypnoea, tachycardia, hypotension, fever, confusion.

100
Q

What is found on auscultation/examination of a patient with pneumonia?

A

Bronchial, harsh breath sounds due to consolidation of tissue around airway.
Focal, coarse crackles due to air passing through sputum.
Dullness to percussion.

101
Q

What scoring system is used in the assessment of CAP severity?

A

CURB65.

102
Q

What factors make up the CURB65 scoring system?

A 
Confusion. 
Urea > 7. 
Respiratory rate ≥ 30. 
Blood pressure < 90 systolic, < 60 diastolic. 
Aged 65 or older.
103
Q

CURB65: Interpret score of 0.

A

Low risk, consider home based care.

104
Q

CURB65: Interpret score of 1.

A

Low risk, consider home based care if sats > 92% and CXR clear.

105
Q

CURB65: Interpret score of ≥ 2.

A

Intermediate risk, consider hospital assessment/admission.

106
Q

CURB65: Interpret score of ≥ 3.

A

High risk, consider intensive care assessment/admission.

107
Q

Give five causes of atypical pneumonia.

A 
Legionella pneumophilia. 
Mycoplasma pneumoniae. 
Chlamydiophilia pneumoniae. 
Coxiella burnetti (Q fever).
Chlamydia psittaci.
108
Q

What mnemonic can be used to remember the atypical causes of pneumonia?

A

Legions of psittaci MCQs.

109
Q

What are the sources of legionella pneumophilia infection?

A

Infected water and airconditioning units.

110
Q

What electrolyte abnormality is seen in legionella pneumophilia?

A

Hyponatraemia.

111
Q

What group of people are particularly affected by chlamydia psittaci?

A

Exposed to infected birds (parrot owner).

112
Q

What are the signs of mycoplasma pneumoniae?

A

Erythema multiform (target lesions).

113
Q

What are the features of chlamydophilia pneumoniae?

A

Wheeze in school aged children.

114
Q

What are the features of coxiella burnetti (Q fever)?

A

Flu-like illness in those exposed to animals (farmer).

115
Q

How is pneumonia managed?

A

Give oxygen and antibiotics.

116
Q

How is atypical pneumonia managed?

A

Macrolides (clarithromycin), fluoroquinolone (levofloxacin), tetracyclines (doxyclines).

117
Q

What is aspiration pneumonia?

A

The result of foreign materials entering the bronchial tree such as oral or gastric contents (food, saliva).

118
Q

What can increase the risk of aspiration pneumonia?

A

Incompetent swallowing mechanism (such as in stroke, multiple sclerosis and intoxication).

119
Q

What lobes of the lung are most affected in aspiration pneumonia and why?

A

The right middle and right lower lung lobes due to a large calibre and more vertical orientation of the right main bronchus.

120
Q

What is the presentation of Covid-19?

A

Loss of smell/taste, fever, cough and shortness of breath.

121
Q

What are risk factors for poor outcomes in Covid-19?

A

Older age, male sex, comorbidities, high BMI and lower socioeconomic level.

122
Q

Describe the pathophysiology of Covid-19.

A

Incompletely understood - hyperinflammatory response to the virus.

123
Q

What are the features of Covid-19 hyperinflammation?

A

Acute respiratory distress syndrome.

Thromboembolic features.

124
Q

What is the non-pharmacological management of Covid-19?

A

Supplemental oxygen, CPAP, mechanical ventilation, proning.

125
Q

What is the pharmacological management of Covid-19?

A

Dexamethasone.
Remdesivir (antiviral)
Tociluzamab (monoclonal antibody).
Anakinra (monoclonal antibody).

126
Q

What is a pleural effusion?

A

A collection of fluid in the pleural cavity.

127
Q

How are pleural effusions classified?

A

Transudate or exudate depending on the protein concentration.

128
Q

What classifies a pleural effusion as transudative?

A

Low protein concentration (< 30g/L).

129
Q

What classifies a pleural effusion as exudative?

A

Raised protein concentration (> 30g/L).

130
Q

Give four causes of transudative pleural effusion.

A

Heart failure.
Hypoalbuminaemia (liver disease, nephrotic syndrome, malabsorption).
Hypothyroidism.
Meigs’ syndrome (benign ovarian tumour).

131
Q

Give four causes of exudative pleural effusion.

A

Infection (pneumonia, TB).
Connective tissue disease (rheumatoid arthritis, SLE).
Neoplasia (lung cancer, mesothelioma, metastases).
Pulmonary embolism.

132
Q

What investigation is most commonly performed in pleural effusion?

A

Chest x-ray.

133
Q

What does chest x-ray reveal in pleural effusion?

A

Blunting of the costophrenic angles.
Fluid in the lung fissures.
Effusions with a meniscus.
Tracheal/mediastinal deviation.

134
Q

What determines the management of pleural effusion?

A

The size - small can be managed conservatively with treatment of the underlying cause.

135
Q

How are large pleural effusions managed?

A

Pleural aspiration.

Chest drain.

136
Q

What is an empyema?

A

An infected pleural effusion.

137
Q

When should you suspect an empyema?

A

A patient recovering from pneumonia but with new or ongoing fever.

138
Q

What does pleural aspiration and analysis reveal in empyema?

A

Pus.
Acidic pH.
Low glucose.
High LDH.

139
Q

What is a pneumothorax?

A

Air enters the pleural space separating the lung from the chest wall.

140
Q

What causes pneumothorax?

A

Often occurs spontaneously in young, thin men due to rupture of subpleural bulla.

141
Q

What is the typical presentation of pneumothorax?

A

Sudden onset shortness of breath and/or pleuritic chest pain in a young, thin man.

142
Q

What clinical signs are present in a patient with pneumothorax?

A

Reduced chest expansion, hyper-resonance to percussion, diminished breath sounds on the affected side.

143
Q

Give examples of causes of pneumothorax?

A

Trauma.
Iatrogenic (lung biopsy, ventilation).
Infection.
Asthma.

144
Q

What is the difference between a primary and secondary pneumothorax?

A

Primary - no underlying lung disease.

Secondary - background lung disease.

145
Q

What investigation is used to confirm the diagnosis of pneumothorax?

A

Erect chest X-ray.

146
Q

What does erect chest X-ray reveal in pneumothorax?

A

Area devoid of lung markings peripheral to the edge of the collapsed lung.

147
Q

What is the management of pneumothorax?

A

All primary pneumothorax and secondary 1-2cm = fine needle aspiration.
Failed aspiration or secondary pneumothorax > 2cm = insert a chest drain into the triangle of safety.

148
Q

Chest drain insertion: What forms the borders of the triangle of safety?

A

5th intercostal space.
Mid axillary line.
Anterior axillary line.

149
Q

Should a chest drain be inserted above or below the rib?

A

Above to avoid the neuromuscular bundle (which runs below).

150
Q

What advice should be given to people following pneumothorax?

A

Cannot fly for at least two weeks (with successful drainage) and can never scuba dive.

151
Q

What is sarcoidosis?

A

A granulomatous inflammatory condition that most commonly affects the lungs (90%) but can affect any organ.

152
Q

Sarcoidosis: What are granulomas?

A

Nodules of inflammation full of macrophages.

153
Q

What is the characteristic presentation of sarcoidosis?

A

Dry cough and erythema nodosum in a black female aged 20-40 years.

154
Q

What are systemic features of sarcoidosis?

A

Low-grade fever, fatigue and weight loss.

155
Q

What are the pulmonary features of sarcoidosis?

A

Mediastinal lymphadenopathy, pulmonary fibrosis, pulmonary nodules.

156
Q

Give examples of extra-pulmonary features of sarcoidosis.

A

Liver - liver nodules, cirrhosis, cholestasis.
Eyes - uveitis, conjunctivitis, optic neuritis.
Skin - erythema nodosum, Lupus pernio.
Heart - bundle branch block, heart block, muscle involvement.
Kidneys - kidney stones, nephrocalcinosis, interstitial nephritis.

157
Q

What serological investigations are performed in sarcoidosis (with results)?

A 
Serum ACE (raised). 
Hypercalcaemia. 
Soluble interleukin-2 receptor (raised). 
CRP (raised). 
Immunoglobulins (raised).
158
Q

What imaging is performed in sarcoidosis (with results)?

A

Chest x-ray (bilateral hilar lymphadenopathy).

159
Q

What is the gold-standard investigation of sarcoidosis (with results)?

A

Bronchoscopy, biopsy of mediastinal lymph nodes with analysis (non-caseating granulomas with epitheloid cells).

160
Q

How is mild sarcoidosis managed?

A

Conservatively - no treatment.

161
Q

What treatment is given in sarcoidosis if indicated?

A

Oral steroids.
Bisphosphonates (to protect against osteoporosis from steroids).
Or methotrexate and azathioprine if steroids contraindicated.

162
Q

What is idiopathic pulmonary fibrosis?

A

A chronic lung condition characterised by progressive fibrosis of the interstitium of the lungs.

163
Q

Idiopathic pulmonary fibrosis: Describe fibrosis.

A

The replacement of normal elastic and functional lung tissue with scar tissue that is stiff and ineffective.

164
Q

What is the clinical presentation of idiopathic pulmonary fibrosis?

A

Progressive exertional dyspnoea, dry cough, digital clubbing commonly seen in men aged over 50.

165
Q

What is heard on auscultation in idiopathic pulmonary fibrosis?

A

Bibasal fine end-inspiratory crepitations.

166
Q

What investigations are performed in idiopathic pulmonary fibrosis?

A

Spirometry.

High-resolution CT chest.

167
Q

What does spirometry reveal in idiopathic pulmonary fibrosis?

A

Restrictive picture: FEV1 normal/decreased, FVC decreased, FEV1/FVC increased.

168
Q

What does high-resolution CT reveal in idiopathic pulmonary fibrosis?

A

Reticular opacities (ground glass appearance) and honeycombing.

169
Q

What is the prognosis and management of idiopathic pulmonary fibrosis?

A

Prognosis is poor. Give supplementary oxygen. Only definitive treatment is lung transplant.

170
Q

What is obstructive sleep apnoea?

A

Collapse of the pharyngeal airway during sleep… characterised by apnoea episodes.

171
Q

Obstructive sleep apnoea: What is an apnoea episode?

A

A person will periodically stop breathing for up to a few minutes (the patient is usually unaware and partner reports symptoms).

172
Q

Give examples of risk factors for the development of sleep apnoea.

A

Middle age, male, obesity, alcohol and smoking.

173
Q

What are the clinical features of obstructive sleep apnoea?

A

Snoring, morning headache, wake feeling unrefreshed, daytime sleepiness, concentration problems.

174
Q

Obstructive sleep apnoea: What investigation can be performed during sleep?

A

Oxygen saturations - they may be reduced.

175
Q

What is the management of obstructive sleep apnoea?

A

Stop alcohol, stop smoking, weight loss.

CPAP.

Finals (11 decks)

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